Paramedic Principles and Practice ANZ: A Clinical Reasoning Approach, 1e [1 ed.] 0729541274, 9780729541275

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PARAMEDIC PRINCIPLES AND PRACTICE ANZ A clinical reasoning approach Matt Johnson, B APP SCI, DIP AMB STUDIES, GRAD DIP EMERG HEALTH, GRAD CERT HEALTH PROF ED, M EMERG HEALTH, FPA Leanne Boyd, DIP APP SCI, B NURS, GRAD CERT CRIT CARE, GRAD CERT HIGHER ED, M NURS, MTEM, PHD Hugh Grantham , ASM, MBBS, FRACGP Kathryn Eastwood, RN, B SC, B NURS, B PARAMED STUDIES, DIP AMB PARA STUDIES, GRAD DIP EMERG HLTH

(MICA), GRAD CERT HIGHER ED, M EMERG HEALTH (MICA), PHD CANDIDATE

Table of Contents Cover image Title page Inside Front Cover Copyright Foreword Preface About the authors Contributors Reviewers The key to improving your clinical practice Acknowledgements CHAPTER 1: Introduction Paramedic principles and practice Essential knowledge Summary

PART 1: PARAMEDIC PRINCIPLES

SECT ION 1: PRINCIPLES OF PARAMEDIC PRACT ICE CHAPTER 2: The paramedic role in healthcare Introduction The role of ambulance services in Australia and New Zealand Professionalism and professional standards Terminology and qualifications The future paramedic role Summary CHAPTER 3: Characteristics of ambulance patients Introduction Who are ambulance patients? From symptom onset to the decision to call an ambulance From calling for an ambulance to ambulance arrival Summary

SECT ION 2: T HE PARAMEDIC’S CLINICAL APPROACH CHAPTER 4: The structured clinical approach Introduction Medicine vs paramedicine? Using a structured approach to combat complexity The emergency model The medical interview model CHAPTER 5: The clinical reasoning process

Introduction Clinical decision making in the face of uncertainty: the paramedic paradigm Problem solving versus decision making The myth of the expert Developing clinical reasoning skills A step-by-step guide to clinical decision making Algorithms and cognitive checks A syndrome approach to patient management Error wisdom Summary CHAPTER 6: The patient interview Introduction The structured patient interview The science and art of communication The paramedic interview setting Paramedic–patient interview structure Barriers to effective communication Summary

SECT ION 3: PAT IENT AND PARAMEDIC SAFET Y CHAPTER 7: Patient safety and paramedicine Introduction The harm caused by healthcare errors Types of medical error

Models of error Reducing diagnostic errors Error defence Error management Evidence-based practice and patient safety EBP, individual patients and clinical reasoning Summary CHAPTER 8: Paramedic health and wellbeing Introduction Wellbeing Paramedic health and safety Stress Managing emotions Fatigue Shift work Occupational violence Injury Student paramedics Getting help Summary

SECT ION 4: PARAMEDIC EDUCAT ION CHAPTER 9: Paramedic education Introduction

Experience versus education The history of paramedic education in Australasia International educational standards Paramedic education in the university setting Course accreditation and professional regulation Continuing professional development and postgraduate education Educational challenges and future directions Summary

SECT ION 5: LEGAL AND ET HICAL CONSIDERAT IONS CHAPTER 10: Legal and ethical considerations in clinical decision making Introduction Ethics and the law Consent Refusal of treatment Elements of consent Case study 1 evaluation Documentation Summary

SECT ION 6: CLINICAL REASONING AND T HE PARAMEDIC MODEL OF PRACT ICE CHAPTER 11: Developing a philosophy of practice Introduction

Models of practice Building a philosophy of practice Summary

PART 2: PARAMEDIC PRACT ICE

SECT ION 7: T HE PARAMEDIC APPROACH T O T HE PAT IENT IN AN ALT ERED CONSCIOUS STAT E INTRODUCTION TO THE PARAMEDIC APPROACH TO THE PATIENT IN AN ALTERED CONSCIOUS STATE IN THIS SECTION AT THE COMPLETION OF THIS SECTION YOU SHOULD BE ABLE TO CHAPTER 12: Hypoglycaemia Introduction Pathophysiology Management of blood glucose At the hospital ED Hospital admission Discharge criteria Hypoglycaemia across the lifespan: paediatric considerations Future research Summary CHAPTER 13: Cerebrovascular accidents Introduction

Pathophysiology Clinical manifestations Ongoing management Investigations Hospital admission Stroke across the lifespan Future research Summary CHAPTER 14: Overdose Introduction Pathophysiology Ongoing treatment Investigations Hospital management Future research CHAPTER 15: Seizures Introduction Pathophysiology Seizure classification Management Ongoing management Hospital admission Summary

SECT ION 8: T HE PARAMEDIC APPROACH T O T HE PAT IENT IN RESPIRAT ORY DIST RESS INTRODUCTION TO THE PARAMEDIC APPROACH TO THE PATIENT IN RESPIRATORY DISTRESS IN THIS SECTION AT THE COMPLETION OF THIS SECTION YOU SHOULD BE ABLE TO CHAPTER 16: Airway obstruction Introduction Pathophysiology Ongoing management Hospital admission Follow-up Summary CHAPTER 17: Asthma Introduction Pathophysiology Ongoing management Follow-up Long-term impact Future research Summary CHAPTER 18: Acute pulmonary oedema Introduction

Pathophysiology Hospital admission Long-term impact Acute pulmonary oedema across the lifespan Ongoing management Ongoing management Future research Summary CHAPTER 19: Chronic obstructive pulmonary disease Introduction Pathophysiology Hospital admission Investigations Follow-up Future research Summary CHAPTER 20: Pneumothorax Introduction Pathophysiology Ongoing management Hospital admission Long-term impact Summary CHAPTER 21: Pulmonary embolism

Introduction Pathophysiology Risk factors Ongoing management Investigations Hospital admission Follow-up Research Summary CHAPTER 22: Pleural effusion Introduction Pathophysiology Ongoing management Investigations Hospital admission Follow-up Summary CHAPTER 23: The paediatric patient with a noisy airway Introduction Pathophysiology Ongoing management Hospital admission Long-term impact Hospital management

Future research Summary

SECT ION 9: T HE PARAMEDIC APPROACH T O T HE PAT IENT SUFFERING A CARDIAC EMERGENCY INTRODUCTION TO THE PARAMEDIC APPROACH TO THE PATIENT SUFFERING A CARDIAC EMERGENCY IN THIS SECTION AT THE COMPLETION OF THIS SECTION YOU SHOULD BE ABLE TO CHAPTER 24: Chest pain Introduction Pathophysiology Myocardial perfusion and myocardial workload Investigations Ongoing management Hospital admission Follow-up Acute coronary syndrome across the lifespan Future research Summary CHAPTER 25: Arrhythmias Introduction Pathophysiology Ongoing management

Hospital admission Arrhythmias across the lifespan Wolff-Parkinson-White Long QT syndrome Commotio cordis Summary CHAPTER 26: Cardiac arrest Introduction Chain of survival Pathophysiology Ongoing management Long-term outcomes Future research Summary

SECT ION 10: T HE PARAMEDIC APPROACH T O T HE PAT IENT WIT H A SEVERE ALLERGIC REACT ION INTRODUCTION TO THE PARAMEDIC APPROACH TO THE PATIENT WITH A SEVERE ALLERGIC REACTION IN THIS SECTION AT THE COMPLETION OF THIS SECTION YOU SHOULD BE ABLE TO CHAPTER 27: Anaphylaxis Introduction Pathophysiology

Investigations Ongoing management Hospital admission Follow-up Long-term role Anaphylaxis across the lifespan Future research Summary

SECT ION 11: T HE PARAMEDIC APPROACH T O T HE PAT IENT PRESENT ING WIT H PAIN INTRODUCTION TO THE PARAMEDIC APPROACH TO THE PATIENT PRESENTING WITH PAIN IN THIS SECTION AT THE COMPLETION OF THIS SECTION YOU SHOULD BE ABLE TO CHAPTER 28: Pain Introduction Pathophysiology Ongoing management Future research Summary CHAPTER 29: Lower back pain Introduction Pathophysiology

Ongoing management Follow-up Outcomes Back pain across the lifespan Future research Summary CHAPTER 30: Renal colic Introduction Pathophysiology Hospital emergency management Investigations Ongoing management Hospital admission Follow-up Long-term role Renal stones across the lifespan Future research Summary

SECT ION 12: T HE PARAMEDIC APPROACH T O T HE T RAUMA PAT IENT INTRODUCTION TO THE PARAMEDIC APPROACH TO THE TRAUMA PATIENT IN THIS SECTION AT THE COMPLETION OF THIS SECTION YOU SHOULD BE ABLE TO

CHAPTER 31: The structured clinical approach to trauma patients Introduction Assessment of the trauma patient Summary CHAPTER 32: Head injuries Introduction Anatomy Pathophysiology Ongoing management Investigations Hospital admission Hospital discharge Head injuries across the lifespan Future research Summary CHAPTER 33: Chest injuries Introduction Pathophysiology Ongoing management Investigations Hospital admission Long-term role Chest trauma across the lifespan Future research

Summary CHAPTER 34: Musculoskeletal injuries Introduction Pathophysiology Ongoing management Investigations Ongoing management of uncomplicated injuries Torn muscle repair Management of specific fractures Complications of musculoskeletal injuries Rehabilitation Long-term impact Future research Summary CHAPTER 35: Traumatic spinal injuries Introduction Pathophysiology Hospital admission Long-term issues and care Life expectancy for SCI survivors Future research Summary CHAPTER 36: Burns Introduction

Pathophysiology ‘Cold burns’ Hospital admission (burns unit) Investigations Ongoing management Follow-up Burns across the lifespan: elderly patients Paediatric airway burns To intubate or not Future research Summary

SECT ION 13: T HE PARAMEDIC APPROACH T O T HE PAT IENT PRESENT ING WIT H ENVIRONMENTAL INJURY INTRODUCTION TO THE PARAMEDIC APPROACH TO THE PATIENT PRESENTING WITH ENVIRONMENTAL INJURY IN THIS SECTION AT THE COMPLETION OF THIS SECTION YOU SHOULD BE ABLE TO CHAPTER 37: Hypothermia Introduction Pathophysiology Ongoing management Future research Summary

CHAPTER 38: Hyperthermia Introduction Pathophysiology Ongoing management Hospital admission Investigations Follow-up and long-term impact Hyperthermia across the lifespan Summary CHAPTER 39: Decompression injuries Introduction Pathophysiology Ongoing management Hospital admission Long-term impact Summary CHAPTER 40: Snake bites Introduction Pathophysiology Ongoing management Hospital management Investigations Hospital admission Long-term impact

Snake bites across the lifespan Future research Summary CHAPTER 41: Spider bites Introduction Pathophysiology Ongoing hospital management Hospital admission Long-term impact Spider bites across the lifespan Summary CHAPTER 42: Marine envenomation Introduction Pathophysiology Hospital management Long-term impact Envenomation across the lifespan Hospital management Future research Summary

SECT ION 14: T HE PARAMEDIC APPROACH T O T HE UNWELL PAT IENT: SPECIFIC CHALLENGES T O PARAMEDIC REASONING INTRODUCTION TO THE PARAMEDIC APPROACH TO THE UNWELL PATIENT:

SPECIFIC CHALLENGES TO PARAMEDIC REASONING IN THIS SECTION AT THE COMPLETION OF THIS SECTION YOU SHOULD BE ABLE TO CHAPTER 43: Acute abdominal pain Introduction Anatomy Pathophysiology Ongoing management Hospital admission Appendicitis across the lifespan Ongoing management AAA across the lifespan Ongoing management Bowel obstruction across the lifespan Summary CHAPTER 44: Sepsis Introduction Pathophysiology Ongoing management Hospital admission Sepsis across the lifespan Research Summary CHAPTER 45: Bleeding from the gastrointestinal or urinary tract

Introduction Pathophysiology Ongoing management GI/urinary tract haemorrhage in the field Hospital management Summary

SECT ION 15: T HE PARAMEDIC APPROACH T O COMPLEX CASES: SPECIFIC CHALLENGES T O PARAMEDIC REASONING AND MANAGEMENT INTRODUCTION TO THE PARAMEDIC APPROACH TO COMPLEX CASES: SPECIFIC CHALLENGES TO PARAMEDIC REASONING AND MANAGEMENT IN THIS SECTION At the completion of this section you should be able to CHAPTER 46: The socially isolated patient Introduction Background Ongoing management Hospital admission Summary CHAPTER 47: The dying patient Introduction Pathophysiology Ongoing management

Hospital admission Death and dying across the lifespan Summary CHAPTER 48: The patient on out-of-hospital dialysis Introduction Pathophysiology Dialysis Ongoing management Follow-up Long-term role ESKD across the lifespan Future research Summary CHAPTER 49: Indigenous Australian patients Introduction Kinship Culture Distribution Epidemiological profile Summary CHAPTER 50: Māori patients Introduction Specific aspects of healthcare for Mori Epidemiological profile

Delayed access to healthcare Death among Mori populations Summary

SECT ION 16: T HE PARAMEDIC APPROACH T O T HE PAT IENT DISPLAYING ABNORMAL BEHAVIOUR INTRODUCTION TO THE PARAMEDIC APPROACH TO THE PATIENT DISPLAYING ABNORMAL BEHAVIOUR IN THIS SECTION At the completion of this section you should be able to CHAPTER 51: The patient displaying abnormal behaviour Introduction Pathophysiology Explanatory models Law and mental health Specific treatment guidelines Investigations Hospital admission Long-term treatment and impacts Mental illness across the lifespan Summary CHAPTER 52: De-escalation in the pre-hospital environment Introduction Theories of aggression

Management of aggression Principles of de-escalation De-escalation in practice

SECT ION 17: T HE PARAMEDIC APPROACH T O OBST ET RIC AND NEONATAL EMERGENCIES INTRODUCTION TO THE PARAMEDIC APPROACH TO OBSTETRIC AND NEONATAL EMERGENCIES IN THIS SECTION AT THE COMPLETION OF THIS SECTION YOU SHOULD BE ABLE TO CHAPTER 53: Imminent birth Introduction Physiology Hospital admission Investigations Follow-up Further research Summary CHAPTER 54: Neonatal resuscitation Introduction Pathophysiology Identifying the newborn at risk of disorders during transition Failure to breathe effectively at birth Failure to establish effective ventilation after birth

Preparing for the birth of a baby Newborn airway management Ongoing management Documentation Birth during transport Discontinuing resuscitation Hospital admission Investigations Follow-up The preterm baby Long-term role Hospital management Future research Summary

PART 3: ESSENT IAL KNOWLEDGE

SECT ION 18: ESSENT IAL CONCEPT S OF PARAMEDIC PRACT ICE INTRODUCTION TO ESSENTIAL CONCEPTS OF PARAMEDIC PRACTICE IN THIS SECTION CHAPTER 55: Perfusion Introduction What is perfusion?

The basics of normal perfusion Disturbances of perfusion Assessment of perfusion Principles of medical management of perfusion Summary CHAPTER 56: The autonomic response Introduction What is the autonomic nervous system? Assessment of autonomic nervous system function Principles of management Summary CHAPTER 57: The inflammatory response Introduction What is inflammation? The basics of normal inflammation Abnormal inflammation Summary APPENDIX 1: Professional role guide APPENDIX 2: Medications commonly encountered in community emergency health Glossary Index

Inside Front Cover Likely dispatch codes Likely dispatch code Abdominal pain Abnormal behaviour Agitated patient Airway obstruction Allergic reaction Altered conscious state Anaphylaxis Animal attack Anxiety Assault Back pain Burns Cardiac arrest Chemical spill Chest pain Choking Collapse Convulsions Deceased patient Diabetic problems Diarrhoea Difficulty breathing Drowning Electrocution Epigastric pain Explosion Fainting Fall Fever Fire Flutter in the chest Fractures Generally unwell Haematuria Haemoptysis Haemorrhage

Chapter reference 30, 43, 44, 45, 46, 53 12, 13, 14, 15, 16, 27, 32, 37, 38, 51 51 16 17, 27, 42 12, 13, 14, 15, 17, 21, 23, 24, 25, 27, 32, 37, 38, 39, 42, 48, 51 41, 42 31 46 32, 49, 50 29, 30, 35, 43, 53 31, 36 17, 21, 26, 37, 42, 48 36 18, 20, 22, 24, 25, 33, 39, 43, 44, 46, 48 16, 17, 23, 27 12, 30, 40, 44 12 47 12 44, 45 16, 18, 19, 41 39, 42 36 43 31 12, 25, 32 31, 32, 33, 34 38 36 25 34 28, 44, 46 45 21 45

Head injury Headache Imminent delivery Infant crying Intoxication Labour Leg pain/numbness Medical problems Melaena Mobility issue Nausea Near fainting Non-breathing (newborn) Not alert Pain Pale and sweaty Palpitations Patient turning blue Post-ictal Psychiatric issues PV (per vagina) haemorrhage (third trimester) Rapid breathing Rash Seizure Seizure, now post-ictal Severe respiratory distress Shooting/stabbing Shortness of breath Snake bite Sting/bite Stroke Sunburn Trauma Unable to move Unconscious Unknown problem Vehicle incident Violent patient Vomiting Weakness Welfare check

32 39, 44 54 28 13 53 35, 43 49, 50 45 29 24, 25 13, 27, 30 54 26 28, 29, 34, 35, 40 24, 25 25 16 15 14, 16, 37, 46, 51 54 47 41 12, 14, 15 27, 32 17 31 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 27, 33, 39, 44, 46, 47 40 42 13, 35, 40 36 28, 31, 33, 34, 35, 49, 50 29 13, 14, 15, 16, 17, 21, 26, 27, 32, 36, 37, 39, 47 44, 46 31, 32, 34 14 40, 42, 44 35, 40 49, 50

Copyright

Elsevier Australia. ACN 001 002 357 (a division of Reed International Books Australia Pty Ltd) Tower 1, 475 Victoria Avenue, Chatswood, NSW 2067 Copyright 2015 Elsevier Australia All rights reserved. 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 permission in writing from the publisher. Details on how to seek permission, further information about the Publisher ’s permissions policies and our arrangements with organizations such as the Copyright Clearance Center and the Copyright Licensing Agency, can be found at our website: 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). This publication has been carefully reviewed and checked to ensure that the content is as accurate and current as possible at time of publication. We would recommend, however, that the reader verify any procedures, treatments, drug dosages or legal content described in this book. Neither the author, the contributors, nor the publisher assume any liability for injury and/or damage to persons or property arising from any error in or omission from this publication. National Library of Australia Cataloguing-in-Publication Data Johnson, Matt, 1964-author. Paramedic principles and practice ANZ: a clinical reasoning approach / Matt Johnson, Leanne Boyd, Hugh Grantham, Kathryn Eastwood. 9780729541275 (paperback) Clinical medicine–Decision making—Textbooks. Emergency medicine—Textbooks. Medical emergencies—Textbooks. Emergency medicine–Diagnosis—Textbooks. Ambulatory medical care—Textbooks. Boyd, Leanne, author. Grantham, Hugh, author.

Eastwood, Kathryn, author. 616.025

Senior Content Strategist: Melinda McEvoy Content Development Specialist: Martina Vascotto Senior Project Manager: Rochelle Deighton Edited by Caroline Hunter, Burrumundi Pty Ltd Proofread by Tim Learner Design by Georgette Hall Permissions by Sarah Thomas and Vijay Rajan Index by Robert Swanson Typeset by Midland Typesetters Printed in China by China Translation and Printing Services

Foreword Matt Johnson, Leanne Boyd, Hugh Grantham, -Kathryn Eastwood and the contributing authors are some of Australia and New Zealand’s most -experienced paramedics, educators, researchers and emergency physicians. So it was with great pleasure that I accepted the invitation to write this foreword for Paramedic Principles and Practice ANZ, a unique and valuable resource that integrates knowledge and decision making in the Australian and New Zealand context that they know and understand so well. Paramedics are required to adapt and improve their range of clinical capabilities to provide care. This brings increased responsibility as professional clinicians to be aware of the potential impact they have on the lives of others. This impact cannot be underestimated. The shift of paramedic education from the vocational to a university model has resulted in clinicians who enter the workforce with a complex understanding of anatomy, physiology, pathology and pharmacology. There is little doubt that this science has been an important step in the development of the paramedic profession. However, new graduate paramedics now have much less clinical exposure where they can learn the art of being a paramedic. I am impressed with the way this text lays out the pathway for graduates to develop and grow to be expert clinicians by bringing together the art and science of paramedicine. The inclusion of real-life stories reinforces this message and brings to life important theoretical models related to developing as an expert clinician and lifelong learner. This text goes beyond the technical aspects of emergency care: it drives and reinforces the importance of professional attitudes, behaviours, clinical competence, teamwork, communication skills and the humanitarian approach required of paramedics. It is a refreshing approach to the complex challenges paramedics face in the context of an ageing population, high instances of chronic health problems, a health system that offers limited access to community-based clinicians and limited technological assistance for paramedic decision making. This book will be a valuable tool for those wanting to provide high-quality, patient-focused care in this challenging healthcare environment. Healthcare starts at the patient, not at the emergency department or at a hospital or clinic door. In this context it is notable that decisions and clinical interventions performed by paramedics often keep patients alive until they can receive more definitive care. Paramedic assessments, decisions and interventions have the capacity to keep patients out of the hospital system entirely, reduce morbidity and reduce the length of hospital stay, all of which have the potential to reduce the social and economic burden on the health system. I recommend this text to you as a resource that will assist you to contribute confidently to the care of your community and to continue to develop your professional practice and career. Excellence is an art won by training and habitation. We do not act rightly because we have virtue or excellence but rather we have those because we

have acted rightly, we are what we repeatedly do. Excellence is not an act but a habit. Aristotle (384–322 BC) Adjunct Professor Ian Patrick, ASM, FPA, LMPA

Preface Medicine is a science of uncertainty and an art of probability. One of the chief reasons for this uncertainty is the increasing variability in the manifestations of any one disease. Sir William Osler (1849–1919) You cannot become a good paramedic by reading a book, regardless of how good the book or how great your memory. Certainly, every case you attend as a paramedic will require you to call upon a detailed knowledge of anatomy, physiology and pharmacology, but to practise effectively in the field of emergency medicine you also need to be able to interpret people and situations. While exams require you to recall facts with certainty, clinical practice is too often lacking in both facts and certainty. To be a safe paramedic you need to elicit accurate information from patients who will differ from you in gender, generation, social situation and health. You then have to determine what (if any) of that information is relevant and finally draw together all of these knowledge sets, skills and attitudes to determine a diagnosis. The process of clinical reasoning is probably the most difficult for students of any medical discipline to learn. Anatomy, physiology and pharmacology will come easily to those blessed with a good memory but will also eventually sink into the minds of the rest of us. Similarly, guidelines and clinical skills can be learned by practice. But how do you take all of this knowledge and use it when you are confronted with a patient? Traditional teaching and texts stretching back 100 years suggest you must first learn the basic biomedical sciences before you engage in solving clinical problems. While the editors of this text do not disagree entirely, it does raise the question: how do you manage a condition if you have not been taught the specifics of the disease that caused it? An alternative method is to apply the clinical reasoning approach to conditions as you learn them. This text does not substitute for other texts which, in far more detail, describe the anatomy, pathophysiology and pharmacology you will need to pass your exams. What the editors hope to offer is a text that allows you to see the links between the pathophysiology of a disease, how this creates the signs and symptoms perceived by the patient and how these need to be managed in the out-of-hospital environment. Clinical reasoning is a real-time, living mystery. Traditional teaching methods offer you the clues that allow you to solve the clinical puzzle. But in real life, paramedics have to extract and sort the clues by importance before they must decide on an answer. To help you to develop this skill, this book is structured in three parts. The chapters in Part 1 articulate the principles that support good paramedic practice: the ability to communicate effectively, gather essential clinical information in difficult environments and use this information to make safe and effective clinical decisions. The chapters in Part 2 present the various conditions that novice paramedics can expect to see as they practise, with each chapter revealing the clinical reasoning process and describing the principles of management for a particular condition. To do this we use a series of case studies, stepping you through each case scenario to link the clues and, importantly, reveal the process of

reaching a safe and effective management plan. Finally, the chapters in Part 3 outline three essential concepts that underpin paramedic practice and are common to a wide range of diseases and injuries: perfusion, the autonomic nervous system and inflammation. The importance of understanding how these concepts integrate into the disease process cannot be overemphasised.

About the authors Matt Johnson Matt joined Ambulance Victoria in 1998 and has practised as a Mobile Intensive Care Paramedic since 2006. He has held the position of Senior Lecturer and Post Graduate Coordinator in the School of Primary Health at Monash University. He is currently the Director of Clinical Education at Cabrini Hospital in Melbourne and holds an adjunct position as Senior Lecturer with HealthPEER (Health Professions Education and Educational Research) in the Faculty of Medicine, Nursing and Health Sciences at Monash University. Leanne Boyd Leanne was appointed as Executive Director Nursing and Cabrini Institute at Cabrini Health in August 2014 and has more than 20 years’ experience in health professional education. Prior to this appointment she worked for Monash University as Director of Academic Programs (Middle East) for the Faculty of Medicine, Nursing and Allied Health and was Head of Department, Community Emergency Health and Paramedic Practice within the School of Primary Health Care. Leanne has Graduate Certificates in Health Professional Education and Critical Care. She also has Masters degrees in Critical Care and Tertiary Education Management. Leanne completed her PhD investigating health program evaluation models in 2009. She has been successful in attracting more than $3 million in tenders/contracts and $2 million in research/consultancy grants during her academic career. She is currently supervising six PhD students. Hugh Grantham Hugh has been passionately involved in paramedic education and professional development since 1987. He was Medical Director of SA Ambulance Service for 18 years prior to taking up his professorial role at Flinders University in 2011. Kathryn Eastwood Kathryn is a Mobile Intensive Care Ambulance (MICA) Paramedic, Registered Nurse (division 1) and Senior University Academic. She is currently completing her PhD in the management of low-acuity patients by ambulance services. She has worked for Ambulance Victoria since 2000 and for Monash University since 2003. Her experience in academia ranges from teaching to curriculum design, subject and course coordination and research. She has been involved in the education of and curriculum design for medical students, nursing students, paramedic students and military personnel. Kathryn has also been a member of the Monash University Human Research Ethics Committee, the Department of Community Emergency Health and Paramedic Practice Research Committee and the Department of Community Emergency Health and Paramedic Practice Course Management Committee for both Undergraduate and Postgraduate Studies.

Contributors Joe Acker, MA (LEADERSHIP), PHD (CANDIDATE), EMT-P (CC), FPA, Senior Lecturer in Paramedic Practice, Charles Sturt University, Port Macquarie, New South Wales, Australia David Anderson, MSTJ, BSC, MBCHB, Fellow, Intensive Care Service, Royal Prince Alfred Hospital, Camperdown, New South Wales, Australia Jason Bendall Rosemarie Boland, RN, RM, MN, PHD Perinatal Educator, Paediatric Infant Perinatal Emergency Retrieval, Victoria, Australia Post-Doctoral Research Fellow, Murdoch Children’s Research Institute, Victoria, Australia Honorary Clinical Senior Lecturer, Faculty of Medicine, Dentistry and Health Sciences, University of Melbourne, Australia Ingrid Ann Brooks, RN, BADVNSG (NURSING EDUCATION), GRADDIPBUSMGT, MEMERGHLTH, FACN, Senior Lecturer, Education Focused, School of Nursing and Midwifery, Monash University, Victoria, Australia Stephen Burgess, BHLTHSC, GRADCERTHLTHPROFED, GRADDIPEMERGHLTH (MICA), MPH, PHD (CANDIDATE), MPA Research and Policy Officer, Benetas, Victoria, Australia MICA Paramedic, Ambulance Victoria, Victoria, Australia Adjunct Senior Lecturer, Department of Community Emergency Health and Paramedic Practice, Monash University, Victoria, Australia Honorary Senior Research Fellow, Geriatric Medicine Aged Care Research Centre, Eastern Health, Victoria, Australia Janet Curtis, MSC (HONS), MEH, MPA, Lecturer, Community Emergency Health and Paramedic Practice, Monash University, Australia Shaunagh Darroch, BSC, MPHARM, GRADCERTACAPRAC, Lecturer, College of Health and Biomedicine, Victoria University, Melbourne, Australia Shaun Ewen, BAPPSC (PHYSIO), MMIL, DED, Professor and Director, Melbourne Poche Centre for Indigenous Health, Faculty of Medicine, Dentistry and Health Sciences, University of Melbourne, Victoria, Australia Philippa Gent, BN, MHPE, GRADDIPPARAMEDICINE, Lecturer in Paramedicine, Australian Catholic University, Victoria, Australia Nick Goodwin, BSC, DIPHLTHSC, MICA Paramedic, Ambulance Victoria, Victoria, Australia Peter Horrocks, RN, ICP, BNURS, MHLTHSC, Senior Lecturer Paramedic Science, School of Clinical Sciences, Faculty of Health, Queensland University of Technology, Queensland, Australia Dianne Inglis, BNURS, DIPHLTHSC (PARAMEDICINE), ADDIPMICP, Clinical Manager, Ambulance Victoria, Australia Paul Jennings, BN, MCLINEPI, GRADCERTBIOSTATS, GCHPE, PHD, FPA, Senior Lecturer, Community Emergency Health and Paramedic Practice, Monash University, Victoria, Australia David Kelly, GRADDIP PREHOSPITAL CARE, BHLTHSC (PARAMEDIC), B PODIATRY MICA Paramedic, Ambulance Victoria, Victoria, Australia Critical Care Paramedic, Queensland Ambulance Service, Queensland, Australia Jeff Kenneally, ASSDIPHLTHSCI (PARAMEDIC), MICA CERTIFICATE, Team Manager, Ambulance Victoria, Victoria, Australia Susan Lee, RN, PHD, MRCNA, Senior Lecturer, Palliative Care Research Team, School of Nursing and Midwifery, Monash University, Victoria, Australia Grainne Lowe, RN, NP, BN (HONS), MN, PHD (CANDIDATE), Lecturer, School of Nursing and Midwifery, Monash University, Victoria, Australia Pip Lyndon-James, MADED, GRADDIP VOCATIONAL WORKPLACE LEARNING, BNURS, ADDIP PARAMEDICAL SCIENCE Lecturer, Paramedicine, University of Tasmania, Sydney Campus, New South Wales, Australia

Intensive Care Paramedic, New South Wales Ambulance Service, New South Wales, Australia Gayle McLelland, RN, RM, MED (I&CT), Lecturer, School of Nursing and Midwifery, Monash University, Victoria, Australia Tegwyn McManamny, BEMERGHLTH (HONS), PHD (CANDIDATE), Lecturer, Department of Community Emergency Health and Paramedic Practice, Monash University, Victoria, Australia Ben Meadley, BAPPSC (HUMAN MOVEMENT), DIPPARAMEDISCI (PREHOSPITAL CARE), GRADDIPICP, GRADDIPEMERGHLTH (MICA), GRADCERTEMERGHLTH (AEROMED RETRIEVAL) Teaching Associate and Unit Coordinator, Department of Community Emergency Health and Paramedic Practice, Monash University, Victoria, Australia Intensive Care Flight Paramedic, Air Ambulance Victoria, Victoria, Australia Paul M. Middleton, RGN, MBBS, DIPIMCRCS (ED), MMED (CLINEPI), MD FRCS (ENG), FANZCP, FCEM, FACEM Clinical Associate Professor, Discipline of Emergency Medicine, University of Sydney, New South Wales, Australia Principal Investigator, DREAM Collaboration, New South Wales, Australia Director, Australian Institute for Clinical Education, New South Wales, Australia Conjoint Associate Professor, Graduate School of Biomedical Engineering, University of New South Wales, New South Wales, Australia Chair, Australian Resuscitation Council, NSW Branch, New South Wales, Australia Chair, Take Heart Australia, New South Wales, Australia Amee Morgans, BAPPSC (HONS), PHD, Senior Research Fellow, Faculty of Medicine, Nursing and Health Sciences, Monash University, Victoria, Australia Alan Morrison, MPET, GRADDIPPADMIN, GRADDIPED, BPARAMEDPRAC, BAPPSC (BIOMEDICAL), DIPHLTHSC, ADVDIPPARASC, MANZCP, MPA Intensive Care Paramedic, New South Wales, Australia Director Education, NSW Ambulance, New South Wales, Australia Adjunct Fellow, School of Science and Health, University of Western Sydney, New South Wales, Australia Adjunct Senior Lecturer, School of Medicine, University of Tasmania, Tasmania, Australia Stephen Mulholland, BPARAMEDSTUD, GRADDIPHLTH (ADMINISTRATION), MICA CERTIFICATE, Senior MICA Team Manager, Ambulance Victoria, Victoria, Australia Stuart Newman, RN, INTCARECERT, DIPTEACHING (NURSING), BED (NURSING), MHA (NSW), MACN, Director, International Programs & Lecturer in Health Services Management, Sydney Nursing School, New South Wales, Australia Paul Oliveri, BHLTHSC (EHS), GCERT ELEARNING Lecturer, School of Medical and Applied Sciences, CQUniversity, Queensland, Australia Practising Paramedic, Queensland Ambulance Service, Queensland, Australia Peter O’Meara, BHA, MPP, PHD, FPA, FANZCP, Professor of Rural and Regional Paramedicine, La Trobe University, Victoria, Australia Virginia Plummer, RN, RM, MSC (HEALTH POLICY & MANAGEMENT), GRADDIP (HEALTH ADMIN), GRADCERTEMERGHLTH (DISASTER PREP & MANAGEMENT), GCHPE, CRITCARECERT, PHD, FCNA, FCHSM, Associate Professor Nursing Research, School of Nursing and Midwifery, Monash University and Peninsula Health, Victoria, Australia Katrina Recoche, RN, MN, BA (SOC/SCI) Lecturer, School of Nursing and Midwifery, Monash University, Victoria, Australia Vice President, Palliative Care Nurses Australia, Queensland, Australia Adam Rolley, GDINTCAREPARAMEDICPRAC, DIPHLTHSC (PRE-HOSPCARE), BCCJ, MPA

Senior Educator, Queensland Ambulance Service, Queensland, Australia Sessional Academic, School of Medicine, University of Queensland, Queensland, Australia Sandra Schmidt, ADVDIPPARAMEDSC, BNURS, GRADCERTAOD, GRADDIPHLTHMGT, MPA, General Manager, Alcohol and other Drugs, Department of Health, Northern Territory, Australia Jade Sheen, BAPPSC (PSYCH) (HONS), GCHE, MCLINFAMTH, DPSYCH (HEALTH), CLINICAL AND HEALTH PSYCHOLOGIST, Senior Lecturer in Clinical Psychology, Deakin University, Victoria, Australia Gavin Smith, PHD, MEH, GRADDIPEMERGHLTH, BPARAMEDSTUD, FPA, MRSV Associate Professor, Paramedicine, Victoria University, Victoria, Australia MICA Paramedic, Ambulance Victoria, Victoria, Australia Brian Stoffell, BA (HONS), LLB (HONS), PHD, Head of Social Health Sciences, School of Medicine, Flinders University, South Australia, Australia Andy Symons David Teuber, BMBS, FACEM, MCLINEPI Senior Lecturer, Emergency Medicine and Prehospital Science, Flinders University, South Australia, Australia Senior Consultant, Emergency Department, Flinders Medical Centre, South Australia, Australia Retrieval Consultant, SAAS-MedSTAR, South Australia, Australia Visiting Medical Officer, Hyperbaric Unit, Royal Adelaide Hospital, South Australia, Australia Vivienne Tippett, BA, GRADDIP PSYCH, MPH, PHD Head, Paramedic Science Program/Director of Research, School of Clinical Science, Queensland University of Technology, Queensland, Australia BNHCRC Lead Researcher, Centre for Disaster and Emergency Management, Queensland University of Technology, Queensland, Australia Deputy Director, JBI Centre for Evidence Based Healthy Ageing, Queensland University of Technology, Queensland, Australia Ruth Townsend, BN, LLB, LLM, DIPPARAMEDSC, GRADDIPLEGALPRACTICE, GRADCERTVET, Solicitor of the Supreme Court of NSW, New South Wales, Australia Mark Trebley, BHSC (PREHOSPITAL CARE), GRADCERTCLINED, GRADCERTINDIGENOUSED, MANZCP, Clinical Training Officer, Intensive Care Paramedic Ambulance, New South Wales, Australia Abigail Trewin, BAPPSC (PARAMEDIC SCIENCE), GDIP IC PARAMEDIC SC, AusMAT Operations Manager, National Critical Care and Trauma Response Centre, Royal Darwin Hospital, Northern Territory, Australia Bronwyn Tunnage, RN, MSC, Senior Lecturer in Paramedicine, School of Clinical Sciences, Auckland University of Technology, New Zealand Tony Ward, RN, PGDIP AERO RT, BHSC, DIPHSC, NZDIPAMB, Programme Leader/Senior Lecturer, Paramedicine, Auckland University of Technology, New Zealand Jason Wasiak Anthony Dennis Weber, ICP, ASSDIPAPPSC (AMBULANCE), ADVDIPHLTHSC (ADVANCED PREHOSPITAL CARE), BHLTH (NURSING), MASTER HLTHSCI (RESEARCH), Deputy Dean (Learning and Teaching) and Paramedic Discipline Lead, School of Medical and Applied Science, CQUniversity, Queensland, Australia Janelle White, BSC, BED, GRADCERT ICP, MN, MANZCP Paramedic Specialist, NSW Ambulance, New South Wales, Australia Senior Lecturer, Bachelor Paramedic Practice, School of Medicine, University of Tasmania, Tasmania, Australia Shaun Whitmore, MICA FLIGHT PARAMEDIC/DIV 1, RN, Air Ambulance Victoria, Victoria, Australia Denise Wilson, PHD, RN, FCNA (NZ), Professor M ori Health, Taupua Waiora Centre for M ori Health Research, Auckland University of Technology, Auckland, New Zealand Fiona M. Wood, FRACS, AM Director of the Burns Service of Western Australia, Western Australia, Australia

Director of the Burn Injury Research Unit, University of Western Australia, Western Australia, Australia Andrea Wyatt, MED, BSC, BPARAMEDSTUDIES, ADIP MICA, PARAMEDIC MICA, Paramedic, Ambulance Victoria, Victoria, Australia

Reviewers Andrew Bell, BPHED, GRADDIPED, DIPPARASC Lecturer in Paramedicine, School of Nursing, Midwifery and Paramedicine, Australian Catholic University, Queensland, Australia Advanced Care Paramedic II, Queensland Ambulance Service, Queensland, Australia Bronwyn Betts, RN, Queensland BAPPSC (NURSING), LLB, LLM, PHD CANDIDATE SeniorASM, Educator, Ambulance Service, Queensland, Australia Sessional Academic, Queensland University of Technology, Queensland, Australia Belinda Flanagan, MMID, BAPPSC (NURSING), GCPROFLEARNING, ASSOCDIPSC (AMBULANCE), Program Coordinator/Lecturer, Paramedic Science, University of the Sunshine Coast, Australia Carole Donaldson, RN, BN (HONS), MAUniversity, Western AdjunctQueensland, Teaching Fellow, Nursing Midwifery and Param edicine, Curtin Australia, Australia Adjunct Lecturer, Medicine and Dentistry, University of Western Australia, Western Australia, Australia Instructor, Australian Resuscitation Council, New South Wales, Australia Susan Furness, MHLTHSC, GRADDIPICPMED, DIPPMED, DIPN, Senior Lecturer, Paramedicine, La Trobe Rural Health School, Victoria, Australia Bill Lord, BHLTHSC, GDIPCBL, MED, PHD, Discipline Leader, Paramedic Science, University of the Sunshine Coast, Queensland, Australia Veronica Madigan, BHLTHSC, MRURALHLTH, PHD Associate Professor, School of Medicine, Notre Dame University, New South Wales, Australia Senior Lecturer, School of Biomedical Science, Charles Sturt University, Bathurst, New South Wales, Australia Paula McMullen, MHPED, PHD, BSN, MANZCP, Head of School, Paramedicine, University of Tasm Tasm Australia JackaSpencer, MBBS, FACEM Senior Emergency Physician, Theania, Alfred Emania, ergency and Traum Centre, Victoria, Australia Retrieval Physician and Coordinator, Adult Retrieval Victoria, Victoria, Australia Tony Walker, ASM, FPA, AFAIMRegional Services, Ambulance Victoria, Victoria, Australia General Manager Adjunct Associate Professor, College of Health and Biomedicine, Victoria University, Victoria, AustraliaTeaching DeborahFellow, Walley,Curtin RN, BSC (HONS), BA (HONS), PGCE Adjunct University, Western Australia, Australia Adjunct Lecturer, Edith Cowan University, Western Australia, Australia Course Director and Instructor, Australian Resuscitation Council, New South Wales, Australia Executive Manager Education, St John Ambulance Western Australia, Western Australia, Australia Howard Wren, RN, BCLINPRACTICE (PARAMEDIC), DIPTEACH (ADULT ED), General Manager—Education, ACT Ambulance Service, Australia Capital Territory, Australia

The key to improving your clinical practice The ability to reach safe and accurate clinical decisions is not solely influenced by the paramedic’s knowledge of disease and dependence on guidelines. The expectations of the patient and their family, the patient’s language, age, gender, experience and fatigue, and the need to manage scarce resources all impact on the paramedic’s ability to exercise effective clinical judgement and deal with the uncertainty that surrounds any diagnosis. This text therefore aims not simply to link pathology with symptoms, but also to contextualise paramedic practice to reveal the unique strategies that experienced paramedics use to practise effectively in the field. Under time and resource pressures, the best paramedics are often unaware of the decision-making process they use to devise treatment plans: this book is designed to reveal this process and provide students with a guide to making safe and effective clinical decisions. To do this, each chapter in Part 2 presents several case studies based on a genuine ambulance dispatch, because in the real world of paramedic practice the problem-solving process starts with the dispatch: differential diagnoses and treatment plans spring to mind the moment a job is received. The initial case study in each chapter describes the typical presentation for a particular condition and the signs and symptoms that should not be missed. It identifies a particular pathology and how this links to the patient’s signs and symptoms, and outlines how the condition commonly presents, the clinical decisionmaking challenges often associated with it and how it can be managed. As each chapter progresses, the presentation becomes less ‘classic’ and the chapter describes how to reach a clinical decision when faced with increasing uncertainty. The subsequent case studies in each chapter thus present less-typical examples, enabling novice practitioners to examine the decision-making processes of more experienced clinicians and to explore how safe and effective clinical decisions can be made. Understanding how you make clinical decisions is the key to improving your skill, and learning why clinicians make errors in collecting or processing information allows you to identify these behaviours in yourself and correct them. Even for experienced clinicians, there is value in understanding the process: when experts are faced with a condition they haven’t encountered before, they may switch to the form of clinical reasoning more often used by novices. This meta-cognition (analysing how you think) is what separates expert emergency clinicians from those with simply a good memory.

Key features

CA SE ST U DY 1 Case 10692, 0006 hrs. Dispatch details: Three males have been assaulted outside a nightclub. One has facial injuries. Police on the scene state that another patient may have been stabbed. Initial presentation: The paramedics find one patient standing outside the nightclub holding a bloodied towel to his face and another two patients sitting in the gutter talking to the police. The police direct the male with facial injuries towards the paramedics. He is distressed but not aggressive and removes the towel to reveal a lacerated lip and a missing tooth. One of the two men sitting in the gutter has a torn shirt but no obvious injuries or blood. Both men are talking calmly to the police. The men who assaulted the group have left the scene.

Case study Each case study is based on a genuine ambulance dispatch and reflects the years of experience of the various chapter authors. The introduction section to each case outlines the dispatch number and call-out time, the dispatch details as noted by the call-taker and the patient’s initial presentation when the paramedics arrive on the scene.

Clinical reasoning steps For every case study we take you through the four-step clinical reasoning process of assess, confirm, treat and evaluate. This process is critical to improving your clinical decision making: although the process is rarely visible in practice, nearly every clinician practising medicine uses this model.

Assess Assessment of patients in the pre-hospital setting is limited in both time and equipment. An accurate history and a structured approach are the two most important elements. Each case study identifies the most pertinent signs and symptoms associated with a particular condition.

Confirm In addition to linking the pathophysiology of a condition with the symptoms, each case study details the various differential diagnoses that should be considered when you are presented with a particular case history. This reflects the way experienced clinicians think: exploring a range of -potential causes for a patient’s condition and systematically

eliminating them until the best management plan is reached.

Treat Each case study outlines the principles of managing the condition with special consideration for the pre-hospital environment. The treatments are not based around a particular skill set, but start with the most basic elements and extend through to an intensive care level.

Ev aluate The evaluation phase is important as the patient’s response to treatment can indicate the accuracy of the initial diagnosis. Not all treatments available to paramedics demonstrate an effect in the timeframes usually associated with emergency care, and in some cases you should expect to see a realistically small or absent response to treatment. In a few cases (as in real practice) the treatment will inevitably be futile and the patient will not survive.

Ongoing management We conclude the case studies with an outline of what happens once the patient arrives at hospital, because understanding where pre-and in-hospital treatments align and differ can assist in determining how aggressive pre-hospital management should be and where transport should be considered as treatment.

Acknowledgements The editors would like to acknowledge the work of the chapter authors: their willingness to share their time and knowledge to assist the next generation of paramedics is greatly appreciated. They would also like to thank Professor Leon Piterman, Pro Vice-Chancellor of the Berwick and Peninsula Campuses and Professor of General Practice at Monash University, and Emeritus Professor Frank Archer. Leon and Frank have been integral in the transition of paramedic practice into a profession and recognised the need for a paramedic text specific to Australian and New Zealand clinical practice. This text could never have been produced without their support and inspiration. The editors would also like to acknowledge their families, close and extended. This text has been the cause of too many solitary evenings and interrupted family functions and holidays for their patience and encouragement to pass without thanks.

CHAP TER 1

Introduction By Matt Johnson

While the media, film makers and many members of the general public view paramedics as constantly rushing to cardiac arrests and patients trapped in crashed motor vehicles, the reality is very different. The chronic disease burden presented by an ageing population, combined with limited access to community-based clinicians (i.e. public nurses and general practitioners [GPs]), has restructured the role of the modern paramedic from emergency first-aider to professional clinician. In Australia and New Zealand, governments and communities now expect paramedics to possess advanced clinical skills and to be able to manage a range of diseases that far exceeds the ‘scoop and scoot’ approach that has characterised the profession for nearly a century. Unlike other clinicians, however, paramedics have to solve their complex clinical problems in full view of the patient’s family and friends, under intense time pressures and using only limited diagnostic equipment. As with medicine and nursing previously, the increased clinical complexity of paramedic practice has led to a shift in paramedic education from a vocational to a university setting. But classrooms struggle to provide students with the complex clinical stories presented by patients in the real world and the challenges involved in untangling these stories to determine safe and effective treatment plans. This text is designed to assist both undergraduate paramedic students and early career paramedics to link the pathophysiology, symptoms and management of acute medical conditions often encountered by paramedics. Written by some of Australia and New Zealand’s most experienced paramedics and emergency physicians, the book reveals through a series of case studies the complex clinical reasoning process that characterises expert clinical practice. This text should act as a valuable resource for any clinician required to deliver high-level care in field.

Paramedic principles and practice W ha t i s cl i ni ca l re a soni ng? The increasing sophistication of medicine has progressively seen each medical profession move away from an apprenticeship model of training to one requiring clinicians to hold a university degree before they can commence practice. The classroom setting provides the complex anatomical, pharmacological and pathological knowledge needed to practise modern medicine but it is widely accepted that it does not produce ‘work-ready’ clinicians on the day of graduation. What separates novice clinicians from experts is not their knowledge or factual recall but rather how they interpret the patient’s various complaints and presentations to reach an accurate conclusion. Clinical reasoning is the hallmark of the expert practitioner (Ritter, 2003) and, tied to experience, it is one of the most difficult skills to teach in a classroom setting. Clinical reasoning is the amalgam of knowledge, critical thinking, judgement and problem solving that allows expert clinicians to make diagnostic leaps that leave novice clinicians wondering what obvious clue they have missed. This text aims to firstly reveal the process of clinical reasoning and then explore the factors that influence our ability to solve clinical problems. By helping you to understand the clinical reasoning process and then explore how your perspective, attitude, communication, preconceptions and philosophy can influence your ability to make safe decisions, we hope to speed your progression towards becoming an expert clinician. We feel that providing this pathway is especially important for paramedics who, as a profession, are not provided with the graduated exposure to critical and undiagnosed cases that characterise the early clinical practice of other medical professions. Unlike doctors and nurses, novice paramedics are expected to respond, with little supervision, to an extremely wide range of conditions from the moment they log onto their first shift (see Fig 1.1). The paramedic workplace is also very different from the hospital environment and this impacts significantly on how paramedics must reason their way through clinical challenges.

FIGURE 1.1 Paramedic students become one half of a fully operational team from their first day of employment. Once paired with an instructor they are subject to whatever cases fall closest to their branch. This is a rich learning environment but it can subject students to considerable pressures. This book is designed as a ‘bridge’ to clinical practice in the field, allowing students and novice paramedics to work through cases, explore differential diagnoses and build an experience base before they are confronted with a patient in actual distress. Source: Image supplied by St John Ambulance WA.

Where paramedics work Perhaps even more so than other medical professionals, paramedics are required to quickly and accurately make clinical decisions based on limited information. So, like all clinicians, paramedics spend much of their time focusing on synthesising the symptoms and clinical findings that each patient presents to them. This clinical decision-making process is complex and challenging in itself, but in addition paramedics must perform this task in an environment that is not conducive to clear thinking. Figure 1.2 illustrates the model that was developed to describe that environment and forms the basis for this text. Solving the ‘clinical puzzle’ is the aim of every paramedic, but gaining a succinct patient history and making safe clinical judgements are not performed in an ideal environment. Failing to appreciate the complexity and variability of this work environment can only compromise the paramedic’s ability to recognise and minimise the

potential for errors in their decision making. This model illustrates that paramedic clinical decision making involves much more than simply recalling a list of symptoms attached to particular conditions.

FIGURE 1.2

Factors in paramedic clinical decision making.

Surrounding the clinical decision-making process are three distinct dimensions that have little to do with the patient’s condition but impact significantly on how the paramedic makes critical decisions. Gaining an awareness of the factors surrounding this decision-making process is critical in recognising the stresses you will experience and how to error-proof your decision making. Immediately surrounding the clinical decision-making process are the personal factors that each paramedic brings to every case they attend. How a case relates to your knowledge and skills will impact on your decisions, but evidence shows that your age, gender, experience and level of fatigue also influence your thought processes and treatment plan. Stepping out one layer, paramedics are influenced by factors generated by the case itself: do you feel safe? Are you the junior member of the crew trying to assess the patient while being assessed yourself? Do the clinical guidelines of your ambulance service allow you to manage the patient safely? Do you have enough resources to deal with the problem at hand? Finally, every case is framed by workplace culture, professional standards and community expectations of paramedic practice. In this text we use this model not only to explore the clinical aspect of decision making but also to identify the external and internal pressures that can cause paramedics to make diagnostic errors.

The paramedic’s clinical approach In Part 1, Chapter 2 discusses the paramedic’s role in healthcare and Chapter 3 looks at ambulance use among patients. Chapter 4 details a structured clinical approach to patient assessment and examines the strengths and weaknesses of the various methods. Chapter 5 outlines the various theories of clinical reasoning (how medical professionals think) and how you can use these theories to develop your own clinical reasoning skills. The chapter introduces two distinct methods of clinical reasoning and where each can most effectively be used. It distinguishes between novice and expert clinical reasoning and gives you insight into how to progress your own clinical reasoning skills. Chapter 6 details the challenge of communication in the health emergency: how to get useful information from your patients. Remember, it is not their job to be good historians; it is your job to ask the right questions in the best manner to get the information you need (see Fig 1.3). Paramedics are especially reliant on communication skills: our diagnostic equipment is limited by portability, there is rarely a written record of the patient’s previous medical examinations at hand and we work in complex situations where acutely ill patients, difficult procedures and high-stimulus environments (noise, weather, family members) combine to create significant cognitive stresses. The chapter develops a medical interview model specifically tailored for the paramedic and describes how to create an environment so that the patient gives you the information you need. Extracting a detailed but succinct patient history is a core requirement for every paramedic and probably the greatest barrier to effective clinical reasoning.

FIGURE 1.3 Experienced clinicians in every medical field make the majority of their clinical decisions based on the patient’s description of their condition. The limitations of time and portable equipment make the ability to elicit an effective description of the patient’s illness an even more important tool for paramedics, but lounge rooms and public streets are not ideal places for a focused and personal narrative. The ability to recognise the hurdles facing paramedics in gaining a patient history must be recognised if they are to be effectively overcome. Subsequent chapters in Part 1 explore the principles of patient safety, how guidelines and practices are developed, the legal and ethical issues faced by paramedics, and education, as well as the cultural challenges that occur in both metropolitan and rural areas. Finally, the part concludes with how to integrate all you have learnt into a concise and well-defined philosophy of practice that will guide the development of your knowledge, skills and attitudes after your formal education is finished (see Fig 1.4).

FIGURE 1.4 A The shift to tertiary education for paramedics has ‘front-loaded’ them with clinical knowledge but provides only limited clinical exposure. One result is a typically segmented practice where the new graduate paramedic focuses on a single component of a case at a time. B The philosophy of practice.

How paramedics think Modern paramedics can no longer rely on a strict adherence to a limited number of protocols to quickly and safely select treatments. In order to practise effectively, paramedics must collect information about the patient, make sense of this disjointed data and apply it to their knowledge of anatomy, physiology and pharmacology before using it to guide a treatment plan. As already noted, this process differs dramatically between novice and expert clinicians: faced with the same case, novices may appear laborious and uncertain, while experts seem to make snap decisions based on little information. Revealing the path all clinicians must take in the journey from novice to expert is the prime intention of this text. The creation of an experience base (and the insight and time to reflect on it) can be a tough road for novice paramedics who, unlike novice nurses or doctors, are not provided with a graduated and resource-rich learning environment. From day one junior paramedics make up half the operational crew that is dispatched to any case. Part 2 builds on the principles outlined in Part 1 and each chapter uses a series of increasingly complex case studies to demonstrate the links between pathophysiology, the patient’s symptoms and the most effective treatment plan. Most importantly, each chapter details the various differential diagnoses that should be considered when you are presented with a particular case history. This reflects the way experienced clinicians think: exploring a range of potential causes for the patient’s condition and systematically eliminating them until the best management plan is reached. Figure 1.5 breaks this process down into four clear steps and this model is used to ‘unpack’ each case study. Although the process is rarely visible in practice, nearly every clinician uses it nonetheless.

FIGURE 1.5

The clinical reasoning model.

Clinical reasoning is notoriously difficult to both teach and learn. The traditional method used by students is to gather ‘all’ the relevant information from the patient, sort the data, apply it to their knowledge base of diseases and decide upon a diagnosis. In recent years, however, studies have found that experienced clinicians start making diagnostic decisions from the very moment they encounter the patient, and the questions they ask (and the tests they perform) are guided by these working hypotheses. Other studies have indicated that very experienced clinicians recognise conditions almost without cognition and seek to disprove rather than prove their hypotheses. What does this mean for the student paramedic still trying to remember the various symptoms of cardiac chest pain, or the novice paramedic struggling to make quick decisions in front of patients? Understanding how you make clinical decisions is the key to improving your skill. Learning why clinicians make errors in collecting or processing information allows you to identify these behaviours in yourself and correct them. Even for experienced clinicians, there is value in understanding the clinical reasoning process: when some experts are faced with a condition they have not encountered before, they switch to the form of clinical reasoning more often used by novices. This meta-cognition (analysing how you think) is what actually separates expert emergency clinicians from

those with simply a good memory. Each chapter in Part 2 starts with a case study based on a genuine ambulance dispatch to help contextualise the decision-making process and create the environment in which decisions must be made, because in the real world of paramedic practice, the problemsolving process starts with the dispatch. Although the crew know that the dispatch may be inaccurate, nonetheless differential diagnoses and treatment plans spring to mind the moment the crew receive a job and it is impossible not to consider them on the way to a case. These cases reflect the years of experience of the various chapter authors.

Where paramedics fit in the health system Although specifically designed for paramedics providing pre-hospital care, this text approaches each case as an episode of care in which the paramedic response may be only a single unit of care (see Fig 1.6). It is an unfortunate characteristic of western health systems that each profession and organisation tends to examine only their own performance in response to a case (e.g. response time, drug guidelines, length of stay, infection rate), when the effective management of patients requires all of these units to work together. Importantly, patients are not necessarily even aware that these separate units exist: they experience the journey from injury to recovery according to how limited or unwell they are and for how long.

FIGURE 1.6

A sample episode of care for chest pain.

The past decade has revealed that the quality of patient care relies more heavily on how well this team of disparate professions work together than on the skills of any one clinician. One patient’s journey from health to a heart attack and then a return to health involves multiple teams with overlapping skills and responsibilities. Importantly, the entire episode of illness starts with the patient’s recognition of the disease and their response to it (see Ch 3), and the patient remains the only common element in every unit of care within this episode. Failing to appreciate how the patient contributes to each unit will restrict each subsequent clinician from accessing all the information they need to perform their role optimally. Although guidelines may vary from state to state and between ambulance services, every paramedic contributes to a patient’s journey through illness, and regardless of how large or small the unit of care delivered by paramedics is, it must integrate into the overall episode without any loss of information or missed management.

Viewed from the perspective of health, the paramedic is an essential component of a multidisciplinary team who provides patient centred care from the first presentation through to recovery (Shaban, Wyatt-Smith & Cuming, 2004). It is easy to think of paramedics working in an isolated silo but the professional paramedic has an everincreasing responsibility to act as part of this multidisciplinary team. Good interprofessional communication and teamwork have a significant impact on the quality of care that patients receive. This text aims to give you an appreciation of the episode of care so that you can function more effectively and understand where your clinical practice fits into overall patient management. The rapidly expanding scope of paramedics in some areas may mean that what currently occurs in the emergency department may soon be being practised in the back of an ambulance.

Beyond paramedics The continuum of care approach used in this text has implications for other professions. Although written specifically for paramedics, the evidence-based, structured clinical approach described here is equally applicable for any medical professional faced with the time-poor, resource-limited and highly emotional nature of emergency medical care. Nurses, GPs and first-responders working in remote areas particularly may find this text useful and the term ‘paramedic’ is used for the sake of simplicity rather than implying a specific skill set or qualification. We have intentionally avoided writing this text according to any particular state or national guidelines, or with a specific definition of ‘paramedic’. Paramedic practice has traditionally been heavily guided by protocols: we were not assumed to have the knowledge to form an independent diagnosis. Today, most paramedic organisations are actively stepping away from local traditions and historical practices and are embracing evidence-based practice. This text therefore does not differentiate between ‘paramedic’ treatment and ‘hospital’ treatment or ‘medical’ treatment: paramedics are simply a unit of care in the much larger episode of care, and we must understand not only our role, but also how it integrates into what comes before and after we attend the patient if we are to practise effectively. Anatomy and physiology do not change according to the building where the patient is located or the uniform worn by the treating clinician. The principles of treatment remain the same and as you read through the case studies in Part 2, where your paramedic practice ends and who takes over the next stage will depend on your level of qualification and the area in which you work. Regardless, it should allow you to place your care in context with what should have come before you arrived on scene and what the patient faces after you hand them over.

Evidence-based practice Detailed in Chapter 7, evidence-based practice is the foundation of modern paramedic care: it provides the scientific rationale for what we do and how we contribute to better patient outcomes. We have tried to follow the best evidence-base available for all the management principles used in the text: if your local practice differs substantially from what you read, explore this difference. Has research already made our efforts out of date,

or is your practice being limited for a particular reason? Should it be changed? Should you submit a new guideline for consideration? Paramedics are part of an increasingly professional body and each case we attend adds to the knowledge base of our profession: seeking evidence will help reinforce what we do and why we do it. Always keep your eyes, ears and mind open for new developments that are supported by evidence.

Essential knowledge A number of essential physiological concepts underpin paramedic practice and are common to a wide range of diseases and injuries. Perfusion, the autonomic nervous system and inflammation are concepts that all paramedics must understand if they are to make safe and effective clinical decisions. To emphasise their importance we have dedicated specific chapters in Part 3 to these concepts and referenced where each of these concepts relates to a specific case study. If these concepts arise in a case study, you will see a reference to the ‘Essential knowledge’ chapters. If you do not fully understand a concept, do not try to push on through the case study: go to the relevant chapter in Part 3, build the foundation upon which you can make effective decisions and then return to the case study. The essential knowledge chapters are exactly that: knowledge essential for making effective decisions.

Summary As a paramedic student you have to collect the knowledge, skills and attitudes that will allow you to perform your work safely and efficiently. Too often, this knowledge is considered to be simply physiology, symptom lists and drug sheets; the skills are thought to be cannulation, intubation and chest tubes; and the required attitudes to be a touch of compassion and a liberal dose of empathy. In truth, this knowledge includes an understanding of why patients have been forced to call an ambulance, what they are experiencing and how to communicate effectively with them in this circumstance so that they will give you the information you need to make an accurate diagnosis. The skills include how to decide between relevant and non-relevant information and how to ask the right question at the right time; and the attitudes include the desire to reflect on your own practice and not rely on others to direct your ongoing learning. This text examines the complex cognitive processes involved in reaching effective clinical decisions in the high-pressure, time-poor environments in which paramedics have to operate.

References Ritter, B. J. An analysis of expert nurse practitioners’ diagnostic reasoning. Journal of the American Academy of Nurse Practitioners. 2003; 15:137–141. Shaban, R., Wyatt-Smith, C. M., Cuming, J. J. Uncertainty, error and risk in human clinical judgment: Introductory theoretical frameworks in paramedic practice. Journal of Emergency Primary Health Care. 2(1), 2004.

PART 1 PARAMEDIC PRINCIPLES O U TL I N E CHAPTER 2: The paramedic role in healthcare CHAPTER 3: Characteristics of ambulance patients CHAPTER 4: The structured clinical approach CHAPTER 5: The clinical reasoning process CHAPTER 6: The patient interview CHAPTER 7: Patient safety and paramedicine CHAPTER 8: Paramedic health and wellbeing CHAPTER 9: Paramedic education CHAPTER 10: Legal and ethical considerations in clinical decision making CHAPTER 11: Developing a philosophy of practice

SECTION 1

PRINCIPLES OF PARAMEDIC PRACTICE O U TL I N E CHAPTER 2: The paramedic role in healthcare CHAPTER 3: Characteristics of ambulance patients

CHAP TER 2

The paramedic role in healthcare By Matt Johnson

O V E RV IE W • Ambulance services are widely recognised as providing an emergency service to patients with life-threatening conditions. • Providing safe transport to hospital in addition to providing emergency pre-hospital care defines the paramedic role and distinguishes the role from that of other health professionals. • Historically, the clinical emphasis of paramedic care has been on stabilising patients for rapid transport to hospital for definitive care. • Ambulances staffed with two crew members are the primary method of service delivery in Australia and New Zealand, but this model is slowly changing. • Paramedic scope of practice has increased significantly over the past 15 years but this is not widely recognised among the public or other health professions. • Ambulance workloads are increasing by about 10% per annum (CAA; Lowthian et al., 2011a). This growth is fuelled by patients suffering chronic conditions rather than the lifethreatening emergencies traditionally associated with ambulance calls. • New models of education, equipment and dispatch are being introduced by some ambulance services to deal with the new caseload. • The traditional ‘Respond, treat and transport’ model of ambulance care is being replaced with ‘Treat and leave’ models. • There is a rapidly growing emphasis on keeping patients out of hospital. This requires paramedics to engage in treatment pathways other than transport to the emergency department (ED). • The complex interactions created when patients have multiple chronic conditions and need to be directed to the safest treatment pathway is increasing the complexity of paramedic clinical decision making. • Paramedics are under pressure to integrate with other healthcare providers and provide patient care in non-emergency community settings. • First responders from volunteer organisations and fire services are now engaging with the traditional ambulance role of responding to health emergencies.

CA SE ST U DY 1 Case 14519, 0947 hrs. Dispatch details: A 74-year-old female with chest pain. The patient has a cardiac history. Initial presentation: The patient is sitting in a chair on the front verandah as the crew arrive. As they approach she coughs vigorously and produces a large volume of purulent mucus that she spits delicately into a tissue. She tells the crew she has had a chest cold for about a week but today she is dizzy when she stands up and her chest hurts.

Introduction To the untrained observer, making clinical decisions probably does not appear to be all that difficult: collect all the information you need, compare it to the known causes of diseases, match it to an appropriate protocol that is based on good scientific evidence and follow the steps described in the protocol. In reality, however, there is well-documented evidence that novice clinicians across a number of medical professions struggle to integrate their knowledge into an effective decision-making strategy (Hoben, Varley & Cox, 2007; Patel & Groen, 1986; Rikers, Loyens & Schmidt, 2004). For paramedic students the challenge is even greater: working with limited diagnostic tools and in a public setting, paramedics are rarely presented with a structured and linear form of clinical information (Shaban, Wyatt-Smith & Cuming, 2004). As has already been noted, paramedics have to make decisions under intense time pressures, with incomplete (and often misleading) information, and with strong emotional and social input from the patient’s family and friends (Shields & Flin, 2012; Wyatt, 2003). Furthermore, due to our ageing population patients rarely have just one disease and many present with complex medical histories (see Fig 2.1). At first glance, the patient described in case study 1 could be suffering from little more than a bacterial chest infection with some dehydration or an ischaemic cardiac event. In actual fact, the patient upon whom this case study was derived was suffering from both: an obvious problem that could have been managed by her GP and another more serious problem that needed urgent intervention.

FIGURE 2.1 The ageing Australian population is expected to contribute to significantly increased spending on healthcare over the next 40 years. Source: Shutterstock/Fotoluminate LLC. Chapter 1 introduced the model shown in Figure 1.1. At the centre of the model lies the actual clinical reasoning and decision-making process where the information gained from assessment is integrated with the paramedic’s knowledge and clinical skill to create a treatment plan. Surrounding this essential skill of emergency medicine (Geary & Kennedy, 2010) is a series of factors that influence the cognitive process of problem solving. As desirable as it might be to remove external influences from decision making, the reality is that we cannot divorce ourselves from the emotions, beliefs and perceptions that frame every decision we make. Just as paramedics are influenced by the factors surrounding a case, so too are patients similarly affected by the people present, the time of day and other factors present at every case. The ability to error-proof our decision making lies in recognising the effects these external influences have and allowing for—not ignoring— them (Croskerry & Wears, 2002). Later chapters elaborate on the internal aspects of clinical decision making (CDM)— how paramedics and their patients think, communicate and respond to emergencies—but before we apply the theory of CDM to the individual, we first need to contextualise the broader environment in which paramedics work: the outside ring in the clinical decisionmaking model. How governments, other health professions and the wider community perceive the role of ambulance services impacts directly on the type of decisions

paramedics are required to make and shapes the way they think.

The role of ambulance services in Australia and New Zealand Em e rge ncy re sponse a nd tra nsport to hospi ta l Like police and fire services, ambulances are a conspicuous part of nearly every community across the globe. Although the levels of skill, training and equipment may vary, the common public perception of ambulance services regardless of where they are based is that they respond to medical emergencies (Lowthian et al., 2011a; Sheather, 2009). Tied intrinsically to this is the notion that ambulances provide rapid transport to hospital for definitive care. For those managing and working in ambulance services it is becoming increasingly obvious that the role of the modern ambulance service will need to extend beyond this paradigm, but for those outside the profession the transport role of ambulance services remains firmly entrenched (see Box 2.1). B O X 2 . 1R e s p o

nd, tr eat and tr anspo r t

The traditional ‘Respond, treat and transport’ model of ambulance services is not as universally applicable to the modern paramedic role as it once was. As ambulance services engage other treatment pathways, the pressure on decision making increases: crews now need to decide which pathway other than transport to ED is most suitable for the patient. With many members of the community expecting every ambulance attendance to result in transport to ED, these new pathways can result in conflict between the treatment the patient expects and what the paramedic is trying to deliver.

P RACT ICE T IP ‘They put wheels on ambulances for a reason’: axiom reminding paramedic students that transport is an integral part of ambulance care—but for how much longer?

P RACT ICE T IP ‘Diesel with the foot flat down is a great paramedic drug’: often quoted by senior paramedics and indicative of an era when the only response to a patient’s clinical deterioration was to transport them to the doctor faster.

Ambulance services in Commonwealth countries share a remarkably similar history. Most started in the early 1900s as small teams of volunteers trained and coordinated by charitable organisations such as St John Ambulance. Based in the major cities, they did not lack work—traumatic and environmental injuries caused by increasing industrialisation were all too common—and the services quickly grew in size (Howie-Willis, 2009). With only rudimentary first-aid skills and virtually no medical equipment, the role of these early agencies was solely response and transport. In fact, an ability to operate the horse or vehicle that carried the patient was often the only essential qualification considered for the role. With most ambulance services structured along military command models (members of the Army Medical Corps often contributed to staffing), the progression from volunteers to paid employees saw the term ‘Ambulance officer ’ become the common descriptor of the role. The fundamental responsibility of providing an emergency response and transport function remains the most obvious and distinctive role of ambulance services worldwide. In Australia and New Zealand, this transport function has not only shaped public perception of the paramedic role, but also influenced the way governments have chosen to develop and use ambulance services. In the early days, it was not uncommon for more than one organisation to offer ambulance services within a major city and support volunteer services in outlying areas. The various ambulance services were eventually incorporated into single state-wide systems under government control (Howie-Willis, 2009). This process of consolidation occurred as early as 1919 in New South Wales and as late as the 1950s in South Australia. Over the succeeding decades the states gradually absorbed within their borders any autonomous regions that delivered independent ambulance services and by the 1980s all Australian states and territories operated statewide ambulance services that recruited and trained their own staff, selected their own equipment and developed their own practice guidelines largely in isolation from the other states. The model varies slightly in Western Australia and the Northern Territory, where the government contracts the delivery of ambulance services to St John. In reality, several of the amalgamated areas within some states still operate with a degree of autonomy, but overall they represent a single organisation staffed by professional ambulance officers in the major cities and towns, with volunteer support in regional centres. Like Australia, the New Zealand ambulance services started as local volunteer organisations but from 1957 the Hospital Act required hospitals to provide an ambulance service to their catchment area. Hospitals gradually contracted the role to St John, which now provides services to nearly 90% of the population. In the Greater Wellington and Wairarapa regions, the Wellington Free Ambulance Service provides coverage. In the late 1960s/1970s a number of research studies suggested that more advanced prehospital emergency care of cardiac and trauma patients could dramatically improve patient outcomes (Boyd & Cowley, 1983; Pantridge & Geddes, 1967). In some countries this led to an increase in the level of patient care, with doctors placed in ambulances, and this remains a standard in many parts of Europe including Germany and France (Dick, 2003). However, in Australia and New Zealand the system remained mostly one of taking the patient to the doctor. Yet there were gradual changes in the education and scope of practice of ambulance officers, and over the past two decades the emergence of the term ‘paramedic’ reflects a shift (real or otherwise) from simply transporting the injured and acutely ill to treating them. In addition, faced with growing demand, a number of ambulance services have contracted the routine transport of low-acuity patients (e.g.

transfers between hospitals) to private ambulance services in an attempt to quarantine their own resources for emergency responses. Regardless of these changes, the emergency response and transport function remains the most visible and defined role provided by the various ambulance services operating in Australia and New Zealand. When patients phone for an ambulance their expectation is that a crew of two ambulance officers will attend, treat them to varying degrees and then transport them to hospital (see Box 2.1). Later in this chapter we explore how this ‘treat and transport’ or ‘pre-hospital’ role of ambulance services is changing and impacts on clinical reasoning and decision making.

Public health Although ambulance services in Australia and New Zealand are based in the public health system (see Box 2.2) and funded almost entirely by government (see Box 2.3), the phrase ‘public health’ as it is used here refers to the concept of promoting and protecting (in addition to treating) the health of the community. The effectiveness of public health programs can be seen by the reductions in the number of cases of lung cancer and heart disease, for instance, due to research and education into factors such as smoking and diet (see Box 2.4). B O X 2 . 2T

he public sec to r am bulanc e m o del

in Austr a lia • Health is a state responsibility. • Ambulance services are organised at a state/territory level. Each state/territory has an ambulance authority (a public agency). Most have an Ambulance Act. Each has a government department that sets standards, monitors ambulance performance and provides the bulk of service funding. Public hospitals are also organised at a state level. All states/territories have a government department that sets standards, monitors hospital performance and provides the bulk of hospital funding. • The various state/territory ambulance authorities meet collaboratively under the banner of the Council of Ambulance Authorities to progress their mutual objectives.

B O X 2 . 3A m b u l a n c

e f unding in Austr a la sia

How the funds for the various Australian and New Zealand ambulance services are collected varies slightly (taxes, levies, subscription), but the services are essentially funded from the public purse. Interestingly, with the exception

of Queensland and Tasmania there is still an expectation to recover fees from patients or insurers to a much greater extent than in public hospitals or other emergency services. Combined with a governance model that links the services directly back to the responsible minister, this has ambulance services competing with other health and emergency services for funding. It also makes them subject to political pressures and policies that may not reflect the best direction for the individual ambulance services. As an example of the funding base provided to Australian ambulance services, in 2010/2011 Ambulance Victoria obtained its revenue as follows: government contribution, $344 million; transport fees, $108 million; membership, $104 million; and other sources (donations, bequests, interest), $12 million (Ambulance Victoria, 2011).

B O X 2 . 4P

ublic health

The results of public health programs can take years to show dividends but the effects can be widespread and ultimately more effective than trying to treat a disease. Tobacco use is estimated to cause more than 5 million deaths worldwide each year (WHO, 2009) and is the leading cause of preventable death. In Australia, sustained public education programs into the dangers of smoking have seen smoking rates fall from 42% of men and 28% of women in 1977 to 23% of men and 19% of women in 2007/2008 (ABS, 2011). Similarly, a recent Australian public awareness campaign on the signs of stroke resulted in a measurable increase in ambulance dispatches for the condition. Stroke is a debilitating and expensive condition, but it often displays symptoms that can act as early warning signs and allow patients to avoid a catastrophic event (Bray et al., 2011)

Given the perceived role of ambulance services in responding to health emergencies, it is not difficult to see the disconnect that exists between the role the ambulance service can provide and the aims of public health to improve the social, political and economic factors that cause illness (Rothstein, 2002). The relationship could be described as one of reactivity, in which ambulance services respond to patients for whom public health initiatives have failed to prevent illness, injury or disability. Yet the role the ambulance service plays in the public health system is far more significant than simply transport and could be described as proactive: for example, ambulance services have been instrumental in initiatives such as the chain of survival, which has dramatically improved rates of survival from cardiac arrest (Eisenberg, Bergner & Hallstrom, 1979; Nolan, Soar & Eikeland, 2006). Developed in the mid-1980s, the first chain of survival concept saw the role of the ambulance as providing a quick response and the early administration of an external defibrillator (see Fig 2.2). Increases in paramedic skills have seen this role expand to include treatments ranging from early post-resuscitation care to the use of inotropes and

therapeutic cooling.

FIGURE 2.2

The original chain of survival. Source: Shutterstock/elenabsl.

The increased prevalence of chronic diseases across the community raises new challenges in both diagnosis and management (see Fig 2.3). Identifying patients who can be managed in the community is a clinical decision that many paramedics struggle with: as a profession, paramedicine has not traditionally engaged in chronic disease management and it remains underrepresented in many vocational and tertiary courses.

FIGURE 2.3 While the training and equipping of paramedics focuses on critical events such as cardiac arrests and terrorist attacks, the vast majority of paramedic work involves responding to patients suffering from the complications of chronic diseases. Source: Image supplied by St John Ambulance WA.

Community education Although early ambulance services grew out of organisations offering first-aid education, very few retain significant public education programs. The emphasis on the emergency response and transport role has seen most modern ambulance services focus their resources in this area and move away from providing first-aid education to the public. This is despite the experience and credibility that paramedics could provide in first-aid training. The approach to providing community education as a public health service (e.g. road accident education), a means of improving emergency care (e.g. CPR and automated external defibrillator [AED] programs) or a funding stream is inconsistent across the ambulance services in Australia and New Zealand.

Paramedic education The past decade has also seen a shift in the way paramedics themselves are educated. Until the early 2000s paramedics were recruited and trained by their local ambulance service. This vocational model involved as few as 4 weeks and rarely more than 20 weeks’ training, and recruited workers mainly from outside the health sector. It provided each ambulance service with a workforce that identified strongly with local guidelines and was especially reliant on protocols to guide decision making. The shift to undergraduate and postgraduate paramedic degrees has substantially increased the knowledge base upon which paramedics can draw to solve clinical problems.

Workplace culture The focus on transport has literally shaped the paramedic workforce: the historical need to load patients onto manually operated stretchers saw ambulance services initially employ an all-male workforce. This contrasted with the long-term recruitment of female nursing staff in hospitals and further differentiated the role of ambulance services until the early 1990s, when female paramedics began to be recruited in significant numbers, probably assisted by the change to university-based education. Up to 64% of undergraduate enrolments in paramedic courses are now female (Williams, 2009). Although many services have revised the recruitment requirements, a significant proportion of the workforce still considers physical strength to be an attribute for performing the role. In a study of clinical placement experiences of paramedic students, 40% of students were told by their supervising paramedic that the paramedic doubted the student’s ability to perform the physical role of the job—and of this group, 36% were advised of this perceived deficiency more than once (Boyle et al., 2008). An assessment of fitness and physical strength is part of the selection process of all ambulance services, but the criteria are not consistent across the board. The shift to university-based education has had other effects on workplace culture. Given that a large number of senior paramedics have been educated within the vocational model (usually a diploma), new university-trained paramedics holding a bachelor ’s degree are, at least technically, educated to a ‘higher ’ level. However, the current university model is struggling to provide students with the necessary quality and amount of clinical placement experience and this has implications for ambulance service planning and delivery. New graduates tend to need clinical support for longer periods, so graduate programs and ‘on-road’ clinical supervision have become a priority. Paramedics generally work in teams of two, and effective communication and consultation are essential. The disparate nature of the old and new staff often means that team members use different knowledge bases, communication styles and decision-making tools. Ambulance services have been slow to embrace postgraduate education, with most failing to link career progression with formal qualifications. The result is a workplace where the majority of senior clinical staff are vocationally trained males over the age of 40 with extensive clinical experience, while the majority of new staff are university-trained females under the age of 25 with little clinical experience (Williams, Onsman & Brown, 2010). In recent years growth of paramedic employment opportunities outside of governmentsponsored ambulance services has been slow but it is steadily increasing. Companies that

provide medical services to industrial sites, sporting events and festivals, as well as private patient transfer operators, are offering paramedic employment and these new operators are likely to create their own workplace cultures that may not be consistent with those in the larger ambulance services. In the not too distant future some paramedics will work for a number of different employers, both public and private.

Patient safety Given that the perceived role of ambulance services is to provide life-saving emergency care, specifically attending to patient safety might seem rather redundant, and some paramedics still consider this to mean removing hazards such as chemicals, heat and bystanders that often present as dangers at an accident scene. In fact, the term ‘patient safety’ is a relatively recent concept that seeks to raise awareness of the risks that health professionals can pose to patients and how these can be mitigated. Although the concept has grown out of the risks created by the complex and segmented nature of healthcare within hospitals, it is increasingly being applied across all healthcare providers. Due to the segmented nature of the health system and clinicians’ concentration on the ever-increasing complexity of their practice, clinicians may unknowingly exclude their patients from the decision-making process or subject them to treatments that may be wellintended but actually result in additional harm. Healthcare organisations are now using a patient-safety framework to mitigate such risk. This patient-centric approach aims to ensure that all healthcare workers have the knowledge, skills, behaviours and systems in place to ensure patient safety (ACSQHC, 2005). Specifically, this has been defined as individuals and organisations recognising the need to: • communicate effectively and involve patients and carers as partners in healthcare, communicating risk to patients and being honest with them after an adverse event (open disclosure); it also reminds healthcare workers and organisations to obtain consent and be culturally respectful and knowledgeable • identify, prevent and manage adverse events and near-misses honestly and openly • employ best-available evidence-based practice and information technology to enhance patient safety by providing accurate and current care (see Box 2.5) B O X 2 . 5E v i d e n c

e-based pr ac tic e

The clinical practice guidelines used by ambulance services are increasingly being scrutinised to ensure they are supported by scientific evidence. As a result, a number of long-held ambulance guidelines have been questioned and either modified or discontinued. Reporting of incidents under a patient-safety framework is designed to reduce the allocation of blame onto individuals and determine whether systematic errors were the cause. This proactive management of adverse incidents and the desire to maximise learning from incidents contrast with the clinical auditing methods traditionally used by some ambulance services.

• understand the human factors that occur in complex organisations and how managing fatigue and stress can impact on patient care • practice ethically and maintain fitness to practise through continued learning (ACSQHC, 2005).

Professionalism and professional standards The notion of a ‘profession’ grew from occupational guilds and early universities and was the recognition that those in a particular profession possessed a unique body of knowledge and a defined role (Cruess, Johnston & Cruess, 2002). Since then, the term has grown to include the concepts of a code of conduct, membership of a professional body and regulation of practice (Sheather, 2009). While it may appear pedantic to some observers, the argument over professionalism in paramedic practice actually has significant implications for how paramedics reach clinical decisions. The increasing complexity of paramedic practice over the past decade has inspired a number of discussions that suggest paramedicine should be considered as a profession (Boyle et al., 2003; Grantham, 2004; Wyatt, 1998). This has been supported by the shift to university-based education, which has standardised the level of knowledge within paramedic practice, and the development of a professional body of knowledge through research. However, until there is a form of national registration and wider membership of professional groups such as Paramedics Australasia, it is arguable whether paramedicine is actually operating as a profession. In other health professions, the professional organisation defines the necessary training, code of conduct, professional behaviours and required body of knowledge. In most ambulance services in Australia and New Zealand paramedics remain subject to the regulation of the various employers of the industry (the state-based ambulance services) and formally they are still described by the Australian Bureau of Statistics (ABS) as associate professionals (ABS, 1997). Furthermore, developing a scientific body of knowledge unique to paramedic practice (the basis upon which clinical decisions are made) is not considered within the scope of many of the current ambulance services. This lack of national regulation in Australia may limit the guidance that paramedics can gain from a code of conduct or a description of professional behaviours, but it is likely the public has a strong opinion on how paramedics should behave and what their role is. For some this status justifies recognition as a profession (Grantham, 2004), but it also relies on recognition and engagement from other health professions. In this sense the past isolation of providing out-of-hospital care has limited interprofessional development of the paramedic role.

Terminology and qualifications Reflecting the lack of national standards of practice, there is also a lack of consistency in the terms used to describe ambulance operations and paramedic care and training. This text adheres to the following descriptions, but the dynamic nature of the profession is likely to see new terms and titles developing.

Ambulance officer In some parts of Australia and New Zealand the term ‘ambulance officer ’ or ‘paramedic’ is used depending on the person’s clinical skills and education, as well their role and legal responsibilities. In other states and regions these two terms are completely synonymous. The term ‘ambulance officer ’ is widely used and because it usually refers to those who were practising before the shift to university-based training, it might be thought suggestive of a lower degree of training and practice. In reality this is not the case and in this text the term is considered synonymous with the term ‘paramedic’.

Paramedic Until a form of national registration is instituted, the specific training and scope of practice of paramedics remains open to interpretation. Since virtually all paramedic positions are in state-based ambulance services, there is a form of professional description, but wide variances exist between the states. In North America the term denotes a higher level of training than the term ‘emergency medical technician (EMT)’ and this sometimes applies in Australia, but in many states the transition from ambulance officer to paramedic involves little more than rebadging existing staff and equipment.

Advanced life support (ALS) paramedic Introduced to recognise a higher level of skills (IV access, use of adrenaline in cardiac arrest, insertion of laryngeal mask airways), this clumsy term has become largely redundant as university-based training has made such skills the basic level of care. When we refer to paramedics in this text we infer that they are accredited with ALS skills, although in some areas the descriptor BLS (basic life support) is still in place for paramedics with less training. (Interestingly, the skills that the term ALS infers in paramedic practice differs from the ALS skill set taught in medical ALS courses.)

Intensive care paramedic (ICP) This term generally refers to paramedics who have undergone additional training after practising as an operational paramedic for a period of time. The selection and training of ICPs was traditionally conducted by the various ambulance services but is gradually moving to a postgraduate model operated by universities. Although ICPs generally practise advanced clinical management techniques and use advanced pharmacology, the significant difference that an ICP brings is in the depth of knowledge and associated

problem solving and judgement.

Extended care paramedic (ECP) This new term refers to paramedics who respond to cases of low acuity where there is a strong possibility that the patient can be treated and left at home or referred to other healthcare providers. Based on a UK model, this role is unique in that it does not intrinsically link ambulance response with patient transport. In fact, its success is often measured by the number of patients not transported to the ED. Models vary from those providing an alternative patient care pathway for well-defined predictable conditions to those collaborating in a multidisciplinary team to provide out-of-hospital care to complex patients who have opted not to go to hospital. This area of work sees paramedics forming close working relationships with palliative care teams providing high-quality care without hospitalisation. At present, most ambulance services in Australia and New Zealand do not use this model as they feel it falls outside their area of responsibility, but the number of services embracing the model (at least in trial form) is increasing. The qualifications to operate as an ECP vary considerably between services although most require an ICP qualification. The scope of practice also varies widely. The acronym ECP has also been used to describe the emergency care practitioner. The phrase ‘practitioner ’ suggests this role in analogous to a ‘nurse practitioner ’. A few extended care paramedics are now undertaking Masters-level education in an interdisciplinary format with nurse practitioners at Flinders University in South Australia. The majority of extended care paramedics are educated in an extended care paramedic education model that is internally accredited by the relevant ambulance service.

First responder This term generally refers to first-aid trained personnel sent to emergency medical cases as part of a coordinated response. In some areas this includes fire crews trained in first aid, while in outlying areas it can include volunteer first-aiders registered with their local ambulance service. The term is also sometimes used to include first-aid–trained bystanders. There is no agreed-upon definition of the role or scope of practice for first responders, but it is generally limited to basic care of the unconscious patient (oropharyngeal airway, bag valve mask ventilation and CPR) and basic assessment of the conscious patient (conscious state, pulse and blood pressure), although in some areas it includes application of AEDs. Participants in volunteer first-responder programs are likely to have an interest in healthcare, and it is not unusual to find highly trained doctors and nurses operating in this field despite the limited clinical guidelines under which first-responder programs operate. Programs using community volunteers are becoming more common in rural and remote areas.

The future paramedic role Over the past 20 years, although paramedic practice has embraced significantly higher standards of education and practice to move far beyond the traditional role (Shaban et al., 2004), the underlying responsibilities of responding to health emergencies and providing transport to hospital have remained largely intact. However, this narrow definition of the paramedic role is unlikely to survive the next 20 years as the profession moves towards registration and into specialist postgraduate education. How the role actually changes will depend on responses to pressures both within the profession and externally.

Internal pressures Ambulance services are being forced to react to two dominant changes: increasing workloads (see Fig 2.4) and decreasing patient acuity (see Fig 2.5). In Australia, demand for services has increased by between 7% and 12.5% per year since the mid-1990s (Ambulance Victoria, 2011; DCS, 2011; Productivity Commission, 2009; CAA, 2008). This is similar to changes faced overseas: demand doubled in London between 1989 and 1999 (Peacock et al., 2005) and increased by 20% in Canada between 2003–2004 and 2008–2009 (BC Ambulance Service, 2009) and by 9% in New Zealand in 2010–2011 (CAA, 2011).

FIGURE 2.4 The Queensland Ambulance Service received 532,950 triple zero (000) calls in 2010–2011—that’s an average of 1460 calls per day. Source: Image supplied by St John Ambulance WA.

FIGURE 2.5 The media portrays paramedic work as a constant parade of acutely ill patients trapped in precarious situations requiring the crew to intervene immediately. However, most patients are suffering from a combination of chronic illnesses, which alone or in combination may be the cause of the current health emergency. To determine a safe treatment plan requires careful collection and sorting of symptoms, vital signs, medical history and the patient’s own description of their condition. Source: Image supplied by St John Ambulance WA. The increase in workload is placing pressure on the politically important performance measure of response times. Although there is no scientific data to support a specific target figure for response times, the public highly values reporting of the percentage of cases attended within the nominated target time and this is therefore a significant performance indicator for ambulance services (Ambulance Victoria, 2011; DCS, 2011). Increasing workloads invariably lead to longer response times unless more ambulances are introduced into service. This rise in demand is commonly attributed to the demands of an ageing population and escalating rates of diseases such as obesity and diabetes (Snooks et al., 1998; Zimmet et al., 2005). The proportion of Australians aged 65 years or older rose from just 4% in 1901 to 13.5% by 2010 and is estimated to reach 21% by 2041 (ABS, 2011). With a strong correlation between age and disability (88% of Australians aged 90 have a disability compared with 40% aged 65–69) this is certainly one factor in increasing workloads, but it is not the only

reason and one study found it contributed to only 25% of the increased workload (AIPC, 2007). The increasing workload is actually multifactorial, with decreasing out-of-hours access to GPs, well-publicised delays at emergency departments, public awareness campaigns into the dangers of stroke (Bray et al., 2011) and chest pain as well as changes to pricing for ambulance attendance all contributing to some degree (Lowthian et al., 2011a). Simultaneously, improvements in public health strategies, medications and motor vehicle safety have reduced the frequency of life-threatening emergencies that have traditionally been identified as core ambulance cases. For example, male death rates from all diseases of the circulatory system decreased from 1020 deaths per 100,000 in 1968 to 234 deaths per 100,000 in 2008, while standardised death rates from motor vehicle accidents fell from 14.8% in 2000 to 9.6% in 2009 (ABS, 2011). A proportion of these decreases are almost certainly attributable to improvements in the pre-hospital care provided by paramedics: for example, the survival rate for out-of-hospital cardiac arrest has improved from 15% to 23% in the past five years in Queensland and is currently 26.3% in Victoria. Clearly, the improvements in some areas of public health are shifting the bulk of paramedic cases from acute to chronic care (Lowthian et al., 2011b). This is further reflected in the evolution of dispatch codes used by some modern ambulance services. Whereas every call for an ambulance was once considered to be an emergency, most ambulance services now recognise that even using a highly risk-adverse triage tool, up to one-third of those who call for an ambulance can be immediately classified as not needing one so urgently that lights and sirens are used in the response (see Fig 2.6). In 2010–2011, the Queensland Ambulance Service responded to 559,461 incidents that were considered to need a lights-and-sirens response and 236,240 cases that were considered to be nonurgent (DCS, 2011). In 2012–2013, Ambulance Victoria received 531,304 emergency calls but classified only 312,021 as requiring a lights-and-sirens response (Ambulance Victoria, 2013). In reality, fewer than 10% of patients are suffering the life-threatening medical events for which the ambulance is so strongly identified (NHS, 2006).

FIGURE 2.6 Research now acknowledges that many patients who receive a fully-equipped, double-crewed ambulance response do not need one. Source: AAP Image/NEWZULU/BJ STROUD.

External pressures The wider public healthcare system is facing demographic and financial challenges. Designed for a past generation, the system is a complex and fragmented collection of services and sectors that lie across multiple layers of government and too often fail to integrate and coordinate effectively (Battersly, 2005; Bray et al., 2011; NHHRC, 2009). Similar to the ambulance service, the system is effective for those suffering acute or emergency problems that can be resolved quickly, but it was not structured to meet the needs of people suffering multiple complex health and social problems (NHHRC, 2009). Unlike the ambulance system, however, the hospital system has passed saturation point and the lack of beds and staff is forcing changes beyond simply trying to increase hospital capacity. The most significant of these changes is the attempt to manage chronic illness in the community rather than in hospitals (NHHRC, 2009; NHS, 2001). This community-based reform is challenging ambulance services to integrate with the wider healthcare system and is changing the fundamental nature of some ambulance responses. This aspect of reform grew out of changes to the National Health Service (NHS) in England (NHS, 2001), which expanded the ambulance role from ‘Respond, treat and transport’ to ‘Respond, treat, leave or refer ’. The reform was driven by local studies, which found that only 10% of people who called for an emergency ambulance actually had a life-threatening

emergency (NHS, 2005) and that while 77% of emergency ambulance calls resulted in a patient journey, only 40% were admitted to hospital (NHS, 2001). This same study found that at least 50% of those transported to hospital could have been treated at the scene or in a community setting (NHS, 2001). These figures are supported by similar studies by the Wellington Free Ambulance service in New Zealand (CAA, 2011). As a result ambulance services in the UK were restructured to operate as mobile coordinators of out-of-hospital patient care. Responses were no longer always by a doublecrewed front-line ambulance and transport was not always to an ED. In addition to being able to treat and discharge patients at the scene, the extended care paramedics (ECPs) were allowed to refer patients to other primary care services such as GPs and local clinics. They were also able to prescribe a wider range of prescription drugs than paramedics had previously administered (NHS, 2001, 2006). The need for improved patient assessment and examination skills, and the ability to treat minor injuries and illnesses, were addressed by the creation of a new position and new training programs. If measured by reductions in ED admissions, the ECP program was certainly successful but it also added an enormous demand to ambulance services for which their staff, training and equipment were initially ill-suited (NHS, 2006). It also saw non-acute patients actively being directed towards ambulance services for the first time (NHS, 2006). The reduction in ED admissions captured the attention of the Australian and New Zealand governments, which were seeking to reduce stresses on the hospital system. New South Wales and South Australia have developed versions of the ECP concept in order to evaluate its effectiveness and safety, while St John in Horowhenua and the Wellington Free Ambulance Service adopted similar models after effective trials. The Victorian and Queensland Ambulance Services are using a modified version of the call-taking process to refer patients identified as low-acuity to other services without dispatching an ambulance at all. In 2010–2011 Queensland’s Secondary Triage and Referral (STAR) system prevented, on average, 46 ambulance transports per week in the Brisbane region (a 53% improvement compared to 2009–2010 when the system was implemented), while the Victorian Triage Referral Service has reduced ambulance dispatches by 12,000, or 8% (Ambulance Victoria, 2011; DCS, 2011).

FIGURE 2.7 The Wellington Free Ambulance has introduced a new concept to provide early intervention for alcohol-related injuries among the city’s late-night revellers. This involves providing a triage service located within the hotel and nightclub district (CAA, 2011). Source: 111 Emergency, CC BY 2.0.

Alternative paramedic roles In Australia and New Zealand the lack of a national standard for training and a scope of practice has largely limited the ability of other industries to engage in the skill set offered by paramedics. The eventual national registration of paramedics should resolve such regulatory barriers and in the future paramedics are likely to find roles outside of the ambulance service. The emphasis that paramedic training and experience places on trauma and acute illness will make paramedics ideally suited to many of these roles. However, the need to assess and manage chronic conditions, as well as to engage with other health providers, will require additional education to augment the current

paramedic skill set (the current Paramedics Australasia role descriptors are presented in Appendix 1). Future roles could include the following.

Industrial paramedic A number of companies in the mining sector already employ paramedics on worksites, ships and offshore drilling platforms. This rapidly growing sector lacks consistent regulatory guidelines regarding what services it must provide and what skill sets and qualification are required.

Community paramedic The awkward nature of this term probably underlines how poorly the currently perceived paramedic role fits into the mostly non-acute model. The role of community paramedic is not well described but is generally targeted at remote and rural communities that cannot attract a higher level of permanent medical care. The role includes primary assessment of acute and chronic conditions, and ongoing management where possible or referral to higher levels of care where required. In reality, the close-knit nature of many rural communities means paramedics already perform these roles (albeit in an unregulated environment), as well as assisting staff at local hospitals in times of need (Mulholland et al., 2009). Some also see the role as including public education activities such as antenatal, rehabilitation and fitness classes. Once again, additional modules will need to be incorporated into training to ensure paramedics can meet expectations.

Humanitarian aid/disaster paramedic The use of paramedics in responses to humanitarian disasters is increasing despite the lack of a regulatory framework. This probably reflects the usefulness of the paramedic skill set, but since some of the required knowledge and skills lies outside the traditional paramedic role, additional training in areas such as wound care, infection control and public health will be required if paramedics are to operate effectively in this role.

Physician assistant Traditional professional roles are strongly guarded in medicine and, despite the success of the role of physician assistant (PA) in other countries, Australia has struggled to introduce this role. Usually aimed at experienced nurses, this qualification is designed to free doctors from minor and straightforward cases by allowing PAs to conduct patient assessments, prescribe some medications, order tests and conduct minor procedures such as suturing. The highly integrated nature of the position in existing healthcare practices does not make the role an obvious extension of paramedic practice, but if the ECP role becomes established with sufficient training, paramedics could foreseeably progress to PA with additional postgraduate education.

Summary The history of paramedic care has impacted strongly on the way governments are developing paramedic resources. The inherent link between emergency response and transport has also shaped the public’s expectations of paramedic services. In addition, the way ambulance services have operated in the past has defined what paramedics expect their role to be in the future. The national health reforms currently underway (see later chapters) are integrating ambulance services into the healthcare system in ways that were not perceived as little as a decade ago. The ‘Respond, treat, leave or refer ’ reforms pose questions about not only training and equipment but also professional practice boundaries, accreditation and how paramedics interact with other health professionals. None of these issues is insurmountable and whatever form the future paramedic role may take, it is almost certain that the need to make safe clinical decisions through effective reasoning is likely to increase as paramedics are faced with more complex patient problems and multiple treatment pathways.

References Australian Bureau of Statistics (ABS) 1220.0. Australian Standard Classification of

Occupations (ASCO). 2nd ed., Canberra: ABS; 1997. Retrieved from www.abs.gov.au/AUSSTATS/[email protected]/66f306f503e529a5ca25697e0017661f/4264B4F35FB85031C

Australian Bureau of Statistics (ABS) Life Expectancy Trends—Australia. Commonwealth of Australia, Canberra, 2011. Retrieved from www.ausstats.abs.gov.au/ausstats/subscriber.nsf/LookupAttach/4102.0Publication23.03.112/$F

Australian Commission on Safety and Quality in Health Care (ACSQHC) National Patient Safety Education Framework. ACSQHC, Canberra, 2005. Retrieved from www.health.gov.au/internet/safety/publishing.nsf/Content/C06811AD746228E9CA2571C600 Australian Institute for Primary Care (AIPC)Factors in Ambulance Demand: Options for Funding and Forecasting (Council of Ambulance Authorities Inc., trans.). Melbourne: LaTrobe University, Australian Institute for Primary Care, 2007. Ambulance VictoriaAnnual Report, 2010–2011. Melbourne: Ambulance Victoria, 2011. Ambulance VictoriaAnnual Report, 2012–2013. Melbourne: Ambulance Victoria, 2013. Battersly, M. W., Health reform through coordinated care: SA HealthPlus. British Medical Journal. 2005;(330):662–666. British Columbia Ambulance Service (BC Ambulance Service)Annual Report. British Columbia Ministry of Health Services, 2009. Boyd, D. R., Cowley, R. A. Comprehensive regional trauma/emergency medical services (EMS) delivery systems: the United States experience. World Journal of Surgery. 1983; 7(1):149–157. Boyle, M. J., Williams, B., Cooper, J., Adams, B., Alford, K. Ambulance clinical placements: a pilot study of students’ experience. BMC Medical Education. 8(19), 2008. Bray, J., Mosley, I., Barger, B., Bladin, C. Stroke public awareness campaigns have increased ambulance dispatches for stroke in Melbourne, Australia. Stroke. 2011; 42(11):2154–2157. Burgess, S., Boyle, M., Chilton, M., Ellis, B., Fallows, B., Lord, B., et alMonash University

Centre for Ambulance and Paramedic Studies (MUCAPS), Submission to the Department of Human Services, in response to the DHS Discussion Paper examining the regulation of the Health Professions in Victoria. Journal of Emergency Primary Health Care. 2003;1(3–4) Croskerry, P., Wears, R. L. Safety errors in emergency medicine. In: Markovchick V.J., Pons P.T., eds. Emergency Medicine Secrets. 3rd ed. Philadelphia, PA: Hanley & Belfus; 2002:29–37. Cruess, S. R., Johnston, S., Cruess, R. L. Professionalism for medicine: opportunities and obligations. Medical Journal of Australia. 2002; 177(4):208–211. Department of Community Safety (DCS)Annual Report, 2010–2011. Brisbane: Queensland Government, 2011. Dick, W. F. Anglo-American vs. Franco-German emergency medical services system. Prehospital Disaster Medicine. 2003; 18(1):29–35. Eisenberg, M. S., Bergner, L., Hallstrom, A. Cardiac resuscitation in the community. Importance of rapid provision and implications for program planning. JAMA. 1979; 4(241):1905–1907. Geary, U., Kennedy, U. Clinical decision-making in emergency medicine. Emergencias. 22, 2010. Grantham, H. Prehospital care as a profession—are we there yet? Journal of Emergency Primary Health Care. 2(2–1), 2004. Hoben, K., Varley, R., Cox, R. Clinical reasoning skills of speech and language therapy students. International Journal of Language, Communication and Communication Disorders. 2007; 42(S1):123–135. Howie-Willis, I. The Australian ambulance system: a historical perspective. In: O’Meara P., Grbich C., eds. Paramedics in Australia: Contemporary Challenges of Practice. Frenchs Forest: Pearson Education Australia, 2009. Lowthian, J. A., Cameron, P. A., Stoelwinder, J. U., Curtis, A. J., Currell, A., Cooke, M., McNeil, J. J. Increasing utilisation of emergency ambulances. Australian Health Review. 2011; 35:63–69. Lowthian, J., Jolley, D., Curtis, A., Currell, A., Cameron, P., Stoelwinder, J., McNeil, J. The

challenges of population ageing: accelerating demand for emergency ambulance services by older patients, 1995–2015. Medical Journal of Australia. 194(11), 2011. Mulholland, P., O’Meara, P., Walker, J., Stirling, C., Tourle, V. Multidisciplinary practice in action: the rural paramedic—it’s not only lights and sirens. Journal of Emergency Primary Health Care. 7(2), 2009. National Health and Hospitals Reform Commission (NHHRC)National Health and Hospitals Reform Commission Report. Canberra: NHHRC, 2009. National Health Service (NHS)Reforming Emergency Care. London: Department of Health, 2001. National Health Service (NHS)Taking Healthcare to the Patient: Transforming NHS Ambulance Services. London: Department of Health, 2005. National Health Service (NHS)NHS Ambulance Services … More Than Just Patient Transport. London: NHS Confederation, 2006. Nolan, J., Soar, J., Eikeland, H. The chain of survival. Resuscitation. 2006; 71:270–271. Pantridge, J. F., Geddes, J. S. A mobile intensive-care unit in the management of myocardial infarction. The Lancet. 1967; 2:271–273. Patel, V. L., Groen, G. J. Knowledge-based solution strategies in medical reasoning. Cognitive Science. 1986; 10:91–116. Peacock, P. J., Peacock, J. L., Victor, C. R., Chazot, C. Changes in the emergency workload of the London Ambulance Service between 1989 and 1999. Journal of Emergency Medicine. 2005; 22(1):56–59. Productivity CommissionSteering Committee for the Review of Government Service Provision. Report on Government Services, 2009. Canberra: Australian Government, 2009. Rikers, R. M., Loyens, S. M., Schmidt, H. G. The role of encapsulated knowledge in clinical case representations of medical students and family doctors. Medical Education. 2004; 38:1035–1043. Rothstein, M. A. Rethinking the meaning of public health. The Journal of Law, Medicine and

Ethics. 2002; 30(2):144–149. Shaban, R., Wyatt-Smith, C. M., Cuming, J. J. Uncertainty, error and risk in human clinical judgment: introductory theoretical frameworks in paramedic practice. Journal of Emergency Primary Health Care. 2(1), 2004. Sheather, R. Professionalism. In: O’Meara P., Grbich C., eds. Paramedics in Australia: Contemporary challenges of practice. Frenchs Forest: Pearson Education Australia, 2009. Shields, A., Flin, R. Paramedics’ non-technical skills: a literature review. Journal of Emergency Medicine. 30, 2012. Snooks, H., Wrigley, H., George, S., Thomas, E., Smith, H., Glasper, A. Appropriateness of use of emergency ambulances. Journal of Accident and Emergency Medicine. 1998; 15:212–218. The Council of Ambulance Authorities (CAA)Annual Report, 2007–2008. Melbourne: CAA, 2008. The Council of Ambulance Authorities (CAA) Annual Report, 2010–2011. CAA, Melbourne, 2011. Retrieved March 2012 from http://caa.net.au/images/stories/caa%20annual%20report.pdf Williams, B. Do undergraduate paramedic students embrace case-based learning using a blended teaching approach? A 3-year review. Australasian Journal of Educational Technology. 25(3), 2009. Williams, B., Onsman, A., Brown, T. Professionalism. Is the Australian paramedic discipline a full profession? Journal of Emergency Primary Health Care. 8(1), 2010. World Health Organization (WHO)Report on the Global Tobacco Epidemic. Geneva: WHO, 2009. Wyatt, A. Toward professionalism—an analysis of ambulance practice. Australasian Journal of Emergency Care. 1998; 5(1):16–20. Wyatt, A. Paramedic practice—knowledge invested in action. Journal of Emergency Primary Health Care. 1(3–4), 2003. Zimmet, P., Magliano, D., Matsuzawa, Y., Alberti, G., Shaw, J. The metabolic syndrome: a

global public health problem and new definition. Journal of Atherosclerosis and Thrombosis. 12(6), 2005.

CHAP TER 3

Characteristics of ambulance patients By Stephen Burgess and Amee Morgans

O V E RV IE W • Knowing who your patients are and understanding how and why they come to be in your care will provide you with an understanding of why they present their illness and what they expect you to do about it. • Calls for ambulance attendance have grown steadily in recent decades but a significant number of patients who need emergency medical care still choose not to use ambulance services. • The reasons for calling an ambulance and the expectations of what will occur when an ambulance arrives are complex and are not always related to physiological emergencies. • ‘Inappropriate use’ of ambulances is probably not as significant as perceived by paramedics and may reflect a lack of understanding of the processes patients use in selecting support in health emergencies. • Understanding the characteristics of patients who choose to engage ambulance services can be a key step in assessing and managing patients. • Understanding the characteristics and intent of the call-taking systems that dispatch ambulance services can also be an important step in assessing, diagnosing and managing patients, and in reducing stress on paramedics. • Having an awareness of what patients experience before and after the ambulance service was called, and appreciating their expectations of what the paramedic will do, is essential in gaining an accurate history and clinical picture.

Introduction Chapter 6 introduces a model of clinical communication that links the patient’s clinical outcomes not just to the paramedic’s clinical knowledge, but also to the paramedic’s ability to communicate effectively. For this communication model to operate successfully, the paramedic needs to use the patient’s expectations and desired outcomes as a tool to gain important clinical information and develop a treatment plan in which the patient is willing to engage. This extends to treatment plans that do not align with what the patient initially perceives will be the outcome: for example, being referred to their GP as opposed to being transported to hospital. The episode of care model introduced in Chapter 1 identifies that the factors that trigger someone to call for an ambulance may occur long before the case is generated or the paramedics arrive. Failing to recognise these events can obscure information that could be used to help reach a clinical decision. Gaining an insight into a patient’s expectations is not easy. The crucial first step, and one that is often overlooked by novice paramedics, involves understanding what leads people to call an ambulance. Simply recognising this process often shows the distance between the paramedic’s expectations of the encounter and the patient’s: many paramedics are frustrated by patients whose condition they perceive to be far from a medical emergency. In this chapter we examine three main areas of patient communication in paramedic practice: • Who are ambulance patients? Who calls an ambulance? Why do they call? What about those who don’t call an ambulance, but should? • From symptom onset to the decision to call for an ambulance. How do patients recognise a health emergency and how do they decide what to do about it? • From calling for an ambulance to the time the ambulance arrives. How do patients interact with the ambulance service? What events can occur between when paramedics are dispatched to a case and when they arrive? How much of the information the patient has provided to the call-taker does the patient think the crew have heard? What won’t they say again because they have already told that part of the story?

Who are ambulance patients? Am bul a nce ca se l oa ds As noted in earlier chapters, there has been a strong and steady growth in demand for ambulance services in Australia and New Zealand in recent years, and services are struggling to cope with annual increases in caseloads of up to nearly 10% (St John NZ, 2011; The Council of Ambulance Authorities, 2010). Yet there are a great many people who could (or should) call for an ambulance but don’t and instead make their own way to an emergency department (ED). The possible outcomes for patients deciding whether to use an ambulance service are shown in Table 3.1. For these outcomes, the patients’ presenting problems were diverse in both cause and severity (Morgans & Burgess, 2011). Table 3.2 shows that of the more than 5.9 million people who presented to an ED in Australia in 2010, only 1.4 million arrived via ambulance, which means that more than 4.5 million made their way by some other means (AIHW, 2010). Of the cases who arrived by ambulance, 2.5% required resuscitation (immediate treatment), 18.4% were emergencies (treatment within 10 minutes), 46.8% were urgent (treatment within 30 minutes), 29.9% were semi-urgent (treatment within 60 minutes) and 2.3% were non-urgent (treatment within 120 minutes). For the patients who did not use the ambulance service, 0.13% required resuscitation, 6.2% were emergencies, 27.8% were urgent, 49.8% were semi-urgent and 15.8% were non-urgent (AIHW, 2010; see Table 3.3). These tables reveal a fascinating story about who uses ambulance services and how sick they are. Less than half (47.5%) of emergency cases arrived by ambulance; only one-third (34%) of urgent cases arrived by ambulance; and just 15.5% of semi-urgent cases arrived by ambulance; while only a small proportion (4.2%) of non-urgent cases arrived by ambulance. TABLE 3.1 Possible outcomes for patients deciding whether or not to use an ambulance service

Used ambulance Didn’t use ambulance

Patient requires medical care and Patient doesn’t require medical care transport to hospital or transport to hospital True emergency patient ‘Inappropriate’ ambulance service user Delay/failure to use when appropriate

Source: Morgans & Burgess (2011).

Non-urgent patient

TABLE 3.2 Non-admitted ED presentations, by triage level and arrival mode, selected hospitals, 2009–2010

Source: Australian Hospital Statistics 2009-2010, Australian Institute of Health and Welfare. Released under a Creative Commons License (CC-BY 3.0 AU).

TABLE 3.3 Triage level and arrival mode selected hospitals, 2009-2010

Source: Australian Hospital Statistics 2009-2010, Australian Institute of Health and Welfare. Released under a Creative Commons License (CC-BY 3.0 AU).

‘Inappropriate’ patients There is a small body of published data on ‘inappropriate’ or non-emergency attendees at hospital EDs; however, the definitions of ‘health emergency’ and ‘inappropriate attendance’ are a matter of debate. A recent Australian study asked randomly selected ED patients to self-rate the level of urgency of their presentation to hospital. Patients typically thought that their life was either under threat or would soon be at risk. When this was compared to their actual level of urgency as assessed at triage, there was no agreement between the two. In other words, what the patients thought was an emergency and what the hospital staff thought was an emergency were completely different (Morgans & Burgess, 2011). This is most probably because patients and health professionals place importance on completely different aspects when deciding on the urgency of a problem. To the health professional, a health

emergency is based on physiological values or metrics that suggest a threat to life (e.g. pulse rate, blood pressure, respiratory rate, level of consciousness). But the layperson is either unaware of these values or unable to interpret their severity and is forced to rely on how he or she feels about the situation to determine its urgency (Morgans & Burgess, 2011). One way to assess people’s perceptions of what constitutes an emergency is to assess what situations prompt them to seek help. One large study showed that most ED attendance was for fever, chest pain or abdominal pain, perhaps indicating that patients perceive these conditions as emergencies (MacLean et al., 1999). Results from another study showed that people identified loss of consciousness, seizure, lack of recognition of one side of the body, paralysis, shock, gangrene, coughing blood, trouble breathing, chest pain and choking as emergencies. Pain—other than renal, colic or chest pain—was not considered an emergency. No symptoms or signs specifically related to gynaecological disorders were considered as emergencies (Li, Galvin & Johnson, 2002).

Psychosocial factors Another study has revealed that patients report making decisions based on the level of discomfort or pain they feel and on the advice of fellow laypeople, such as family and friends (Morgans, Archer & Allen, 2008). The patients in this study classified symptoms as an emergency not based on physiological criteria, but rather on when they were beyond the capabilities of the patient to control and manage. Patients did not recognise medically significant symptoms as prompting them to seek emergency help, instead focusing on the nature of the presenting symptoms. Symptom onset that was sudden and severe was interpreted as urgent, whereas slow onset or mild and intermittent symptoms were interpreted as less urgent. This tendency to focus on rapid development rather than medically significant symptoms is a key difference between the medical and nonmedical categorisations of urgency. It may explain why patients report non-life-threatening symptoms as potentially serious and present ‘inappropriately’ with symptoms that are of little medical urgency, or alternatively neglect to seek prompt help for slow-onset or intermittent symptoms of a potentially serious nature, such as chest pain or shortness of breath (Morgans & Burgess, 2011).

Why do people avoid ambulances? Some people actively avoid seeking ambulance services. Table 3.4 shows the results of a survey of patients who attended EDs in Melbourne (Morgans, Archer & Allen, 2008). There are many reasons given for not calling an ambulance, but the most common may be classified as social or perceptual barriers: lack of knowledge (not sure if it was an emergency); ambulance is just for transport (could be driven by others); and embarrassment (didn’t want to make a fuss). To make things even more complex, a health emergency is difficult to define, as changes in health conditions are dynamic and may vary in urgency over time. Interestingly, most researchers agree that there are no demographic factors that directly predict patterns of health service use (Lowthian et al., 2011).

TABLE 3.4 Reasons patient did not call an ambulance Reason % of responses Unsure if it was an emergency 27.0 Could be driven to hospital by others 22.0 Did not want to cause a fuss 14.7 Too embarrassed to call an ambulance 7.0 Don’t want to go to hospital 7.0 Ambulance would take too long to arrive 4.5 Rather call local doctor 4.0 Costs: not an ambulance subscriber 4.0 Rather drive myself 3.0 Costs: not sure if covered 1.0 Source: Morgans, Archer & Allen (2008).

W HY P AT I E NT S CA L L What triggers a patient to call an ambulance varies widely across the population, but in almost every case it results from a sense of loss of control and an inability to manage a situation. To paramedics, the circumstances may appear trivial or far from a medical emergency, but that is not how the patient perceives the situation.

From symptom onset to the decision to call an ambulance The decisions made during a health crisis can directly affect a patient’s chances of survival. When a health condition unexpectedly becomes life-threatening, it is often up to the patient or a bystander to recognise a health emergency and decide to seek medical help. In these unexpected cases, such judgements usually lie in the hands of people with no medical training. Yet the ability to recognise life-threatening symptoms is a skill usually associated with health professionals.

Calling an ambulance due to chest pain The decisions made by people during health emergencies, and the important consequences that flow from them, was investigated in the 1970s when it was noted that almost 50% of patients delayed seeking medical help for an acute myocardial infarction (AMI) for up to 4 hours after the onset of symptoms (Feinleib & Davidson, 1972). Delay in seeking help for AMI is a significant problem as early treatment can greatly minimise permanent damage to the heart and prevent fatal arrhythmias. In response to the increased risk of death over time, the ‘chain of survival’ concept was developed and promoted in the 1980s (Newman, 1989; see Fig 2.1). At that time the chain of survival described the optimal treatment for an AMI and cardiac arrest as early access to emergency medical services (ambulance services). As the consequences of delaying treatment became more established, aspects of the hospital and ambulance systems were improved. This included faster in-hospital triage and improving health professionals’ knowledge of cardiac symptoms (Clawson & Martin, 1990; Clawson, Martin & Hauert, 1994); improvements in life-saving thrombolytic drugs and cardiac surgical interventions (e.g. angioplasty) (Cannon, Sayah & Walls, 1999); and making ED staff aware of the importance of early treatment for AMI and cardiac arrest (Valenzuela et al., 1997). Despite these initiatives, almost 20 years later it was found that patients suffering AMI were still delaying calling for help for 6 hours on average (Dracup, McKinley & Moser, 1997). So to improve patient outcomes the chain of survival process was reassessed and ‘early recognition and response’ was added as a new key first link (Newman, 1998; see Fig 3.1). It is clear that if patients do not recognise a health emergency and therefore fail to seek appropriate medical help promptly, the remaining links in the chain are weakened and patients will continue to have poorer health outcomes than if they had sought treatment earlier (Penny, 2001). An article on prehospital treatments for AMI, however, illuminated the lack of definitive research to improve patient recognition and response, and concluded: ‘most of the delay occurs before the patient contacts the ambulance service. However, no strategy has been identified that encourages patients to present earlier …’ (Leitch, 2003).

FIGURE 3.1 The revised chain of survival. Source: Adapted from Shutterstock/elenabsl.

Education is not enough Contrary to what we might expect, improved patient education about AMI and the importance of seeking early treatment does not reduce patient delay in seeking help (Dracup et al., 2009). The finding that education strategies are unable to reduce these delays has been supported by a Cochrane Collaboration review of the effectiveness of educational interventions (Grilli et al., 2000). Even more surprisingly, first-hand experience does not help either: patients with a history of AMI delay seeking medical help for longer in a subsequent AMI than previously (Pattenden et al., 2002). This suggests that AMI patients have not understood the medical urgency of their previous health emergency, or that their experience of the treatment or management was so off-putting they would risk death to avoid experiencing it again. More recent research shows that patients with chest pain continue to delay seeking help and avoid ambulance use (Ingarfield et al., 2005; Taylor et al., 2005). Although the chain of survival concept was developed for AMI and cardiac arrest, evidence suggests that the issue of delay in seeking help is not unique to AMI patients. Many patients with asthma similarly do not seek medical help until symptoms become lifethreatening (Kolbe et al., 1996; Lavoie et al., 2010). Even when patients with chronic asthma are taught to recognise important symptoms and how to act in a health emergency, they do not act appropriately in the event (Lavoie et al., 2010). It seems that patient delay in seeking help may be quite common across a range of acute medical conditions. This generates many questions about patients’ recognition and understanding of a health emergency and the actions they need to take at the time. So, why do patients delay seeking help in health emergencies? The research literature has consistently demonstrated that neither previous experience nor education changes patients’ behaviour. If patients’ decision-making processes involved simply weighing up the benefits of getting treatment versus the potential for death or disability without prompt medical care, patients would logically opt to seek treatment. Yet many do not. This suggests that predicting and explaining patient behaviour through a ‘rational action’ model in the setting of a health emergency is unhelpful. The observations about patient

behaviour suggest that in reality their decision-making process is not an empirical costbenefit analysis. Thus we need to try to understand what patients actually do and why they do it, so that when we respond we can communicate effectively and (hopefully) meet their needs in the best possible way.

What factors lead patients to call for ambulance care? A recent Australian study (Morgans, Archer & Allen, 2008) identified a combination of factors that distinguish those people who are more likely to call an ambulance for a health problem from those who use alternative methods of transport to hospital (see Table 3.5). Ambulance users are more likely to: possess a pension card; score higher on the ‘powerful others’ subscale of the health locus of control scale (indicating that they attribute a significant amount of control over their health to powerful others, such as health professionals); and use ‘maladaptive’ avoidance coping skills, particularly emotional discharge techniques like crying, to deal with the situation. This suggests that ambulance users are people who cope poorly when experiencing a health emergency. Rather than using thoughtful approaches to find a solution, they respond to their emotions related to the situation and defer responsibility to the available emergency healthcare resources. TABLE 3.5 W ho is qualified to decide when it is time to call an ambulance? A doctor? A paramedic? The hospital? The patient? Relatives, parents or friends? A bystander (e.g. police)?

A doctor calls an ambulance in 14.4% of cases A paramedic calls an ambulance in 0% of cases The hospital calls an ambulance in 0% of cases The patient calls an ambulance in 19.8% of cases Relatives or friends call an ambulance in 50.4% of cases Bystanders (e.g. police) call an ambulance in 15.4% of cases

Source: Morgans, Archer & Allen (2008). We ought not to be surprised that users of ambulance services are more likely to have a pension card. People who are poorer or socioeconomically disadvantaged in other ways generally live shorter lives and suffer more illness and reduced quality of life than those who are well-off (AIHW, 2006). Also, someone holding a pension card is more likely to be older and as we age we experience more health problems, so it stands to reason that, as a group, pensioners of all types (age, disability, veteran, etc) will have greater health needs and so will be more likely to need emergency healthcare. Conversely, the same study found that people who use alternative means of transport to hospital are more likely to combine the coping styles of cognitive avoidance and positive reappraisal. This means that they actively avoid thinking about the current situation and its potential implications (like death or disability) and instead frame the situation in a more positive manner, expressing the view that the situation could be worse. The interesting

thing about this group is that while they actively cope with their health emergency by selfmedicating, seeking alternatives to ambulance care and contacting family and friends for advice and support, they actually waited a dangerously long time to arrive at a source of healthcare and in some cases had poorer outcomes as a result. So a ‘poorer ’ coping style of crying, or panicking and calling an ambulance would have been more beneficial for some patients than trying to deal with the situation by relying on their own resources.

Patient decision-making processes in health emergencies The process to call (or not to call) an ambulance during a health emergency involves a series of decisions. Understanding this process is essential in developing effective approaches (including education campaigns) to improve patients’ decision-making strategies, outcomes and subsequent health behaviours. One study that investigated people who arrived at EDs found a number of areas where decision making can fail (Morgans, Archer & Allen, 2008). The study included: a survey of patients, some of whom used ambulances and some of whom didn’t; interviews with volunteers who had experienced a health emergency in the previous 12 months; and discussions with groups of health professionals, including ED staff, GPs and paramedics, around wider health system experiences with patient patterns of seeking healthcare. The process of deciding to call an ambulance can be described as four discrete steps.

Step 1: Recognise that things are not normal Recognising that their health is far from normal proves rather difficult for some patients and the study by Morgans and colleagues (2008) found that patients use the following strategies to determine whether they have something to be worried about: • Compare current health situation to ‘normal’ status. • Identify symptoms. • Identification of symptoms is harder for people with chronic illnesses such as angina and asthma as these patients experience frequent exacerbation of symptoms. • Mild symptoms are perceived as less serious. • Intermittent symptoms can be confusing for patients. • Identification of important symptoms depends on layperson knowledge of important symptoms, which varies greatly among patients and illnesses. • Identify any pain. Experiencing pain or discomfort tells a patient that things are not normal. Some patients may self-medicate, which can impact on the symptoms. • Identify any traumatic mechanism of injury (e.g. fall, accident). Once patients have decided that they are experiencing something abnormal, they have to decide whether or not to do something about it.

Step 2: Identify the situation as an urgent health issue Defining an event as an emergency was difficult for most study participants and often involved consultation with another layperson for advice and reassurance. An emergency was deemed to have occurred when patients felt that the situation was beyond their

ability to control and manage. The outcome of this stage thus depends mostly on coping style and is affected by whether the illness is acute, chronic or acute on chronic. Key factors that impact on whether patients classify their symptoms as urgent include the following: • Sudden-onset symptoms are deemed as more urgent than those of gradual onset. • If there is a traumatic mechanism of injury, the situation is quickly identified as urgent, even when the injury is minor. • In chronic illnesses such as chest pain, abdominal pain, diabetes, asthma and COPD symptoms can fluctuate and patients find it harder to evaluate the urgency of their symptoms. 〉 Patient quote: ‘I get chest pain most days, some days are worse than others. At what point do I call an ambulance? When I can’t handle it anymore.’ (Morgans, Archer & Allen, 2008) As noted earlier, patient perceptions of urgency have absolutely no correlation with inhospital measures of medical urgency (Morgans & Burgess, 2011). Patients in the study did not generally consider medical issues when defining a health event as an emergency, instead focusing on social, personal and psychological responses to illness. When seeking healthcare for a perceived emergency condition, patients reported a belief that they were seriously unwell, required emergency medical care and expected to be admitted to hospital for medical assessment and treatment. Once patients have determined that a situation is urgent, they have to decide what to do about it.

Step 3: Decide to get help One in five people from the study contacted an ambulance as soon as they identified an event as an emergency—meaning that four out of five called someone else first. In fact, contacting a layperson (family and/or friends) was usually the first action taken by patients, followed by consideration of the healthcare services available at the time and seeking permission to use those services. Contrary to the beliefs of paramedics and hospital-based health professionals, seeking a source of medical healthcare was usually achieved only after arduous personal and social considerations by the patient. This was also the stage where patients expressed the most confusion and difficulty making decisions. The types of actions taken by patients in the study once they had decided to seek help included: • calling a friend or relative: 55% of callers to ambulance services had called a friend or relative first to seek health advice and ‘permission’ to use emergency health resources • self-medicating to try to relieve the symptoms: this included taking pain relief such as paracetamol or ibuprofen, anginine/GTN spray for chest pain or salbutamol for asthma. Self-medicating was particularly common in acute-on-chronic illnesses, including cardiac and respiratory problems, and significantly contributed to the delay in seeking ambulance care • seeking permission to use emergency health resources: in an Australian study, 40% of patients with chest pain tried to contact their GP before attending the ED (Ingarfield et al., 2005). Once patients have decided to seek healthcare, they need to decide whether to call an ambulance, present to an ED or attend their GP.

Step 4: Decide w here to get emergency medical help Health professionals in the study emphasised a variety of factors that they thought influenced patients’ decisions regarding which health service to approach and when. They believed that patients accessed the ED because a sense of urgency compelled them to bypass their GP. However, the data showed that almost 10% of ambulances were actually called by patients’ GPs, and some patients reported that their GP had advised them to go to the ED. According to the study: • in 21% of cases the ambulance service was the patient/carer ’s first point of contact • in only 20% of cases did patients themselves call the ambulance—in the vast majority of cases relatives called the ambulance service (indicating the important role of family and friends in such situations) • patients reported waiting a long period of time with acute pain, shortness of breath or discomfort in the hope that they would regain control over their symptoms and avoid a hospital stay—the reasons given for avoiding a hospital stay included a loss of personal autonomy, fear of long-term admission, discomfort and convenience factors • some patients indicated that they did not use an ambulance service as they considered it to be a means of transport only and therefore equated it with being driven by others • the time of the day, the day of the week, access to a GP and the availability of alternative sources of help affected patients’ decisions to attend ED or use an ambulance • some patients see their GP regularly, whereas others seek care only when they are experiencing an acute health crisis • the influence of previous health experiences such as being sent home from ED previously without being admitted as an inpatient leads patients to believe that the outcome will be the same this time and therefore the situation isn’t really urgent • insurance/subscription status affected 2% of cases, so in the Australian context cost was not a barrier to seeking healthcare • the average time from symptom onset to contacting the ambulance service was 4.6 hours. The reality is that patient decision making in prehospital health emergencies is a layperson’s decision-making process. It is affected by psychosocial factors rather than demographic or medical factors. Patients who seek emergency healthcare generally believe that what they are experiencing is a genuine emergency and that they are seeking the most appropriate source of care—which directly relates to their perception of the roles and responsibilities of the providers of emergency healthcare services. In the study by Morgans and colleagues (2008), patients and their carers reported that they found the emergency health experience frightening and worried about the experience and its outcomes for a long time after the event. Such fears were also evident in the proportion of people who tried to avoid hospital attendance because they dreaded a forced hospital stay. This helps to explain why it took patients on average 4.6 hours to identify their symptoms, define them as an emergency, seek help and advice, and then make the decision to pick up the phone to call the ambulance service.

From calling for an ambulance to ambulance arrival It is important to remember that patients are involved with the ambulance service as soon as they dial the emergency number, and that many (often complex) things happen in the time between calling for help and the arrival of paramedics. This component of the patient’s healthcare journey is often ignored and its importance overlooked. However, during this time the patient is part of the emergency health system and will receive help such as triage of case urgency, resource allocation and clinical skills dispatch, pre-arrival instructions, and advice and reassurance. This will have an influence on the patient, whether they (or the attending paramedics) know it or not. To gain a better insight into a patient’s state and to best meet their needs, it is important that you are aware of these influences.

The process of calling an ambulance in Australia and New Zealand Once a person calls 000 in Australia or 111 in New Zealand, their call is answered by an operator who will ask which service they require—police, fire or ambulance—and their address. The operator then connects the call to the appropriate service in the relevant state or region. There are slight variations with regard to the call-taking process, but in most centres now the use of trained paramedics as call-takers has largely been replaced by teams of non-paramedics supported by a paramedic clinician. Victoria, Queensland, New South Wales, South Australia, Western Australia and Tasmania use a computer-aided dispatch system known as the Medical Priority Dispatch System (MPDS), which automatically prompts the questions to be asked. All cases begin as follows: • Where is your emergency? [Confirmation of address and cross-streets or landmark] • What is the problem? Tell me exactly what has happened. • Is the patient conscious? • Is the patient breathing? If it is determined that the patient is conscious and breathing, a structured process of medical classification and triage begins. If the patient is not breathing and is not conscious, they are presumed to be in cardiac arrest and an emergency ambulance response is sent immediately.

Medical triage Medical triage of ambulance calls is generally governed by a structured process such as MPDS and involves identifying the primary problem and determining its severity. The triage depends on what the caller reports to the call-taker. The aim is to determine what resources the patient needs and the level of clinical urgency compared to other patients. For example, if there are two cases and one ambulance, triage is used to determine which case the ambulance is sent to first. Automated triage systems like MPDS are designed to ensure a consistent level of resource allocation and efficient prioritising of large numbers of

patients simultaneously. Once the primary symptom has been identified, the call-taker can provide pre-arrival instructions to help the caller or the patient before the ambulance arrives. Instructions are commonly given for the following: • childbirth • CPR • control of bleeding • airway management • scene safety. The role of call-takers and ambulance dispatchers is vital: they are responsible for obtaining key information about the patient’s condition and allocating the appropriate resources to the patient. Many patients at this time are distressed and still evaluating their changing symptoms. Similarly, many patients call an ambulance because they have reached the point where a long-term illness or situation has become beyond their control and they may therefore be emotional and exhausted. This provides a challenging environment for call-takers and patients alike. Cases 1 and 2 are examples of transcripts of ambulance calls and illustrate the call-taking process.

Summary If you look back to Figure 3.1, you can see that ‘early recognition and response’ is the first link and therefore the key to the rest of the chain of survival. Even with excellent clinical management and highly-skilled paramedics, if a patient delays calling an ambulance or avoids using an ambulance, they can have a much poorer health outcome. It can also be difficult for patients to evaluate their symptoms and make a decision about what to do in a health emergency. For all the cases that you attend as a paramedic, there will always be a proportion of cases that are not emergencies, but could have been. It is important to consider the situation from the patient and carer ’s perspective, even when at your most frustrated. There are many misconceptions about what patients do or not do and why they behave the way they do in a health crisis. Even experienced health professionals may not understand the situation. In some ways this is not surprising: in many situations we assume that others think just like we do, so we may be surprised, even exasperated, when they act in ways that we do not expect. The key is to remember that patients do not make judgements about their symptoms from a position of specialised medical knowledge. Most patients who seek the help of paramedics do so on the basis of how they feel about their situation and genuinely believe they are experiencing a health emergency. We cannot expect patients to make a decision to seek help in the same way that a health professional would.

Case 1 John, a 39-year-old man, develops some chest pain while driving a forklift at a large manufacturing company. He goes to the first-aid room and the receptionist in administration decides to call an ambulance when the chest pain gets worse. Emergency ‘Police, fire, or ambulance: which service do you require?’ operator: Receptionist: ‘Hello? We need an ambulance, he’s got chest pain.’ Emergency ‘Which state or territory are you in?’ operator: Receptionist: ‘What? I’m in Deer Park and I need an ambulance please.’ Emergency ‘Is that Deer Park, Victoria?’ operator: Receptionist: Yes. YES! Victoria! That’s what I said!’ Ambulance ‘Ambulance. Where is your emergency? call-taker: Receptionist: ‘I already told them this. We need an ambulance please; there is a man here with chest pain.’ Ambulance ‘What address do you want the ambulance to come to?’ call-taker: Receptionist: ‘Plasticmakers Manufacturing, 59 Jones Street, Deer Park.’ Ambulance ‘Plasticmakers Manufacturing, 59 Jones Street, Deer Park. Is that

call-taker: near the intersection of Westall Road? Receptionist: ‘Yes, entrance B is just off Westall Road. Tell them to come in through entrance B … and hurry, I think he is getting worse, he looks terrible.’ Ambulance ‘What is the problem? Tell me exactly what has happened.’ call-taker: Receptionist: ‘He’s been here in the office, he has chest pain and he needs an ambulance.’ Ambulance ‘How old is he?’ call-taker: Receptionist: ‘About 35, I think.’ Ambulance ‘Is he conscious?’ call-taker: Receptionist: ‘Yes.’ Ambulance ‘Is he breathing?’ call-taker: Receptionist: ‘Yes, but he’s sort of gasping now, he’s really struggling. Are they on their way?’ Ambulance ‘Is he completely awake and able to talk?’ call-taker: Receptionist: ‘Yes, he’s struggling to talk, but he’s awake.’ Ambulance ‘And you said he wasn’t breathing normally, is that right?’ call-taker: Receptionist: ‘Yes, he’s breathing hard.’ Ambulance ‘I have an ambulance organised for you coming to Plasticmakers call-taker: Manufacturing, 59 Jones Street, Deer Park, entrance B off Westall Road. I have a couple more quick questions to help the ambulance, OK?’ Receptionist: ‘OK.’ Ambulance ‘OK. Is he changing in colour?’ call-taker: Receptionist: ‘Well, he looks pale, almost a bit grey, and he’s sweaty.’ Ambulance ‘Does he have any history of heart problems?’ call-taker: Receptionist: ‘Have you got heart problems, John? … He said he hasn’t, no.’ Ambulance ‘Is he on any medications?’ call-taker Receptionist: ‘Are you on medication, John?… He says he is on blood pressure medication but he can’t remember what it’s called.’ Ambulance ‘OK, we have an ambulance organised; will someone be out the call-taker: front to direct the ambulance to the right place?’ Receptionist: ‘Yes, I can make them do that.’ Ambulance ‘That’s good. Now you need to keep a careful eye on John, make call-taker: sure he keeps breathing regularly and is awake and talking to you. If anything changes, you need to call me back immediately on 000. The ambulance is on its way to you now. OK?’ Receptionist: ‘OK, thanks.’

Case 2 Roger, a 53-year-old male cyclist, is hit by a car. Emergency operator: Vehicle driver: Ambulance call-taker: Vehicle driver.

‘Police, fire, or ambulance: which service do you require?’ ‘Ambulance, in Brisbane please.’ ‘Ambulance. Where is your emergency?’

“I’m on the freeway exit, there’s an old man … a man here; he’s come off his bike.’ Ambulance ‘What address are you at—which freeway?’ call-taker: Vehicle driver: ‘I haven’t killed him, he’s alive, but he’s pretty banged up. Are they far away? He’s bleeding …’ Ambulance ‘What address are you at—which freeway?’ call-taker: Vehicle driver: ‘I’m. driving to work. I’m on the Gateway Motorway—just past Logan Road.’ Ambulance ‘So you are on the Gateway Motorway, just past Logan Road? Are call-taker: you heading towards the Pacific Motorway?’ Vehicle driver: Yes, I think so.’ Ambulance ‘Can you see the bus station from where you are?’ call-taker: Vehicle driver: ‘Yes, I am near the bus station; he pulled out from the bus station, I didn’t see him in time, it just happened so fast…’ Ambulance ‘So you have hit a male cyclist with your car, is that right?’ call-taker: Vehicle driver: ‘Yes, that’s right.’ Ambulance ‘How old is he?’ call-taker: Vehicle driver: ‘About 60, I think.’ Ambulance ‘Is he conscious?’ call-taker: Vehicle driver: ‘Yes.’ Ambulance ‘Is he breathing?’ call-taker Vehicle driver: ‘Yes, he’s moaning, he’s sitting in the gutter … you alright, mate? I didn’t see you…’ Ambulance ‘Is he completely awake and able to talk?’ call-taker: Vehicle driver: ‘Yes, he’s giving me a bit of lip; he’s not happy.’ Ambulance ‘I have an ambulance organised for you coming to the Gateway call-taker: Motorway, at the bus station just past Logan Road.’ Vehicle driver: ‘OK.’

Ambulance call-taker: Vehicle driver: Ambulance call-taker: Vehicle driver: Ambulance call-taker: Vehicle driver: Ambulance call-taker: Vehicle driver:

‘Is he breathing normally?’ ‘Yes, he’s breathing fine.’ ‘And you said he’s sitting in the gutter—he’s not trapped by the vehicle or anything?’ ‘No, nothing like that. I just can’t believe it.’ ‘Are there any hazardous materials—petrol from the car or anything?’ ‘No, no.’ ‘Can you tell me about his injuries?’

‘Well, his helmet is in pieces, so I think he belted his head pretty hard; he’s got grazes on his leg and both his arms.’ Ambulance ‘OK, we have an ambulance organised.’ call-taker: Vehicle driver: ‘Actually it’s here—I can hear the siren, and the police are here too. Oh my God. What a mess.’ Ambulance ‘That’s good—can you see the ambulance?’ call-taker: Vehicle driver: ‘Yep, they’re just pulling up now.’ Ambulance ‘OK then, I’ll leave you in the care of the paramedics.’ call-taker: Vehicle driver: ‘OK, thanks.’

It is also worthwhile remembering that patients are not in a state of suspended animation once the call to the ambulance service has been made: the patient’s encounter with the ambulance service starts with the telephone call, not when the paramedics arrive on the scene. Many (often complex) things happen in the time between calling for help and the arrival of paramedics. Effective communication is unarguably a cornerstone of good clinical practice.

References Australian Institute of Health and Welfare (AIHW)Australian Hospital Statistics 2009– 2010. Canberra: AIHW, 2010. Cannon, C. P., Sayah, A. J., Walls, R. M. Prehospital thrombolysis: an idea whose time has come. Clinical Cardiology. 1999; 22:10–19. Clawson, J. J., Martin, R. L. Modern priority dispatch. Emergency. 1990; 22(1):32. Clawson, J. J., Martin, R. L., Hauert, S. A. Protocols vs. guidelines: choosing a medicaldispatch program. Emergency Medical Services. 1994; 23(10):52–60. Dracup, K., McKinley, S., Moser, D. K. Australian patients’ delay in response to heart attack symptoms. Medical Journal of Australia. 1997; 166:233–236. Dracup, K., McKinley, S., Riegel, B., Moser, D. K., Meischke, H., Doering, L. V., et al. A randomized clinical trial to reduce patient prehospital delay to treatment in acute coronary syndrome. Circulation Cardiovascular Quality & Outcomes. 2009; 2(6):524–532. Feinleib, M., Davidson, M. J. Coronary heart disease mortality. A community perspective. JAMA. 1972; 222(9):1129–1134. Grilli, R., Freemantle, N., Minozzi, S., Domenighetti, G., Finer, D. Mass media interventions: effects on health services utilisation. Cochrane Database Systems Review. 2, 2000. [CD000389.]. Ingarfield, S. L., Jacobs, I. G., Jelinek, G. A., Mountain, D. Patient delay and use of ambulance by patients with chest pain. Emergency Medicine Australasia. 2005; 17:218–223. Kolbe, J., Vamos, M., Fergusson, W., Elkind, G., Garrett, J. Differential influences on asthma self-management knowledge and self-management behavior in acute severe asthma. Chest. 1996; 110(6):1463–1468. Lavoie, K., Bouthillier, D., Bacon, S., Lemière, C., Martin, J., Hamid, Q., et al. Psychologic distress and maladaptive coping styles in patients with severe vs. moderate asthma. Chest. 2010; 137(6):1324–1331. Leitch, J. Changing times in the treatment of myocardial infarction. Medical Journal of

Australia. 2003; 178:381–385. Li, J., Galvin, H. K., Johnson, S. C. The ‘prudent layperson’ definition of an emergency medical condition. American Journal of Emergency Medicine. 2002; 20(1):10–13. Lowthian, J. A., Cameron, P. A., Stoelwinder, J. U., Curtis, A., Currell, A., Cooke, M. W., McNeil, J. J. Increasing utilisation of emergency ambulances. Australian Health Review. 2011; 35(1):63–69. MacLean, S. L., Bayley, E. W., Cole, F. L., Bernado, L., Lenaghan, P., Manton, A. The LUNAR project: a description of the population of individuals who seek health care at emergency departments. Journal of Emergency Nursing. 1999; 25(4):269–282. Morgans, A., Archer, F., Allen, F. Patient decision making in prehospital health emergencies: determinants and predictors of patient delay. Journal of Emergency Primary Health Care. 2008; 6(3):1–16. Morgans, A., Burgess, S. What is a health emergency? The difference in definition and understanding between patients and health professionals. Australian Health Review. 2011; 35:284–289. Newman, M. Defibrillation shakes the nation: results of the Journal of Emergency Medical Services 1988 National Early Defibrillation Study. Journal of Emergency Medical Services. 1989; 14:50–59. Newman, M. The chain of survival revisited. Journal of Emergency Medical Services. 1998; 23(5):46. Pattenden, J., Watt, I., Lewin, R., Stanford, N. Decision making processes in people with symptoms of acute myocardial infarction: qualitative study. British Medical Journal. 2002; 324:1006. Penny, J. Editorial. Patient delay in calling for help: the weakest link in the chain of survival? Heart. 2001; 85:121–122. St John NZCaring in Many Ways: Annual Report. Wellington: St John, 2011. Taylor, D. M., Garewal, D., Carter, M., Bailey, M., Aggarwal, A. Factors that impact upon the time to hospital presentation following the onset of chest pain. Emergency Medicine

Australasia. 2005; 17(3):204–211. The Council of Ambulance Authorities. Annual Report, 2009–2010. Findon, South Australia: The Council of Ambulance Authorities (Australia), 2010; 1–84. Valenzuela, T., Roe, D., Cretin, S., Spaite, D., Larsen, M. P. Estimating effectiveness of cardiac arrest interventions: a logistic regression survival model. Circulation. 1997; 96:3308– 3313.

SECTION 2

THE PARAMEDIC’S CLINICAL APPROACH O U TL I N E CHAPTER 4: The structured clinical approach CHAPTER 5: The clinical reasoning process CHAPTER 6: The patient interview

CHAP TER 4

The structured clinical approach By Matt Johnson

O V E RV IE W • Using a structured clinical approach is an effective tool for combating the complex nature of patient assessment. • The clinical approach that has been developed for use in hospitals and clinics is optimised for gathering information in low-stimulus environments where the roles of clinicians and patients are well defined. This does not describe the paramedic’s clinical decision-making environment. • To safely and effectively gather information in the high-stimulus environment in which paramedics work, paramedics must be aware of the strengths and weaknesses of using a structured approach. • Understanding and utilising the process of the clinical assessment can lower the cognitive load that paramedics have to deal with and allow them to concentrate on the content or the information generated by the assessment and incorporating that information into their decision-making process.

CA SE ST U DY 1 Case 12714, 2047 hrs. Dispatch details: A 72-year-old male attending a wedding has collapsed. The patient is reportedly unconscious. Initial presentation: The ambulance crew find the patient sitting on a chair at a crowded wedding reception. He is pale but conscious and surrounded by concerned family and friends. He is telling everyone that he is okay, but when the crew arrives they are told by family members that the patient complained

of feeling hot before his eyes rolled back. He then fell forwards onto a table and suffered a brief seizure. He regained consciousness as soon as he was laid on the ground. He has since insisted on sitting back in his chair. As the father of the bride he has been celebrating and has enjoyed at least four glasses of champagne, plus wine and beer. His wife and daughter are insisting that he goes to hospital but he is adamantly refusing.

Introduction The list of possible causes of this patient’s collapse is long and diverse. In terms of severity, the causes range from benign and self-righting (e.g. intoxication) to serious and requiring intervention (e.g. cardiac arrhythmia). Between the two extremes are a multitude of conditions that could feasibly be the cause of the events described. In this crowded setting of high emotion, anxiety and conflict, the paramedic crew must determine the cause of the patient’s collapse and then, depending on their decision, institute a treatment plan that will almost certainly upset some of those involved in the situation. This is the first in a series of chapters that use a typical ambulance dispatch case to examine how paramedics can reach a safe and accurate clinical decision and initiate their preferred management plan with the support of everyone involved. This chapter focuses on the process of gathering the information that paramedics need to make effective clinical decisions. In describing the steps involved in gathering information, it can become difficult to separate the process from the content that the process generates: the human mind instinctively interprets what is presented to it, and thus subsequent chapters explore both the strengths and the weaknesses of how we use the information we collect. In the turbulent world that is pre-hospital medicine, using a structured clinical assessment gives you a road map to guide you from the moment the patient encounter begins to undertaking your treatment plan (see Fig 4.1). Employing this process for every patient will reliably provide you with the information you need to safely apply the knowledge and clinical skills you have attained during your education.

FIGURE 4.1

Using a standardised approach provides the

paramedic with a road map through the assessment process. Using this step-by-step approach to patient assessment, the paramedic has only one thing to do at a time; by completing these steps in the right order, paramedics can obtain the physical information they need to build safe and accurate diagnoses. Source: Image courtesy St John New Zealand. Casting a wide net to capture information is an essential skill for modern paramedics as the rapid expansion of the paramedic skill set, combined with an ageing population, has created clinical challenges far beyond what paramedics experienced as little as a decade ago. Increasingly, patients have multiple chronic health problems with overlapping pathologies and symptoms as opposed to a single, sudden episode with a clear cause. Simultaneously, the choice of treatment pathways and interventions available to paramedics has also become much larger and more complicated. Even the old adage of ‘treat for the worst’ no longer applies universally: like all health professionals, paramedics are part of a healthcare system that must use clinical judgement to carefully allocate increasingly scarce resources to achieve cost-effective care (Binder, 1995). In some cases this will require the paramedic to engage patients in treatment plans that do not involve transport to hospital (e.g. referral to their general practitioner [GP]), while at other times the expectation will be that the paramedic crew are so accurate in their assessments that they will bypass the nearest hospital to ensure that their patients receive specialist care for the conditions they have diagnosed. Unfortunately, the unpredictable and mobile nature of paramedic work also means that our diagnostic equipment is limited by what can safely be carried by hand. In short, paramedics are expected to make fast, accurate, high-stakes clinical decisions with little technical support in time-poor and highly emotive situations (see Fig 4.2). It is this overwhelming complexity that makes a structured clinical approach so valuable.

FIGURE 4.2 The paramedic workplace environment is characterised by an excess of stimuli (noise, crowds, smells, family) and a lack of clinical information. The difference between paramedic cases and those faced by doctors who work in general practice or hospital settings does not imply, however, that we cannot learn from the experience and research that have developed the clinical assessment process used by other health professions. In fact, the acceptance of a structured approach in low-stimulus environments should only reinforce how important the structured clinical approach can be to paramedic patient outcomes.

Medicine vs paramedicine? Before we examine case study 1, think about most places where medicine is practised. Try to recall your last visit to your GP, for instance: chances are you phoned to make an appointment and, on arrival, were directed to a waiting room until the doctor was ready to see you. While there you probably contemplated your ailment, went over the timeline of your symptoms and structured an idea of what would happen: a prescription for antibiotics for your sore throat, a medical certificate because your back was playing up or a referral for an ultrasound for the shoulder you crushed playing touch-football last week. Finally, when your doctor was ready, you entered a quiet room where a folder on the desk or computer was labelled with your name and contained your known medical history. It is unlikely the waiting room was crowded with friends and relatives keen to theorise on your condition: almost certainly your interaction with the doctor was conducted just between the two of you. In other words, the interaction was planned, private and optimised for the GP to obtain an accurate history and conduct a physical examination. Even the lack of predictability associated with an emergency department (ED) is (generally) well controlled. Access to a doctor is restricted by a triage and admission process that collects personal details and quickly assesses each patient’s complaint without the clinician having the pressure of making a specific diagnosis or initiating treatment. Once inside the department, areas are clearly delineated, information is strategically placed and roles are well defined: staff, patients and visitors are easily distinguished. In addition, patients have nametags attached to their arms and are placed in cubicles where everything required is (relatively) conveniently located and back-up staff are easily available. Information collection is further compartmentalised with nurses normally completing basic physical observations such as pulse, blood pressure and temperature, before the doctor collects and collates the detailed information required to reach a clinical decision. Now compare this with case study 1. What does the paramedic crew know about the patient before they meet him—and his family? His name? Medical history? Is the environment of a wedding reception conducive to gathering information or conducting a detailed physical examination? Does the patient even want to be assessed, or will he insist that he is fine and the wedding should not be interrupted? Is the family likely to help the assessment with succinct, accurate information, or will their version be distorted by shock and fear for the patient’s health? The paramedic’s workplace is very different from a GP’s clinic or hospital ward as shown in Table 4.1. A GP consultation is constructed to reduce distracting stimuli while simultaneously providing the doctor with as much information as possible. In contrast, the paramedic’s clinical assessment is characterised by high levels of stimulus, but precious little information. It is usually noisy, emotional and unfamiliar, and in most cases the paramedic does not even know the patient’s name (see Fig 4.3).

TABLE 4.1 Comparison of GP versus paramedic cases GP cases Paramedic cases Private, in GP’s office Public, in front of family Scheduled Unexpected Patient requests the appointment Most often, others call 000 on the patient’s behalf Patient prepares history for GP Patient uncertain of events GP can take notes and refer to charts Paramedic unable to take notes and refer to charts Non-acute Acute (probably acute on chronic) Timely Urgent Supported by sufficient staff Usually insufficient staff All necessary equipment available Equipment limited by portability

FIGURE 4.3 Even regular medical consultations are stressful events and most institutions have worked hard to create an environment that makes it as quick, easy and safe as possible to establish a diagnosis for each patient. This is not the world of the paramedic, who has to enter someone else’s home at a time of high stress to ask the most personal questions. Source: Image supplied by St John Ambulance WA. However, if information is the key to making effective decisions, then paramedics must find a way of reducing stimuli while simultaneously collecting as much accurate information as possible. One way to do this is to use the structured clinical approach for every patient. This approach guides the paramedic through the assessment to ensure that vital clues to the patient’s condition are not omitted, while its predictability allows the paramedic to focus on the information gathered and not on determining the next question to ask.

Using a structured approach to combat complexity A few years before the outbreak of World War II, aircraft manufacturer Boeing assembled a crowd of politicians, reporters and military officers to reveal a stunning new aircraft. The result of a competition to build a new heavy bomber for the US air force, the recently completed plane was expected to easily win the lucrative contract. On this flight it was to be piloted by Major Ployer Hill, one of Boeing’s most experienced test pilots. Tragically, shortly after take-off the plane banked sharply and crashed into the ground, killing Hill and another member of the crew. Despite his experience, Hill had forgotten to disengage a new locking system on the control surfaces at the rear of the plane. Hill’s crash changed the way pilots operate. Compared to earlier aircraft, Hill and his fellow pilots were being confronted by aircraft with multiple engines, hydraulic systems, radios and more instrumentation than they had ever known. In short, the planes had become too complex and pilots were no longer able to safely ‘fly by the seat of their pants’. As a result of Hill’s crash standardised aircraft checklists were introduced: a process so logical now that it seems difficult to understand why it was not implemented earlier. At the time, however, it was simply assumed that pilots ‘knew’ how to fly and could work through any problem they encountered. Using a checklist reduces a complex task to one simple essential task at a time to be performed in a specified order to achieve a predictable outcome or solution. The process is supported by both cognitive load and situational awareness theories (Endsley, 1995; Nolan, 2000; Paas, Renkel & Sweller, 2004); it is very effective in high-risk and high-cost industries such as aviation, shipping, nuclear power generation and construction, but is often resisted in medicine (Gawande, 2009).

P RACT ICE T IP In an effort to combat inconsistencies and poor patient outcomes, major hospitals are now introducing pre-surgery and pre-intubation checklists that need to be completed prior to commencing the procedures.

One of the reasons that clinicians may struggle to consistently implement a structured clinical approach is the variety of presentations that can occur among patients. The WHO (2010) has categorised more than 13,000 distinct diseases and injuries so the permutations of signs and symptoms between individual patients is beyond the recall of any clinician. But far from reducing the usefulness of a structured approach to patient assessment, the variability of how patients can present actually increases the need for a structured assessment. Compared with operators working from written checklists, however, and due to the variability of injury and disease presentations (and how patients describe them), paramedics must not only follow a structured approach but also understand the purpose of the structure itself (see Fig 4.4). This allows them to operate within the structure, using

its key elements to ensure that vital information is captured, but without being restricted too tightly to a specific order so that they can adapt to the uniqueness of the situation. Over the next few pages we step you through a structured clinical approach developed for the emergency medical setting.

FIGURE 4.4 Shaping a patient encounter into a defined structure is a difficult skill to learn and novice paramedics will instinctively stick much more closely to the prescribed order than expert practitioners who are more familiar with the process and are able to move easily within the structured approach. Source: Image courtesy St John New Zealand.

The emergency model Although the terminology may vary between ambulance services, the major steps in the emergency model can be summarised as follows: 1. the primary survey 2. the vital signs survey 3. the physical exam 4. the differential diagnosis.

The primary survey The primary survey (see Fig 4.5) is the perfect example of a tool that can be used to reduce the decision-making load while simultaneously providing essential information. It is used to quickly establish whether a patient is dead or dying or alive. Faced with an unconscious patient, the primary survey removes any tendency for the paramedic to start considering complex causes and directs them to just one task: A, B, C or H. A = clearing the airway. Once the airway is cleared, the paramedic’s only task is assessment of breathing: B. If the patient is not breathing, the only task is to commence intermittent positive pressure ventilation. If, once ventilation has been established, the patient has no pulse (C, circulation), the paramedic must commence chest compressions. If A, B and C are intact, controlling any obvious external haemorrhage (H) is the paramedic’s next priority.

FIGURE 4.5

The primary survey (ABCH).

Over the past decade two additional aspects have been added to some versions of the primary survey: disability (D) and exposure (E). To assess disability the responder needs to conduct a rapid neurological assessment, while to assess exposure the responder has to undress the patient to reveal any injuries. Although these aspects fit neatly into the primary survey in an alphabetical sense, for paramedics both involve complex assessments and procedures (e.g. to be conducted safely, exposing a trauma patient can take several minutes and a small team). Thus, in the primary survey these additional aspects are generally more suitable for first responders who have limited clinical decisions and interventions to initiate. For paramedics, disability and exposure are explored in the vital signs survey and secondary survey, which are conducted once the primary survey has been completed and any actions it specifies have been commenced. Since more than 90% (QAS, 2011) of ambulance service patients are conscious when

paramedics arrive, the primary survey quickly exhausts its ability to guide the decisionmaking process. Thus, to determine how sick the conscious patient may be, paramedics rely on the vital signs survey.

The vital signs survey While the primary survey establishes whether a patient is dead/dying or alive, the vital signs survey (VSS) provides a qualitative measure of how sick the patient is and quickly identifies patients who may soon deteriorate. The human body is capable of maintaining relatively normal activities despite significant injury or illness—it does this by various compensation mechanisms such as increasing the heart rate, redistributing blood from the skin to the vital organs, or altering the rate or rhythm of ventilation. As a result, a patient may outwardly appear relatively well despite a severe underlying injury or disease. The paramedic uses the VSS to detect signs of these compensatory changes. The VSS is also a valuable triage tool that can be used to rank patients in terms of severity in a multicasualty environment. The order and composition of the survey may vary slightly between ambulance services. The VSS is made up of three components: a respiratory status assessment (RSA), a cardiovascular status assessment (CVSA, or perfusion status assessment, PSA) and a neurological status assessment (see Tables 4.2–4.4). In addition to observing and talking to the patient, the VSS requires the paramedic to measure the patient’s pulse rate and quality, determine their blood pressure and auscultate the sounds produced by ventilation.

TABLE 4.2 Respiratory status assessment

Source: Adapted from Ambulance Victoria (2008). Clinical Approach V3 CPG A0101.

TABLE 4.3 Perfusion status assessment

TABLE 4.4 Neurological status assessment

P RACT ICE T IP Most vital signs surveys specify a ‘normal’ range, but some patients fall outside these values even when they are healthy. The very fit, the very slight or the very old may have heart rates and blood pressures that fall outside of the ‘normal’ range, but don’t assume that outside of ‘normal’ is a healthy variant: explore the patient’s background (previously assessed heart rates and blood pressures) to ensure what is discovered does not have a pathological cause.

The 15-point Glasgow Coma Scale is almost universally accepted as a useful tool for assessing a patient’s conscious state, but its utility and predictive value in the emergency environment are increasingly being questioned (Green, 2011). As a result, some ambulance services are now using a more simple four-point assessment tool known as AVPU, whereby patients are categorised as being alert (A), responding to voice (V) or pain (P), or unresponsive (U).

The physical examination For patients presenting with traumatic injuries, this stage includes a head-to-toe physical examination looking for evidence of injuries. Commonly called the secondary survey, this can be a challenging process on fully clothed patients who are anxious and in pain. For patients suffering a medical complaint, this stage may include measurements such as blood glucose level (BGL), oxygen saturations, temperature and ECG recordings. It is important to enquire about any pain or discomfort the patient is feeling. Where pain is located, how it is described and how it evolves over time are all essential clues in determining the cause of the pain and whether it represents a serious threat to the patient. A structured approach in the form of a mnemonic is commonly used to explore pain: DOLOR is (conveniently) Latin for pain and provides an excellent structure for pain assessment (see Table 4.5). A more detailed description of pain assessment can be found in Chapter 28.

TABLE 4.5 DOLOR

P RACT ICE T IP Exposing a trauma patient to the environment to conduct a secondary survey is not always possible or wise, but rather than neglect this step entirely until a ‘full’ survey can be completed, try to conduct the survey as best you can through the patient’s clothes if access is limited. Broken bones and other injuries that are hidden can often be identified by gentle, systematic palpation. The survey can be completed once the patient is more accessible.

The differential diagnosis It was not so long ago that paramedics did not require this fourth stage: if a patient was conscious, it was time to transport them. Expectations have changed, however, and paramedics now need to identify and manage any alterations detected in the VSS and physical exam. In addition, most clinicians will take the opportunity during the VSS and physical exam to seek a past medical history and a history of what has occurred to generate the ambulance call. Although the terms may vary, the approach described in Figure 4.6 should be familiar to most paramedics and it forms the basis of the structured approach. Based on the precept that the patient is severely ill or injured, the emergency model prioritises the most important and least subjective assessments and leaves the less critical elements until last. For the patient suffering a life-threatening medical emergency it forms a sound approach, but is it as effective for paramedics confronted with patients who present with less severe but more complex problems?

FIGURE 4.6 The emergency model. This structured approach to patient assessment prioritises the most important and least subjective assessments of the primary survey. Once these have been cleared the algorithm directs the clinician to collect a set of vital signs to identify any physiological distress. Only once these essential tasks have been completed should the clinician consider collecting the more subtle information to support a diagnosis and inform a management plan.

A CU T E ON CHRONIC The term ‘chronic’ implies a steady state of a condition that is painful or uncomfortable but is not life-threatening. In contrast, ‘acute’ suggests a sudden onset of a new condition. However, many patients suffering a chronic disease are far from stable and suffer frequent sudden exacerbations of their condition: this is referred to as an ‘acute on chronic’ presentation. The challenge is determining whether the acute presentation is in fact an extension of the chronic condition or an entirely new condition.

Let’s try applying this model to the patient described in case study 1. He is conscious and talking and not obviously bleeding, so the primary survey is effectively completed as the paramedic approaches. To assess his perfusion status you will need to take his blood pressure. To record that accurately requires removing his coat, but he insists he does not need to be assessed. Similarly, establishing an accurate Glasgow Coma Scale score will require his cooperation, and performing an ECG will require him to unbutton most of his shirt. Do you think he will agree to these assessments or might your insistence on conducting your assessments inflame his reaction? Thus, the emergency model may struggle to provide an effective pathway when the patient is resistive to treatment and where the verbal history of events is more illustrative of the condition than physical tests. The dramatic shift in ambulance workloads from severe, acute health emergencies to complex, acute on chronic cases has altered the demands on paramedics. These days ambulance patients are rarely unconscious but are often confused, anxious and reluctant to engage in assessments. Paramedics therefore require more than just physical clinical assessment skills such as taking a blood pressure or auscultating chest sounds: communication is a vital tool in gaining the information required to make an accurate diagnosis (this is elaborated on further in Chapter 6). Paramedics may also need to adapt their traditional emergency-based approach for chronic patients. A standardised clinical approach that takes a wider perspective than just immediate threats to life may offer a better tool for modern paramedic practice.

The medical interview model Although little has been written about paramedic assessment of patients, the past 30 years have seen intensive research into how doctors and other health professionals can more effectively assess their patients. Much of this research has been driven by findings linking the quality of assessment not only with better clinical outcomes, but also with ethical decision making, patient compliance and patient satisfaction (O’Toole, 2008; Rosenburg, Lussier & Beaudoin, 1997; Silverman, Kurtz & Draper, 2008). Most importantly for paramedics, there is strong evidence that despite the advances in diagnostic technology, it is the combination of the patient’s story and the basic physical exam that is the most powerful tool in reaching a clinical decision (Silverman et al., 2008). Given this wealth of knowledge, it is worthwhile considering whether the medical interview model is better suited for most paramedic patients. Like the emergency model, the medical interview model provides a structured approach aimed at gathering quality information in order to make an accurate clinical decision. But unlike the action-focused emergency approach, which forces the practitioner to conduct a physical exam almost immediately, the medical interview model prioritises the patient’s history and symptoms. This approach supplies the paramedic with context against which the observations recorded during the VSS and physical exam can be considered (see Ch 6 for more detail about how this can affect the quality of the information gained and the patient’s response to decisions made by the paramedics). The medical interview model structures the approach into four stages (Silverman et al., 2008): 1. initiating the assessment 2. gathering information 3. the physical exam 4. planning and treatment. Importantly, this approach (see Fig 4.7) should not be seen as superior or inferior to the emergency model: it is simply another guided assessment tool that may be more suitable for ambulance patients who are fully conscious.

FIGURE 4.7 The medical interview model. The emergency model of patient assessment is ideally suited to patients who have suffered traumatic injuries but the medical interview model provides a structured approach for non-trauma patients. Compared with the emergency model it aims to gather high-quality clinical information to make an accurate clinical diagnosis. Unlike the action-focused emergency approach, which forces the practitioner to conduct a physical exam almost immediately, the medical interview model prioritises the patient’s history and symptoms.

Initiating the assessment

The purpose of the assessment initiation phase is to learn the patient’s name, introduce yourself and ask the patient to describe what they consider the problem to be. Seeking the patient’s view serves a number of purposes, the most important of which is that is reveals the patient’s preferred outcome for the encounter. This patient-centric approach is developed more fully in subsequent chapters.

Gathering information Next, the paramedic should establish details of the patient’s past medical history, medications, allergies and, most importantly, the pertinent history of what happened that required an ambulance.

The physical exam With the pertinent details established, the physical exam is contextualised with the information already gained. Compared with the emergency model this phase is often easier to complete, as patients feel they have already conveyed their story and so become more cooperative.

Planning and treatment The assumption underpinning the emergency model is that patients are so ill that they will willingly consent to whatever treatment plan the paramedic chooses. In reality, patients not only have the right to be involved in the decision-making process, but many insist on it. Preferred hospital, notification of family and use of medications are all common causes of unnecessary conflict between paramedics and patients because this phase of the interaction is simply not considered by the paramedic.

P RACT ICE T IP Learning how paramedics should respond when a patient replies, ‘Nothing’s wrong: these people are just worrying about nothing. I’m fine!’ is covered in Chapter 6.

While both models offer the advantage of providing a structured clinical approach to help guide the paramedic through the information-gathering process, each has its inherent strengths. Recognising and using these strengths will ensure you get the right information to make the right decision.

References Binder, L. S. Clinical diagnosis in emergency medicine: Lost art, or lost cause? Academic Emergency Medicine. 1995; 2:622–629. Endsley, M. R. Toward a theory of situational awareness in dynamic situations. Human Factors. 32(64), 1995. Gawande, A.The Checklist Manifesto: How to Get Things Right. London: Profile Books, 2009. Green, S. M. Cheerio, laddie! Bidding farewell to the Glasgow Coma Scale. Annals of Emergency Medicine. 58(5), 2011. Nolan, T. W. System changes to improve patient safety. British Medical Journal. 2000; 18(320):771–773. O’Toole, G.Communication: Core Interpersonal Skills for Health Professionals. Sydney: Elsevier, 2008. Paas, F., Renkel, A., Sweller, J., Cognitive load theory: Instructional implications of the interaction between information structures and cognitive architecture. Instructional Science. 2004;32(1), doi: 10.1023/B:TRUC.0000021806.17516.d0. Queensland Ambulance Service (QAS)Department of Safety Annual Report. Brisbane: State of Queensland, 2011. Rosenburg, E. E., Lussier, M., Beaudoin, C. Lessons for clinicians from physician-patient communication literature. Archives of Family Medicine. 1997; 6:279–283. Silverman, J., Kurtz, S., Draper, J. Skills for Communicating with Patients, 2nd ed. Oxon, UK: Radcliffe, 2008. World Health Organization (WHO). International Statistical Classification of Diseases and Related Health Problems, 10th rev ed. Geneva: WHO, 2010.

CHAP TER 5

The clinical reasoning process By Matt Johnson

OVERVIEW • Paramedics and other clinicians working in emergency medicine must be able to accurately assess a wide range of conditions using limited diagnostic tools, time and resources. • The process of paramedic clinical decision making has not been well researched. • The ability to effectively solve complex clinical problems differentiates novice from expert clinicians. The greater depth of factual knowledge that expert clinicians have to call upon does not adequately explain this difference. • Traditional analytical models of clinical decision making do not fully describe how expert clinicians solve clinical problems with more accuracy than novices. • Expert clinicians are generally unaware of the cognitive processes that drive their decision making (Geary & Kennedy, 2010). • Two distinct models or systems of clinical reasoning appear to exist: one is rapid, instinctive and unconscious; the other is slow, analytical and controlled. Experts primarily use the instinctive/rapid method, whereas novices are more likely to use the slow/analytical approach. • The integration of factual knowledge and clinical experience into ‘scripts’ or ‘exemplars’ that describe typical disease presentations summarises the progression from novice to expert clinical reasoning. • Neither the rapid/instinctive system nor the slow/analytical system is suited to every circumstance. Both have inherent errors and the most effective method is to recruit the strengths of each in reaching a clinical decision. • Recognition of the two systems should enhance a paramedic’s ability not only to progress towards expert reasoning but also to detect when errors occur and to maintain patient safety in the face of diagnostic uncertainty.

Introduction It doesn’t matter what field of health you practise—medicine, nursing, paramedicine, surgery or physiotherapy—being a novice is a difficult phase. Full of fresh knowledge and skills, and armed with an overwhelming desire to look after your patients, at times it can seem that you are playing by a different set of rules to everyone else. Your more experienced colleagues seem to walk into a room and pluck a diagnosis out of thin air—and too often for your liking, it proves to be right. You, meanwhile, are struggling to complete a thorough assessment and ask all the right questions and are cautiously trying to decide what factors are the most important in differentiating a particular diagnosis. The shift of ambulance education to the university setting has undoubtedly increased the novice paramedic’s scientific knowledge and clinical skills. But the ability to implement this knowledge effectively is limited by the novice’s ability to make fast and accurate decisions (Shaban, 2005). Almost every health professional faces a degree of uncertainty with clinical decisions but for those working in emergency health fields the risk of error is compounded by stress and a lack of time and resources (Shaban, Wyatt-Smith & Cuming, 2004). Although the clinical decision-making process has not been well-researched among paramedics, it has been well-described in both nursing and medicine (Shaban, WyattSmith & Cuming, 2004). This chapter examines established clinical reasoning and decisionmaking processes and reveals that, perhaps even more so than for doctors and nurses, clinical judgement for paramedics is far more complex than a simple data-processing sequence. Clinical decision making is not solely analytical or reliant on the clinician’s recall of facts: it is a complex cognitive process that develops according to the clinician’s experience and, importantly, how that experience is integrated into the clinician’s personality and beliefs (McCarthy, 2003). This chapter presents two conflicting systems of clinical reasoning that must be integrated for the clinician to make safe decisions in the uncertain world of emergency health. We compare the clinical reasoning of novice paramedics with that of expert paramedics and examine how paramedics move towards expert decision making as they gain experience. We also discuss why, when confronted with especially challenging cases, some expert paramedics consciously revert back to the novice system in order to choose the best patient management plan.

CA SE ST U DY 1 Case 12648, 1016 hrs. Dispatch details: A 55-year-old male, severe respiratory distress, no history. Initial presentation: On arrival the student paramedic and his clinical instructor find the front door of a typical suburban house ajar. Inside they see a

slightly overweight 55-year-old male sitting on a lounge chair. He is in obvious respiratory distress, able to speak only a word or two at a time. He is very anxious. He is fully conscious, has a respiratory rate of 42 BPM and a pulse of 157 that is regular. He shakes his head when asked if this has ever happened before. ‘Never ’, he says between breaths. His pulse oximetry on oxygen at 8 L/min is 94%. Having determined that the patient is conscious, the student paramedic commences a vital signs survey (VSS) and finds the patient has a BP of 100/60 and is in sinus tachycardia with normal ST segments. His face is very flushed but he is otherwise pale, cool and clammy to touch. He nods to affirm the shortness of breath came on suddenly but shakes his head when asked if he has pain in his chest. His shortness of breath is the most obvious problem. The student paramedic listens to the patient’s lungs. After listening carefully he turns to his instructor and says, ‘There’s a little wheeze; it could be asthma?’ ‘He’s having a PE’, replies the clinical instructor as she places a Hudson mask over the patient’s face. ‘I’ve already called for back-up.’

Clinical decision making in the face of uncertainty: the paramedic paradigm To those unfamiliar with the world of medicine, it would appear that clinical reasoning and decision making would not differ greatly from standard problem-solving models (see Fig 5.1): collect the data, consider the causes, decide on the most likely explanation and then implement a solution (Eva, 2004; Shaban, 2005). In reality, however, paramedics rarely have the time or the equipment to compare different causes of diseases. For example, while a blood test might confirm paramedics’ suspicions of meningococcal septicaemia, the situation they face requires an immediate decision and, like doctors working in emergency departments (EDs), the need for expedient treatment requires paramedics to make cognitive ‘short cuts’ in the face of significant uncertainty (Geary & Kennedy, 2010).

FIGURE 5.1

Problem solving.

To the bystander, paramedicine is extremely task focused—actions rather than thoughts: applying oxygen masks, inserting IV lines, drawing up medications, transporting patients. This conspicuous technical skill set is undoubtedly important to patient care, but compare the ability of novice and expert paramedics to perform their clinical skills or test their basic knowledge and the differences are likely to be small. In fact, given the changes in paramedic education, it is actually likely that the student in case study 1 could describe the pathology of a pulmonary embolism (PE) better than his clinical instructor, but that greater knowledge doesn’t necessarily translate into a diagnosis. The significant difference between novices and expert clinicians lies in the invisible cognitive processes that drive the decision-making process, which determines what skills are needed, in what order and to what degree (Wyatt, 2003). Like doctors staffing EDs, the spectrum of conditions that paramedics are required to assess ranges from simple to immediately life-threatening and in the modern setting their role can extend from life-saving interventions to assessing seemingly mundane complaints for early signs of serious disease. This is why we need to carefully consider how paramedics

make decisions on behalf of patients. Thankfully, we are not alone in this challenge. Although clinical decision-making skills have been studied for nearly four decades their relationship to clinical competency has only recently re-emerged as a critical factor in clinical performance and patient outcomes (Greaves & Grant, 2000; Ledley & Lusted, 1959; Norman, 2000; Shaban, Wyatt-Smith & Cuming, 2004). This neglect is generally attributed to the rapid growth of scientific diagnostic tools over the same period, as the ability of the sole practitioner to decipher complex medical conditions was increasingly considered unimportant in the face of these new diagnostic tools. But for paramedics who work largely without these tools, we suggest that knowing how you think (and how to use other forms of reasoning) is just as important as your ability to embed all those disease pathologies, signs and symptoms was to passing your exams (Croskerry, 2000).

Problem solving versus decision making While it could appear that medical researchers have only recently discovered that we can struggle with solving problems when we are not able to collect all the necessary information, the comparison between carefully reasoned problem solving and instinctive decision making has been going on for centuries. Laplace suggested in 1814 that ‘good minds know by a sort of instinct without being able to explain how in precision’ (Gigerenzer & Hoffrage, 1995). Then in the 1950s two American professors produced a seminal paper on analytical decision making in medicine (Ledley & Lusted, 1959). Almost certainly driven by their interest in early computers (one of them later went on to invent the whole-body CAT scanner) they were seeking to establish the cognitive pathway that leads to an accurate diagnosis. They proposed a two-stage model of clinical reasoning that started with a hypothesis-generation stage (I think this patient may be having a heart attack) and was followed by a hypothesis-evaluation stage (Do his symptoms confirm a heart attack?). They were interested in how formal analytical techniques could be applied to the hypothesis-testing phase, but their theory failed to adequately address two significant questions: how is the hypothesis developed in the first place (and what factors influence that creation); and, what factors make us able to safely eliminate one hypothesis from another? Many people would suggest that this model uses evidence and probability to develop the diagnosis and this classical reasoning process would be familiar to most students as the method they apply to solve the case studies presented in lectures and tutorials (Freshwater-Turner et al., 2007). Known as Bayesian analysis, its linking of probability, evaluation of clinical evidence and careful analysis creates an inherent scientific appeal and it endows any finding with a degree of certainty—at least in the mind of the clinician. Development of Ledley and Lusted’s paper subsequently produced the more elaborate hypothetico-deductive reasoning model (Elstein, Shulman & Sprafka, 1978; Eva, 2004). Deductive reasoning is also known as deductive logic because it generates a supposedly certain conclusion from a set of general principles: • All men are mortal. • Tony is a man. • Therefore, Tony is mortal. This is an example of deductive logic. While the ‘certainty’ of a deductive conclusion is appealing, for deductive reasoning to be foolproof the premises on which it is based must be true and clear. The problem with this model for paramedics and other health professionals is that the ‘truths’ about a patient may not be known and some degree of uncertainly nearly always pervades the process. This could be because the ‘truths’ cannot be discovered with the tools available or, more likely for the novice, it relies on the assumption that the clinician possesses all the required knowledge to firstly create all the possible diagnoses and then to correctly interpret all the methods used to test the hypothesis (Croskerry, 2000).

P RACT ICE T IP When confronted with the patient in case study 1, the clinical instructor did not formally go through either an inductive or a deductive process: she just

looked at the patient and ‘knew’ he was having a pulmonary embolism. The diagnosis arose without rigorous analysis in exactly the same way that we make decisions every day based on impressions and intuition, and without conscious effort. Is this form of clinical reasoning safe?

Inductive reasoning, by contrast, draws a specific conclusion from general principles. That is, the finding is probably correct but not necessarily so. It can be useful to think of inductive reasoning as a statistical approach to decision making: • 90% of humans are right-handed. • Joe is human. • Therefore, Joe is almost certainly right-handed. By inducing from findings not necessarily specific to Joe we are able to make an educated guess that Joe is right-handed. Unlike deductive reasoning where the conclusion must be true if the premises are true, inductive reasoning allows that the conclusion may be false even if all the premises are true. Rather than being considered valid or invalid, inductive conclusions can be regarded as strong or weak, probable or improbable. Although most of us consider our diagnostic process to be deductive (based on ‘truths’), the reality is we are forced to work by inductive reasoning far more often. Consider this example of inductive reasoning: • 25% of myocardial infarctions present with no chest pain. • Peter has no chest pain. • Therefore, there is a 25% chance that Peter might be having a myocardial infarction. If Peter is a 25-year-old who has presented with a sprained ankle this conclusion is weak and of little help to the paramedic. If Peter is an 80-year-old male complaining of shortness of breath and nausea, it could be a useful diagnostic tool that reminds the paramedic to investigate the possibility of an infarction. So, both deductive and inductive reasoning can be useful tools for problem solving, but an inability to collect accurate information (or indeed to interpret it) does not explain how expert clinicians are able to make fast, accurate decisions. There is also the issue that, when used by humans, Bayesian analysis may not be as accurate as the mathematical nature of the processes implies (see Box 5.1; Gigerenzer & Hoffrage, 1995). B O X 5 . 1B a y e s i a n

a n a lysis

Bayesian analysis is inherently appealing to scientific minds as it appears to offer a mathematical pathway to an answer. In the setting of emergency health, however, it has a number of significant limitations: namely, that most clinicians don’t actually know the formula, but also, just as importantly, that like deductive reasoning it requires known values for the probability of a disease occurring and the reliability of a particular test for that disease. Finally, it doesn’t necessarily produce an answer: it simply provides a probability that a disease is present. So, if you have more than one hypothesis (say, asthma versus acute pulmonary oedema) you have to complete the formula for each one and compare the probabilities. Disturbingly, even when clinicians are given the data

they need to complete the formula (unlikely in the field), they are very poor at estimating the outcome and get it right in only 15% of cases (Eddy, 1982; Gigerenzer & Hoffrage, 1995; Kurzenhäuser & Hoffrage, 2002; Lewis & Keren, 1999). In case you want to test yourself, the formula is as follows:

P(H|E) is the Probability of a Hypothesis, given the Evidence. This is the figure we are ultimately seeking: what is the probability our patient has a disease (hypothesis) based on a test (evidence) where we know the accuracy of the test? Bayes refers to this as the ‘posterior probability’: how often the disease will be present when the test returns a positive result. To calculate it we have to know and complete the following: P(E|H) calculates the conditional probability: the probability that having the disease (hypothesis) will produce a positive test (evidence). Remember, very few tests are 100% sensitive. P(H) is the prior probability of the hypothesis: the probability that our patient has the disease regardless of the test result. P(E) is the prior probability of the evidence: the probability of a positive regardless whether the disease is present. See Figure 5.2.

FIGURE 5.2

Bayesian analysis.

As a result, the best we can hope from this analysis is the probability that a patient has a particular condition based on the accuracy of a particular test. As complicated as this is, it is also not very intuitive. For example, if you took a disease that affects 1 in every 10 people and you had a test that is 90% accurate in detecting that disease (i.e. it returns a positive result nine times when tested on 10 people who have the disease), what are the odds that a person who tests positive has the disease? If you answered 90% you are picking the most common, but not the correct, answer. (The correct answer is actually 50%.) Even when confronted with a specific formula, our unconscious biases and beliefs affect our decisions. Another example of our poor instinctive assessments of probability was found by Kurzenhäuser and Hoffrage (2002). Supplied with the following details, they asked medical students to assess the probability that a pregnant woman would give birth to a child with Down syndrome given a positive ultrasound test: • Probability of Down syndrome: 0.15% • Probability of ultrasound test detecting Down syndrome: 80% • False positives for ultrasound test (test says the syndrome is present but it isn’t): 8% Seventy-six per cent of students gave a spontaneous estimate exceeding 50%. (The correct answer is 1.5%.) A similar magnitude of error was recorded when experienced doctors were asked to estimate the probability of breast cancer given a positive mammogram (Eddy, 1982). Remember, these overestimations occurred when the clinicians were aware not only of the test results, but also how effective the test actually was—a rarity in paramedic practice.

The myth of the expert Nearly every profession has a story in which a complex problem that baffles all who are confronted by it is solved in an instant by an expert who just happens to walk past. The near-mystical nature of these events has even inspired best-selling books (Gladwell, 2005; Kahneman, 2012). Is it because these experts simply ‘know’ more? Has their experience raised the odds so that they have seen something similar before? Did they use deductive or inductive reasoning but simply complete the task so quickly that they (and everyone else) were unaware of it? If so, how were they able to make a decision without having all the information available to those who had been trying to solve the problem beforehand? Before we can answer such questions and integrate this knowledge into our paramedic practice we need to briefly examine how our minds store, recall and use knowledge. Imagine you are preparing dinner with your partner when he or she drops a bowl of freshly prepared salad on the floor. The bowl smashes and the salad scatters across the floor. Your reaction is instantaneous: without consciously calculating the value of the bowl, the fact that your partner had a bad day at the office or how much mess has been made, you start to respond and unconsciously integrate all you know to anticipate your partner ’s anger and frustration and prepare a conciliatory response. The mental work of dealing with this situation occurs largely in silence and without appreciable delay. This is a very different response to problem solving compared with deductive or inductive reasoning. A less emotional example involves reading in your everyday language: you don’t need to recall the rules of grammar to understand a sentence—that occurs automatically. But try reading in a language that you are yet to master and suddenly you become aware of grammatical rules that distort the context of a sentence until you pause and construct the meaning. This suggests that a decision in an area where you understand the concepts is not a deductive action-reaction sequence, and that a decision in an area of expertise is a complex cognitive process that occurs without actual conscious reasoning strategies (Geary & Kennedy, 2010). The contrast between the rapid, unconscious problem solving that we use every day and the considered, thoughtful process of solving difficult tasks has interested psychologists for decades. One theory that attempts to explain and integrate the different types of reasoning is dual process theory or DPT (Evans, 2008; Stanovich & Toplak, 2012—see Fig 5.3). This states that clinical decisions can be reached by either a fast, intuitive pathway or a slower, analytical pathway. Clinicians who recognise the pattern of symptoms instinctively use the fast pathway, while novices, unfamiliar with a patient’s presentation, have to work through the slower pathway to reach the same conclusion. In case study 1 the two individuals use these different pathways when confronted with the same problem: the clinical instructor ’s experience allows her to recognise the pattern of a PE (shortness of breath, poor perfusion, normal chest sounds, cyanosed face) so she takes the automatic and fast pathway; the student is still working through the slow and considered pathway when the instructor reaches her decision. In the field of medicine DPT explains much of the difference between expert and novice clinical reasoning skills (Stanovich & West, 2000).

FIGURE 5.3 Clinical decisions can be reached by either a fast, intuitive pathway or a slower, analytical pathway. Source: Adapted from Croskerry (2003) and Croskerry et al. (2009). Within DPT psychologists refer to the rapid processing of information and retrieval of knowledge that we unconsciously use to make continuous judgements about our surroundings as system 1 decision making (Norman, Young & Brooks, 2007). This system is responsible for creating a continuous ‘coherent interpretation of what is going on around us’ (Kahneman, 2012) and is also referred to as intuitive decision making (Shaban, 2005). Psychologists reflect that the richness and complexity of the process is invisible to most people because it occurs without conscious thought (Kahneman, 2012; Norman, Young & Brooks, 2007; Stanovich & West, 2000). On the other hand, system 2 decision making involves what most of us consider to be reasoning and judgement. Unlike the automatic and complex responses of system 1, system 2 processing is slow, deliberate and ordered, and occurs at the very forefront of our consciousness. Commonly listed properties of system 1 and system 2 processing are illustrated in Table 5.1. While system 1 decision making occurs without thought or effort, system 2 processing requires concentration—and the harder the task, the more concentration is needed.

TABLE 5.1 Commonly listed properties of system 1 and system 2 processing System 1 processing Holistic Automatic Relatively undemanding of cognitive capacity Relatively fast Acquisition by biology, exposure and personal experience Parallel Evolutionarily old Implicit Often unconscious or preconscious Lower correlations with intelligence

System 2 processing Analytical Controlled Capacity demanding Relatively slow Acquisition by culture and formal tuition Sequential Evolutionarily recent Explicit Often conscious Higher correlations with intelligence

Source: Stanovich & Toplak (2012). In fact, system 2 processing of difficult tasks may demand so much of your attention that you cannot perform another task simultaneously. This is infamously illustrated in a video whereby observers recording the number of simple but varied tasks being performed fail to notice the presence of an extremely unusual event that also occurs (Simons & Chabris, 1999). Another example of system 2 processing requiring concentration is the difficulty you would have had trying to perform any other task while calculating the Bayesian probability task earlier in the chapter. In the medical field this state of being unable to perform a routine task if you are occupied with a problem that requires system 2 processing is recognised in the relationship between interruptions during a task and the number of errors made by clinicians (Hitchen, 2008; McGillis Hall, Pedersen & Fairley, 2010). Although it has long been widely recognised that expert clinicians can be distinguished from novices by their effective clinical reasoning (Boshuizen & Schmidt, 2000; Cholowski & Chan, 2001; Gaba, Fish & Howard, 1994), what is only just becoming accepted is that experts don’t just ‘know’ more, but by relying on system 1 decision making they use their information differently from novices (Croskerry, 2000). Rather than long lists and probability equations, their experience creates a network of knowledge that describes the conditions they regularly encounter (Sibert et al., 2002). As opposed to recalling individual facts about a disease they have learnt the pattern it presents. Expertise is not, it seems, magical or possibly even linked to intelligence or memory; it is simply an ability to see the pattern within a complex situation, which not only negates having to sort through all the information but actually makes all but the most important data disappear, leaving only the answer. The question remains, however: how do you turn your fresh paramedic knowledge into expertise?

Developing clinical reasoning skills Before you despair that memorising long lists of signs and diseases is somehow the wrong way to learn, it is important to remember two things. Firstly, the path to expert reasoning skills necessitates walking the hard novice trail—although simply recognising that you need to think differently and not just know more will act as a short cut. Secondly, perhaps the most important aspect of creating expert practice is to realise that you already operate at this level in many areas of your life. Driving home in light traffic is a great example of how you operate under system 1. Although you are not aware of it, you are in fact processing large amounts of information on road conditions, the drivers around you and the time it will take to get home. You are not, as you did when you first learnt to drive, struggling to maintain a safe distance from the car in front of you or indicating too early because you are overwhelmed with processing all the information around you. The ability to process large amounts of information and use it to make effective decisions requires two basic ingredients: experience and insight. Inadequate amounts of either simply won’t allow you to develop to expert level. Again, think of all the areas you consider yourself to be ‘expert’ at (not just good, but expert) and you will find that you have performed and thought about the role extensively. It is well-recognised that the contemporary tertiary medical education model is not a particularly effective method for developing clinical reasoning skills (Newcastle University, 2009), but the paramedic workplace can also be a difficult place to gain either experience or the perspective to review your experience appropriately. There is no control over what cases you will attend as a novice or whether these cases will be typical of a disease’s normal presentation. Similarly, the role can be so overwhelming that it can be difficult afterwards to remember what decisions you actually made and why. Watching your partner is often of little guidance as their reasoning is mostly invisible to outsiders—and often themselves (Wyatt, 2003). Nonetheless, a number of studies have identified that clinical reasoning is a skill that can be learnt and, with insight into the process, the transition from novice to expert can be shortened (Higuchi-Smith & Donald, 2002; Kamin et al., 2003). This chapter elaborates on the two different cognitive systems because, as a novice, you need to accept that your decision making will initially be slow and (often) full of uncertainty. But this stage is essential in building towards expert practice. You also need to understand that imitating expert practice by making ‘snap’ decisions is unsafe if you do not have the experience base to draw upon (Hatala, Norman & Brooks, 1999). This text has been created specifically to provide you with both requirements necessary to improve your clinical reasoning (experience and insight) in a safe environment. It cannot fully replace real-life experience, but each case presented here should help create networks within your academic knowledge and allow you to safely develop expert clinical practice.

System 1 processing Although we know that experts are less likely to use hypothetical-deductive reasoning or system 2 thinking compared with novice clinicians (Norman, 2005), there is less certainty over exactly how experts turn their experiences into instantaneous decisions. While there may in fact be more than one process occurring in system 1 reasoning (Stanovich & Toplak,

2012), most of the theories that try to explain the ‘expert phenomenon’ share the concept of the creation of a ‘schema’, an ‘illness script’ or an ‘exemplar ’ (Croskerry, 2000; Norman, 2005; Norman, Young & Brooks, 2007). It is assumed that experts have more knowledge than novice practitioners with regard to disease processes and should therefore perform better in clinical reasoning regardless of which system they use to make a clinical decision. Unfortunately, this supposed greater knowledge is not always demonstrated in standardised testing (Day et al., 1988) and it appears that expert clinicians rarely make use of the basic scientific concepts at their disposal when making complex decisions (Norman, 2005). Instead, experts take the long, isolated lists of causes, signs and symptoms they graduated with as students and turn them into ‘story-like narratives’ that describe and connect the typical presentation of each disease (Bordage et al., 1997). Unlike the lists and facts recited by students when questioned about a disease process, experts provide a succinct description of the links between causes, signs, symptoms and treatment (Norman, 2005). Once these ‘scripts’ have been formed, each subsequent case adds to the narrative by either conforming to the existing story or being reconciled by reflection (see Chapter 11). Understanding that experts and novices use different systems to reach clinical decisions (Boshuizen & Schmidt, 2000) is an important step in developing your practice because it means that the key to expert practice is not necessarily remembering more facts about more diseases. Experts are able to use intuitive decision making because they have changed the structure of their knowledge. Rather than long lists of symptoms or ranges of physiological values, experts have narratives that contain large amounts of integrated information (see Table 5.2). TABLE 5.2 Developing expert clinical reasoning

Source: Adapted from Boshuizen & Schmidt (2000). The concept is consistent with the categorisation model in psychology in which new information is memorised not in complete detail, but simply in how it differs from examples that already exist. Another way to describe this process is ‘pattern recognition’: you don’t need to recall the intricacy of a pattern to recognise that one is similar to another. The need to construct your clinical knowledge in this form is re-shaping medical education and assessment in many areas (Eva, 2004).

The flaw s of system 1 While all clinicians may aim to operate at the level of an expert, there are dangers in relying solely on system 1 decision making and there are times when even experts should

revert to system 2 processing. The most common human factors that negatively affect clinical decision making are outlined below (see also Box 5.2). B O X 5 . 2C h a r a c

ter istic s o f the em er g enc y

health se ing and per so nnel that m ay lead to diag no stic er r o r External • High communication load • High noise levels • Inadequate staffing • Poor feedback • Inexperience • Inadequate supervision

Internal • High levels of diagnostic uncertainty • High decision density • High cognitive load • Narrow time windows • Multiple interruptions/distractions • Circadian dyssynchronicity • Fatigue • Novel or infrequently occurring conditions

Personal • Gender • Risk-taking behaviour • Maladaptive group pressures • Maladaptive coping behaviour • Underconfidence • Overconfidence • Authority gradient effects • Likelihood of detection Source: Adapted from Croskerry & Sinclair (2001), Croskerry & Wears (2002) and Croskerry et al. (2009).

The law of small numbers While system 1 processing is consistent with expert practice, making decisions based on inadequate or poorly formed ‘illness scripts’ is dangerous. A number of studies have demonstrated that cases presented early in students’ careers disproportionately affect their

decision making, with students adhering to their initial exemplar regardless of how typical or correct it is (Hatala et al., 1999; Norman, Young & Brooks, 2007). If the primary symptom of your first experience of a patient with a myocardial infarction is shortness of breath, it is likely you will disproportionally correlate shortness of breath with myocardial infarction until your experience develops and you discover it is relatively rare. This law does not only affect novice practitioners: paramedics who have been practising for many years are unlikely to have experienced every disease presentation and some of their ‘illness scripts’ may be formed on a single case.

Bias Because system 1 processing occurs at a subconscious level, we are not aware of the biases that exist within its processing or how they affect our decisions (McCarthy, 2003; Norman, Young & Brooks, 2007). The number of identified biases has steadily increased as the decision-making process has been researched, and several are particularly common in cases where paramedics attend (see Box 5.3). The most critical bias, however, is the belief that any decision made by this process is unbiased. Unlike deductive reasoning where we at least have the opportunity to determine whether the premises are true, we are blind to the premises that inform our decisions in system 1 processing. The danger this presents is the tendency to adhere to a diagnosis made intuitively, even when the information gained during the patient assessment does not agree with this decision (Croskerry, 2003, 2005). (See the section on cue-criteria mismatching below.) B O X 5 . 3T

o err is human: the human fac to rs

i n vo l ve d i n c l i n i c a l d e c i si o n m a k i n g That medical errors occur relatively often is not surprising given the complexity of situations that present in emergency medicine (Victorian Auditor General, 2005). Some errors are unavoidable but rare: incorrect test results due to machine failure, or a patient who deliberately distorts their disease description. Other errors are systemic and occur as a result of the workplace rather than the individual: protocols or forms are incorrect. The final category of errors is the type we are most interested in: errors of judgement. Although novice practitioners fear that they do not know enough to make good decisions, this awareness can act as a safety net, prompting them to make conservative choices until they become more confident. Of greater concern are the errors in judgement that occur when clinicians fail to appreciate how much their personality affects their decision making. System 1 processing allows us to condense large amounts of information to make good intuitive decisions, but since much of this processing happens unconsciously, there is an opportunity for ‘human factor ’ errors to slip unnoticed into our practice. Some experts refer to these unconscious ‘colourings’ of our decision-making processes as a ‘bias’. While the term is probably accurate in that it carries connotations of prejudice or judgement, it can create resistance in those who feel they would not be subject to such unprofessional reactions. The less subjective term, cognitive dispositions to respond (CDRs), is also used to describe this reaction

(Croskerry et al., 2009), but in reality, we are all subject to beliefs that form as a result of our experiences and these then form part of the premises that shape how our system 1 processing responds to situations (McCarthy, 2003). The best we can do is to recognise that these biases (or CDRs) exist and allow for them in our clinical reasoning process. Cases 1–3 (all drawn directly from our clinical experience) expose some common biases that can exist in the pre-hospital environment. While you are primed to suspect the worst in each case, try to imagine yourself in each situation and the assessments you would have made about each patient.

Belief When experts are faced with a situation they are familiar with, the instinctive and invisible processing of system 1 produces an answer that feels (and is usually) correct. System 1 processing may also produce an answer in a difficult situation, but it is less likely to be correct. The instinctive attempt to create a plausible explanation in any situation can suspend disbelief in nonsensical situations. Hopefully, the clinician will identify the lack of sense and revert to system 2 processing in an attempt to reconcile the situation, but in instances where the answer is not entirely ludicrous (or system 2 is otherwise occupied) this initial belief may not be questioned. Again, most experienced clinicians will recall numerous cases where something was discovered during a patient assessment that on retrospect clearly did not make sense, but at the time seemed to fit into their schema of the situation. In most instances these cases involve high workloads and the paramedics are often task-saturated. Similarly, the complexity of human emotions may bias an answer to make it palatable to the clinician despite it being no more likely to be correct. Studies have shown that given indeterminate information over the likelihood of a patient suffering a severe illness, doctors will more often choose the less serious alternative (Groopman, 2007). The invisible nature of system 1 can make you think the answer ‘no’ relates to the question of whether a patient has cancer, when in fact the question being answered is ‘Do I want to tell the patient he has cancer?’

System 2 processing While we have described system 2 processing as slow and effortful, the ability to recognise when it is the best method to reach a treatment plan is an essential part of the expert paramedic’s armoury.

The strengths of system 2 Back-up When faced with decisions where system 1 cannot produce an acceptable answer, the slow and cumbersome system 2 is the safe (and only) alternative. Only system 2 can consciously compare alternatives, weigh statistical likelihoods, follow rules and make informed choices. When faced with a problem they have not encountered before, truly

expert practitioners will recognise the situation and take the time to go through a system 2 analysis of the problem. System 1 is good at recognising patterns but you need to invoke system 2 when you discover a new pattern.

Cue-criteria mismatching While most experienced clinicians will initially make an intuitive decision about a patient, they will notice any difference between the cues identified by their system 1 processing and the criteria described by that condition. This separation from their ‘typical illness script’ will prompt them to step away from system 1 processing and into the more analytical system 2 method (see Fig 5.4). The ability to see and respond to the cue-criteria mismatch relies solely on the paramedic’s insight and ability to understand their decisionmaking process. Every experienced clinician can recall a case when their instinctive reasoning provided them with an instantaneous diagnosis: the patient fitted the ‘script’ for (say) asthma perfectly. The patient was young (mid-30s), had become increasingly short of breath overnight with a wheeze, had a history of asthma and had been using an inhaled reliever for little effect. In the past 15 minutes her conscious state had deteriorated rapidly and the crew had been dispatched to an ‘asthma attack’. On arrival the crew found the patient with a respiratory rate of 32, a pulse of 156, a BP of 105/90 and a GCS of 12. System 1 says ‘asthma’, but on completing a vital signs survey the experienced paramedic noted that the lung wheezes were mild and air entry to both lungs seemed adequate. While all the ‘cues’ for asthma were present, on close examination the patient did not actually meet the ‘criteria’ to be diagnosed with the disease. The slow, considered process of system 2 reasoning can resolve the conflict that can occur when system 1 recognises a pattern incorrectly. This patient was in fact suffering from septicaemia secondary to a lung infection.

FIGURE 5.4 Any separation from their ‘typical illness script’ will prompt expert clinicians to step away from system 1 processing and into the more analytical system 2 method. Source: Adapted from Croskerry (2003) and Croskerry et al. (2009). In this text, the first chapter cases are typical presentations of a condition. The links between the pathology, signs, symptoms and treatment are logical. We reveal the reasoning process behind each case and this should start to form the ‘schema’ for your future system

1 practice. (We would hope that, if you were to return to the text after gaining some experience, you would wonder why we had bothered to explain the clinical reasoning behind these cases because it is so obvious.) Subsequent case studies in each chapter add to the clinical ‘schema’ and, combined with your clinical experience, should eventually help you to add depth and understanding to your ‘disease narrative’. Since this is a textbook and the patients outlined here are not reliant on us to make immediate clinical decisions, we have used a very structured system 2 approach to discuss each case. Until you build a substantial level of clinical experience, this is the process your instructors will expect you to use. After we have described the clinical reasoning process used, we explain the dangers of adopting system 1 practice too soon.

A step-by-step guide to clinical decision making In order to expose the clinical reasoning process, we use the four-step model of assess, confirm, treat and evaluate (see Fig 1.5).

Step 1: Assess Chapter 4 described using a standardised assessment process to reduce the cognitive workload in the high-stimulus environments that paramedics find themselves working in. This is equally important for novices and experts. Regardless of whether you have wellformed ‘illness scripts’ or not, you will inevitably find yourself creating hypotheses about the cause of a patient’s condition during the assessment process: it’s just the way the human minds works. These judgements may occur before you even meet the patient, based on dispatch details, the patient’s age, their appearance or the way they meet you at the door. Using all this information to create possible causes for a patient’s presentation is advisable, but make sure you finish the assessment process, even if you are confident of your clinical decision (see Box 5.3). Never make a decision based on incomplete information. By the end of your assessment process you will find, using system 1 or system 2, you will have made a clinical decision about the patient’s condition.

Step 2: Confirm Judgement can be described as ‘the assessment of the alternative’ (Dowie, 1993) and it forms an essential step in clinical decision making. Given the uncertainty and time pressures associated with most paramedic cases, the rush to reach a diagnosis and begin treatment can lead to premature diagnostic closure (see Box 5.3). Nearly all experienced paramedics will admit that at one time or another they have failed to pay attention to aspects of the assessment that have not met their preferred diagnosis (cue-criteria mismatch) and have focused on those features that do match. This ‘cognitive check’ stage (Croskerry et al., 2009) is rarely represented in traditional clinical problem-solving models, but is an essential safety check when making decisions in a diagnostically limited environment. For every case presented in this text we suggest alternatives for each condition, because once you start to develop your ‘illness scripts’ you will still be subject to the law of small numbers and you need to review your intuitive response before you proceed to treat any patient. In cases where the omission of a condition could endanger the patient we include a red flag as a warning. Most of the alternative diagnoses offered should be able to be eliminated quickly, but a few may require you to return to the

assessment stage and conduct further assessment. This ‘backward step’ should be considered a success, not a failing of your reasoning process. In some case studies we step you through the DENT process before proceeding any further. The mnemonic DENT is a cognitive tool to help select and eliminate differential diagnoses (see Box 5.4 for further details). B O X 5 . 4P

u ing a DENT in it

You can use the mnemonic DENT to help you break down the judgement phase of the four-step clinical decision-making process. It is especially useful for analysing your decision-making process in case studies or during tutorials. Define the presentation. Based on your assessment, summarise what factors about the patient’s presentation are abnormal. Explore possible solutions. List the conditions that could cause all or one of these abnormal presentations. Narrow your choices. Consider the questions or tests you could use to eliminate or confirm the conditions in your list of hypotheses. Test your solution. Consider how quickly and effectively your proposed treatment should change the presentation if you are correct. If those changes don’t occur in your proposed time frame, this may indicate you have chosen incorrectly.

Step 3: Treat Clinical decision making must extend into the treatment phase (remember, treatment doesn’t necessarily mean treating with medications or procedures—it can include transport, advice or referral). You need to determine whether the treatment is safe and acceptable to the patient.

Step 4: Evaluate Although the effectiveness of medical treatments can vary, most conditions will respond to appropriate treatment. How a patient responds to your treatment plan is invaluable information about the accuracy of your initial assessment and the results should feed back into the decision-making loop (Geary & Kennedy, 2010). When a patient fails to respond to treatment, it might indicate that your initial assessment was incorrect: take this new information and reassess your patient and your decision making. This text should provide

you with a guide as to how responsive each condition is to correct treatment.

Algorithms and cognitive checks While the use of guidelines and protocols may appear to conflict with intuitive decision making, the process of developing clinical guidelines is usually supportive of both intuitive and thoughtful clinical reasoning (Croskerry et al., 2009). For example, algorithms are excellent at distinguishing between classic presentations of a disease (e.g. acute myocardial infarction versus thoracic aneurysm) and can summarise the experience of hundreds of cases collected by researchers for a paramedic who may not yet have experienced either type of case. In high-acuity, task-heavy cases such as cardiac arrest, treatment algorithms lower the cognitive load on individuals and allow teams to operate more effectively without needing detailed instructions (Geary & Kennedy, 2010). Cognitive checks are also commonplace in all forms of clinical practice and address some of the shortcomings associated with both intuitive and thoughtful reasoning (Croskerry et al., 2009; Geary & Kennedy, 2010). Novice radiologists are constantly reminded, ‘The most commonly missed fracture is the second fracture’. This idiom can be described as a cognitive forcing strategy (Croskerry, 2000): it recognises that clinicians looking for the reason why a patient is complaining of pain in a particular area will be satisfied when they find a fracture that explains the pain—and won’t see a second fracture in the same area. Similarly, paramedic students are told never to ignore the patient who is cold, pale and clammy, because ‘the skin never lies’ and the strong sympathetic response required to produce this state is indicative of physiological distress. That medicine makes common use of such idioms is recognition of the fallibility of human thought processes and the need to keep patients safe in spite of our cognitive flaws.

A syndrome approach to patient management Given the limitations of the equipment carried by paramedics it is inevitable that there will be times when even the most experienced clinician will not be able to determine the exact cause of a patient’s condition, regardless of which form of clinical reasoning they employ. But the imperative to treat the patient remains. In these circumstances it is important to remember that the end point is effective patient management and not necessarily a definitive diagnosis. A hypotensive patient whose cause cannot be determined does not require a diagnosis before the syndrome of poor perfusion can be treated (see Fig 5.5).

FIGURE 5.5 The inability to reach a specific diagnosis, even after thoughtful system 2 processing, is not uncommon in the pre-hospital setting, but the lack of diagnostic tools should not preclude treatment. After completing the history, vital signs survey and secondary survey and finding no clear cause, clinicians can revert to a ‘systems’ or ‘syndrome’ approach. Most paramedic services provide broad guidelines for the management of poor perfusion, hypoxia, alterations of conscious state, etc. Where a definitive diagnosis cannot be reached, these guidelines can be used to direct treatment.

Case 1 A 63-year-old female presents to a local doctor in a country town complaining of shortness of breath. She is a tourist on a bus trip and does not speak English as a first language. The tour guide explains that the patient has been unwell for 24 hours and is now complaining of shortness of breath. She has had some mild relief from an asthma inhaler given to her by another

passenger. She has no other medical history. On examination by the GP the patient is oriented but drowsy and can only speak single words because her respiratory rate is 42. She has mild wheezes in the mid-zone of her right lung. Her blood pressure is 100/70 mmHg and her pulse is rapid and regular at 170 BPM. The GP commences her on oxygen and inhaled salbutamol and calls for an ambulance to transfer her to a hospital 50 kilometres away. On arrival the ambulance crew find the patient has deteriorated and is now in an altered state of conscious. Her BP has fallen to 80/60 mmHg. They quickly establish an IV line and transfer her to a stretcher. They assess her and continue with the doctor ’s treatment for asthma. Shortly before they depart, however, they notice that she is inhaling and exhaling a normal volume of air. Despite the mild wheeze this is not consistent with asthma and they examine the ECG more closely. They cannot find any evidence of atrial activity on the ECG (no P waves) and suspect the patient is suffering from a rapid arrhythmia known as supraventricular tachycardia (SVT). This is consistent with her symptoms and they commence treatment with antiarrhythmic medications. These are unsuccessful and the patient is unchanged on arrival at hospital. The crew hand over to the ED medical staff, who try a different medication to treat the SVT. They are also unsuccessful and are contemplating their next step when a senior staff member arrives and inquires about the patient’s temperature. With temperature not being a criteria for either asthma or SVT, it has not been a priority for the ambulance crew or the hospital staff. To the newly arrived doctor, however, the patient appears to be suffering from septicaemia. A tympanic temperature of 41.2°C confirms her suspicions and the patient is started on antibiotics and steroids.

Bias Triage cueing and anchoring are two very strong cognitive biases that occur when teams of medical staff are involved and can lead to premature diagnostic closure —whereby each team accepts a diagnosis from the previous carer that they themselves would not support if they had assessed the patient from the beginning. In this case, trying to communicate with the patient and the severity of the patient’s condition occupied the clinicians and distracted them from completing a full assessment (they had already been told what was wrong with the patient, remember). The patient’s failure to respond to treatment was another cue-criteria mismatch that was not picked up until a ‘fresh set of eyes’ that was not distorted by the triage was able to assess the patient.

Case 2 At 9.30 am on a Sunday a mother calls for an ambulance for her 21-year-old daughter who is suffering from a headache and vomiting. The experienced crew arrives to find the patient sitting at the kitchen table looking miserable. They are told she went out with friends last night but did not drink excessively

and was in bed shortly after midnight. She awoke as normal but soon after developed a severe headache and vomited twice. She has taken two Panadol and the headache has been relieved slightly. She has no medical history and the family has never called an ambulance previously. The crew advise her to continue with Panadol and to attempt to maintain her fluid intake. They leave her in the care of her family. Four hours later her mother finds her unconscious in her bedroom. Investigation later at hospital finds that she has suffered a subarachnoid haemorrhage (SAH).

Bias Representative error occurs when a disease presents atypically. It is especially dangerous in cases such as SAH, where there is a well-defined set of symptoms familiar to all emergency clinicians: sudden onset of severe pain (‘worst in my life’) during exertion, collapse, vomiting and an altered conscious state. In fact, the condition often shows early signs similar to those identified by this patient and as a result is misdiagnosed in up to 25% of cases who present to hospital (Edlow & Caplan, 2000). In this case, the ‘script’ for SAH used by the crew was distorted by its focus on the acute, severe presentation and did not include the prodromal symptoms. Attribution error, whereby the patient is judged as being responsible for their condition, may also have occurred here and distorted the paramedics’ response. The paramedics logically included a ‘hangover ’ in their differential diagnosis but failed to explore any cue-criteria mismatches with this diagnosis. Ascertainment biases are discussed in Chapter 6.

Case 3 A 32-year-old female calls for an ambulance complaining of central chest pain. When the crew arrive she is conscious, talking and clearly anxious. Her heart rate is 120 BPM, her BP is 120/90 mmHg, and she is cool, pale and clammy to touch. Her respiratory rate is 22 BPM, her lungs sounds are normal and she has oxygen saturations of 99%. She says the pain came on suddenly and feels like ‘tightness’ in her chest. She has no other medical history and has not taken any drugs or medications. She has no known allergies.

Bias Base rate neglect refers to our inherent tendency to assume that the prevalence of a disease follows exactly what we have been exposed to in our career. It is the reverse of forming an ‘illness script’: ‘I’ve never seen a young female have a heart attack; therefore young females don’t have heart attacks.’ Although females make up only 10% of myocardial infarction cases that occur in people under the age of 45 (Morillas et al., 2002), they suffer a greater mortality rate (Canto et al., 2012). While young females are less likely to suffer risk factors such as hypertension and obesity, they are at higher risk of hypercoagulable states

from diseases such as lupus or from oral contraceptives (Egred, Viswanathan & Davis, 2005). Given our limited ability to calculate Bayesian probability when we actually ‘know’ the rates of disease and the accuracy of testing, base rate neglect further distorts our accuracy. This patient would clearly be assessed as having ‘cardiac chest pain’ if she were older and male, but in this case it is too easy to ignore the symptoms and focus on conditions more often associated with her gender and age. Of course, the opposite can be true: if every patient you have attended for the past month complaining of shortness of breath has had an underlying chest infection, for the next patient you attend with shortness of breath you will ‘almost certainly’ find a chest infection. This response is closely related to search satisfaction, one of the more common biases in emergency health. Search satisfaction is reflected in the radiographic idiom, ‘The most commonly missed fracture is the second fracture’, whereby the radiologist stops looking for other abnormalities once they find a fracture that explains the patient’s condition. Search satisfaction can occur at both ends of paramedic assessment. It may mean that we see only those cues that match our provisional diagnosis and either ignore or stop looking for other information (also known as confirmation bias, which can lead to premature diagnostic closure). Or it may mean that we are unsure about a diagnosis but identify a symptom for which we have a treatment protocol. This may be sound judgement in some cases, but if we then ‘confine’ a patient to that protocol and fail to keep exploring, there may be aspects we miss. Finally, some aspects of our personality are shaped by our place in society and our views of the world. A number of studies have shown that gender affects clinical decision making, with women making more conservative judgements than men when diagnosing chest pain (Borges & Osmon, 2001; Pearson et al., 1995).

Error wisdom The list of possible cognitive biases is growing as research in this field expands and indeed many overlap (Croskerry et al., 2009). The biases illustrated here are far from a comprehensive list and fail to even address the impact of fatigue, stress, cognitive overload and supervision on the clinician’s ability to make strong decisions. However, they illustrate that human reasoning is inherently error-prone and that if we are to manage our patients safely we need to recognise our less-than-perfect abilities and devise conscious strategies to overcome them.

Summary Like others who work in the field of emergency medicine, paramedics are required to assess and initiate treatment on a staggeringly wide range of health conditions. To do this safely and effectively they must accept the error-prone and biased nature of human decision making and use a range of cognitive processes, from intuitive to analytical, to develop effective management plans for their patients. Despite the lack of historical support for instinctive decision making in medicine (Hamm, 2004), it is becoming clear that it forms the basis of expert clinical reasoning. The ability to recognise the potential for errors and to choose the correct decision-making tool for the circumstance requires paramedics to understand their own thinking and to continually examine their decision-making processes as their knowledge and skills develop with experience.

References Bordage, G., Connell, K. J., Chang, R. W., Gecht, M. R., Sinacore, J. M. Assessing the semantic content of clinical case presentations: studies of reliability and concurrent validity. Academic Medicine. 1997; 72:S37–S39. Borges, N. J., Osmon, W. R. Personality and medical specialty choice: technique orientation versus people orientation. Journal of Vocational Behaviour. 2001; 58:22–35. Boshuizen, H. P.A., Schmidt, H. G. The development of clinical reasoning expertise. In: Higgs J., Jones M., eds. Clinical Reasoning in the Health Professions. Edinburgh: ButterworthHeinemann; 2000:15–22. Canto, J. G., Rogers, W. J., et al. Association of age and sex with myocardial infarction symptom presentation and in-hospital mortality. JAMA. 307(8), 2012. Cholowski, K. M., Chan, L. K.S. Prior knowledge in student and experienced nurses’ clinical problem solving. Australian Journal of Educational and Developmental Psychology. 2001; 1:10–21. Croskerry, P. The cognitive imperative: thinking about how we think. Academic Emergency Medicine. 7(11), 2000. Croskerry, P. When diagnoses fail: new insights, old thinking. Canadian Journal of CME. Nov, 2003. Croskerry, P. The theory and practice of clinical decision-making. Canadian Journal of Anesthesia. 56(6), 2005. Croskerry, P., Cosby, K. S., Schenkel, S. M., Wears, R. L.Patient Safety in Emergency Medicine. Philadelphia: Lippincott Williams & Wilkins, 2009. Croskerry, P., Sinclair, D. Emergency medicine: a practice prone to error? Canadian Journal of Emergency Medicine. 2001; 3:271–276. Croskerry, P., Wears, R. L. Safety errors in emergency medicine. In Markovchick V.J., Pons P.T., eds.: Emergency Medicine Secrets, 3rd ed., Philadelphia, PA: Hanley & Belfus, 2002. Day, S. C., Norcini, J. J., Webster, G. D., Viner, E. D., & Chirico, A. M. (1988). The effect of

changes in medical knowledge on examination performance at the time of recertification. Paper presented at the Proceedings of the 27th Conference in Research into Medical Education, Chicago, IL. Dowie, J., Clinical decision analysis: background and introductionLlewelyn H., Hopkins A., eds. Analysing How We Reach Clinical Decisions. Royal College of Physicians: London, 1993 Eddy, D. M. Probabilistic reasoning in clinical medicine: problems and opportunities. In: Kahneman D., Slovic P., Tversky A., eds. Judgment under Uncertainty: Heuristics and Biases. Cambridge: Cambridge University Press, 1982. Edlow, J. A., Caplan, L. R. Avoiding pitfalls in the diagnosis of subarachnoid hemorrhage. New England Journal of Medicine. 2000; 342:29–36. Egred, M., Viswanathan, G., Davis, G. K. Myocardial infarction in young adults. Journal of Postgraduate Medicine. 2005; 81(962):741–745. Elstein, A. S., Shulman, L. S., Sprafka, S. A.Medical Problem Solving: An Analysis of Clinical Reasoning. USA: Harvard University Press, 1978. Eva, K. W. What every teacher needs to know about clinical reasoning. Medical Education. 2004; 98:98–106. Evans, J. S. Dual-processing accounts of reasoning, judgment, and social cognition. Annual Review of Psychology. 2008; 59:255–278. Freshwater-Turner, D. A., Boots, R. J., Bowman, R. N., Healy, H. G., Klestov, A. C. Difficult decisions in the intensive care unit: an illustrative case. Anaesthesia and Intensive Care. 2007; 35:748–759. Gaba, D. M., Fish, S. K., Howard, S. K.Crisis Management in Anesthesiology. New York: Churchill Livingstone, 1994. Geary, U., Kennedy, U. Clinical decision-making in emergency health. Emergencias. 2010; 22:56–60. Gigerenzer, G., Hoffrage, U. How to improve Bayesian reasoning without instruction: frequency formats. Psychological Review. 1995; 102(4):684–704.

Gladwell, M.Blink: The Power of Thinking without Thinking. USA: Black Bay Books, 2005. Greaves, J. D., Grant, J. Watching anaesthetists work: using the professional judgments of consultants to assess the developing clinical competence of trainees. British Journal of Anaesthesia. 2000; 84:525–533. Groopman, J.How Doctors Think. New York: Houghton Mifflin, 2007. Hamm, R. M. Theory about heuristic strategies based on verbal protocol analysis: the emperor needs a shave. Medical Decision Making. 2004; 24:681–686. Hatala, R. M., Norman, G. R., Brooks, L. R. Influence of a single example upon subsequent electrocardiogram interpretation. Teaching and Learning in Medicine. 11, 1999. Higuchi-Smith, K., Donald, J. Thinking processes used by nurses in clinical decisionmaking. Journal of Nursing Education. 2002; 41(4):145–154. Hitchen, L. Frequent interruptions linked to drug errors. British Medical Journal. 2008; 336:1155. Kahneman, D.Thinking, Fast and Slow. England: Penguin, 2012. Kamin, C., O’Sullivan, P., Deterding, R., Younger, D. A comparison of critical thinking in groups of third-year medical students in text, video and virtual case modalities. Academy of Medicine. 2003; 78(2):204–211. Kurzenhäuser, S., Hoffrage, U. Teaching Bayesian reasoning: an evaluation of a classroom tutorial for medical students. Medical Teacher. 2002; 24(5):516–521. Ledley, R. S., Lusted, L. B. Reasoning foundations of medical diagnosis. Science. 1959; 130:9– 21. Lewis, C., Keren, G. On the difficulties underlying Bayesian reasoning: a comment on Gigerenzer and Hoffrage. Psychological Review. 106(2), 1999. McCarthy, M. Detecting acute confusion in older adults: comparing clinical reasoning of nurses working in acute, long-term, and community health care environments. Research in Nursing and Health. 2003; 26:203–212. McGillis Hall, L., Pedersen, C., Fairley, L. Losing the moment: understanding interruptions

to nurses’ work. Journal of Nursing Administration. 2010; 40(4):169–176. Morillas, P. J., Cabadés, A., et al. Acute myocardial infarction in patients under 45 years. Revista Espanola Cardiology. 55(11), 2002. Newcastle UniversityClinical reasoning instructor resources. Newcastle: School of Nursing and Midwifery, 2009. Norman, G. R. The epistemology of clinical reasoning: perspectives from philosophy, psychology, and neuroscience. Academic Medicine. 2000; 70:S127–S133. Norman, G. R. Research in clinical reasoning: past history and current trends. Academic Medicine. 2005; 39:418–427. Norman, G. R., Young, M., Brooks, L. R. Non-analytical models of clinical reasoning: the role of experience. Medical Education. 2007; 41:1140–1145. Pearson, S. D., Goldman, L., Orav, E. J., Guadagnoli, E., Garcia, T. B., Johnson, P. A., Lee, T. H. Triage decisions for emergency department patients with chest pain: do physicians’ risk attitudes make the difference? Journal of General Internal Medicine. 1995; 10(10):557–564. Shaban, R. Theories of clinical judgment and decision-making: a review of the theoretical literature. Journal of Emergency Primary Health Care. 3(1), 2005. Shaban, R., Wyatt-Smith, C. M., Cuming, J. J. Uncertainty, error and risk in human clinical judgment: introductory theoretical frameworks in paramedic practice. Journal of Emergency Primary Health Care. 2(1), 2004. Sibert, L., Charlin, B., Corcos, J., Gagnon, R., Grise, P., Van der Vleuten, C. Stability of clinical reasoning assessment results with the Script Concordance test across two different linguistic, cultural and learning environments. Medical Teacher. 2002; 25(5):522–527. Simons, D. J., Chabris, C. F. Gorillas in our midst: sustained inattentional blindness for dynamic events. Perception. 1999; 28:1059–1074. Stanovich, K. E., Toplak, M. E. Defining features versus incidental correlates of Type 1 and Type 2 processing. Mind & Society. 2012; 11:3–13. Stanovich, W., West, R. Individual differences in reasoning: implications for the rationality

debate? Behavioural and Brain Sciences. 2000; 23:645–726. Victorian Auditor GeneralManaging Patient Safety in Public Hospitals. Melbourne: Victorian Government, 2005. Wyatt, A. Paramedic practice: knowledge invested in action. Journal of Emergency Primary Health Care. 1(3–4), 2003.

CHAP TER 6

The patient interview By Matt Johnson

OVERVIEW • Like other medical consultations, the paramedic–patient encounter is inherently unbalanced in that the paramedic holds the scientific knowledge required to diagnose the patient, but requires the patient to describe their symptoms and history in order to apply this knowledge. The patient is unlikely to understand the significance or importance of all their symptoms in enabling the paramedic to reach a diagnosis. This remains true despite advances in diagnostic technology (O’Toole, 2008). • Effective clinician–patient communication is fundamental to collecting sufficient information to determine an accurate diagnosis and gaining the support of the patient for the preferred treatment (Groopman, 2007; O’Toole, 2008). • In the diagnostically limited environment of emergency health, the paramedic’s ability to communicate effectively is the primary tool to gather information that will assist in developing a treatment plan (Groopman, 2007). • The clinician’s ability to explain the nature of the disease to the patient and the best method to manage this episode will not only affect the patient outcome but also may be the most significant factor in reducing complaints against clinicians (Stewart et al., 1999). • The use of a structured patient interview plan can provide a ‘map’ to ensure important data is gathered while the patient’s concerns are considered (Lipkin, Putnam & Lazare, 1995; Silverman, Kurtz & Draper, 2008). • The ability to communicate effectively is not a personality trait. Being a good communicator outside the medical interview setting does not always translate into the ability to gather a comprehensive patient history and integrate that data into effective clinical reasoning. However, there is now a substantive body of evidence that suggests that effective medical communication can be taught and improved (Hausberg et al., 2012).

Introduction Despite the increasingly technological nature of medicine, the ability to obtain an accurate history from the patient remains possibly the most essential skill for any health professional (Engel, 1987; O’Toole, 2008). In fact, experienced medical practitioners across a number of specialities will testify that there are many conditions where the physical examination or laboratory investigations are unlikely to yield anything useful and it is the patient’s story that offers the only route to reach a diagnosis (Groopman, 2007). That is not to say that patients know what is wrong with them: their stories are often distorted by anxiety, fear, pain and prejudice. But to sort through these distractors and reach a diagnosis may require paramedics to explore (rather than ignore) the patient’s perceptions and experiences of their illness. This requires an open-minded and flexible approach that does not always come naturally to the independent-minded clinicians drawn to emergency medicine. Good clinicians are able to extract an appropriate history from the patient and use it to formulate a diagnosis while simultaneously establishing sufficient trust with the patient so that they approve the clinician’s preferred management strategy. Studies have shown that effective communication is linked to improved patient outcomes (Stewart, 1995; Stewart et al., 1999) and fewer malpractice claims (Levinson et al., 1997) and medication errors (Kohn, Corrigan & Donaldson, 2000). Yet, despite the significant impact on patient outcomes that a paramedic’s interpersonal and communication skills can have, some studies suggest that communication skills actually decline during the health professional’s education (Rider, Hinrichs & Lown, 2006) as students focus on learning the science of their discipline—that is, the pathophysiological pathways, the management protocols and the appropriate drug regimens rather than talking and listening to patients. However, research also shows that effective medical communication is a skill that can be learned. This chapter outlines the essential communication skills and a structured approach to communicating with patients. Together these should enable you to extract the right information from patients in a timely manner.

The structured patient interview In Chapters 1–5 we described the underlying challenges of delivering community-based emergency healthcare as a paramedic. We outlined the role of paramedics in modern society and indicated that an ageing population and the associated chronic disease burden have increased both the workload and the complexity of the paramedic’s role, and have moved it away from the high-acuity cases (heart attacks and trauma) that most people associate with the profession. Understanding and managing chronic diseases are now essential paramedic skills. We also explained that patients who engage in paramedic care do so unexpectedly and as such often do not have a full understanding of their symptoms or how they should be managed. In many cases, it is the patient’s friends or family who call the emergency services and the patient may not want to be assessed by the paramedics. In this highly emotive setting paramedics have to make safe and accurate decisions. In Chapter 4 we introduced the structured clinical approach, a ‘road map of patient assessment’ designed to give paramedics a step-by-step approach to collecting the information necessary to make the most appropriate management plan. This approach was described as the process of patient assessment and in Chapter 5 we explored how the content generated by this process can be used (or misused) to reach a diagnosis or management plan. The process we described in Chapter 4 is not complete, however, as it focused primarily on the clinical tasks required of the paramedic: the patient there was entirely passive and almost irrelevant to the process. In reality, patients are far from passive: they may have strong ideas about their condition and will express these ideas when they feel it is most relevant. From the moment paramedic and patient meet they are trying to express their needs to each other: too often, the competing nature of this interaction results in lost information or misunderstandings, or even conflict. In this chapter we add a structured approach to the patient interview to the standardised assessment introduced in Chapter 4. We also explain how the beliefs, roles and actions of both the patient and the paramedic affect the quality of information exchange and the subsequent quality of care.

‘Patient interview’ vs ‘taking a history’ In this chapter we use the phrase ‘patient interview’ rather than the more common paramedic description of ‘taking a history’. The tasks involved in taking a traditional case history (see Box 6.1) are not well attuned to the paramedic environment where time and resources are limited; and the word ‘take’ suggests the clinician does little more than scribe what the patient offers (Lipkin, Putnam & Lazare, 1995). Such an outdated description of the assessment process is no longer valid. Cognitively, the structure of the traditional history-taking process is also longer and more complicated than it needs to be for many diseases: some aspects provide no diagnostic worth, yet consume the clinician’s time and attention. The phrase ‘patient interview’, although uncommon in paramedic circles, reflects the true nature of the modern clinician–patient encounter: both parties interacting and sharing information to reach a mutually acceptable understanding of what needs to occur and how it will progress.

B O X 6 . 1T

h e h isto r y-ta k in g p r o c e ss

Traditional medical history structure 1. Chief complaint 2. Immediate illness history 3. Past medical history 4. Medications 5. Allergies 6. System review 7. Family medical history 8. Childhood diseases The importance of the prodromata (what happened before) in diagnosing illness is described in medical texts as far back as Roman times (Prioreschi, 1998), but it was the explosion of scientific medical knowledge in the 19th century, particularly the attribution of diseases to specific organs, that inspired a formal approach to gathering medical information from patients. Klemperer ’s (1903) 57-point ‘scheme of assessment’ would easily pass for a modern hospital-based case history today. Created at a time when the increasing complexity of medicine required a list to avoid ‘mistakes of omission’, this template was based purely in science and optimistically assumed that only gathering objective facts would lead to an accurate diagnosis. Ignoring that medical science was (and still is) incomplete, some scholars argue the unemotional nature of the ‘historytaking process’ also contributed to its success (Roter & Hall, 2006). The scientific structure of the process removed the doctor from any emotional interaction with the patient and disguised the uncertainty of the diagnosis from both the patient and the clinician. By shifting the focus from the patient to the disease, this checklist approach created a ‘low-context’ environment that allowed doctors to retreat away from the emotional impact of the illness to a position of ‘pure rationalism’ (Roter & Hall, 2006).

The science and art of communication If we were all identical in beliefs, experiences and physiology, clinicians would not need to focus so closely on communicating with patients. They would simply need to ask a series of standard questions, perform the necessary tests and process the data and it would always lead to a logical conclusion. But while medicine is based in science, it is a human undertaking that is practised in a world mired with beliefs, values, opinions and inconsistent levels of knowledge (Saunders, 2000; Tolana, 2007; see Fig 6.1). Clinical decisions are rarely based on scientific values alone: the variability of human bodies and disease presentations does not allow that degree of certainty. We need the rich details of the patient’s story to assist us in reaching a diagnosis.

FIGURE 6.1 What we say, how we say it and what we expect to hear is usually shaped before either party speaks a word. Look at the above images and you cannot help but attribute the style of conversation you would have with each individual. A uniform sharpens that effect by reducing the impact of gender, age and physical appearance and defining the role of the wearer. Source: Top: Thinkstock/moodboard; Thinkstock/Ingram Publishing; bottom: Thinkstock/lukas_zb; Thinkstock/AntonioGuillem. The notion that the patient’s description of their illness has more diagnostic power than modern technology does not sit easily with all clinicians and many novice paramedics will quickly suggest the ECG as a definitive tool in the assessment of chest pain (see Fig 6.2). The challenge of determining whether a patient’s chest pain is related to their heart is a task most city-based paramedics will perform three or four times per shift, and the notion

that a machine is both sensitive and specific enough to identify the nature of this pain fits easily into our view of modern medicine. Unfortunately, the ECG’s sensitivity to identify early evidence of damage to heart tissue has been shown to be 69% at best (Kudenchuk, Maynard & Cobb, 1998) and possibly as low as 13% (Rouan, Lee & Cook, 1989). In reality, the paramedic’s decision regarding the most appropriate management plan for a patient will be determined on the basis of the patient’s description of their pain and other symptoms.

FIGURE 6.2 Many novice paramedics will quickly suggest the ECG as a definitive tool in the assessment of chest pain.

Parson’s affect neutral model How we express ourselves (verbally and non-verbally) is very dependent on the role we perceive we have in the circumstance: this is especially true when we communicate with people we have never met. Historically, the roles of patient and clinician are strongly ‘socially legitimised’ and were first described by American sociologist Talcott Parsons in 1950 (Parsons, 1951a). According to Parsons, the clinician is the holder of medical knowledge while the patient is the seeker of that knowledge. The clinician should dispense their knowledge without favour, undue profit or concern for anything other than the patient’s welfare. The clinician asks the questions; the patient answers them honestly. The clinician dispenses advice; the patient should accept and adhere to that advice (see Table 6.1). This active–passive divide attributed well-defined rights and obligations to both parties and characterised the interaction between them for much of the second half of the last century. But because it attributed complete control of the interaction to the doctor it was rarely a construct that allowed the clinician to fully understand the patient’s presentation. That it survived (and in some places grew) as a model of communication was probably due to its alignment with the social norms of the era and the aspirations of the medical profession in maintaining a distinct professional separation.

TABLE 6.1 Traditional clinician–patient role relationship Patient Clinician Passive Active Seeks help Provides help Needs medical knowledge Holder of medical knowledge Information supply (answers) Information collection (asks) Complies with advice (cooperation) Provides advice (guidance) Key to this traditional role structure was that the clinician had to remain neutral to the patient’s personal or social attributes and focus only on the disease (Lipkin, Putnam & Lazare, 1995). The model also suggested that any failure in the consultation was a result of either party failing to adhere to their roles and responsibilities. It was quickly noted, however, that the distinct role division was actually a cause of conflict between the two parties: patients were not completely unaware of their illness—they formed ideas as to the cause, possible investigations and treatment (Katon & Kleinman, 1980). When their ideas of their illness were not addressed, they felt the clinician was either uncaring or incompetent (DiMatteo & Hays, 1980; Valentine, 1991). In such cases they were less likely to follow the clinician’s advice, regardless of how appropriate it may have been. The concept of the patient as the unknowing seeker of medical advice was probably never entirely true but it is now rapidly decaying. Patients’ ability to access medical information has rapidly accelerated over the past decade, with one study finding that 41% of participants were influenced by the Internet about seeking medical care, treating an illness or questioning the advice they received from their doctor (Forkner-Dunn, 2003). Parson’s model also placed the responsibility of collecting information on the clinician and directly contributed to the traditional history-taking method: long lists of questions, often grouped by organ system, but excluding personal data, patient interpretations or expectations (Lipkin, Putnam & Lazare, 1995). Simultaneously, the increasing corporatisation of medicine has seen all clinicians— doctors, paramedics and nurses—become more subject to economic pressures. This inherently challenges the concept of a value-neutral clinical decision made solely on the best interests of the patient, but also fails to take into account that the implications of all clinical decisions radiate outwards from the individual patient to the public healthcare system and ultimately to the entire community (Masse et al., 2001; Saunders, 2000). While the social distinction and power imbalance between patient and clinician described by Parsons is still evident today (and still actively pursued by some clinicians), the asymmetrical model describing the relationship between clinician and patient fails to accurately describe the actual encounter or act as a tool to build effective communication.

The Explanatory Model Just as Parson’s model was published, other attempts were made to describe the clinician– patient relationship. Less authoritarian than the active-passive relationship described by

Parsons, the Explanatory Model acknowledges not only the value of the patient’s input into the interview but also how it can lead to conflict. The Explanatory Model recognises that nearly all patients have an understanding of the cause, severity and expected treatment for their illness (Carrillo, Green & Betancourt, 1999; Kleinman, Eisenberg & Good, 1978). This explanation may be based on culture, beliefs and past experience more than scientific evidence, but unless it is recognised and addressed there is no means of developing a satisfying and effective management plan (Baer et al., 2008; Haidet et al., 2008). While Parson’s model bestowed professional expertise and authority on every clinician by virtue of their role, patients are actually reluctant to trust those who they consider have not listened to or understood their description of their illness (Roter & Hall, 2006). The vital distinction that the Explanatory Model makes is between illness and disease (see Table 6.2). Patients are primarily concerned with illness: why they are ill, how the condition affects their lives, what it doesn’t allow them to do—and they may create a narrative that explains all of these aspects. Paramedics are primarily focused on the biological dimensions of disease: linking the pathology to the abnormal function of tissues and extending this to the creation of specific symptoms (Stewart et al., 1995). Paramedics use this ‘narrative’ to create a coherent and logical story in their minds that identifies the underlying disease. As a result, there is enormous potential for conflict between the two explanations if they are not explored and expressed appropriately (Kleinman et al., 1978). In reality, neither explanation has to be the sole focus of the interview and to ignore one or the other will leave one party unsatisfied. It shouldn’t belittle the clinician to allow the patient to express their understanding of the illness as it is the only tool the paramedic has to develop a shared understanding of the disease and to negotiate a successful resolution of the health problem (see Box 6.2; Baer et al., 2008; Haidet et al., 2008). It may be difficult for some novice clinicians to accept that their role is not simply to diagnose the disease, nor is it the patient’s role to accept that diagnosis with blind faith. To ensure that the patient believes their illness is being appropriately managed, paramedics may have to not only implement the correct treatment, but also convince the patient that their diagnosis is in fact correct. B O X 6 . 2S h a r e d

va l u e s

Although we communicate with people every day, the encounter between clinician and patient is not a typical social encounter. In addition to the stresses of pain and illness, any exchange between clinician and patient is framed by specified roles and responsibilities: the clinician as the caregiver and the patient as the care receiver. When we communicate we constantly send and receive messages, encode and decode, and respond consciously and subconsciously in what can be described as a ‘transactional’ model (Buckman, 2002). This communication occurs in a fluid state: neither party is certain where it will go, and both parties are constantly trying to read and respond to the messages they are receiving. All this happens against background noise and requires perception, interpretation, filtering and modification, all contextualised by biases and prejudices, values and beliefs.

To be an effective communicator you therefore need to analyse the other person’s frame of reference. You also need to develop an awareness of the other person’s perceptions, biases and preferred techniques—and become aware of your own. Finally, you need to become fluent in a range of communication strategies (see Fig 6.3).

FIGURE 6.3 The transactional model of communication suggests that each party is trying to express their needs until a mutual point of understanding is reached or one party is able to dominate the decision-making process. Reaching a mutual understanding of the outcome is quicker if we understand the needs behind both party’s attempts to influence the decision process.

TABLE 6.2 Explanatory clinician–patient relationship Patient Clinician Expert on illness Expert on disease Has concept of cause Yet to form concept of cause Needs concerns addressed Needs to develop a management plan

Case 1 A 75-year-old retired schoolteacher calls for an ambulance at 0900 on a weekday complaining of shortness of breath. He is surprised when two young female paramedics arrive to assess him but he explains clearly that for the past 2 days he has been short of breath when he exerts himself. He states the last time this occurred was due to fluid accumulating in his lungs as a result of a problem with his heart and that he spent nearly a week in hospital. He was started on a new medication after this event which he takes every day and has had no reoccurrence of the problem until 2 days ago. He feels he may have developed a tolerance to his medication and needs to go to hospital as he ‘nearly died’ last time. On assessment, the paramedics find no evidence of acute pulmonary oedema (APO; fluid on the lungs), and the patient’s pulse and blood pressure are normal, as is his ECG. He states the shortness of breath hasn’t disturbed his sleep and occurs only when he walks briskly and that he has had a productive cough of purulent sputum for a week or so following a head cold. He appears well, is talkative, is not currently short of breath and his temperature is normal. His respiratory rate is 16 and his oxygen saturation is 98. On auscultating his lungs the paramedics find a small area of coarse irregular crackles in the midzone of his left lung that alter after a cough. The patient shows none of the signs of APO but has a well-localised chest infection that may require antibiotics. The paramedics suggest that the best management plan would be for the patient to attend his GP but he insists they are wrong and he needs to go to hospital—immediately.

Case 2 A young mother calls for an ambulance in the early hours of the morning for her 2-year-old son. The boy has woken with a barking cough after being unwell with a runny nose for 2 days. She tells the crew she believes he is suffering from asthma as his father had asthma as a child. She is very distressed because she feels asthma is a serious disease and will restrict her son’s activities for life, just

as it has for her husband. The crew find the child conscious but in moderate respiratory distress. His has an inspiratory stridor but his tidal volume is unaffected. His lungs are clear with no wheeze and he has a mild temperature. The signs and symptoms are consistent with croup, a viral infection of the upper airways that affects young children. What would you say to the mother to relieve her incorrect diagnosis? Would she believe you?

The notion of the patient interview as a negotiation challenges many clinicians who instinctively feel patients should comply with expert opinion. However, the interview is not a negotiation in the commercial sense whereby, for example, two parties seek ownership of property, but is rather a negotiation to resolve the conflict between the clinician’s and the patient’s explanatory models. The result allows the paramedic to provide optimal clinical care, while the patient feels what they have received is in their best medical and personal interests (Buckman, 2002; Haidet et al., 2008; Lipkin, Putnam & Lazare, 1995). The ability to reach a negotiated ‘truth’ becomes the purpose of the interview.

CA SE ST U DY 1 Case 11274, 1147 hrs. Dispatch details: A 72-year-old female is complaining of chest pain. Initial presentation: The ambulance crew finds the patient sitting on a chair at a crowded food-court in a major shopping centre. She is pale but conscious and surrounded by concerned friends. The patient is telling everyone she is ‘fine’, but friends tell the crew that the patient suddenly complained of feeling unwell and that she had chest pain. The patient and her friends are on a shopping tour prior to leaving on an overseas cruise in 2 weeks’ time.

The paramedic interview setting In most locations where medicine is practised there is order and function. Emergency departments (EDs) are full of signs and labels: spaces are clearly delineated, information is strategically placed and roles are easy to identify (O’Toole, 2008)—it is unlikely anyone will confuse a doctor with a patient or a nurse with a family member. Similarly, GP consultation rooms are private and the layout makes it obvious where the patient is to sit and what role they are to assume. Compare this with the crowded noisy environment in case study 1 where friends are surrounding a patient who has yet to accept she is even ill. Although regular medical consultations may be stressful events, most institutions have worked hard to create an environment that makes it as quick, easy and safe as possible to extract the best possible information from the patient. The paramedic’s workplace is very different and is frequently a place of high stimulus and precious little information (see Fig 4.1). In this noisy, emotional and unfamiliar environment the paramedic may not even know the patient’s name before having to commence their assessment. If it is in a public place there may be many people to judge the paramedic’s actions and words. For this reason, developing a structured approach to the interview portion of the patient assessment is essential. Most ambulance services use a form of the standardised assessment (including collecting a verbal history) introduced in Chapter 4, as it reduces the stimulus on the paramedic by providing a step-by-step approach to patient assessment. The paramedic completes one task at a time and, by doing the steps in order, the resultant data should provide the information necessary to build a safe and accurate differential diagnosis. While some components of the standardised approach involve clinical skills such as taking a pulse or blood pressure or auscultating lungs, most of it involves asking questions and then —most importantly—listening to the answers.

Paramedic–patient interview structure Using the various social models that describe the clinician–patient interview, numerous researchers have developed guidelines and checklists to assist clinicians to conduct effective patient interviews (see Fig 6.4) and gain accurate diagnostic information (CohenCole, 1991; Makoul, 2001; Novack, Dube & Goldstein, 1992; Riccardi & Kurtz, 1983; Stillman, Sabars & Redfield, 1976; van Thiel & van Dalen, 1995). For the unique nature of the paramedic–patient interview we have adapted the Calgary-Cambridge guide (see Fig 6.5; Kurtz et al., 2003; Silverman et al., 2008). This framework has been chosen because it doesn’t simply overlay communication skills on top of the traditional model of taking a medical history. Instead, it integrates the communication tasks into the process of gathering a history and recognises that there are phases in the patient interview where the paramedic needs specific, detailed information, and moments when the patient should be encouraged to tell their story. It also recognises that the intrusive and intimate nature of the physical examination (pulse, blood pressure, ECG) is both part of information gathering and a form of communication and relationship building between paramedic and patient.

FIGURE 6.4 Paramedic–patient interview structure. Source: Adapted from Kurtz et al. (2003).

FIGURE 6.5 Structuring the patient interview provides the clinician with a road map to guide and provide landmarks where specific communication tools need to be used. Performed effectively, it addresses the patient’s need to feel their story is understood. Source: Adapted from Kurtz et al. (2003). The framework provides a logical, structured approach to the patient interview that directs the paramedic towards a conclusion but also ensures that important information is not missed (Nolan, 2000). It recognises that specific communication skills need to be used at specific times and for specific goals. Apart from providing landmarks that the paramedic can return to if interrupted, by dividing the interview into distinct phases it also delineates points where the paramedic’s communication style needs to change if it is to be effective. Finally, the framework decreases the cognitive load for the paramedic by dividing the interview into small acts, each of which is finished before the next is started, while simultaneously building a rapport with the patient. This structured framework builds the interview using five basic steps: 1. initiating the session 2. gathering information 3. physical examination 4. explanation and planning 5. closing the session. Each of these can be further divided by activities and tasks (see Fig 6.5). Performed correctly, these steps should provide the paramedic with accurate information collected in a form that is easier to contextualise while also addressing the patient’s concerns.

Step 1: Initiating the session Errors that occur early in the interview impact on the paramedic’s clinical decision making, but the first few moments also shape the patient’s view of the clinician’s competence (see Box 6.3). In terms of stimulus versus information, this is the phase where possibly the greatest imbalance exists, and communication in this early stage cannot simply conform to social conventions and politeness. The information and trust gained at this point will have ongoing effects on the accuracy and efficiency of the interview (Silverman et al., 2008). B O X 6 . 3F

ir st im pr essio ns c o unt

‘Real communication occurs when the evaluative tendency is avoided, when we listen with understanding. It means to see the expressed idea and attitude from the other’s point of view, to sense how it feels to him, to achieve his frame of reference in regard to the thing he is talking about’ Rogers (1961) For the paramedics involved, cases commence when the dispatch is received. For patients, however, the events leading up to a call may stretch back weeks or even years. Failing to appreciate why a patient has engaged an ambulance service and what that process will do to their communication style impedes many paramedics from conducting a successful patient interview. Probably the most obvious impact of the patient’s state of mind on their ability to communicate effectively is the case of a patient who is experiencing severe pain. In such a case no-one would be surprised that a normally quiet and reserved person could respond with anger or impatience towards those trying to assist them. Fail to gain a patient’s trust, or make them feel as if you do not understand their situation, and they will consider you to be unprofessional and poor at your job. Remember, the patient doesn’t know how well you followed the guidelines or how accurately you performed their chest auscultation. They only know how much you seemed to care and listen.

Preparation Paramedics usually work in teams so there is an opportunity to brief cases before being confronted with a patient. For novice paramedics, this is an opportunity to read the dispatch details and start preparing a list of likely differential diagnoses. For case study 1 the crew might consider the common causes of chest pain and determine what information (signs, symptoms, diagnostic tests) could be used to differentiate between them. This process can also identify causes for which the paramedic does not have a strong ‘illness script’ prepared and would thus unknowingly not include in their

differential process. As you drive to a case you can assess how you are feeling and if this could lead to a cognitive disposition to respond (see Ch 5). Are you hungry, tired, cold or not working well with your partner, or did you miss an obvious cause the last time you attended a similar case? This will impact on how you communicate with the patient and how you make clinical decisions. You may not be able to alleviate all such issues, but being aware of your biases could minimise their impact.

P RACT ICE T IP The patient interview has three prime functions: 1. gather information 2. respond to the patient’s needs/emotions 3. influence behaviour (Lipkin, Putnam & Lazare, 1995).

Observ ation Given the stress of driving under ‘lights and sirens’, it is easy to arrive at a case and continue the sense of urgency. Remember, effective paramedics use structure to reduce stimulus and seek to gain information wherever they can. While you are collecting your gear from the vehicle take a moment to observe the environment: is it a well-kept house with an immaculate garden or is it overgrown and poorly tended? This can give you clues as to the patient’s normal level of activity and the expectations they will have regarding treatment and outcome. Numerous photos of family members can indicate levels of social support—as can a shopping expedition with friends! Take a moment to absorb your surroundings, as they will probably contextualise what you find during the patient interview and examination.

Establishing initial rapport: introduction and role clarification Start by introducing yourself and your partner: Hello, my name is Sarah and this is my partner, Tom. We’re from the ambulance service. What is your name? While media and public impressions of paramedic practice are of task-driven care of critically ill patients, the reality is that more than 90% of patients are conscious when paramedics arrive (QAS, 2011). Paramedics may deploy their life-saving ‘technical skills’ such as chest decompression or defibrillation only once or twice a year, but every day they have to sort through the complex medical histories of (usually) elderly patients suffering from multiple diseases before they can determine an appropriate management plan. Most paramedics (and indeed most medical practitioners) make the false assumption that patients feel relieved by the arrival of a health professional. Research suggests, however, that patient responses to medical emergencies are much more complex (refer to Fig 6.6) and, unless these responses are understood, the paramedic risks making assumptions that will restrict their ability to gain an accurate history (Gallagher et al., 2005). Patients often face a series of events (onset of pain) and decisions (take medication, call family, call emergency number) before the paramedics arrive. For many patients, the

arrival of two (or more) uniformed medical professionals carrying equipment only confirms their worst fears: that they are, in fact, seriously ill. Offering a calm, relatively standard greeting can normalise the situation for the patient.

FIGURE 6.6 It’s widely assumed that patients feel relieved when paramedics arrive at a scene. Research suggests, however, that patient responses to medical emergencies are much more complex. The arrival of paramedics can add to the patient’s fear or their sense that the situation is even worse than they thought. Failing to understand the patient’s emotion can limit the quality of information paramedics extract during the interview. Paramedics should also remember that patients who have called for help have reached a point where they have admitted that they or their family can no longer cope with their illness or the situation confronting them (Morgans, Archer & Allen, 2008). This can evoke feelings such as vulnerability, shame and embarrassment. That they have resorted to calling strangers for help can act to reinforce their sense of helplessness or isolation. Identifying yourself as paramedics can be vital when dealing with elderly patients who may struggle to differentiate one uniform from another due to failing eyesight. Not knowing who has arrived or what role they play can be extremely unsettling (Silverman et al., 2008)—often it is not the patient who has called the ambulance but friends or family members after the patient has complained of feeling unwell. Paramedics should not assume that the patient knows who they are or why they have been called. The shift to university training has dramatically altered the demographic of paramedics practising in Australia and New Zealand, and many elderly patients will be surprised when young or female paramedics arrive to manage their health emergency (see Fig 6.7). For these patients, offering a professional introduction and referring to the patient respectfully (Mr or Mrs as opposed to Darl, Pet, Sweetie, Mate etc) will overcome their suspicion that the paramedic is too inexperienced to manage their condition.

FIGURE 6.7 Elderly patients are often surprised when young female paramedics arrive to attend to them. While being young and female does not impact on job performance, ignoring the fact that patients may have such an initial reaction will affect how much a patient will trust the crew’s advice. As a result, many young paramedics need to portray themselves (visually and with language) more professionally than older paramedics. Source: Image courtesy St John New Zealand.

Effective communication at this point of the interview is dependent on the paramedic’s ability to analyse and accept the patient’s frame of reference (see Fig 1.3 in Chapter 1). Each party brings their past experiences, prejudices and social status to every communication event. In the prehospital environment these are just some of the factors that contextualise how patient and paramedic will express themselves in the setting of a health crisis and this is further complicated by the stress of the situation and other environmental factors. Effective paramedics take into account their own and the patient’s backgrounds to determine ‘what the patient is trying to express’ and what methods they can use to display understanding and to communicate their own needs. Without this perception it is difficult to achieve understanding between the parties. The way we react to a situation is dependent on our past experiences, beliefs and values. These determine not only how we create an ‘explanation’ of our situation for ourselves, but also how we express that explanation to others. While the ability to recognise our cognitive biases is vital to effective clinical decision making, our ability to recognise the biases of our patients is also essential if we are to gain their trust and support. A young paramedic who achieved excellent grades at university may feel confident in her ability to care for her patients, but unless she accepts that her patients may not instinctively share that belief she will not address the discrepancy. Remember, patients are almost certainly unaware of the paramedic’s adherence to clinical guidelines when being treated: they do not know whether the correct drug was administered, in the correct dose, at the correct time. Instead, they will judge the paramedic’s clinical ability on the basis of his or her ability to listen and display empathy. It is difficult to overstate the importance at this stage of gaining the support, trust and involvement of the patient in helping you develop a management plan.

Identifying the reasons for the consultation It’s nice to meet you, Mrs Jones. Why have you called an ambulance today? While the question of identifying why the patient requires medical attention fits logically into the interview structure for doctors, it often creates tension between patient and paramedic. Again, the key is to seek the patient’s perspective of the events that have led up to this point. Many patients have already explained their situation to the emergency call-taker and assume the paramedics are fully aware of it, so the paramedics asking this question can immediately cast the crew as not fully understanding the situation. The worth of having a structured approach is often revealed at this point, when many novice paramedics, lacking a specific question, phrase the query as they would in normal social circumstances: How are you going? Too often, the reply is an abrupt and confidenceshaking: I’m terrible, that’s why I called an ambulance! This vague question can also allow the patient scope to answer in broad terms: I’m terrible, my back hurts, I can’t sleep properly, my eczema is playing up and I just feel terrible. Why have you called an ambulance today? is often a question patients feel they have already answered to the call-taker and one the paramedics should already know. While there is no ‘correct’ opening question for all circumstances (Gafaranga & Britten, 2003), How can we help you today? displays both interest and concern, but is usually specific enough to guide the patient towards a description of why an ambulance was called in this instance. Whatever question is chosen, clinicians need to carefully consider the impact of how they start the interview (Silverman

et al., 2008).

Env ironmental control Considerations of where the interview should be conducted are not addressed in the Calgary-Cambridge framework as most medical interviews are scheduled to occur in appropriately private locations. Interviews conducted by paramedics, however, tend to occur in public spaces. The ability to elicit frank and honest answers from patients and to conduct a physical examination is dependent on how comfortable the patient feels in that environment, and paramedics may need to exclude bystanders or move the patient to make it more conducive. Even when the patient is physically and psychologically comfortable, paramedics can create a more conducive interview setting by reducing background noise or adjusting ambient lighting, for example. Importantly, assuming a position close to the patient and at the same height reduces the power imbalance inherent in the interview and suggests that the paramedic is not only focused on the patient but is also willing to devote time to their assessment (Silverman et al., 2008).

Step 2: Information gathering With the tone of the interview set, the next stage addresses two overlapping needs: the patient’s need to convey what they feel is important about their illness; and the paramedic’s need to identify the underlying disease. Accordingly, the paramedic adaptation of the Calgary-Cambridge model divides this phase into two distinct components that require different communication skills. In the initial patient-centric phase the skill of active listening is essential; while controlling the subsequent paramediccentric phase with directed questions ensures the collection of accurate information specific to the disease process.

Listen to the patient’s opening statement (patient-centric phase) As already discussed, patients assess and engage with the paramedic based on their belief that the paramedic ‘understands’ what is happening to them. For this to occur, the patient must have the opportunity to present their explanation of the illness. While allowing the patient to fully explain the nature of their illness may seem obvious, it rarely translates into reality: studies have found that doctors allow their patients the opportunity to complete their opening statement of concerns in only 23% of cases before interrupting them with a question directed towards a specific concern—with the average time to interruption ranging between 12 and 23 seconds (Beckman & Frankel, 1984; Marvel et al., 1999; Rhoades et al., 2001). Interestingly, female doctors were found to interrupt their patients less often than male doctors, but female patients were interrupted more frequently by both genders compared with male patients (Rhoades et al., 2001). While discredited in its ability to generate a good history and address the patient’s concerns, Parson’s patriarchal description of the doctor–patient encounter certainly seems to align with instinctive human behaviour. Some clinicians may be concerned that, left unchecked, patients will take so long to describe their situation that it will impact on patient care and scheduling. However, a number of studies have indicated that patients allowed to complete their opening

statement without interruption take less than 10 seconds longer on average than those who are redirected during their description (Marvel et al., 1999), and even patients with a complex history are able to fully describe their condition in less than 2 minutes (Langewitz et al., 2002). In order to benefit from the patient’s opening statement requires more than just silence on behalf of the paramedic. Listening doesn’t simply comprise being able to recite what a patient has said. For the patient to feel you are listening, they need to feel you are present ‘psychologically, socially and emotionally’ (Egan, 1990). This engagement is not easy for paramedics who feel their role is to supply medical expertise, but patients list traits such as honesty, respect and empathy as being equal to competency in what they are seeking from a medical consultation (Ley, 1998). Most of the cues patients use to determine whether the paramedic is listening come from the paramedic’s body language (Silverman et al., 2008). Important among these is eye contact, and taking notes has been shown to reduce the patient’s belief that the clinician is paying full attention to all their concerns (Ruusuvuori, 2001). Expressing your concern can be supplemented by the use of facilitative phrases such as, ‘yes’, ‘good’, ‘uh-huh’ and ‘I understand’ (Silverman et al., 2008). By the end of this phase the paramedic should be able to understand the patient’s perspective on their illness: their concerns, their understanding of the cause and their expectations for this episode. The shift from the patient-centric phase to the paramedic-centric phase of information gathering reflects the shift from an understanding of the illness to determining the underlying disease. Before this commences it is important to provide the patient with a summary of your understanding of the illness. Critically, this demonstrates to the patient that you have absorbed and understood their explanation. This may be vital if you are to later present a conflicting explanatory statement about the disease: the patient’s ability to accept a ‘negotiated truth’ will depend on their belief that you have integrated their ‘truth’ (Haidet et al., 2008). For example: So, Mrs Jones, from what you have described, you’ve had 3–4 days of chest pain that comes when you walk but goes away when you rest. It’s only occurred during the day but you’ve never had it before last Wednesday. You think the pain is muscular because you fell playing bowls on Tuesday, but your friend told you it sounds more like heart pain. Today the pain came on again after you climbed some stairs and your friend insisted on calling an ambulance. From what you’ve said, the pain has almost completely gone but might just be there a little bit. At once, this paraphrasing demonstrates your listening and understanding of the patient’s perspective. Importantly, this is not the time to challenge any of the patient’s ideas—regardless of how inaccurate you perceive them to be.

Seek the biomedical perspectiv e (paramedic-centric phase) Determining the underlying disease process requires the paramedic to assume more control over the interview but does not mean that the patient becomes completely passive. The aim is to gather ‘accurate, complete and mutually agreeable’ information (Silverman et al., 2008). Whereas the patient-centric phase required a single open question (How can we help you today?), this phase requires careful use of closed and open questioning techniques. Closed questions are specific and can usually be answered with a single word: Is the pain sharp or dull? Do you have pain at the moment? They are invaluable when trying to differentiate between conditions. An important skill in phrasing closed questions is not to

suggest to the patient that one answer is better than another. Patients rarely intentionally act to deceive, but they will have their own explanations and expectations of their condition and may tend to align their answers if they feel this fits with their explanation. Open questions allow the patient to introduce information on conditions that the clinician may not have considered previously: Tell me about this pain you’ve been having. They have been shown to produce more information more quickly than a series of closed questions (Takemura et al., 2005). The use of open questioning to gain information without influencing the answers and then using closed questions to refine the answers has been described as the open-to-closed cone (Goldberg et al., 1983). In structure, the biomedical perspective aligns closely with the traditional medical history used commonly in both medicine and paramedicine: 1. key history (immediate sequence of events leading to the consultation) 2. symptom investigation.

Key history The sequencing and progression of symptoms can be strongly indicative of a particular disease process: shortness of breath from APO tends to manifest in the early hours of the morning after several hours of lying supine, whereas asthma presents acutely at any time but rarely when the patient is asleep and unable to expose themselves to an allergic trigger factor. Thus, identifying when particular symptoms occurred and their severity can help identify the underlying disease. If the patient has been allowed to describe their illness, much of this information will already have been extracted. The patient’s opening statement will often present most of the key history.

Symptom inv estigation A number of mnemonics have been developed to assist clinicians in creating the open-toclosed cone required to fully investigate a patient’s symptoms. The most commonly used mnemonic in paramedic practice is DOLOR (which conveniently is Latin for pain): Description of pain/discomfort Onset Location Other signs and symptom Relief Two other mnemonics that may be used are shown in Box 6.4. B O X 6 . 4H i s t o

r y-g a th e r in g a id s

Aside from DOLOR, there are other mnemonics that can be used to investigate a patient’s symptoms:

WWQQAA + B Where When Quality

Quantity Aggravating and relieving factors Associated manifestations Beliefs

OPQRST Onset Provocation Quality Region, relief, radiation, recurrence Severity Time

Description The description or nature of the pain is strongly diagnostic. For example, chest pain described as ‘heavy’ or ‘tight’ is strongly suggestive of inadequate blood supply to the heart. Start your exploration with an open question: Paramedic: Mrs Jones, can you describe the pain you had? What was it like? Patient: It’s in the middle of my chest; it felt like my chest became very tight. Shifting to a closed question can add accuracy: Paramedic: So, if asked to describe it as either sharp or heavy, you would say? Patient: Oh, definitely as a heavy feeling. Offering the patient an option that contradicts your initial diagnosis (‘sharp’) is one method of avoiding a search satisfaction bias in your clinical decision making. Onset This may have been covered in the opening statement but now is the time to gain more detail. Again start with an open question: Paramedic: What were you doing when you first felt the pain today? Patient: I was walking up those stairs. Focus with a closed question: Paramedic: Were you carrying anything? Or holding onto anything with your arm? Patient: No, just walking. Paramedic: Does using the arm you fell on last week cause the pain to appear? Patient: No.

And another: Paramedic: Did the pain come on suddenly or did it build up gradually? Patient: No, it just hit me suddenly and I felt quite sick. Location By the time most paramedics get to determine the location of pain they often have a strong hypothesis for the cause of the pain (cardiac, pleuritic or musculoskeletal) and may rush this stage by asking a closed question, such as: Is the pain just in your chest or does it radiate? To gain diagnostic information it is better to ask an open question: Paramedic: Mrs Jones can you show me with your hand where the pain is? Patients will either point to a specific location or illustrate a large area. This is a valuable differential tool that can then be elucidated with a closed question: Paramedic: So the pain is right across your chest? Patient: Yes. Other signs and symptoms How this question is phrased is often an indicator of whether a paramedic is able to assume the patient’s perspective. ‘Signs and symptoms’ are paramedic terms and most patients would not be sure what the paramedic was seeking if they were asked: Were there any other signs and symptoms? A better way to gain this information is to start with an open question: Paramedic: When the pain started, did you feel anything else that is not normal for you? Patient: I felt a little dizzy and I thought I might actually be sick. Vomit, that is. If there are specific symptoms that help differentiate between diseases these can be asked about in closed questions. Only enquire about one symptom at a time, otherwise it can be difficult to identify which symptom the patient is agreeing to: Paramedic: So you felt dizzy and nauseous. Were you sweaty? Patient: A little, just for a couple of minutes. Paramedic: Did you feel short of breath? Relief This is also a question that paramedics may ask about from their own frame of reference, for example: Does anything give you relief from the pain? Patients often interpret this to mean a response to pain-relief medications, when paramedics need much more detailed information if they are to discern the causes of pain. This is best detailed in specific closed

questions: Paramedic: Mrs Jones, does the pain change in location or severity if you take a big breath? Patient: No. Paramedic: What if you press on the area where you showed me the pain is? Does that change the pain at all?

Step 3: Physical examination Provided patients have been asked to provide a key history and to explain the details of their symptoms, most will not question having a physical examination at this point. In many cases, this compliance will extend to allowing the paramedic to expose the patient’s chest for auscultation or ECG recording. (Even patients who initially resist relinquishing control will become compliant if the paramedic gains their trust.) However, paramedics have to balance their need for information against preserving the patient’s dignity: in many cases such diagnostic examinations can be delayed until the patient is in a more private location such as the ambulance.

Step 4: Explanation and planning After completing the assessment but before commencing the treatment plan is the time to present your explanatory statement to the patient and seek to align their expectations with your clinical expertise. Clinicians who are unable to assess the patient’s perspective or their own biases may use this opportunity to force their clinical expertise and power onto the patient: Paramedic: You don’t think it’s your heart, Mrs Jones, but I’ve seen a lot of heart problems in my time and I think it is your heart causing this pain, so you need to come with us to the hospital. I’m not sure you’ll be going on that cruise. However, paramedics who have gained an awareness of the patient’s concerns will phrase their explanatory statement so that it aligns, rather than confronts, the patient’s perspective. By not exerting their power over the patient they are more likely to find a cooperative response: Paramedic: Mrs Jones, I understand that you don’t think this pain is being caused by your heart, but I can’t completely rule it out with the equipment I have here with me. I’d like to take the safest path and take you to hospital for some more tests. If we’re wrong and the pain is coming from your fall, then you can go on the cruise with your mind completely at ease. Incorporating the patient’s perspective into your statement shows the patient that you are seeking similar outcomes despite your different views.

Step 5: Closing the session Patients presenting with acute pain or injuries are less likely to resist treatment or transport to hospital, but the increasingly chronic nature of paramedic work now requires paramedics to explain to patients that transport to an ED is not always the most appropriate management plan for their condition. Such a difference between the patient’s perceived outcome (transport to hospital) and the paramedic’s preferred management (referral to another treatment pathway) can be a source of conflict for paramedics who lack the insight and communication skills to develop the patient interview to the point of shared understanding. Closing the session is thus increasingly necessary for paramedics whose scope of practice allows them to ‘treat and leave’ patients as opposed to the traditional role of ‘treat and transport’. An important aspect of closure is to provide the patient with a pathway for the expected outcome of treatment as well as what should be considered an inadequate response to treatment. For example, in the case of a young male treated with an antiemetic for acute gastroenteritis: Paramedic: This medication won’t make you feel normal but it should reduce the nausea and vomiting. The vomiting should subside over the next 12 hours. If it persists any longer, make an appointment to see your GP.

Barriers to effective communication There are a number of barriers to communication that are effectively amplified in the prehospital environment. Recognising these barriers is the first step to minimising their effect.

Signal vs noise The concept of signal versus noise in terms of information gathering is probably best described using the analogy of an old AM radio: in between the stations only static can be heard (noise), but when the radio is tuned in to the correct frequency the broadcast is clear (signal). If a station isn’t quite tuned in, the mix of signal and noise makes it hard to discern what the announcer is saying. In fact, the amount of data we receive is exactly the same whether the station is correctly tuned in or not: the difference is that we can only understand the information if the signal is clear and there is no static. Arriving at a case presents a similar problem for paramedics: a lot of data is being presented but only some of it is actually useful in determining what is wrong with the patient. Separating the signal from the noise is actually why paramedics use a standardised assessment and interview process: they are an attempt to ‘tune’ themselves into the signal. However, not all structured assessments are useful in this situation. For example, the mnemonic SAMPLE Symptoms Allergies Medications Pertinent past history Last oral intake Events is easy to remember, but it risks adding too much noise to the signal. This is because, in addition to the illogical order (the events leading up to the illness are last), some of the information actually pertains to what the paramedic needs to know after they have made their clinical decision: an allergy to morphine will guide the paramedic to choose another form of pain relief, but adding this information during the diagnostic phase is unnecessary and can distract from the actual information needed to make the clinical diagnosis. Similarly, there are times when the patient’s prescribed medications are valuable tools in determining the diagnosis, but at other times the medications have no impact on clinical decision making. Either way, obtaining the medications is often far from simple: they may be at hand, but the patient may have to leave mid-assessment to locate them or they may be in an unlabelled dosette box. Thus, such a question can take several minutes to answer and often provides more opportunity to miss information than to collect it. In addition, ‘Last oral intake’ is rarely applicable to paramedic care. Different professions use different models of a ‘history’ depending on what they are seeking to learn and how long they have to gain that information. It is important for an anaesthetist to discover when the patient last ate or whether the patient has any lung problems. For the social worker it is vital to know if the patient lives alone or with others who can assist them in their daily activities. What is noise for some is signal for others: attempting to collect everything is simply adding to noise.

Compared with the mnemonic DOLOR, which is used for symptom analysis, using the mnemonic SAMPLE can disrupt the interview, create an illogical timeline and generate unnecessary information. However, a mnemonic such as SAMPLE may be useful when the paramedic is reaching the end of the interview to act as a memory aid to ensure that the interview has been comprehensive.

Empathy While it is often easy to express sympathy for the illness that a patient is suffering, empathy describes the ability to understand another person’s experiences and, vitally, convey that sense of understanding to the person. The unsuitability of a checklist approach to traditional history taking is obvious when we consider that patients primarily judge the competence of their clinicians by how much empathy they feel from the clinician during the interview process—and patients appear to be remarkably adept in detecting real from forced expressions of empathy (Ley, 1998). Empathy means expressing that you recognise another ’s situation, feelings and motives, but how do you communicate empathy? Responding to emotions is usually intrinsically linked to how we feel about the other person in the conversation, and for paramedics who have not considered how different communicating with patients is compared with communicating with friends and family, responding empathetically to a stranger can add to the emotional burden when continually being confronted with distressed patients. Expressing empathy doesn’t require the paramedic to personally experience the patient’s fear or frustration any more than it requires the paramedic to experience the patient’s chest pain in order to diagnose it (Buckman, 2002). The three steps to expressing empathy are not difficult but must be recognised if they are to be incorporated into the interview without burdening the paramedic with the actual emotional response: Step 1: Identify the emotion. Step 2: Identify the source. Step 3: Respond to show you have made the connection between the first two steps (Buckman, 2002). Consider the following conversation: Patient: I don’t want to go to hospital. Paramedic: But you have to go, that’s the only way we can determine if the pain is from your heart. The paramedic’s response is logical and scientific, but it does not identify or manage the emotion that is causing the patient to have the reaction she is expressing. Now consider this alternative version of the conversation:

Patient: I don’t want to go to hospital. Paramedic: Why don’t you want to go to hospital, Mrs Jones? Patient: They’ll keep me there and I won’t be able to go on my trip. And I have to be home tomorrow: my grandchildren are coming to stay the night. Paramedic: Mrs Jones, the tests will only take a few hours and if they don’t find anything you won’t be kept in hospital. It’s better to get it sorted so you can look after your grandchildren without worrying about getting sick. They won’t ask you to stay in hospital unless you really need to. Displaying empathy when you don’t share the beliefs, experiences or values of the person you are communicating with doesn’t require you to artificially create expressions of concern. Far from fearing any emotional expressions from patients, you should see such expressions as valuable insights into patients’ feelings and consider them as opportunities to express your understanding.

Wait time and language One of the dangers of a structured interview process is that the presence of the ‘next question’ in the mind of the clinician can cause them to rush forwards without considering the information contained in the answer to the current question. Focusing on driving the interview forwards can also impact on the quality of information gained from elderly patients, who may require longer to process their thoughts than clinicians are willing to wait. This commonly manifests itself during symptom investigation, when the paramedic asks an open question then rushes to a closed question when an answer isn’t immediately forthcoming: Paramedic: How would you describe your pain? [Brief pause] Is it sharp or dull? Delayed cognitive function is a characteristic of ageing even without any underlying disease process such as dementia or Alzheimer ’s disease, and doctors have been shown to be poor in detecting cognitive changes during patient assessments (Woodford, 2007). Combined with hearing and/or language difficulties this can cause patients to take longer to form answers than paramedics are willing to wait.

Culture Culture is not limited by ethnicity, language or birthplace. It can be described as a system of shared values, beliefs and behaviours that shape how we contextualise our world (Carrillo et al., 1999). Religion, age, education, gender and sexual preference all contribute to culture and, if not appreciated, can create barriers to effective clinical communication (Carrillo et al., 1999). Of course, it simply isn’t practical to learn all of the cultural nuances that could impact on patient care (who to address, how to address them, whether to shake hands or not etc)—and anyway, such a notion fails to recognise that individuals within a culture are unique and respond differently to illness. Beyond recognising that cultural barriers exist, the key is to ask (directly but politely) about the patient’s beliefs and preferences (Carrillo et al., 1999).

Paramedics, in fact, form a very strong cultural group described by a common understanding of disease processes, hierarchy, responsibility and processes. Historically, the paramedic culture consisted entirely of middle-aged males, and today novice female paramedics are often subjected to cultural biases from patients. As unfair as cultural stereotyping is (regardless of the direction it flows), it does exist and the key to mollifying its effects are to firstly recognise the bias and secondly to seek or provide information to reduce its impact.

Personality Parsons’ (1951b) model of doctor–patient interaction was based on the premise that the doctor was untouched by the patient’s traits, personality, culture or education (Roter & Hall, 2006). In fact, numerous studies have shown that clinicians’ beliefs, education and prior experiences affect not only how they make clinical decisions but also how they communicate with their patients (Ainsworth-Vaughn, 1992; Dale et al., 2008; Kaplan et al., 1996; Sandhu et al., 2008).

Summary Despite the advances in technology associated with medicine in general, a clear and accurate history remains the most important tool in the paramedic’s diagnostic armoury. Although communication styles are closely linked to personality, the ability to conduct an effective ‘medical interview’ involves a mix of skills and behaviours that can be developed and learned. Distorted by anxiety, fear, pain and a lack of understanding, patients often construct descriptions of their illnesses that are difficult for clinicians to correlate, and paramedics need to use a structured approach if they are to formulate a diagnosis while simultaneously establishing sufficient trust with the patient that they will approve the clinician’s preferred management strategy.

References Ainsworth-Vaughn, N. Topic transitions in physician–patient interviews: power, gender, and discourse change. Language in Society. 1992; 21(3):409–426. Baer, R. D., Weller, S. C., Garcia, J. G., Rocha, A. L. Cross-cultural perspectives on physician and lay models of the common cold. Medical Anthropology Quarterly. 2008; 22(2):146–148. Beckman, H. B., Frankel, R. M. The effect of physician behavior on the collection of data. Annals of Internal Medicine. 1984; 101(5):692–696. Buckman, R. Communications and emotions. British Medical Journal. 2002; 325(7366):678– 682. Carrillo, J. E., Green, A. R., Betancourt, J. R. Cross-cultural primary care: a patient-based approach. Annals of Internal Medicine. 1999; 130:829–834. Cohen-Cole, S. A.The Medical Interview: A Three Function Approach. St Louis, MO: Mosby-Year Books, 1991. Dale, J., Sandhu, H., Lall, R., Glucksman, E. The patient, the doctor and the emergency department: a cross-sectional study of patient centredness in 1990 and 2005. Patient Education and Counseling. 2008; 72:320–329. DiMatteo, M. R., Hays, R. The significance of patients’ perspectives of physician conduct. Journal of Community Health. 1980; 6:18–34. Egan, G.The Skilled Helper: A Systematic Approach to Effective Helping. Pacific Grove, CA: Brooks Cole, 1990. Engel, G. L. How much longer must medicine’s science be bound by a seventeenth century world view? In: White K.L., ed. The Task of Medicine: Dialog at Wickenburg. Menlo Park, CA: The Henry J. Kaiser Foundation, 1987. Forkner-Dunn, J. Internet-based patient self-care: the next generation of health care delivery. Journal of Medical Internet Research. 5(2), 2003. Gafaranga, J., Britten, N. ‘Fire away’: the opening sequence in general practice consultations. Family Practice. 2003; 20(3):242–247.

Gallagher, T. J., Gregory, S. W., Bianchi, A. J., Hartung, P. J., Harkness, S. Examining medical interview asymmetry using the expectation status approach. Social Psychology Quarterly. 2005; 68(3):187–203. Goldberg, D., Steele, J. J., Smith, C., Spivey, L.Training Family Practice Residents to Recognize Psychiatric Disturbances. Rockville, MD: National Institute of Health, 1983. Groopman, J.How Doctors Think. Melbourne: Scribe Publications, 2007. Haidet, P., O’Malley, K., Fharf, B., Gladney, A., Gresinger, A., Stret, R. Characterizing explanatory models of illness in healthcare: development and validation of the CONNECT instrument. Patient Education and Counseling. 2008; 73:232–239. Hausberg, M. C., Hergert, A., Kröger, C., Bullinger, M., Rose, M., Andreas, S. Enhancing medical students’ communication skills: development and evaluation of an undergraduate training program. BMC Medical Education. 12(16), 2012. Kaplan, S., Greenfield, S., Gandek, B., Rogers, W., Ware, J. E. Characteristics of physicians with participatory decision-making styles. Annals of Internal Medicine. 1996; 124:497–504. Katon, W., Kleinman, A. Doctor–patient negotiation and other social science strategies in patient care. In: Eisenberg L., Kleinman A., eds. The Relevance of Social Science for Medicine. Boston: Reidel, 1980. Kleinman, A., Eisenberg, L., Good, B. Culture, illness, and care: clinical lessons from anthropologic and cross-cultural research. Annals of Internal Medicine. 1978; 88:251–258. Klemperer, G.The Elements of Clinical Diagnosis. Macmillan, 1903. Kohn, L. T., Corrigan, J., Donaldson, M. S.To Err is Human: Building a Safer Health System. Washington, DC: National Academy Press, 2000. Kudenchuk, P., Maynard, C., Cobb, L. Utility of the prehospital electrocardiogram in diagnosing acute coronary syndromes: the myocardial infarction triage and intervention (MITI) Project. Journal of the American College of Cardiology. 1998; 32:17–27. Kurtz, S., Silverman, J., Benson, J., Draper, J. Marrying content and process in clinical method teaching: enhancing the Calgary-Cambridge guides. Academic Medicine. 2003; 78(8):802–809.

Langewitz, W., Denz, M., Keller, A., Kiss, A., Rüttimann, S., Wössmer, B. Spontaneous talking time at start of consultation in outpatient clinic: cohort study. British Medical Journal. 2002; 325:682–683. Levinson, W., Roter, D., Mullooly, J. P., Dull, V. T., Frankel, R. M., Physician-patient communication. Journal of American Medical Association. 1997;277(7):553–559 Ley, P.Communicating with Patients. Improving Communication Satisfaction and Compliance. London: Chapman & Hall, 1998. Lipkin, M., Putnam, S. M., Lazare, A.The Medical Interview. New York: Springer, 1995. Makoul, G. Essential elements of communication in medical encounters: the Kalamazoo Consensus Statement. Academic Medicine. 2001; 76(4):390–393. Marvel, K. M., Epstein, R. M., Flowers, K., Beckman, H. B. Soliciting the patient’s agenda. Have we improved? JAMA. 1999; 281(3):283–287. Masse, R., Legare, F., Cote, L., Dodin, S. The limitations of a negotiation model for perimenopausal women. Sociology of Health and Illness. 2001; 23(1):44–64. Morgans, A., Archer, F., Allen, C. Patient decision making in prehospital health emergencies: determinants and predictors of patient delay. Journal of Emergency Primary Health Care. 6(3), 2008. Nolan, T. W. System changes to improve patient safety. British Medical Journal. 2000; 18(320):771–773. Novack, D. H., Dube, C., Goldstein, M. G. Teaching medical interviewing: a basic course on interviewing and the physician-patient relationship. Archives of Internal Medicine. 1992; 152:1814–1820. O’Toole, G.Communication: Core Interpersonal Skills for Health Professionals. Sydney: Churchill Livingstone, 2008. Parsons, T.The Social System. Glencoe, Illonois: The Free Press, 1951. Parsons, T.Toward a General Theory of Action. Harvard University Press, 1951. Prioreschi, P.Roman Medicine. Horatius Press, 1998.

QASDepartment of Safety Annual Report. Brisbane: State of Queensland, 2011. Rhoades, D. R., McFarland, K. F., Finch, W. H., Johnson, A. O. Speaking and interruptions during primary care office visits. Family Medicine. 2001; 33(7):528–532. Riccardi, V. M., Kurtz, S. M.Communication and Counselling in Healthcare. Springfield, IL: Charles C. Thomas, 1983. Rider, E., Hinrichs, M., Lown, B. A model for communication skills assessment across the undergraduate curriculum. Medical Teacher. 28(5), 2006. Rogers, C. R.On Becoming a Person: A Therapist’s View of Psychotherapy. Boston: Houghton Mifflin, 1961. Roter, D., Hall, J. A.Doctors Talking with Patients/Patients Talking with Doctors. Westport: Praeger, 2006. Rouan, G., Lee, T., Cook, F. Clinical characteristics and outcome of acute myocardial infarction in patients with initially normal or non-specific electrocardiograms. American Journal of Cardiology. 1989; 64:1087–1091. Ruusuvuori, J. Looking means listening: coordinating displays of engagement in doctorpatient interaction. Social Science in Medicine. 2001; 52(7):1093–1108. Sandhu, H., Adams, A., Singleton, L., Clark-Carter, D., Kidd, J. The impact of gender dyads on doctor–patient communication: a systematic review. Patient Education and Counseling. 2008; 76:348–355. Saunders, J. The practice of clinical medicine as an art and as a science. Medical Humanities. 2000; 26:18–22. Silverman, J., Kurtz, S., Draper, J. Skills for Communicating with Patients, 2nd ed. San Francisco: Radcliffe, 2008. Stewart, M. Effective physician–patient communication and health outcomes: a review. Canadian Medical Association Journal. 1995; 152(9):1423–1433. Stewart, M., Brown, J. B., Boon, H., Galajda, J., Meredith, L., Sangster, M. Evidence of patient–doctor communication. Cancer Prevention Control. 1999; 3(1):25–30.

Stewart, M., Brown, J. B., Weston, W. W., McWhinney, I. R., McWilliam, C. L., Freeman, T. R.Patient-centered Medicine: Transforming the Clinical Method. Boston: SAGE, 1995. Stillman, P. L., Sabars, D. L., Redfield, D. L. Use of parprofessionals to teach interviewing skills. Paediatrics. 1976; 57:769–774. Takemura, Y., Sakurai, Y., Yokoya, S., Otaki, J., Matsuoka, T., Ban, N., et al. Open-ended questions: are they really beneficial for gathering medical information from patients? Journal of Experimental Medicine. 2005; 206:151–154. Tolana, P. C.Decision Making in Medicine and Health. New York: Nova Biomedical Books, 2007. Valentine, K. L. Comprehensive assessment of caring and its relationship to outcome measures. JAMA. 1991; 266:1831–1832. van Thiel, J., van Dalen, J.MAAS-Global criterialijst, versie voor de vaardigheidstoets Medisch Basiscirriculum. Maastricht: Universiteit Maastricht, 1995. Woodford, H. J. Cognitive assessment in the elderly: a review of clinical methods. QJM. 100(8), 2007.

SECTION 3

PATIENT AND PARAMEDIC SAFETY O U TL I N E CHAPTER 7: Patient safety and paramedicine CHAPTER 8: Paramedic health and wellbeing

CHAP TER 7

Patient safety and paramedicine By Paul Jennings

OVERVIEW • Patients deserve to receive high-quality healthcare and healthcare providers generally go to extreme lengths to provide it. • Despite diligence and competence, all clinicians are subject to error. • Medical errors are pervasive, substantial and affect all types of people, in all settings, receiving all types of treatment. Medical errors are not uncommon. • Cultural issues such as blame and avoidance affect the number of medical incidents and nearmisses that are reported. • Disclosure of adverse events should be made easier and less punitive in order to identify and correct errors. • The science of patient safety describes the extent of medical error and examines means to reduce risk and alter personal and organisational culture. • Patient safety is intrinsically linked to evidence-based practice and the formation of clinical protocols and guidelines that support clinical practice, but will always require effective clinical reasoning.

Introduction It is often confusing to new medical, nursing and paramedic students that there is a discipline within healthcare known as patient safety. After all, the notion of healthcare is that it helps patients to recover from illness or injury. Indeed, the Hippocratic Oath (Collier, 1910) states ‘Never do harm to anyone’. It is perhaps this disconnect—that caring for patients could actually harm them—that allowed a culture to develop whereby medical errors went largely unreported until the 1990s, when a series of disturbing studies discovered that medical errors were both more common and more serious than people had ever anticipated (Brennan et al., 1991; Thomas et al., 2000; Kohn, Corrigan & Molla, 1999). Far from being rare, one American study found that if medical errors were classified as a disease, they would be the sixth most common cause of death in the United States (National Center for Health Care Statistics at the Centers for Disease Control, 2005). In Australia, medical errors result in as many as 18,000 unnecessary deaths and more than 50,000 people becoming disabled each year (Weingart et al., 2000). As a result, the process of identifying why medical errors occur and what can be done to prevent them has developed into a specific discipline and a specialised form of risk management concerned with monitoring, analysing and preventing these errors. Consumers of healthcare have the right to expect that they will receive high-quality and safe care regardless of the setting in which it is delivered—hospital, GP or prehospital setting. Errors occur because those who are responsible for the provision of healthcare are human. Every day, competent, careful and conscientious people commit errors as a result of systemic or individual failures. For paramedics providing healthcare in the diagnostically limited and often chaotic environment of prehospital emergency care, understanding the factors that contribute to errors and threaten patient safety is essential if such errors are to be avoided. This chapter examines the common causes of medical errors and how effective clinical reasoning is one tool that can be used to reduce both the frequency and the severity of errors.

The harm caused by healthcare errors Until relatively recently, the notion of ‘patient safety’ was inseparable from ‘patient care’: it was assumed that by looking after their patients that clinicians were intrinsically making them safe. Patient safety is generally defined as, ‘the avoidance or reduction to acceptable levels of actual or potential harm from health care or the environment in which healthcare is delivered’ (AIHW, 2009). This definition is equally applicable to all healthcare settings and disciplines. The cornerstone of patient safety is the systematic identification and monitoring of adverse events, or medical errors, and the improvement of healthcare through redesigning education and processes. The Harvard Medical Practice Study in the mid-1980s was one of the earliest studies reporting on adverse events (Brennan et al., 1991). The study screened a random sample of patient notes from 51 acute care facilities in New York State in order to identify records that contained an adverse event. The researchers found that some 13.6% of patients died as a result of an adverse or negligent event in hospital (Brennan et al., 1991; Leape et al., 1991; Localio et al., 1991). In a similar study conducted in Utah and Colorado in the early 1990s (Thomas et al., 2000) the authors found that 15.4% of adverse or negligent events caused death. This study also identified that the ED had a much higher error rate than other areas within hospitals due to the type and volume of work, and the staff involved. The Quality in Australian Health Care Study in the mid1990s was the first Australian study to examine medical errors. The authors examined the incidence of adverse events, the likelihood these events might have led to death and the possibility that the events might have been prevented using patient records from 28 Australian hospitals across two states. The authors found that 4.9% of adverse events caused death and 51% of adverse events could have been prevented (Wilson et al., 1995). The prehospital environment is probably the health setting most analogous to the ED (see Fig 7.1) and the most recent study aiming to detect and reduce adverse events in the ED was reported in 2002. In this Victorian study, 2.85% of patient attendances were screened positive for one or more adverse events, and an adverse event was later confirmed in 1.24% of patient attendances, with 32.4% of these events being deemed severe. After implementing various quality improvement activities (mostly changes to hospital policy and work practices), the number of adverse events fell dramatically (Wolff & Bourke, 2002).

FIGURE 7.1 The concept of separating the process of treating patients from exposing them to risks has not been an easy transition for hospitals, but it is now a well-established practice that supports clinical care. Source: Shutterstock/beerkoff. Even though the magnitude of errors and adverse events has now been recognised, the degree to which they are acknowledged varies between settings. While there is considerable literature examining incident monitoring and adverse event tracking in the hospital environment (i.e. anaesthesia, operating theatres and intensive care units), there is scant literature relating to adverse events and incident reporting in the prehospital environment. The findings of a systematic literature review conducted in 2009 found 88 papers covering seven themes of patient safety in paramedic practice (Bigham et al., 2011; see Table 7.1).

TABLE 7.1 Patient safety themes emerging from the literature

Source: Department of Health, Victoria (2010).

Types of medical error While the factors that lead to medical errors are rarely simple or singular, medical errors can be classified into four categories: diagnostic, treatment, failure and preventive (Assaf et al., 2003). • Diagnostic errors include a delay in making the correct diagnosis, missing a diagnosis and making an incorrect diagnosis that leads to patient harm (Singh et al., 2012). The rate of diagnostic errors is estimated to be between 10 and 15% (Graber, Franklin & Gordon, 2005; Shojania et al., 2003). It is this category of error that our text primarily seeks to address (see Fig 7.2).

FIGURE 7.2 Working in the community setting, surrounded by distractions, it is likely that paramedics are at greater risk of making diagnostic and treatment errors than medical professionals working in controlled environments. Being aware that errors will pervade their clinical management at some point is the first step paramedics must make in reducing the potential consequences of any error. Source: Shutterstock/paintings. • Treatment errors result in harm because of mistakes in a procedure such as a biopsy, suturing or intubation, but they also include medication errors. Because medication

administration is so common, giving an incorrect drug dose, via the wrong route or even the wrong medication, is the most likely cause of medical error and subsequent patient harm (Assaf et al., 2003). • Failure errors occur when a process or piece of equipment fails to function as designed. Instinctively this suggests the failure of equipment such as ventilators or monitors, but poor communication at handover, erroneous record keeping and patient misidentification are all typical failure errors in which people contribute to an error. • Preventive errors are the instances when patients are harmed by a failure to deliver drugs or procedures that are known to reduce complications. Wound infection due to delayed changing of surgical dressings or omission of post-operative antibiotics are common examples of preventive errors.

Models of error That errors occur frequently and patients are harmed have strongly motivated researchers to develop error mitigation strategies and a number of authors divide errors into two main models of causation: errors of the person, and errors of the system (Graber, Gordon & Franklin, 2002; Nolan, 2000; Reason, 2000). The person approach examines errors as a result of aberrant behaviour—care providers being forgetful, careless or even negligent. This model attributes blame to the person, and mitigation strategies introduced by organisations to address this type of error include educational programs, newsletters and posters aimed at coercing individuals to conform to newly devised procedures or protocols. Viewing errors solely by this model can see organisations create an environment of fear to promote adherence to policy and, where errors are identified, implementing a program of naming, blaming, shaming and retraining (Nieva & Sorra, 2003; Reason, 2000). The systems approach, on the other hand, accepts that individuals are not infallible and that errors will inevitably occur, irrespective of the will of organisations and clinicians. Humans will make mistakes, especially when the culture or system in which they are operating does not recognise the risk (Nieva & Sorra, 2003). In this approach, errors are seen as ‘consequences rather than causes’ (Reason, 2000), most often resulting from failures in systems or processes rather than individual inattention. Countermeasures are based on developing safety measures and processes that reduce the likelihood of clinicians making an error—engineering the risk out of risky situations and tasks. When errors do occur, the focus is not on who made the error, but rather why the defences failed (Reason, 2000).

Reducing diagnostic errors This text is primarily focused on reducing diagnostic errors by improving information collection and clinical reasoning skills. Chapters 4–6 identified specific areas, concepts and skills that can be developed to limit the perceptual and thought processes that lead to human error. However, it is important to realise that in addition to the personal and systemic factors that contribute to diagnostic error, there is also a category of ‘no-fault’ errors (Graber et al., 2002) that must be considered. These errors occur because no diagnostic test is infallible, diseases can present atypically and patients are (very) occasionally non-compliant in providing an accurate description of their condition. Most ambulance services implement a system-level protection by ensuring that novices work with experienced paramedics. This is an example of a layered approach to error mitigation and it reduces, but does not completely mitigate, the chances of error.

Error defence Reason (2000) is probably best known for his Swiss cheese model of system accidents (see Fig 7.3). This model shows how most systems offer a series of defences, barriers or safeguards that block an error from progressing too far. However, despite a process, task or situation having a number of layers of defence (or cheese), errors can still occur. The defence layers (or countermeasures) may be engineered (physical barriers or alarms), may rely on people (paramedics, doctors, nurses) or may consist of procedures, protocols or administrative controls. The model illustrates that often the various layers of defence function independently of each other, with varying degrees (or indeed opportunities) for communication. Furthermore, despite the best intentions of each of the countermeasures, they may not be 100% infallible. While the countermeasures are generally effective in preventing hazards (or errors or incidents) from occurring, it is possible that some errors could slip through the holes, resulting in an adverse event. In the medical setting some holes in the cheese can be thought of as active failures of systems or individuals (e.g. distraction), while others are latent and exist across the whole organisation.

FIGURE 7.3

The Swiss cheese model of system accidents. Some holes can be thought of as active failures of systems or individuals, while others exist across the whole organisation. Source: Adapted from Reason, J. (2000).

P RACT ICE T IP Opioids administered for pain relief also have sedative and respiratory

effects. When administered in hospitals at night, the sedation may be mistaken for a normal sleeping pattern and a patient may subsequently develop a hypoxic head injury due to a combination of airway occlusion and respiratory depression.

P RACT ICE T IP Sodium and potassium chloride are harmless and dangerous medications, respectively, but they are often prepared in identical ampoules distinguished only by tiny type. Paramedics often wrap potassium chloride ampoules in tape when they stock them in their kit so that they can easily be identified in poor light or when crew are tired or distracted.

Error management The inception of patient safety as a discipline has seen the introduction of a structured approach to reducing errors but, because it recognises that errors can never be totally avoided, it also demands that systems can tolerate and learn from any errors that do slip through. One of the most significant changes as a result has been the shift from a person approach to a systems view of errors. This enables individuals involved in errors to report the error into a constructive rather than a punitive environment and allows the organisation to respond by adapting the system rather than punishing the individual (Nieva & Sorra, 2003). It is now widely accepted that in addition to having a responsibility to be vigilant in the provision of patient care, all healthcare practitioners have an equal responsibility to report any errors through the appropriate channel. Unfortunately, many errors go unreported, often resulting in lost opportunities for process or training improvements. A recent study undertaken in the prehospital environment identified six main reasons why clinicians are reluctant to report errors: • the burden of reporting • fear of disciplinary action • fear of potential litigation • fear of embarrassment • fear of breaches of anonymity or confidentiality • concern that ‘nothing would change’ even if the incident was reported (Jennings & Stella, 2011). For the safety of our patients it is vital that these barriers are overcome to ensure complete and timely notification of errors, adverse events and near-misses. In some ambulance services support for reporting errors and near-misses, and building them into a continuous quality improvement link, is well-established, but in others it remains bound by a culture of blame.

Open disclosure The culture of safety that has developed in some organisations that have embraced error management has extended beyond staff to include patients and their families. In healthcare systems that have a fully evolved culture of safety, the identification of hazards, adverse and sentinel events is rewarded and staff are shielded from punishment, while weaknesses in the system are rectified (Nieva & Sorra, 2003). However, the notion that patients should be informed openly and honestly about adverse events as soon as possible after they occur is alarming to clinicians working in organisations where error disclosure is primarily linked to disciplinary action (Hebert, 2001).

Sentinel events Sentinel events are the most severe healthcare-related errors and must be notified to a health service provider ’s governing body, often the state Department of Health. In Australia a sentinel event is defined as ‘a relatively infrequent, clear cut event that occurs independently of a patient’s condition; it commonly reflects hospital system and process

deficiencies, and results in unnecessary outcomes for the patient’ (Department of Health, Victoria, 2010). Box 7.1 lists the eight Australian sentinel event classifications. These classifications are clearly more relevant to hospital and inpatient health settings, but ambulance services must be aware of their statutory responsibilities of reporting such incidents. Some health departments add an additional classification, such as ‘other catastrophic event’, to capture additional cases that meet the classification of a sentinel event (Department of Health (Victoria), 2010). It is into this classification that the majority of paramedic sentinel events fall. B O X 7 . 1N a t i o

n a l se n t i n e l e ve n t

c lassific atio ns • Wrong procedure or body part • Haemolytic blood transfusion • Infant discharged to wrong family • Suicide in an inpatient unit • Medication error • Intravascular gas embolism • Retained instruments • Maternal death Source: Adapted from Department of Health, Victoria (2010).

Monitoring patient safety Responsibility for ensuring patient safety must be shared between clinicians, health administrators, clinical leads and healthcare consumers (patients). There are a number of guiding principles around patient safety that ambulance organisations should focus on (see Box 7.2). As a minimum, ambulance managers should ensure that clinicians are involved in the development of clinical guidelines, designing systems and processes and monitoring the clinical effectiveness of their organisation. Clinicians should also actively participate in quality improvement activities and embrace error reporting, peer review and clinical audit. The historical nature of ambulance services offering low-level clinical care saw many develop without a strong culture of clinical auditing. The self-contained nature of many services also resulted in auditing processes that were entirely internal and failed to seek broader clinical expertise. This was not that different from what most hospitals experienced when they started to embrace the notion of a patient safety system, and most of the patient safety auditing tools introduced by progressive ambulance services have come from the hospitals. Nonetheless, the move to such a system usually represents a cultural shift that is often difficult for both management and operational staff. B O X 7 . 2G u i d i n g

princ iples o f ambulanc e

o r g a n isa tio n s f o c u se d o n im p r o vin g patient saf ety • Clinicians are empowered to improve clinical care delivery. • Clinicians actively involve consumers as partners in their care. • Clinicians participate in designing systems and processes. • Quality improvement activities are planned, prioritised and have sustainability strategies in place. • Clinical care delivery is evidence-based. • Standards of clinical care are clearly articulated and communicated. • Performance of clinical care processes and clinical outcomes are measured. • Clinical performance measures, peer review and clinical audit are used to evaluate and improve performance. • New procedures and therapies assuring quality and safety issues are considered. Source: Department of Health, Victoria (2010).

CA SE ST U DY 1 Case 1807, 2250 hrs. Dispatch details: An advanced life support crew are dispatched to a 22year-old female suffering from respiratory distress. The address is a nightclub and the call has come from club staff who state she appears to be hyperventilating. Initial presentation: On arrival the crew find a young woman with a raised respiratory rate who appears to be confused and is not able to answer questions. Her pulse is 110, blood pressure 110/80 mmHg and respiratory rate 30; and the pulse oximetry reads 100%. No-one at the club can give any details about her previous medical history or the events leading up to the ambulance being called. Apart from hyperventilation there is no other obvious abnormality. It seems that she has psychogenic hyperventilation so the crew try to slow her breathing down. She is placed on oxygen via a mask while they attempt to reassure her and slow her respiratory rate. Her blood glucose isn’t checked at the scene as it is not deemed to be relevant. As she doesn’t seem to be responding, the crew decide to transport her a short distance to the local ED. On arrival at the ED a routine blood glucose reveals her blood sugar to be 35 and the hospital staff comment on the strong smell of ketones. No long-term harm seems to have been done and luckily the crew decided

to transport the patient; however, they misdiagnosed ketoacidosis as psychogenic hyperventilation.

Patient safety and organisational culture The development of a patient-safety culture is critical to reducing patient risk (Nieva & Sorra, 2003). One effective way to inspire cultural change is through case reviews— recounting actual or realistic stories where clinicians were involved in an incident that resulted in actual or potential harm. Case study 1 is an example of a vignette that can be posed, followed by questions to focus discussion. Clinicians are often able to relate to such events and help raise awareness of the learning principles. Organisations that have a culture of blame or avoidance of error may benefit most from honest, open discussion of realistic stories that describe the fallibility of humans and systems.

Case study reflection The patient’s diabetic ketoacidosis was missed by the ambulance crew at the scene. If they had taken a blood sugar reading as routine for a patient in an altered conscious state, the diagnosis would have been clear. Similarly, if they had picked up the smell of ketones at the scene it would have raised the suspicion of diabetic ketoacidosis. Although no harm occurred on this occasion, the possibility exists that this could have been an error with significant consequences. The paramedics were dispatched to a case labelled as ‘hyperventilation’ in a nightclub and it is possible that this created a preconceived idea. Preconceptions can lead to premature diagnostic closure (discussed in Ch 5) and missing the clinical diagnoses. The environment, with its extraneous odours and variable light, did not lend itself to obtaining good-quality observations and might account for why the smell of ketones was missed. Interestingly, the sensitivity to detect ketones in exhaled breath is variable and may have a genetic component (Forrai et al., 1981; Laska & Hubener, 2001), so both members of the crew might have been unable to detect ketones by smell. As detailed in Reason’s model, such factors aligned like the holes in Swiss cheese to enable this error to slide through. Luckily this was a near-miss situation rather than an error with major consequences, but it should nevertheless be followed up. Reviewing the case will suggest controls to prevent the situation occurring again for other patients or crew.

Risk management controls The strongest controls to prevent a risk situation being repeated are mechanical controls, which remove human behaviour completely from the equation. An example of this is a safety handle on a piece of heavy machinery that automatically shuts the machine down if the handle is not pressed continually. However, mechanical controls are difficult to arrange in a clinical environment. Procedural controls are also strong. Occasions when procedures or protocols create a safer environment than relying on paramedic reasoning and understanding include the

first stages of a cardiac arrest (e.g. the NZRC/ARC cardiac arrest guidelines—see Fig 7.4) and high-intensity, low-frequency roles like neonatal resuscitation. Similarly, many ambulance services have a protocol that requires a blood glucose to be taken for all patients with an altered conscious state. In order for this control to work the behaviour needs to be driven by the protocol rather than relying on paramedic reasoning and understanding.

FIGURE 7.4 The NZRC/ARC guidelines for managing adult cardiac arrest are a good example of a guideline created on the basis of evidence that provides clinicians with a ‘scaffold’ to support them in a high stimulus, high-workload environment. Source: © 2014 Australian Resuscitation Council. However, a procedure is useless unless it is followed and that is the function of education and clinical governance. Organisations must ensure adequate education of staff and auditing of procedures to identify individual or system weaknesses. Education can help us to make a strong link between the clinical experience we have just had (or hopefully somebody else had and told us about) and the reasons why we need to modify our behaviour in future: we now know why we should always remember the blood glucose. The weakest controls are individually-focused disciplinary approaches in which the individual is left in no doubt that they have made an error but no supporting education or system is put in place. Unfortunately, this disciplinary approach to risk management has been a feature of health service culture in the past. Clinical practice for all professions is, in reality, a mixture of procedures or protocols and guidelines that are supported by clinical reasoning. In high-stress circumstances, a wellconstructed guideline is an important element to patient safety and provides a scaffold for our clinical reasoning. In this sense guidelines are a function of evidence-based practice

and risk management control.

Evidence-based practice and patient safety Throughout the whole of medicine there is a move to base clinical guidelines on the best evidence available, and evidence-based practice (EBP) is considered by some to be an essential element of patient safety. EBP is the systematic process by which the best available evidence on a topic is used to underpin the decision-making process for a relevant treatment, action or task (Doherty, 2005). Founded during the 1970s, EBP was influenced by two independent but intertwined movements. The first of these was led by epidemiologist Dr Archie Cochrane. Dr Cochrane called for systematic reviews of current research across all medical specialities so that evidence from scientific studies could be made more accessible for healthcare practitioners (Melnyk & Fineout-Overholt, 2005). The success of this initiative continues today and the results are published in the Cochrane Collaboration. Secondly, in conjunction with this production of clinical reviews, a new approach to medical practice was developed, known as evidence-based medicine (Guyett & Drummond, 2002). Initiated by clinical epidemiologists David Sackett, Brian Haynes, Peter Tugwell and Victor Neufeld at McMaster University in Canada, this new philosophy brought scientific decision making to the bedside and by the early 1990s it had spread to other areas including allied health and nursing (Guyett & Drummond, 2002). EBP includes data from a wide variety of evidential levels. Although some evidential levels are considered more reputable than others, EBP is selective, not exclusionary between different types, recognising the diversity of evidence available. Practitioners gathering evidence incorporate data from sources such as randomised control trials (RCTs), systematic reviews, documented experiences, theories, documented patient reviews, role models, policy directives and expert opinion (le May, 1999). As a minimum, practitioners need to refer to more than one paper in order to refer to their practice as evidence-based (Birnbaum, 1999; Doherty, 2005; Melnyk & Fineout-Overholt, 2005). Relying on only one paper does not recognise research differences and runs the risk of making recommendations on evidence that is not reputable, reliable or reproducible.

P RACT ICE T IP Old clinical guidelines can be used to identify where EPB has been employed in paramedicine. For example, aminophylline for asthma, isoprenaline for bradycarycardia and atropine for cardiac arrest are all medications that were once routinely used in prehospital medicine but have been replaced or simply excluded as either ineffective or harmful.

EBP, individual patients and clinical reasoning The relationship between EBP and patient safety appears fundamental: patients will be diagnosed and receive treatment based on the results of large studies where the tests and interventions have been proven to be safe and effective (Savage & Williams, 2008). In terms of developing guidelines and protocols this can be extremely useful to paramedics working in information-and time-poor settings: they can rely on the guidelines to reduce the cognitive load of decision making and ensure the management plan is generally beneficial. However, guidelines—even those developed by strong studies—should never completely negate clinical reasoning. One of the weaknesses of EBP is that even a welldesigned trail is a summary of the ‘net’ effect of the test or drug: how did the majority of patients respond to the intervention? For interventions that are standard or routine this uniformity is undoubtedly beneficial: for example, the guideline that all patients in an altered conscious state should have their blood glucose level tested will ensure any episodes of hypo-or hyperglycaemia are captured. In routine procedures the essential element is including reliable interventions that provide a distinct treatment path—that is, for an altered conscious state test for hypoglycaemia; if hypoglycaemia is present, treat with IV glucose. Where EBP cannot replace clinical reasoning is in acknowledging that the design of clinical trials aims to both reduce variables and identify a common response. In practice, clinicians will see cases that present or respond abnormally, and they will also be confronted by patients with multiple (acute and chronic) comorbidities that may influence their presentation or reaction to treatment (Savage & Williams, 2008). For paramedics, guidelines developed by EBP provide a simple solution for routine cases, but it remains the paramedic’s responsibility to determine whether a patient can be described as ‘routine’. Rather than criticise EBP for its inability to deal with ‘special cases’, perhaps a better view is to embrace its utility to reduce the cognitive workload and decision making in the majority of cases, and allow the clinician to detect the ‘special cases’ through effective reasoning and then integrate their knowledge of physiology and treatment to select the best management plan for that patient.

Summary Medical practice is inherently complex. While it is the intent of all clinicians to protect their patients, this complexity can lead to errors. Medical errors are not usually caused by clinicians initiating the wrong treatment through a lack of knowledge; threats to patient safety are more often the result of clinicians working within flawed systems. The process of recognising and improving systems in healthcare is proving challenging as it can conflict with traditional clinical governance models that do not recognise error and tend to attribute blame to individuals rather than the system. Nonetheless, over the past decades there has been a significant change in the way some hospitals identify medical errors and seek to prevent them recurring. This should lead to much safer patient care in the longer term and has already been adopted by some ambulance services. Consumers of healthcare have the right to expect the care they receive to be safe, regardless of the setting in which it is delivered. The current generation of clinicians being educated are the first to have concepts of human factors, error wisdom and patient safety embedded into their curriculums and, provided they are supported in the workplace, they should be the safest clinicians yet to enter practice.

References Assaf, A. A.F., Bumpus, L. J., Carter, D., Dixon, S. B. Preventing errors in healthcare: a call for action. Hospital Topics. 2003; 81(3):5–12. Australian Institute of Health and Welfare [AIHW]Towards National Indicators of Safety and Quality in Health Care. Cat. no. HSE 75. Canberra: AIHW, 2009. Bigham, B. L., Morrison, L. J., Maher, J., Brooks, S. C., Bull, E., Morrison, M., et al. Patient safety in emergency medical services. advancing and aligning the culture of patient safety in EMS: Canadian Patient Safety Institute. Canadian Journal of Emergency Medicine. 2009; 13(1):13–18. Birnbaum, M. L. Guidelines, algorithms, critical pathways, templates, and evidence-based medicine [comment]. Prehospital & Disaster Medicine. 1999; 14(3):114–115. Brennan, T., Leape, L., Laird, N., et al. Incidence of adverse events and negligence in hospitalised patients: results of the Harvard Medical Practice Study I. New England Journal of Medicine. 1991; 324(6):370–376. Collier, P.F., Son. Oath of Hippocrates. Harvard Classics, Vol. 38. Boston: Harvard Press, 1910. Department of Health, Victoria. (2010). Building Foundations to Support Patient Safety. Sentinel event program annual report, 2009–2010. State of Victoria. Doherty, S. Evidence-based medicine: arguments for and against. Emergency Medicine Australasia. 2005; 17(4):307–313. Forrai, G., Bánkövi, G., Szabados, T., Papp, E. S. Ketone compound smelling ability: study in Hungarian twins. Acta Medica Academiae Scientiarum Hungaricae. 1981; 38(2):153–158. Graber, M. L., Franklin, N., Gordon, R., Diagnostic error in internal medicine. Archives of Internal Medicine. 2005;165(13):1493–1499 Graber, M. L., Gordon, R., Franklin, N. Reducing diagnostic errors in medicine: what’s the goal? Academic Medicine. 2002; 77(10):981–987. Guyett G., Drummond R., eds. User ’s Guide to the Medical Literature. Chicago: AMA

Press, 2002. Hebert, P. C. Disclosure of adverse events and errors in healthcare. Drug Safety. 2001; 24(15):1095–1104. Jennings, P. A., Stella, J. Barriers to incident notification in a regional prehospital setting. [Comparative Study Research Support, Non-U.S. Gov’t.]. Emergency Medicine Journal. 2011; 28(6):526–529. Laska, M., Hubener, F. Olfactory discrimination ability for homologous series of aliphatic ketones and acetic esters. Behavioural Brain Research. 2001; 119:193–201. le May, A.Evidence-based Practice Nursing Times Monographs. London: Emap Healthcare, 1999. Leape, L., Brennan, T., Laird, N., et al. The nature of adverse events in hospitalised patients: results of the Harvard Medical Study II. New England Journal of Medicine. 1991; 324(6):377–384. Localio, A. R., Lawthers, A. G., Brennan, T. A., et al. Relation between malpractice claims and adverse events due to negligence: results of the Harvard Medical Practice Study III. New England Journal of Medicine. 1991; 325(4):245–251. Melnyk, B., Fineout-Overholt, E.Evidence-Based Practice in Nursing & Healthcare: A Guide to Best Practice. Philadelphia: Lippincott Williams & Wilkins, 2005. National Center for Health Care Statistics at the Centers for Disease Control. Deaths/Mortality. Retrieved March 2013 from www.cdc.gov/nchs/fastats/deaths.htm, 2005. Nieva, V. F., Sorra, J. Safety culture assessment: a tool for improving patient safety in healthcare organizations. Quality and Safety in Health Care. 2003; 12(Supp II):ii17–ii23. Nolan, T. W. System changes to improve patient safety. British Medical Journal. 2000; 18(320):771–773. Reason, J. Human error: models and management. British Medical Journal. 2000; 320(7237):768–770.

Savage, G. T., Williams, E. S., Evidence-based medicine and patient safety: limitations and implicationsSavage, G.T., Ford, E.W., eds. Advances in Health Care Management: Patient Safety and Health Care Management, Vol. 7. Bingley, UK: Emerald Group, 2008. Shojania, K. G., Burton, E., McDonald, M., Goldman, L. Changes in rates of autopsydetected diagnostic errors over time. JAMA. 2003; 289:2849–2856. Singh, H., Graber, M. L., Kissam, S. M., Sorensen, A. V., Lenfestey, N. F., Tant, E. M., et al. System-related interventions to reduce diagnostic errors: a narrative review. BMJ Quality and Safety. 2012; 21:160–170. Thomas, E. J., Stoddert, D. M., Burstin, H. R., et al. Incidence and types of adverse events and negligent care in Utah and Colorado. Medical Care. 2000; 38(3):261–271. Kohn, L. T., Corrigan, J. M., Molla, S.To Err is Human: Building a Safer Health System. Institute of Medicine, 1999. Weingart, S. N., Wilson, R. M., Gibberd, R. W., Harrison, B. Epidemiology of medical error. British Medical Journal. 2000; 320(7237):774–777. Wilson, R. M., Runciman, W. B., Gibberd, R. W., Harrison, B. T., Newby, L., Hamilton, J. D. The Quality in Australian Health Care Study. Medical Journal of Australia. 1995; 163(9):458– 471. Wolff, A. M., Bourke, J. Detecting and reducing adverse events in an Australian rural base hospital emergency department using medical record screening and review. Emergency Medicine Journal. 2002; 19:35–40.

CHAP TER 8

Paramedic health and wellbeing By Tegwyn McManamny

OVERVIEW • Paramedics are exposed to highly stressful situations every shift. • The unpredictable nature of the paramedic workplace can require crews to operate for long hours in uncomfortable environments without adequate nutrition or rest breaks. • There is a unique physical and emotional toll associated with working as a paramedic. • Both internal and external stressors are present at almost every case to which paramedics respond and they will influence the clinical decision-making process. • A paramedic’s ability to recognise and adapt to the internal and external stressor will have an impact on patient care as well as paramedic wellbeing. • Developing an awareness of the stressor involved in paramedic work and a self-awareness of how you respond is essential for paramedics and paramedic students alike to practise selfawareness. • Signs and symptoms of prehospital stressors are well described and strategies have been developed on how to monitor and prevent negative impacts on paramedics.

Introduction Paramedics work in a dynamic, uncontrolled environment, caring for people with varying states of physical and psychological suffering (Argentero & Setti, 2008), and it is unreasonable to suggest that this environment has no physical or psychological impact on the paramedics themselves (see Fig 1.1). The decisions paramedics make and their subsequent actions have a significant bearing on the health outcomes of their patients. In Chapter 1 we introduced a model of paramedic decision making that placed the actual decision-making process at the centre of a field of external influences. In subsequent chapters we examined a number of these influences more closely: the role of the paramedic, workplace culture, the patient’s perceived outcome, how the patient communicates and the paramedic’s education. In Chapter 7 we discussed how failures in both people and systems can affect patient safety, and in this chapter we examine the effect that occupational stressors may have on the paramedic’s ability to make safe and effective clinical decisions. We look at the paramedic’s ‘emotional capacity’ and how it impacts on both the patient and the paramedic. Unlike some of the other factors involved in clinical decision making, emotional capacity is one of the most labile, and it can fluctuate significantly within a single shift. Gaining an awareness of how the role affects the paramedic physically and emotionally will not only lead to safer clinical decisions but can also help maintain the health of the crew.

Wellbeing Wellbeing goes beyond feeling physically healthy—it is a multidimensional concept involving every part of a person: emotional/psychological, spiritual, intellectual and physical (Beebe & Myers, 2010). This implies that many factors influence wellbeing and that difficulties in one area may cause overall imbalance. Wellbeing in all its forms is beneficial: for example, an emotionally well person is resilient to challenge and can make grounded decisions; a physically well person can withstand illness and use their body fully; a spiritually well person is secure in their existence and purpose; and an intellectually well person is comfortable in exercising their mental abilities.

Paramedic health and safety Paramedics are exposed to a range of health and safety concerns that may affect their wellbeing, such as: • exposure to contagious and infectious diseases from patients • exposure to contagious or infectious diseases by sharps such as needles • exposure to chemicals used in medical procedures such as methoxyflurane, nitrous oxide and industrial cleaning products • physical tasks that involve awkward postures, repetition, force or overexertion • exposure to extreme temperatures and inclement weather • risk of injury from fire, explosions, unstable structures and surfaces, falling objects, traffic and occupational violence • slips, trips and falls—often compounded by the fact that the paramedic is carrying a patient on a stretcher or in a wheelchair • transport dangers including driving at high speeds, often in difficult traffic or weather conditions • shift work and extended workdays • periods of intense psychological stress or trauma (Canadian Centre for Occupational Health and Safety, 2004). These issues can present significant challenges for paramedics, who have to balance such welfare concerns with managing the health and wellbeing of their patients. Making good decisions that have positive impacts on patient wellbeing involves being physically, mentally and emotionally healthy.

Stress A paramedic’s health and wellbeing can be significantly influenced by stress. A stressor is any condition or event (physiological, psychological or environmental) that causes a stress response (Girdano, Dusek & Everly, 2008). A stress response occurs when a person is confronted by a perceivably threatening situation, leading to the sympathetic arousal of the autonomic nervous system. This arousal has been termed the ‘fight or flight’ response. It causes the release of catecholamines (adrenaline and noradrenaline) from the adrenal medulla, preparing the body to stay and defend or to run away. The ‘threat’ message is conveyed initially through the autonomic nervous system (see Box 8.1) but is sustained by a hormonal response that involves the release of adrenocorticotrophic hormone (ACTH) and glucocorticoids such as cortisol. Although stress is generally considered to be a psychological response, it has significant biological components, both short and long term. B O X 8 . 1S h o

r t-ter m eff ec ts o f str ess

• Increased heart rate • Increased blood pressure • Pupil dilation • Sweating • Increased blood sugar levels • Inhibition of digestive secretions • Peripheral vasoconstriction • Bronchodilation

Long-term effects of stress The health impacts of stress in the long term can be significant. Increased cortisol levels over a prolonged period of time lower the efficiency of the immune system, making the body more susceptible to infection and slowing the rate of wound healing (Martini, 2006). Chronically high levels of stress hormones trigger remodelling in cardiac and vascular tissue and can result in hypertension. Tiredness, sleep disorders, headaches, chronic pain and psychological difficulties such as anxiety, depression and panic attacks are also attributable to chronic exposure to stress hormones, as are changes in the brain structures involved in cognition and mental health (Lupien et al., 2009).

Acute and chronic stress Much has been written about stressors and the effects of stress on healthcare workers, especially those working in emergency situations. Prehospital stress is often divided into two categories: acute stress, usually related to exposure to critical incidents and traumatic events; and chronic stress, which is often linked to cumulative stress, burnout and everyday job-intrinsic stress (Hamilton, 2009).

Acute stress Exposure to acute stressors such as critical incidents and traumatic events is often an integral part of the job for paramedics and other emergency workers (see Fig 8.1). A critical incident is defined as any event or circumstance that caused or could have caused (a ‘near miss’) unplanned harm, suffering, loss or damage (National Health Service, 2006). It can be extended to include any incident that overwhelms/threatens to overwhelm the individual’s usual method of coping (Alexander & Klein, 2001).

FIGURE 8.1 Number of incidents attended and those deemed critical. Source: Alexander & Klein (2001). The highest levels of critical incident stress appear to come from exposure to ‘chaotic, tragic or gruesome circumstances’ (Donnelly & Siebert, 2009). For paramedics, incidents involving children, suicides and grotesque mutilation are cited as being the most distressing (Gallagher & McGilloway, 2007). Paramedics may attend tragic and poignant scenes where they are confronted with deceased and dying patients, multi-casualty accidents and paediatric resuscitations including cases of sudden infant death syndrome (SIDS)—also known as sudden unexpected death of an infant (SUDI). The effects of such exposure are unique to the person experiencing them. Emotional reactions such as uncontrolled weeping, panic and emotional numbing with a blank stare (Linton, Webb & Kommor, 1992) may result initially, but later effects can include nightmares, flashbacks and changes in mood. It is important to recognise the significant impact that critical incidents and traumatic events can have, and to be alert for signs of critical incident stress in yourself and your colleagues.

Chronic stress While exposure to critical incidents and traumatic events can have a tremendous impact

on the physical and mental wellbeing of paramedics, everyday operational duties can be just as stressful. Chronic stress, the ‘enduring problems, conflicts and threats that many people face in their daily lives’ (Pearlin, 1989), can be an ever-present background noise that paramedics must manage as an adjunct to the provision of emergency healthcare. Causes of chronic stress in paramedics include: • operational concerns such as organisational mismanagement, inadequate backup and dispatch errors (Alexander & Klein, 2001) • lack of support from or conflict with colleagues (Donnelly & Siebert, 2009) • shift work and sleep disruption • working in hazardous conditions; exposure to violence • constant physiological arousal (when responding to or anticipating an incident) (Linton, Webb & Kommor, 1992) • high workload.

The stress of not being stressed It is commonly perceived that paramedics spend their days managing one acutely unwell patient after the other, saving lives in difficult circumstances and responding to crisis after crisis. However, the changing nature of the paramedic role (Joyce et al., 2009) has shown that paramedics are increasingly responding to low-acuity jobs where the assistance they provide is often a listening ear and transport to a medical facility rather than any lifesaving intervention. This can be a challenge for paramedics, who are trained in advanced life-support skills and may feel that they are not contributing to patient healthcare in the way they anticipated. Somewhat paradoxically, this lack of exposure to critically ill patients can be stressful for paramedics, who feel their training and skills are being wasted. In reality, the routine and mundane prehospital care provided by paramedics can generate its own form of stress. The cumulative effect of exposure to both acute and chronic stressors has been associated with negative outcomes for paramedics. These include ill health, burnout, premature mortality (Young & Cooper, 1995) and high levels of workforce absenteeism (Mitchell & Dyregrov, 1993). Paramedics responding to call-outs are inadvertently affected by the chronic stressors around them, and it is important for individuals to recognise the impacts of this ‘background noise’ on their moods, decision making and clinical practice.

CA SE ST U DY 1 Case 14593, 0230 hrs. Dispatch details: A 17-year-old female patient has been drinking with friends. She has collapsed and is now unconscious. Initial presentation: On arrival, the inner city crew finds the patient in the toilets of a nightclub. The club is crowded and very noisy. The patient has

vomited on her clothes and the floor. There are four friends in attendance: they are loud and obnoxious, appearing intoxicated, and are using their phones to photograph the patient. They state she has been drinking vodka shots for several hours. The patient localises and groans to painful stimuli before vomiting again. Suddenly, one of the patient’s friends holds her iPhone in the face of the attending paramedic and attempts to take a photo of him. He grabs the phone and throws it against the wall. The paramedic’s partner is shocked by the action as the paramedic concerned is renowned for his calm and polite nature. This shift is the crew’s second nightshift in succession and the patient is the fourth intoxicated patient of the evening. Neither crew member has eaten since the start of the shift.

In case study 1 we can see the effects of stress, and perhaps a dwindling emotional capacity, on the attending paramedic. He is tired and hungry, and the several intoxicated patients the crew has attended already have proven emotionally draining without providing a sense of professional pride. When the bystander pushes a mobile phone near his face it proves to be the tipping point, with the build-up of a busy shift causing a peak in his stress levels, triggering an outward reaction in response.

Managing emotions Several authors discuss the concept of an emotional bank account or emotional pie (e.g. Hanna, 2009). According to this concept, our feelings of stress and wellbeing are rarely constant: the world and the people we interact with are constantly making deposits or withdrawals on our sense of wellbeing (in the case of the bank account metaphor), or consuming parts of our ‘pie’. When your emotional wellbeing is high you have a deep reserve to draw on before you are affected. But if the people and situations around you all demand an emotional investment from you, your reserve will run down (see Fig 8.2). Your reserves can be replenished by positive experiences and interactions, boosting your emotional wellbeing.

FIGURE 8.2 Our feelings of stress and wellbeing are constantly being challenged by the world and the people with whom we interact. When your emotional wellbeing is high your emotional reserves can be considered whole and you have the resilience to deal with stresses that suddenly present. But the same stress on a day when your wellbeing has been challenged by other ‘withdrawals’ can generate a large (and others may perceive) disproportionate reaction. Small stresses that reduce your positive balance may have little or no effect when your reserve is deep, but if your reserves are low the same stresses can generate a large (and,

others may perceive) disproportionate reaction. Experiencing traumatic incidents, negative interactions with people around you or long tiring days may not trouble you as much when your emotional wellbeing is high, but as your reserves dwindle you may find yourself responding in a more emotional or seemingly ‘out of character ’ manner. Recognising the potential for this to occur is an important step towards self-awareness. If you can recognise that your reserves are being challenged, you can take steps to protect yourself from running out completely and having a meltdown like the paramedic in case study 1.

Running on empty For paramedics facing a long shift full of emotionally charged situations, maintaining a degree of self-awareness and monitoring their stress and emotion levels throughout the shift become essential in avoiding triggers. You need to learn to recognise early what situations may deplete your reserves—not having your meal break on time, interacting with traumatised relatives of patients, communicating poorly with your work partner and facing busy nightshifts, for example.

DEF INIT IONS Stressor: Physical, psychological or social force that puts real or perceived demands on the body, emotions or mind of an individual. Occupational risk factors: The hazards and risks that workers are exposed to through their profession. Examples include physical or psychological injury, bullying, harassment, violence and stress. Occupational violence (or workplace violence): Violence associated with work; it may involve ‘incidents where staff are abused, threatened or assaulted in circumstances related to their work … involving an explicit or implicit challenge to their safety, wellbeing or health’ (Wynne et al., 1997).

Replenish your reserves Early in a paramedic’s career, when the excitement and novelty of the role are rich, it is difficult to imagine being run down. But after a few years the break between shifts can seem too short to fully recharge before the cases start rolling in again. Recognising this and using your downtime to positively recharge yourself are essential if you are to enjoy a long career in the field. Some crews have to work together for long periods. While this can be a stress in itself, it also offers the opportunity (and responsibility) to watch for stresses and reactions in your work partner. While most crews maintain an unspoken mutual agreement to keep an eye out for each other, a head’s up before a shift (‘I’;m just not in the mood to deal with difficult patients tonight!’) can help your partner keep you away from triggers that on other nights would not affect you.

Protect yourself The paramedic role by nature involves a series of small stressors punctuated by the occasional large stressor. One of the keys to managing these stresses is to recognise the unique nature of the job (no-one calls an ambulance because they are happy) and to actively protect yourself at the start of every shift. Unlike other jobs where commercial or creative successes can actually make a day entirely positive, paramedics (like a number of healthcare roles) are subject to a series of patients all suffering from a crisis. Prepare yourself. If you know that you react badly to conflict when you are hungry, carry muesli bars and some fruit in your ambulance kit bag so that you can eat on the run, even if your meal break is late. If you know you have some extra night shifts coming up, set aside time for a decent sleep and time-out beforehand (perhaps a long walk in a quiet area). If things have been rough at home or you are experiencing personal difficulties, ensure you let your work partner know so that he or she can keep an eye out for you at work, and consider other options for getting your wellbeing back on track, such as counselling or other support. It is important to realise that some situations may affect you more than others owing to past experiences and encounters. For example, a paramedic who is a keen cyclist may feel more empathy for cases involving bicycle crashes at work. Paramedics with young children are likely to find scenes with patients the same age as their children more challenging. In case study 2 we can see that Joe is particularly affected by the condition of his elderly patient. This may be because he has associated the situation with that of a relative, who was similarly affected by a stroke. Perhaps today’s patient and her family reminded him of his own experiences. If you are aware that some situations will challenge you more than others, it is important to remember the ‘emotional reserve’ concept and endeavour to keep your balance topped up. Recognise your emotions, speak to your work partner about any potential difficulties and consider addressing the root cause of your distress through counselling or other support services.

CA SE ST U DY 2 Case 10778, 0730 hrs. Dispatch details: A 65-year-old female with sudden onset of slurred speech and left-sided numbness. Initial presentation: On arrival the crew finds family members sitting around the patient, who was eating breakfast when she experienced the onset of symptoms. The patient is now unable to move her left arm and leg. The patient’s family are supporting her from falling to the left. She is conscious, has an obvious left-sided facial droop and is speaking with slurred words. Joe, who is attending the patient, begins his primary assessment but soon turns to his partner and says he has to step outside for a moment. He appears shaken and

upset, and asks his partner to take over.

It is natural for paramedics to have an emotional reaction to the incidents they encounter. However, crossing the boundary between sympathy and empathy can result in a risky emotional attachment, leaving the paramedic’s emotional state vulnerable. It is important to maintain a professional relationship with patients, understanding their needs without becoming too emotionally involved.

Fatigue Fatigue has been defined as ‘a state of tiredness, affecting both mind and body; where an individual is unable to function at their normal level of abilities’ (Sofianopoulos et al., 2011). It is more than just being tired after a poor night’s sleep, and can be caused by a variety of influences including sleep disturbances, shift work, poor lifestyle and occupational stress. Fatigue is a health and safety issue that paramedics are confronted with daily. It can significantly affect their physical and psychological wellbeing, which has implications for patient care. The symptoms of fatigue vary for each individual, and it is important to understand how fatigue affects you and the people around you. Reading the signs (see Boxes 8.2 and 8.3) will help you know when to take action and make positive changes to ensure your health and safety, and that of your colleagues. B O X 8 . 2G e n e r a l

sig ns o f f atig ue

• Constant yawning • Heavy or sore eyes, rubbing your eyes • Trouble keeping your head upright • Delayed reactions • Irritability • Daydreaming • Taking longer than usual to perform simple tasks

B O X 8 . 3S i g

n s o f d r i ve r f a t i g u e

• Drifting over lanes • Difficulty remembering driving the last few kilometres • Driving at varying speeds • Dim or fuzzy vision • Unintentional increases or decreases in speed • Fumbling for gear changes • Missing turn-offs

In case 1 below, Tom finds himself nodding off behind the wheel while stopped at the traffic lights. His past few days have been busy, sleepless and exhausting, leading to accumulated fatigue that has manifested itself in several ways. The risks to himself, his work partner and their patients are of serious concern. Whether you are driving or attending to a patient, you have a duty of care to ensure the safety of everyone in your ambulance. If you recognise the signs of fatigue in yourself or your partner, act! Take a

break wherever possible, ensure you are well-nourished and hydrated, and monitor your condition. In case 1 we can also see the effect that the paramedic’s fatigue can potentially have for the patient. An error in drug administration could be detrimental to patient safety. Tom may have been working on autopilot, his normally sharp senses dulled: studies indicate that judgement, alertness and concentration are all affected by fatigue (Dowson & Zee, 2005). Additionally, work performance is decreased due to changes in problem solving and decision making (Jansen et al., 2003): this has significant ramifications for patient care in the prehospital setting.

Case 1 Tom finished a busy nightshift at 7 am and had a poor after-shift sleep because of the noise of his neighbours renovating next door. Driving to his second nightshift that afternoon he already feels grumpy. He forgot to bring his dinner and has to settle for takeaway—again. Tom and his work partner are flat out all night. Several cups of coffee don’t seem to help. Tom feels nauseated. At 3 am Tom finds himself nodding off while the ambulance is stopped at a red light. It might seem innocuous except that Tom is the one behind the wheel. At the crew’s next job Tom’s partner asks him to check the drug dosage they’d calculated and draw up the IV medication. Only when Tom handed the syringe back did he realise he’d drawn up the wrong drug by mistake.

How to manage fatigue Paramedics can help reduce their fatigue, and recover more effectively from shift work, by remaining self-aware and monitoring themselves. Key factors in the management of fatigue include: • practise good sleep habits (leave adequate time for sleep, and set up the room for sleep during daylight with heavy curtains and noise insulation) • maintain a healthy diet, low in fat and high in fresh fruit and vegetables • maintain good physical fitness through regular exercise • restrict your caffeine and alcohol intake, and avoid using tobacco • ensure that your family and friends understand the demands of the paramedic lifestyle and can provide a supportive home environment.

Shift work Paramedics work a variety of shift patterns to provide continuous emergency care for their communities. This results in a combination of long hours, overnight duties, rotating schedules, early starts and broken (or absent) nocturnal sleep (Patterson et al., 2010). Shift work has been identified as contributing to paramedic burnout (Mock et al., 1999) as well as hampering patient safety and having ‘detrimental consequences’ on the health and wellbeing of paramedics (Sofianopoulos et al., 2011). The discordant sleep patterns that result from rotations between day, afternoon and night shifts make it difficult to maintain consistently high sleep quality and natural circadian rhythms (Joyce et al., 2009). This misalignment of the work–rest cycle is associated with many health problems, including decreased alertness, elevated levels of fatigue and poorer cognitive performance, potentially leading to poor occupational performance and workplace mishaps (Courtney, Francis & Paxton, 2010). As a novice paramedic you may not feel the impact of shift work immediately: partially due to the excitement and nervous energy you will no doubt feel when beginning your career but also because the long-term effects are yet to accumulate. To reduce these effects it is important to establish good work/rest habits from the beginning—by prioritising sleep, a healthy diet and exercise. These are all regarded as protective factors, helping to mediate the effects of shift work.

Look after yourself There are some simple things you can do to positively contribute to your health and wellbeing and ensure your longevity in the career you have chosen: • Catch up on sleep. Ensure you get plenty of rest both before and after your shifts, particularly nightshifts. Hang heavy curtains in your bedroom to block out light and noise, and use earplugs for afternoon naps. • Watch your diet. Large meals and foods rich in fat and carbohydrates can make you feel drowsy as your body attempts to process them. Choose plenty of fresh vegetables with lean protein for your meals, and have snacks such as nuts and fruits within easy access. Stick as closely as you can to your normal eating pattern—avoid those 2 am dim-sims where possible! • Nap. Studies have found that strategic napping during downtime on shifts (particularly nightshifts) can reduce fatigue and the adverse effects on physiological functions (Takeyama et al., 2009 ). Use your downtime to rest and regain some energy. • Speak up! If you are fatigued, let your partner know so that they are aware of how you are feeling and can help monitor your condition. If your fatigue is likely to cause an accident or negatively impact on patient outcomes, you should let your employer know immediately so that steps can be taken to ensure you get a much-needed break as soon as possible. • Seek help. Having social supports and relationships are vital to wellbeing, and discussing your experiences can be a valuable debriefing tool. Ambulance services also provide psychological support, counselling and critical incident debriefing for their staff. If your physical or psychological health deteriorates, seeking professional assistance can be difficult, but a good first step is discussing any concerns with your local doctor, who can

point you in the direction of further assistance where required.

Occupational violence The degree of exposure to occupational violence varies widely across occupations, but jobs requiring face-to-face contact with patients present a greater risk (Mayhew & Chappell, 2005) and paramedics in particular have a high risk of exposure (Boyle, Koritsas & Coles, 2007; Mayhew & Chappell, 2009; Pozzi, 1998). This is result of both their role and where it is practised: isolated sites, domestic premises, emotionally charged scenes and ‘situations where the potential patients and bystanders [are] affected by illicit drugs or alcohol’ (Mayhew & Chappell, 2009)—all potential risk factors for occupational violence. Research indicates that fully qualified paramedics are more likely to experience violence than student paramedics (Boyle et al., 2008; Koolhaas et al., 2011; Koritsas, Boyle & Coles, 2009) due to the protection provided by the more-experienced paramedic partner intervening or mediating during an incident in the interests of the less-experienced student paramedic they supervise. Verbal abuse is the most common form of occupational violence experienced by paramedics (Boyle et al., 2008; Koritsas, Boyle & Coles, 2009; Pozzi, 1998; Suserud, Blomquist & Johansson, 2002). Paramedics are more likely to experience verbal abuse if they have many hours of direct patient contact, work as part of a two-person crew and are fully qualified (Koritsas, Boyle & Coles, 2009).

CA SE ST U DY 3 Case 12583, 0024 hrs. Dispatch details: A 32-year-old male has sustained a ‘major haemorrhage’. Details are unclear but it appears he is bleeding from the abdomen. Initial presentation: On arrival, paramedics Shaun and Simon park the ambulance out the front of a suburban boarding house. They note the blood splattered on the footpath. They are met by a dishevelled female who smells of alcohol and appears intoxicated. She has blood on her shirt. She tells the crew her boyfriend has been stabbed in a dispute. The crew ask for further information but the female insists they treat her boyfriend immediately. Simon attempts to ascertain who stabbed the patient and where the offender may be now, while Shaun quietly radios dispatch and asks for police assistance due to the nature of the incident. However, the female becomes agitated and starts swearing and screaming at the crew to ‘hurry up and help’ her boyfriend. Suddenly, she grabs Simon’s shirt and attempts to drag him down the driveway. As he pushes her away her behaviour escalates and she launches herself at Simon, screaming and attempting to scratch his face.

Intimidation and physical abuse are the second most common forms of occupational violence experienced by paramedics. Female paramedics encounter this form of violence more commonly than their male counterparts (Koritsas, Boyle & Coles, 2009). Gender appears to be a common predictor of other forms of occupational violence (sexual harassment and sexual assault) and this may be due to women being seen as ‘easy targets’ for workplace violence (Koritsas, Boyle & Coles, 2009). Although fortunately not prevalent, physical assault of ambulance staff does occur, with some paramedics reporting being subject to a form of physical violence in their workplace (Boyle et al., 2008; Brough, 2005; Corbett, Grange & Thomas, 1998; Grange & Corbett, 2002; Hafeez, 2003; Koritsas, Boyle & Coles, 2009; Mayhew & Chappell, 2009; Pozzi, 1998; Suserud et al., 2002). Examples of physical assault include being hit, kicked, slapped, dragged by the hair and gripped by the throat, or, in the case of Simon in case study 3, scratched. Box 8.4 discusses ways to protect yourself from violence in the workplace. B O X 8 . 4O c

c u p a tio n a l vio le n c e : p r o te c tin g

yo u r se lf 1. Recognise patients or bystanders who might pose a risk to you or your partner (such as those affected by drugs or alcohol, relatives at emotionally charges scenes and those suffering acute psychotic illness). 2. Minimise risk prior to exposure: know where your duress alarms are and how to use them. Be aware of ‘flagged’ locations where violence has been reported in the past and ensure police assistance is sought if required. 3. Know your access and egress points and plan with your partner your approach to potentially unsafe scenes (remote areas, isolated sites, areas where egress is difficult and locations involving multiple persons such as brawl scenes). Stand to the side of a patient’s front door after knocking, not immediately in front of it. This gives you room to move if the door is opened to reveal a threat, such as an angry dog or a person with a weapon. 4. Carry your equipment bags in your hands or off one shoulder, not draped across your body. This allows you to drop them easily if running and also provides the option of using them in a defensive manner if required. 5. Park your ambulance in such a way that you can leap in and drive away immediately if you are threatened. If a difficult reversing manoeuvre and a three-point-turn are required to leave a scene, you are exposing yourself to avoidable risk. 6. If you are threatened, attacked or feel in danger, leave the scene immediately. Seek cover in the ambulance and retreat from the area. 7. If you are exposed to occupational violence, ensure you report the incident to your employer and the police, and take steps to seek help to mitigate the effects of any physical, emotional or mental health disturbance.

In case study 3, Shaun and Simon are exposed to two forms of occupational violence: verbal harassment and physical assault. They considered their safety when approaching the scene: they parked the ambulance at the front of the property, pointing in the direction of retreat should they need to leave the scene in a hurry. In addition, it can be assumed that each was carrying an equipment bag, which they could drop at the feet of a potential attacker, acting as an obstacle to allow them a few more vital seconds to escape. Simon could also use his bag as a shield, to prevent the emotional and intoxicated female from getting too close. Finally, Shaun has radioed for police assistance, in the hope of circumventing any further issues, as there is potentially an armed offender on scene. This situation escalated very quickly, increasing in volatility due to the concerns of the patient’s girlfriend. Simon and Shaun could have taken a few additional steps to safeguard their approach: • If someone outside a venue could be of concern, or if responding to a suspicious job, do an initial drive-by in the ambulance to size up the scene. • Wind down the window enough to hold a conversation with the person outside, so that you can gather enough information to make an informed decision about what is going on. If the scene is dangerous, you can drive away and contact the police. Occupational violence is unfortunately a feature of the prehospital setting that paramedics may be exposed to. However, as part of ‘D’ for dangers, safeguarding your approach is pivotal and will help reduce the risk of unwanted situations.

CA SE ST U DY 4 Case 00522, 1030 hrs. Dispatch details: A 54-year-old male has fallen down some steps and sustained a leg injury. He is conscious and breathing but in significant pain. Initial presentation: On arrival, paramedics Lauren and Amy are shown to the back patio of a suburban house by the patient’s wife. The patient is lying at the foot of the patio stairs. He states that he has fallen down five steps, a distance of approximately 1 metre. His only injury is to his lower right leg, which is bent underneath him. While Lauren assesses the patient and begins administering analgesia, Amy retrieves the stretcher from the ambulance. The patient is quickly made comfortable and his leg is splinted. As Lauren and Amy attempt to get the patient onto the stretcher, Amy feels a tearing pain in her shoulder and is subsequently unable to lift her arm.

Injury Paramedics, like other healthcare professionals, may be affected by injury or illness in the course of their work (see Fig 8.3). Back and extremity injuries appear to be the most common forms of physical injury reported by paramedics in the course of their employment (Gentzler & Stader, 2010; Schwartz, Benson & Jacobs, 1993). The most common causes of prehospital workplace injury involve reaching for overhead equipment, pulling patients from bed to stretcher, lifting patients on spineboards from the floor and seated tasks that require bending and twisting (Gentzler & Stader, 2010; Lavender et al., 2000). Paramedics carry vital equipment from ambulance to patient—equipment such as trauma bags, resuscitation packs with oxygen bottles, defibrillators, spineboards, wheelchairs and stretchers. This equipment can be bulky and heavy, and may need to be carried up and down stairs, into cramped spaces and for long distances. Patients who are immobile, injured or obese require additional help, putting further strain on the physical capabilities of paramedics.

FIGURES 8.3 The obvious dangers of exposure to bodily fluids and needle-stick injuries have generally been wellmanaged and it is the unique dangers of working in the community setting that now contribute to the majority of paramedic injuries. Lifting patients from awkward positions after falls and working in confined spaces such as overturned cars are unavoidable activities but paramedics need to recognise the risks and mitigate them by using equipment or teams as effectively as possible. Source: Image supplied by St John Ambulance WA. Workplace injuries are disruptive and expensive to both the paramedic sustaining the injury and their ambulance service. Injury management and rehabilitation can be timeconsuming and frustrating for paramedics, who may have to undertake alternative duties as their injury heals. Many ambulance services provide primary injury prevention

programs in an effort to educate paramedics about the risk of workplace injury and to minimise its incidence and effects. Box 8.5 outlines ways to reduce your risk of workplace injury. B O X 8 . 5H o

w to r e d u c e yo u r r isk o f

wo rkplac e injury • Wear appropriate personal protective equipment (PPE) such as gloves, safety glasses and face masks to reduce your risk of exposure to body fluids. • Ensure you are trained how to operate equipment so that you can use it properly without threat to your health and safety. If you don’t know how to use a certain piece of equipment, seek advice. • Utilise ergonomic resources. If your ambulance service provides lifting aids such as walk/lift belts, stair chairs and lift mattresses, use them! If a nursing home you attend has a lifting machine, ask trained staff to use it to move the patient onto the ambulance stretcher. • Talk through lifts, slides and other movements with your work partner and with other personnel who may be on scene to help you (such as the police and firefighters). Ensure that everyone who is contributing to the exercise understands how it will be carried out and what their role is. This is particularly important for difficult extrications. • Seek help. Never attempt lifts, slides or other movements with heavy equipment or patients when alone. • Warm up prior to lifting: stretch the muscles you anticipate using, such as your back, arm and leg muscles. Don’t attempt to perform sudden heavy movements when your muscles are cold and inflexible. Also, stretch and try to move around when you find yourself in the same position for some time, such as when you get a break after performing CPR, or when you are sitting in a cramped position in the back of an ambulance. • Bend your knees! Practise your lifting technique, maintaining a straight back and using your legs: it should be a movement you know well and can utilise when called upon. • Adjust the position and height of your seat in the ambulance to suit your body. Use a lumbar support if required. • Don’t jump out of the ambulance carelessly: stepping down carefully will reduce the likelihood of ankle and knee injuries. • Maintain good physical fitness including weight-bearing exercise to maintain bone and muscle strength and good posture. • Report hazards to your employer to protect yourself and others from potential injury.

In case study 4, Lauren and Amy are attempting to move an injured patient from the ground to the stretcher. Immediately they are in a vulnerable position, as they want to

provide excellent patient care but this is offset by the fact that the patient is some distance from the stretcher. Moving the stretcher as close as possible to the patient will reduce the distance they need to cover. If the patient is able to move themselves, they could be encouraged to do so, but this patient has a potentially fractured leg and as a result is less likely to be able to bear weight. If the paramedics had a lifting aid such as a walk/lift belt, they could use it to assist with the movement. If not, they may have to radio dispatch and ask for another crew to assist with the lift. While this may seem like a time-consuming and resource-heavy method of lifting, it is one way to be sure that the crew’s wellbeing is not compromised by injury.

Student paramedics Being a new paramedic or studying to become one is an exciting time in your career journey. There are new challenges to face and new rewards on offer. This chapter has already discussed the occupational stressors that can impact on paramedics in general, but there are also specific stressors that are more likely to affect students as they try to find their place in a busy and stressful work environment. Seniority is one of the case-specific factors in clinical decision making. This factor is particularly pertinent to student paramedics who not only are trying to determine the nature of the patient’s problems but also feel the pressure of being assessed by the senior crew member. As well as adding to the student’s cognitive load this can distort the decision-making process if the student tries to second-guess what the senior member would do. Moving from the security of the classroom to the chaos of the prehospital world can be confronting to students who have not yet developed coping abilities or stress management strategies (Young, 2012). It is important to recognise the challenges that paramedic students, both undergraduate and newly employed, may face. These include: • financial concerns • academic pressures, including exams and study • personal commitments, including relationships • sourcing and maintaining part-time work • living arrangements • power imbalances with supervisors, preceptors and clinical instructors • clinical rounds (placements) • adjusting to the cultural and organisational nuances of the prehospital environment.

Case 2 Lee is a first-year undergraduate studying paramedicine. As part of his study he is required to undertake clinical placements in prehospital and hospital environments to familiarise himself with his intended workplace. His first placement is at a rural ambulance station. He rings the station doorbell and is let in by a tired-looking paramedic. Inside, the other paramedics are talking and laughing, and Lee isn’t sure whether he should interrupt them to introduce himself. Instead he sits at the table and gets his study books out. The station manager arrives and gives Lee a quick tour before the pager goes off and Lee follows the dayshift crew to the ambulance for their first job. Lee sits in the rear seat but can’t hear the other paramedics because the engine is so loud. He wonders what job they are going to …

It is important to give yourself time to adjust to your new lifestyle. As well as studying and undertaking assessments and exams, your learning curve will steepen with the introduction of scene safety and awareness, patient and interprofessional communication, patient assessment and management, clinical reasoning and teamwork—the ‘on-road’

components of your chosen profession.

Clinical placements Undergraduates undertake emergency ambulance clinical placements, or clinical rounds, throughout their degree course. These clinical placements are designed to provide on-thejob skill acquisition (Michau et al., 2009) and link theory with practice (Boyle et al., 2008). These placements are often the first opportunity students have to be part of the prehospital environment and interact with patients and qualified paramedics. It is not uncommon to experience anxiety before and/or during clinical placements, with students often having high self-expectations and low clinical experience, and trying to balance academic and clinical demands concurrently. This is a normal part of student life, and your supervisor, preceptor or clinical instructor will be there to guide you through your clinical placement experiences. There are several key premises that may make your journey easier: 1. Be organised. Know the date and time that your shifts start well in advance, and find out the exact location of the branch or station. Plan your route there beforehand so that you aren’t stressing at 6.30 am on your first day trying to figure out where to go. Pack your lunch and snacks for the day as well as the gear your university or organisation may require you to have on hand (such as safety glasses, your name badge, a reflective vest and a hardhat). You will need to ensure you are aware of your responsibilities regarding both your university and the prehospital organisation you are on placement with. 2. Look the part. You are representing an emerging profession and will be accompanying your supervising paramedics into people’s homes, workplaces, places of worship and other public places. Ensure you turn up for your placement wearing the correct uniform and appropriate footwear and looking neat and tidy. 3. Introduce yourself. Fronting up to your first placement not knowing anyone can be very daunting, so start the day on a good note by introducing yourself, and also mention to your supervisor or preceptor what level you are at. If this is your first placement your responsibilities will be different from those of a third-year student who is about to graduate. Your supervisor should explain your role. For example, on your first placement you may be observing, while after some practice you may be allowed more opportunities to have input into patient management. In case 2 Lee is on the first day of his clinical placement. He can look forward to an interesting day on the road, but he needs to ensure that he communicates well with his supervising paramedics. Lack of communication will lead to uncertainty and potentially a poor educational experience for Lee. 4. Speak up. If you are uncertain about something, or a direction you are given does not make sense, check immediately with your supervisors. They are your source of information and guidance and are a wonderful resource, so use them to their full potential! 5. Wind down. Clinical placements can be stressful. Ensure you take the time when you get home to relax and wind down. Make a list of anything you’d like further explanation on or anything you didn’t understand and take it with you to your next placement, where your supervising paramedics should be able to help you. Get a good night’s sleep and take care of your physical and psychological health.

First exposure to traumatic incidents

Paramedics may be first on the scene of traumatic incidents such as a motor vehicle accidents, SIDS fatalities and violent deaths. Responding to such events is emotionally difficult and distressing. Some paramedics say you never get used to it, whereas others find that dealing with such scenes becomes easier with time, due to improved coping mechanisms and emotional resilience. If you are called out to an event that sounds like it has the potential to be of a serious nature, let your supervisors know if it is your first time dealing with such a call-out. This is particularly important if it is your first time at the scene of a fatality. By communicating that this will be a new experience for you, you are helping your supervisors to understand what support or resources they may need to provide you before, during or after the callout. If you become distressed at a scene, give yourself some distance rather than remaining in close proximity to what has challenged your emotions. Let your supervisors know how you feel and make sure you debrief with either the paramedic crew or an independent source (such as ambulance peer support) after the event.

Balance Finding a balance between the demands of study, clinical placements and having a personal life (including maintaining relationships and attending social events) can be challenging. This chapter has already provided some ideas regarding stress management and how to top up your ‘emotional pie’. In addition, ensure you take time out to do something you love and that relaxes you. You are just starting what will hopefully be a long and rewarding career, and you need to look after yourself!

Getting help Extensive literature points to the psychological effects of accident and emergency work, with a strong indication that paramedics are at greater risk of developing physical and mental stress-related disorders (Donnelly & Siebert, 2009). Exposure to occupational violence can have serious emotional and mental health consequences for operational paramedics, with studies finding that negative impacts accumulate with repeated exposure to workplace violence (Mayhew & Chappell, 2009). Recognising changes in mental and physical health will help ensure that problems can be addressed early—vital for long-term wellbeing. Prehospital organisations have a responsibility to their employees in terms of preparing them for traumatic incidents as well as providing support post-incident. Paramedics suffering burnout, depression, anxiety or posttraumatic stress disorder (PTSD) require access to support and interventions to decrease stress, promote posttraumatic growth and increase resilience. Programs that address the stressful nature of the job at an organisational level may focus on support after critical incidents as well as management of chronic stress and burnout.

Critical incident stress management In an acknowledgement of the distress experienced by paramedics and firefighters responding to traumatic incidents, a debriefing tool was created to facilitate their recovery (Mitchell, 1983). While controversy exists as to its effectiveness, many organisations use it worldwide. Critical incident stress debriefing (CISD) is conducted by trained facilitators. The process involves participants sharing their experiences of the event and reporting any symptoms, with the facilitator working to normalise stress responses and link participants into further aid if required (Halpern & Maunder, 2011).

Organisational help Prehospital organisations offer a wide array of other support services to their staff, including peer support, follow-up and referral services (to trained psychologists and counsellors), as well as education regarding emotional and mental health and how to obtain help. Educational programs may encourage self-awareness and monitoring of self and others, increasing awareness of stress and psychological health. It is important that such management tools are easily accessible for staff, and that emotional and psychological wellbeing is prioritised.

Personal strategies It is important to remember the potential for positive experiences post-stress and the increased resilience and growth that may result. You need to monitor yourself for signs of stress, recognising when it is present and what has contributed to it. Identifying stress early on allows you to seek help as soon as possible, creating the potential for growth and promoting psychological health. In addition, seeking assistance early helps you to learn

effective coping strategies, rather than relying on poor mechanisms like denial, substance abuse and withdrawal (Clohessy & Ehlers, 1999). The value of support services in the form of colleagues, friends and family can never be underrated. The people you know and trust, who know you well, can be a wonderful source of support. Spending time with family and friends, engaging in activities you enjoy, is a form of stress management that many find effective. Look for opportunities to improve your coping and stress management strategies, and never be afraid to seek help when you feel overwhelmed.

Summary While a range of occupational, psychological and social factors may impact on paramedics in their workplace, it is possible to take steps to reduce the risk of any adverse effects. Being aware and recognising occupational risk factors such as stress, occupational violence and injury can help paramedics to make safe choices and decisions to support their health and wellbeing. The decision-making process and patient care can be influenced by a range of factors confronting paramedics; therefore, optimal wellbeing, in all its forms, is vital to ensure the safety of patients and paramedics alike. Undergraduate students face particular challenges that can affect their wellbeing and it is important that support is accessible during this period of their journey. Self-awareness and monitoring help you to recognise stress and other psychological concerns, and lead to improvements in managing negative stress and promoting growth and resilience.

P OST T RA U M AT I C GROW T H Posttraumatic growth (PTG) refers to the positive psychological changes a person may experience after experiencing a traumatic event. Personal growth, adaptation and life awareness may be increased, and previous assumptions challenged (Tedeschi & Calhoun, 2003). Another term for PTG is ‘growing out of ashes’.

References Alexander, D. A., Klein, S. Ambulance personnel and critical incidents: impact of accident and emergency work on mental health and emotional wellbeing. British Journal of Psychiatry. 2001; 178(1):76–81. Argentero, P., Setti, I. Job perception, work conditions and burnout in emergency workers. [Comparative Study]. Giornale Italiano di Medicina del Lavoro Ed Ergonomia. 2008; 30(1 suppl A):A64–A70. Beebe, R., Myers, J.Workforce Safety and Wellness. Professional Paramedic, Volume I: Foundations of Paramedic Care. Clifton Park, NY: Delmar, Cengage Learning, 2010. Boyle, M., Koritsas, S., Coles, J. A pilot study of workplace violence towards paramedics. Emergency Medicine Journal. 2007; 24:760–763. Boyle, M. J., Williams, B., Cooper, J., Adams, B., Alford, K. Ambulance clinical placements: a pilot study of students’ experience. BMC Medical Education. 2008; 8:19. Brough, P. Workplace violence experienced by paramedics: relationships with social support, job satisfaction, and psychological strain. Australasian Journal of Disaster and Trauma Studies. 2005; 2:1–12. Canadian Centre for Occupational Health and Safety. Occupations and workplaces: paramedics. Retrieved 16 November 2011 from www.ccohs.ca/oshanswers/occup_workplace/paramedic.html, 12 August 2004. Clohessy, S., Ehlers, A. PTSD symptoms, response to intrusive memories and coping in ambulance service workers. British Journal of Clinical Psychology. 1999; 38(Pt 3):251–265. Corbett, S., Grange, J., Thomas, T. Exposure of prehospital care providers to violence. Prehospital Emergency Care. 1998; 2:127–231. Courtney, J., Francis, A. P., Paxton, S. J. Caring for the carers: fatigue, sleep, and mental health in Australian paramedic shiftworkers. Australian and New Zealand Journal of Organisational Psychology. 2010; 3(1):32–41. Donnelly, E., Siebert, D. Occupational risk factors in the emergency medical services. Prehospital & Disaster Medicine. 2009; 24(5):422–429.

Dowson, D., Zee, P. Working hours and reducing fatigue-related risk: good research vs good policy. JAMA. 2005; 294(9):1104–1109. Gallagher, S., McGilloway, S. Living in critical times: the impact of critical incidents on frontline ambulance personnel—a qualitative perspective. International Journal of Emergency Mental Health. 2007; 9(3):215–223. Gentzler, M., Stader, S. Posture stress on firefighters and emergency medical technicians (EMTs) associated with repetitive reaching, bending, lifting, and pulling tasks. Work. 2010; 37(3):227–239. Girdano, D. A., Dusek, D. E., Everly, G. S. Controlling Stress and Tension, 8th ed. San Francisco, CA: Pearson Benjamin Cummings, 2008. Grange, J., Corbett, S. Violence against emergency medical services personnel. Prehospital Emergency Care. 2002; 6(2):186–190. Hafeez, S. The relationship of violence-related trauma and length of trauma exposure to posttraumatic stress disorder in emergency medical services personnel. Dissertation Abstracts International: Section B: The Sciences and Engineering. 2003; 63(11B):5517. Halpern, J., Maunder, R., Acute and chronic workplace stress in emergency medical technicians and paramedicsLangan-Fox J, Cooper C, eds. Handbook of Stress in the Occupations. Edward Elgar: Cheltenham, 2011 Hamilton, L. Managing emotion, work and stress. In: O’Meara P., Grbich C., eds. Paramedics in Australia: Contemporary Challenges of Practice. Sydney: Pearson Education Australia, 2009. Hanna, H. Communication and team work in paramedic practice. In: O’Meara P., Grbich C., eds. Paramedics in Australia: Contemporary Challenges of Practice. Sydney: Pearson Education Australia, 2009. Jansen, N., Van Amelsvoort, L., Kristensen, T., Van den Brandt, P., Kant, I. Work schedules and fatigue: a prospective cohort study. Occupational and Environmental Medicine. 2003; 60(Supp1):i47–i53. Joyce, C. M., Wainer, J., Pitermann, L., Wyatt, A., Archer, F. Trends in the paramedic workforce: a profession in transition. Australian Health Review. 2009; 33(4):533–540.

Koolhaas, J., Bartolomucci, A., Buwalda, B., de Boer, S., Flugge, G., Korte, S., et al. Stress revisited: a critical evaluation of the stress concept. Neuroscience and Biobehavioral Reviews. 2011; 35(5):1291–1301. Koritsas, S., Boyle, M., Coles, J. Factors associated with workplace violence in paramedics. Prehospital & Disaster Medicine. 2009; 24(5):417–421. Lavender, S. A., Conrad, K. M., Reichelt, P. A., Johnson, P. W., Meyer, F. Biomechanical analyses of paramedics simulating frequently performed strenuous work tasks. Applied Ergonomics. 2000; 31(2):167–177. [T.]. Linton, J. C., Webb, C. H., Kommor, M. J. Critical incident stress in prehospital emergency care. West Virginia Medical Journal. 1992; 88(4):146–147. Lupien, S. J., McEwen, B. S., Gunnar, M. R., Heim, C. Effects of stress throughout the lifespan on the brain, behaviour and cognition. Nature Reviews Neuroscience. 2009; 10(6):434– 445. Martini, F. Fundamentals of Anatomy and Physiology, 7th ed. San Francisco, CA: Pearson Benjamin Cummings, 2006. Mayhew, C., Chappell, D. Violence in the workplace. Medical Journal of Australia. 2005; 183(7):346–347. Mayhew, C., Chappell, D. Ambulance officers: the impact of exposure to occupational violence on mental and physical health. The Journal of Occupational Health and Safety Australia and New Zealand. 2009; 25(1):37–49. Michau, R., Roberts, S., Williams, B., Boyle, M. An investigation of theory-practice gap in undergraduate paramedic education. BMC Medical Education. 2009; 9:23. Mitchell, J. When disaster strikes … The critical incident stress debriefing process. Journal of Emergency Medical Services. 1983; 8(1):36–39. Mitchell, J. T., Dyregrov, A. Traumatic stress in disaster workers and emergency personnel: prevention and intervention. In: Wilson J.P., Raphael B., eds. International Handbook of Traumatic Stress Syndromes. New York: Plenum Press; 1993:905–914. Mock, E. F., Wrenn, K. D., Wright, S. W., Eustis, T. C., Slovis, C. M. Anxiety levels in EMS

providers: effects of violence and shifts schedules. American Journal of Emergency Medicine. 1999; 17(6):509–511. National Health Service. Standards for critical incident reporting in critical care. Retrieved 1 March 2011 from www.library.nhs.uk/GUIDELINESFINDER/ViewResource.aspx? resID=299638, 2006. Patterson, P. D., Suffoletto, B. P., Kupas, D. F., Weaver, M. D., Hostler, D. Sleep quality and fatigue among prehospital providers. [Research Support, N.I.H., Extramural]. Prehospital Emergency Care. 2010; 14(2):187–193. Pearlin, L. I. The sociological study of stress. Journal of Health and Social Behaviour. 1989; 30:241–256. Pozzi, C. Exposure of prehospital providers to violence and abuse. Journal of Emergency Nursing. 1998; 24(4):320–323. Schwartz, R. J., Benson, L., Jacobs, L. M. The prevalence of occupational injuries in EMTs in New England. Prehospital & Disaster Medicine. 1993; 8(1):45–50. Sofianopoulos, S., Williams, B., Archer, F., Thompson, B. The exploration of physical fatigue, sleep and depression in paramedics: a pilot study. Journal of Emergency Primary Health Care. 9(1), 2011. Suserud, B. O., Blomquist, M., Johansson, I. Experiences of threats of violence in the Swedish ambulance service. Accident and Emergency Nursing. 2002; 10:127–135. Takeyama, H., Itani, T., Tachi, N., Sakamura, O., Murata, K., Inoue, T., et al. Effects of a modified ambulance night shift system on fatigue and physiological function among ambulance paramedics. Journal of Occupational Health. 2009; 51(3):204–209. Tedeschi, R., Calhoun, L. Routes to posttraumatic growth through cognitive processing. In: Paton D., Violanti J., Smith L., eds. Promoting Capabilities to Manage Posttraumatic Stress: Perspectives on Resilience. Springfield, IL: Charles C Thomas, 2003. Wynne, R., Clarkin, N., Cox, T., et alGuidance on the Prevention of Violence at Work. Luxembourg: European Commission, 1997. Young, K. M., Cooper, C. L. Occupational stress in the ambulance service: a diagnostic

study. Journal of Managerial Psychology. 1995; 10(3):29–36. Young, R. EMS Stress and Paramedic Students. Tema Conter Memorial Trust. Toronto: Humber Institute of Technology and Advanced Learning, 2012; 1–3.

SECTION 4

PARAMEDIC EDUCATION O U TL I N E CHAPTER 9: Paramedic education

CHAP TER 9

Paramedic education By Peter O’Meara and Stuart Newman

OVERVIEW • Australia and New Zealand lead the world in paramedic education. • The increased scope of paramedic practice over the past two decades has been a driver in transitioning paramedic education from a vocational system to a university-based system. • The establishment of university-based education provides the research foundation to link evidence and practice to guide the future development of paramedic roles and approaches to clinical problem solving. • The university model of paramedic education requires students to retain a large body of scientific knowledge that they must then be able to apply in highly stressful situations. • The volume of knowledge delivered in a course may exceed students’ capacity to integrate it into effective clinical practice. Modification of paramedic education is necessary to provide students with expertise in clinical decision making. • The current employment model transitions students from university to practising paramedic almost instantaneously, without the support structures provided to medical, nursing and allied health students. • The ability to develop clinical reasoning skills to apply theoretical knowledge while still a novice practitioner is more important for paramedics than for other clinicians, who are able to transition gradually from novice practice, shielded from high-acuity and difficult cases by senior clinicians. • To lessen the ‘shock’ of attending serious cases while still a novice, paramedic students must integrate clinical reasoning skills into their knowledge base during their training. • Mentoring of graduate students during their early career is an essential element in the maturation of the paramedic’s clinical reasoning skills.

Introduction In less than a generation the paramedic profession has evolved from skills-based ambulance drivers who were not expected to understand underlying pathophysiology to today’s paramedics who are required to integrate their knowledge into safe and effective clinical decision making. In the past there was no expectation that ambulance drivers would take on clinical management decisions that required high levels of judgement or reasoning: most approaches to emergency medicine were based on commencing treatment once the patient arrived at hospital. But today’s professional paramedics need to understand and apply judgement in order to commence treatments in the field— something that would have been unheard of a generation ago. Education has been a major force in supporting this transformation (Joyce, Wainer & Piterman, 2009; Willis & McCarthy, 1986). Today there is a vast range of university courses in Australia and New Zealand that aspiring and experienced paramedics can undertake to gain entry-level qualifications or to advance their knowledge and skills through degreeconversion and postgraduate courses. The shift to tertiary education has, however, presented challenges for both students and the profession. The body of scientific knowledge (anatomy, physiology, pathology, pharmacology) now required to practise is both wide and deep, and like other medical professions this knowledge must be integrated with skills and attitudes to enable it to function in the field. Like medicine and nursing beforehand, paramedic educators are now realising that while classrooms may be an efficient method of transferring basic knowledge, they struggle to provide the context and complexities of genuine paramedic cases (Cox et al., 2006). In clinical terms paramedics have climbed from the wide and safe paths in the valley of medicine and must now carefully pick a new path along the higher ridges, where mistakes are both serious and costly.

P RACT ICE T IP In most people disruption of blood flow through the right coronary artery restricts blood supply to the inferior aspect of the heart. The inferior wall lies close to the vagus nerve and ischaemia in this area can trigger gastrointestinal (GI) symptoms that can cloud the diagnosis of a myocardial infarction.

This chapter explores the state of paramedic education and training within Australia and New Zealand. It identifies that although the level of scientific education has increased substantially as a result of the shift to university education, the development of expert clinical reasoning skills extends beyond classroom-based education.

FIGURE 9.1 Forming the safest and most effective treatment plan needs an understanding of pathophysiology, but the ability to apply that knowledge requires paramedics to work in complex environments with multiple interactions.

Experience versus education In case study 1 Pip can almost certainly describe the diagnostic criteria of both atrial fibrillation and inferior myocardial infarction far better than Greg. She might also be able to quote that the first ECG in patients suffering a myocardial infarction is only between 13% and 69% sensitive (Speake & Terry, 2001)—or the frequency that gastrointestinal symptoms are associated with myocardial infarctions (El-Shafie, 2007; McLean, Preston & Flapan, 2008; Smith & Carley, 2001). But critically, Pip is yet to develop the ‘scripts’ (see Ch 5) that enable her to put these facts together when confronted with a patient presenting with an unusual collection of symptoms. Greg, on the other hand, cannot explain Doris’ symptoms to a cellular level but he has seen this collection of supposedly benign symptoms before and knows their combination is probably far more serious than any of the symptoms in isolation. He possesses a tacit knowledge, gained from experience and applied unconsciously, that enables him to initiate a safe treatment plan (Cianciolo et al., 2006). This example is not meant to show that experience alone is the best education: the following day the same crew could attend a patient where Pip’s deeper knowledge of pharmacology will allow her to identify the reason why the patient is unwell. Given the complex nature of out-of-hospital, unscheduled care and the diversity of healthcare situations encountered, modern paramedics must be well educated, skilled and knowledgeable practitioners in a range of subjects and be able to appraise and adopt an enquiry-based approach to the delivery of care (British Paramedic Association, 2005; Norman et al., 2006). Paramedic education programs should produce graduates with an educational base and attributes appropriate to these emerging needs, as well as the level of qualification and specified level of competence required.

CA SE ST U DY 1 Case 10497, 1122 hrs. Dispatch details: A 78-year-old female with no specific symptoms; complaining of feeling generally unwell. Initial presentation: Pip finds the patient, Doris, sitting calmly in her lounge room. She is fully conscious and outwardly appears well. She is well-dressed, the house is clean and neat and it is immediately obvious that she lives alone. Pip commences a thorough and structured assessment, determining that the patient’s skin is pale but warm, her BP is 115/80 mmHg, her pulse is 102 and her GCS is 15. Pip notices that Doris’ pulse is slightly irregular and she asks Greg to record an ECG. It reveals nothing other than that the patient is in atrial fibrillation—a relatively common and usually benign arrhythmia in elderly people. Further examination reveals Doris is not febrile, her respiratory effort and sounds are normal and oxygen saturations are excellent. Several times during the assessment she burps and appears profoundly embarrassed. Her

only complaint is feeling lethargic and nauseous but she does not highlight the persistent burping. She states that both the nausea and the burping started shortly after she awoke. She has not had breakfast. Doris says she regularly visits her GP for a check-up and that she takes no medication. Pip is surprised when Greg tells Doris she needs to go to hospital by ambulance and starts setting up for an IV. Background: The ambulance crew for this case consists of a new student, Pip, and her very experienced clinical instructor, Greg. As with most recent graduates, Pip is acting as the lead clinician for nearly all of the cases the crew attend. Pip has proven to be an excellent paramedic, reflecting the high grades she attained at university. Greg is approaching retirement after more than 30 years on the road. He joined the ambulance service at 32 after working as a motor mechanic.

The history of paramedic education in Australasia Voca ti ona l course s Until the early 1990s nearly all ambulance services in Australia and New Zealand provided industry-specific training courses for their staff. These ‘in-house’ courses were the standard form of ambulance officer education and ranged from volunteer first-aid programs to accrediting professional staff to an intensive care level. Courses consisted of block courses of a few weeks and some distance education requirements, followed by both theory and practical examinations. Some supervisory and management training was offered through ambulance education centres. Admission to these programs of study and management of the curriculum and educational standards were under the direct control of the respective ambulance services, which often had operational and political imperatives to satisfy that could be in conflict with educational objectives. One of the consequences of these courses was the lack of accreditation portability for applicants transferring between states, moving from the defence forces or moving from overseas. Another effect of having so many services training their staff to a specific scope of practice has been a lack of standardisation with regard to titles and skills. The terms ‘advanced life support’, ‘intensive care’ and even ‘paramedic’ describe different skills sets in different regions. Compared to the employer-specific programs provided in Australia, New Zealand offered a standardised national program through the National Ambulance Officers Training School, which opened in 1977. The early to mid-1970s saw the introduction of intensive care paramedic courses for ambulance officers in Melbourne and Sydney, following developments in the United Kingdom and the United States (Eisenberg, Pantridge & Cobb, 1996; Willis & McCarthy, 1986). These developments greatly changed the expectations that ambulance officers and other health professionals had of the ambulance officer education system (see Fig 9.2).

FIGURE 9.2 The evolution of tertiary-based paramedic education has enabled today’s paramedics to play a key role as members of the health team. Like many educational systems the value of its components is often not appreciated until the learner has integrated academic and practical learning to achieve true mastery of the subject. The breadth and depth of paramedic education can often be better appreciated from the viewpoint of a qualified paramedic than a student. Source: Courtesy of the Government of South Australia/SA Health.

P RACT ICE T IP The scope of medications that paramedics were once able to administer was often limited to those that had no or very mild side effects (so no harm would be done if they were administered in error) or that could be administered orally. As skills in intramuscular injection and IV access were established, paramedics began treating a wider range of conditions.

Throughout the 1980s most Australian in-house courses received accreditation from vocational education and training bodies in their respective jurisdictions (Department of Health and Community Services, 1994; Field, Battersby & Hodge, 1999; Hotchin, 1986; Pammenter, 1978) and these courses gradually progressed from certificate courses to associate diplomas, diplomas and advanced diplomas as further content and rigour was added to ambulance officer education. One of the original vocational qualifications, the Diploma of Paramedicine (the National Diploma in New Zealand) is still offered and accepted as an entry-level qualification for paramedics in some Australian and New Zealand ambulance services and the Australian Defence Forces. Historically these early in-house qualifications ‘locked’ staff into employment with a small number of employers and they very rarely attracted credits in university or other vocational courses. Although the move to vocational education and training during the 1980s and early 1990s saw significant changes in the depth of education provided to ambulance staff (Battersby, 1999; Department of Health and Community Services, 1994; Grantham, 2004) and brought with it some level of recognition and flexibility, it still lagged behind educational developments in other health professions, which by then had migrated to the higher education sector—most notably nurse education, which transferred directly from hospital-based programs to university degrees in the late 1980s (Francis, 1999).

Tertiary education The transfer of ambulance education to the higher education sector commenced during the mid-1990s. In Australia it began in New South Wales, with the development of a Bachelor of Prehospital Care at Charles Sturt University in collaboration with the Ambulance Service of New South Wales (Field, 1994; Lord, 2003). A little later, Victoria University and Monash University established programs in Victoria; and in South Australia, the South Australian Ambulance Service and Flinders University developed a paramedic university program that first accepted students in 1998. In New Zealand, the Auckland Institute of Technology developed a Bachelor of Health Science (Paramedic) degree, while the Wellington Free Ambulance created a paramedic degree delivered by Whitireia Community Polytechnic. All of these early university programs had a strong emphasis on distance education during the establishment phase as means of upgrading existing ambulance officers, so that those already practising in Australia, New Zealand and parts of the United Kingdom and Canada could undertake ‘conversion degrees’. Since that time paramedic education has been progressively transferred to higher education institutions where it sits alongside other health professions. Current paramedic education programs in Australia and New Zealand are now almost completely located in the higher education sector (Wilde, 1999). Paramedic students often sit in the same classes as other health science students (deWit, 1997; Field, 1994, 1995)—for example, at La Trobe University, paramedic, nursing and allied health students undertake a common first year before undertaking discipline-specific subjects. The aim of such an approach is to provide students with greater career flexibility and to introduce students to interprofessional learning early in their educational development. In concert with these changes in the education model we have seen ambulance providers challenged to move from a primarily transport model to a more definitive prehospital medical treatment, primary health and social care model (Ball, 2005; Blacker,

Pearson & Walker, 2009). Both changes are still in progress and present many challenges to ambulance authorities, educators and paramedics.

International educational standards In most parts of the world sub-degree programs are the norm. In many countries, emergency medical technician and paramedic education programs remain tied to the learning of specific motor skills with little emphasis on the formation and acquisition of underlying knowledge or independent clinical decision-making skills. In the United States and Canada, for instance, most paramedic training is provided in community college systems; there are a relatively small number of university programs. While the acquisition of technical skills is very good in many of these sub-degree programs, their duration and structure make it difficult to include a broader and more comprehensive curriculum that covers the foundation biosciences and social sciences that form the basis of the clinical reasoning required when confronted with complex cases. These vocational courses also tend to omit the public health subjects that form a cornerstone of other professional health science degrees in medicine, nursing and allied health. Training of paramedics follows a similar structure in some parts of Europe, with students undertaking programs that emphasise technical, protocol-driven skills for entrylevel paramedics. In the United Kingdom and Ireland paramedic education and training have been moving towards degree-level programs for some time, either within universities or in partnership with them. The estimated 21 programs at 16 universities in England are a mixture of two-year foundation degrees and three-year Bachelor (Hons) degrees. In Ireland, the University of Dublin in collaboration with ambulance providers offers twoyear diplomas for entry-level students and experienced paramedics wishing to upgrade their qualifications. In addition, it offers a research Master of Science degree for paramedics.

Paramedic education in the university setting University education has developed largely in partnership with the statutory ambulance authorities, which recognise the strategic need to increase the depth of knowledge and understanding that paramedics require as they are confronted with a wider range of cases and, particularly, the comorbidity complexities of chronic diseases. Although some ambulance services still employ staff prior to enrolling them in educational programs, most statutory ambulance services in Australia and New Zealand almost exclusively employ university graduates from accredited paramedic programs. Today there are around 22 entry-level paramedic programs on offer or planned throughout both countries at 16 university campuses. While the courses vary in name, structure and length they all produce graduates with similar competency levels that are theoretically accepted as baselevel qualifications by the ambulance authorities. The most common program structure is a three-year undergraduate degree program, although in some cases accelerated progress is possible through trimester course structures and credits for past studies. There are also four-year double degree programs at Monash University, Queensland University of Technology and the Australian Catholic University, which provide a dual qualification in paramedicine and nursing. La Trobe University offers a four-year combined Bachelor/Masters qualification that incorporates health science, public health and paramedicine. Both Charles Sturt University and the University of Ballarat offer postgraduate pathways for nurses wishing to make the transition to a paramedic career. At the base of all paramedic programs are the underlying sciences and social sciences that are common to medicine, nursing and allied health courses (Willis et al., 2010). While the structure of individual courses may vary, they all include specific subjects in anatomy and physiology, pathophysiology, pharmacology from the biosciences; sociology, psychology and management from the social sciences; and specific clinical and emergency management subjects related to paramedic practice. In recognition of the clinical reasoning challenges faced by paramedics, most programs are working to modernise their programs through the adoption of non-traditional pedagogical approaches, such as casebased and enquiry-based learning approaches that emphasise independent learning and autonomous clinical practice. As healthcare needs become more complex, delivering effective healthcare, particularly primary care, requires health professionals to work together in a collaborative manner to meet the needs of patients (Hallikainen et al., 2007). Improvements to continuity and coordination of care in practice require a team-based approach across the professions, something that paramedics may battle with as they tend to be more independent and autonomous than some other health professionals (O’Meara, 2011a). The introduction of interprofessional learning opportunities is a strategy that has been widely implemented to produce adaptable and flexible practitioners with the interpersonal skills to work effectively in collaborative teams. Other emerging developments in paramedic education include greater use of simulated learning environments, further development of competency-based training to better reflect contemporary needs and a greater emphasis on improving the quality of the

education taking place while students are undertaking clinical placements. It is only through a concerted effort in all these areas that universities, the profession and employers can ensure that the paramedic curriculum and pedagogy will meet the needs of tomorrow’s paramedics through better integration and active learning, and an interprofessional practice approach.

Academic competence vs professional mastery: the challenges of the tertiary education model Although widely supported, the increased complexity of paramedic scope of practice combined with the transition to tertiary education presents a number of challenges to both institutions and students. Not surprisingly, these challenges have been shared by professions such as nursing and medicine, which have led a similar path from vocational to tertiary education. The most obvious challenge is providing students with the ability to link the large body of scientific knowledge bestowed during their course with the ability to solve complex clinical problems when confronted with a patient (see Fig 9.3). So much of any undergraduate course involves recalling information for exams that it is easy for students and teachers to forget that the test of any clinician’s education is ultimately judged not on what they know, but what they do with what they know (Cox et al., 2006). Given the complexity of the modern medical degree, for example, it is easy to forget that until the mid-19th century doctors were trained as apprentices. For these students the link between theory and practice was entrenched in daily tasks that were authentic, and the motivation to learn was embedded in the need to provide treatment to genuine patients (Steketee & Adrian, 2007). By literally looking over the shoulders of their mentors, these students received feedback on their skills as well as a role-model of professional behaviour, and by learning through doing they gained an understanding of the ‘complexities, pitfalls, customs and rituals common to that environment’ (Honebein et al., 1993). Until recently, this was almost the exact model experienced by ambulance officers who, after a few weeks of introductory theory, were placed on an operational ambulance as part of a two-person crew and dispatched to whatever cases occurred closest.

FIGURE 9.3 At the end of their undergraduate degree, although students’ theoretical knowledge is generally excellent, the ability to integrate this knowledge into practice requires more experience than clinical placements can provide. It will take even the best students a considerable time before they gain enough patient exposure to fully integrate their knowledge into practice. Source: Courtesy of the Government of South Australia/SA Health. Interestingly, not long after medicine transitioned from the vocational model to a

university-based curriculum, reports began to surface that although the new students may have been achieving academic success, they were struggling to apply the theoretical knowledge to a patient’s presentation and to form a judgement as to the cause (Cox et al., 2006).

From experienced student to novice clinician The ability to reason a diagnosis from a set of complex and often ill-defined symptoms is often described as the difference between novice and expert clinicians (Ajjawi & Higgs, 2008; Bowen, 2006). There is an argument that universities can at best produce competent novice clinicians who tend to focus on the certainty of technical skills as they struggle with the uncertainty of clinical reasoning (see Fig 9.4).

FIGURE 9.4 An advanced paramedic student will not only be comfortable with the pathophysiology and evidence base underpinning a management strategy but will also take into account the larger picture, which includes the patient’s social circumstances and logistical and environmental factors. Source: Image supplied by St John Ambulance WA. For paramedic students who are now subject to the rigours of tertiary education similar challenges exist, but they can be mitigated if the student is able to recognise the limitations of the various learning environments and take advantage of other settings (such as clinical placements) to develop their clinical reasoning skills. Perhaps rather than considering themselves as ‘competent novices’, students finishing their university education should

recognise their status as ‘expert students’ who possess a strong theoretical knowledge base but an underdeveloped set of ‘illness scripts’. Kramer (1974) has described the process of ‘reality shock’ for nursing students who are suddenly exposed to the rigours of clinical practice and find it impossible to transition from student to clinician. Recognising that there will be a ‘practice gap’ (see Fig 9.5) is essential if students are to protect themselves during the transition phase and take full advantage of learning from the complex and confusing patients they will encounter. It is these patients who will create the ‘illness scripts’ that will ultimately link theory to practice (Billet, 2009; Bowen, 2006).

FIGURE 9.5 Clinical placements during undergraduate study provide an invaluable opportunity to integrate theoretical knowledge with practice. However, limited clinical placement hours, inconsistent workloads and a lack of formal education support during placements can limit the quality of experience gained by students.

Course accreditation and professional regulation With the burgeoning of university-based education programs in paramedicine, the Australasian Council of Ambulance Authorities Inc. has documented paramedic competencies to underpin the assessment of courses. These competencies are largely based on those developed in the United Kingdom by the College of Paramedics and they follow the same structure, documenting the knowledge, skills and attitudes that graduates should be able to demonstrate at the completion of their studies. This development was based on the premise that paramedics are independent practitioners working, to their specified level of competence, with patients of all ages, with individuals and in groups, and they are essential members of interdisciplinary and interagency teams. Effective practice requires paramedics to recognise and understand their patients’ social and economic contexts (see Fig 9.6). Given the complex nature of out-ofhospital, unscheduled care and the diversity of healthcare situations encountered, paramedics must be well-educated, skilled and knowledgeable in a range of subjects and be able to appraise and adopt an enquiry-based approach to the delivery of care (British Paramedic Association, 2005).

FIGURE 9.6 A comprehensive tertiary education enables paramedics to make sophisticated evaluations of situations and implement patient-focused decisions that are based on objective evidence-based evaluations. Source: Courtesy of

the Government of South Australia/SA Health. Accreditation of paramedic programs is an external process of evaluation designed to ensure that entry-level paramedic education programs meet accepted standards. The aim is that entry-level programs will be responsive to the needs of industry, the profession and communities, with consistent and acceptable educational standards (Pearson, 2011). The current accreditation program was conceived as a partnership between Australian and New Zealand ambulance authorities, the profession (Paramedics Australasia) and those universities that had already entered the field. The current accreditation system for entrylevel programs in Australia and New Zealand has three stages: • Preliminary approval. Preliminary approval of a new entry-level paramedic education program should be sought prior to the commencement of teaching the course; approval is normally granted prior to, or commensurate with, the entry of the first cohort into the program. • Provisional accreditation. A new program that has been granted preliminary approval will be eligible for provisional accreditation after the first year of teaching, subject to successful annual review. Provisional accreditation may also be granted where conditions are attached following assessment for full accreditation. • Full accreditation. A program is eligible for full accreditation for a period of 5 years when the first cohort of graduates has at least 12 months of practice experience following graduation. The development and implementation of the accreditation guidelines was an important milestone in the professionalism of the paramedic role. By the end of 2011 nine university programs had been fully accredited, with other programs at various stages of the accreditation process. A number of training providers offer vocational qualifications, such as the Diploma in Paramedicine for ambulance sector workers. Some of these providers claim to offer qualifications that will enable graduates to be employed in statutory ambulance authorities but this is incorrect, as the Australasian Council of Ambulance Authorities has made it clear that the organisations it represents will only accept qualifications from their own training centres or accredited universities. While the Australian Defence Forces continue to offer the Diploma of Paramedicine to their medics, the New Zealand Defence Forces have transitioned to a degree-level qualification in partnership with Auckland University of Technology.

Continuing professional development and postgraduate education Following graduation and employment with a statutory ambulance authority, many graduates are required to undertake an extended induction program, sometimes presented as a formal graduate paramedic program (see Fig 9.7). These programs are intended to facilitate the transition from tertiary institution to paramedic clinical practice. The underlying premise is that while graduates are qualified academically, they are not capable of practising safely without some form of supervision and perhaps even further education (McDonell, Burgess & Williams, 2009). This is in marked contrast to the situation in the United Kingdom, where paramedic university graduates are considered work ready and registered under the Health Professions Council (Health Professions Council, 2007).

FIGURE 9.7 Paramedics working within the healthcare system today are required to evaluate and make judgements at a professional level. As the clinical expectations of paramedics have increased, so has the need for a paramedic education that supports this level of evaluation and reasoning. Source: Courtesy of the Government of South Australia/SA Health. Continuing professional development helps all health professionals to maintain, improve and broaden their knowledge, expertise and competence. In the event that paramedics become a registered health profession under the Australian Health Practitioner Regulation Board, practising paramedics will be required to undertake approved continuing education programs. The requirements for continuing professional development will be detailed in the registration standards for the profession, and any additional guidelines in professional codes and guidelines. While some of these requirements will be fulfilled through employer-sponsored education activities, much of the responsibility for continuing professional development lies with the individual paramedic, who will need to undertake self-directed learning activities. The existence of a paramedic-specific body of knowledge is central to the capacity of paramedics to satisfy these professional requirements. Texts such as this are an essential part of a sustainable and respected place for paramedics among the health professions (O’Meara, 2011b). Graduate paramedics have access to a wide range of postgraduate courses through both coursework and research. Throughout Australia and New Zealand growing numbers of paramedics are studying or have graduated from research degrees at either doctoral or masters level that enable them to contribute to the knowledge base of the discipline and to take up academic positions in universities. Many are well published and some are notable contributors to this text. In addition to the continued availability of postgraduate programs in management, education and a myriad other disciplines, the enthusiastic paramedic can undertake a wide range of discipline-specific courses at universities offering paramedic programs. These include programs in intensive care, disaster management, leadership, aero-medical retrieval, community paramedicine and clinical education.

P RACT ICE T IP The scope of practice in some Australian states allows paramedics to perform clinical procedures such as rapid sequence intubation. Where these advanced skills are tied to extensive education, the performance and outcomes are excellent, but in other areas where the skills have been introduced without adequate training the outcomes are poor.

These postgraduate programs are crucially important to the paramedic profession and to the future sustainability of university paramedic programs. However, the relative lack of

suitably qualified academics is putting a major burden on those paramedics already employed as academics, who are juggling large teaching loads, pressure to publish in peerreviewed journals and very often the completion of their own higher degrees (O’Meara, 2006). These pressures are also being felt in other parts of the world where paramedic programs remain dependent on a small number of paramedic academics with the support of other health professionals.

Educational challenges and future directions The move towards tertiary education for paramedics in Australia and New Zealand has been a success, with graduates emerging who are more adaptable than the vocationally trained ambulance officers of the past. Yet there are many challenges and opportunities that need to be met before the transition is complete, particularly the ongoing task of creating a body of knowledge on which the profession can continue to grow and evolve. Until the transition is complete, paramedics will remain partially anchored in the past. This can be observed in the continuing tension between the concept of the universityeducated paramedic professional and the practical technician of the past. There remains a view that theoretical knowledge and practice in the field are incompatible with each other—even though other health professions have successfully melded the two concepts together. It is as if perceptions have not made the transition from the ‘working-class’ origins of the ambulance driver to the paramedic of today (Willis & McCarthy, 1986). However, throughout Australia and New Zealand there are promising strategies being implemented to progress the profession. These include the growing number of practising paramedics and paramedic academics undertaking research degrees and other postgraduate education, joint university/ambulance service appointments, secondments, efforts to improve the quality of clinical placement and the conduct of a wider range of research activities. Of particular note has been the increase in the number of textbooks with paramedic editors and authors (Curtis et al., 2011; Griffiths & Mooney, 2011; McDonell, Burgess & Williams, 2009; Reynolds, 2009; Sheather, 2009; Stirling, 2009). As members of this new and evolving profession it is largely up to you, the readers of this book, to bridge the gap between the past and the future, ensuring that we do not lose the values and history of the past but also that we are not held back by it.

Summary Students undertaking the journey from beginner to mastery benefit from a sound broadbased academic education upon which subsequent learning and development can occur. Today’s students in many ways end up following the same process of evolution as the paramedic profession has undergone. Beginning students are introduced to the fundamentals of anatomy and physiology relevant to paramedic practice, as well as the industry and basic skills necessary to participate in clinical placement in the field. As they progress through their education, more complex issues requiring greater depth of knowledge and judgement are introduced. The basic skills are then underpinned with knowledge of how the pathophysiology and the complex patient’s social and emotional environment all impact on management.

References Ajjawi, R., Higgs, J. Learning to reason: a journey of professional socialisation. Advances in Health Science Education. 2008; 13:133–150. Ball, L. Setting the scene for the paramedic in primary care: a review of the literature. Emergency Medicine Journal. 2005; 22:896–900. Battersby, D. The future of ambulance officer education and training in the UK. Prehospital Immediate Care. 1999; 3:113–114. Billet, S. Conceptualizing learning experiences: contributions and mediations of the social, personal, and brute. Mind, Culture and Activity. 2009; 16(1):32–47. Blacker, N., Pearson, L., & Walker, T. (2009). Redesigning paramedic models of care to meet rural and remote community needs. Paper presented at the 10th National Rural Health Conference, Cairns. Bowen, J. L. Educational strategies to promote clinical diagnostic reasoning. New England Journal of Medicine. 2006; 335(21):2217–2225. British Paramedic AssociationCurriculum Framework Consultation Document. London: British Paramedic Association, 2005. Cianciolo, A. T., Matthew, C., Sternberg, R. J., Wagner, R. K. Tacit knowledge, practical intelligence and expertise. In: Ericsson K.A., Charness N., Feltovic P.J., Hoffman R.R., eds. The Cambridge Handbook of Expertise and Expert Performance. New York: Cambridge University Press, 2006. Cox, M., Irby, D., et al. American medical education 100 years after the Flexnor Report. New England Journal of Medicine. 2006; 355:1339–1345. Curtis, K., Ramsden, C., Lord, B., et alEmergency and Trauma Care for Nurses and Paramedics. Sydney: Elsevier, 2011. Department of Health and Community ServicesReview of the Ambulance Officers’ Training Centre. Melbourne: Department of Health and Community Services, 1994. deWit, A. ‘Against the odds’. Tertiary education for ambulance paramedics in Victoria,

Australia. Australasian Journal of Emergency Care. 1997; 4(3):19–22. Eisenberg, M. S., Pantridge, J. F., Cobb, L. A. The revolution and evolution of prehospital cardiac care. Archives of Internal Medicine. 1996; 156:1611–1619. El-Shafie, K. Belching as a presenting symptom of angina pectoris. Sultan Qaboos University Medical Journal. 2007; 7(3):257–259. Field, J. Establishment of ambulance education in a university context. Australasian Journal of Emergency Care. 1994; 1(1):13–15. Field, J.Designing a curriculum in prehospital care. Bathurst: Charles Sturt University, 1995. Field, J., Battersby, D., Hodge, D. Professional qualifications for ambulance officers: a case study. Australian Journal of Emergency Care. 1999; 6(2):11–16. Francis, B. Rationalisation and professionalisation: a comparison of the transfer of registered nurse education to higher education in Australia and the UK. Comparative Education. 1999; 35(1):81–96. Grantham, H. Ambulance education past present and future. Journal of Emergency Primary Health Care. 2004; 2(1–2):1–2. Griffiths, P., Mooney, G. P. The Paramedic’s Guide to Research: An Introduction; Volume 1. McGraw-Hill, Berkshire, UK, 2011. Hallikainen, J., Väisänen, O., Rosenberg, P. H., et al. Interprofessional education of medical students and paramedics in emergency medicine. Acta Anaesthesiologica Scandinavica. 2007; 51:372–377. Health Professions CouncilStandards of Proficiency: Paramedics. London: Health Professions Council, 2007. Honebein, P., Duffy, T., et al. Constructivism and the design of learning environments: context and authentic activities for learning. In: Duffy T.M., ed. Designing Environments for Constructive Learning. New York: Springer-Verlag, 1993. Hotchin, L., Career structure: ambulance training in Victoria. Response 1986; 11–15 Joyce, C. M., Wainer, J., Piterman, L. Trends in the paramedic workforce: a profession in

transition. Australian Health Review. 2009; 33(4):533–540. Kramer, M.Reality Shock: Why Nurses Leave Nursing. Philadelphia: Mosby, 1974. Lord, B. The development of a degree qualification for paramedics at Charles Sturt University. Journal of Emergency Primary Healthcare. 1(1–2), 2003. McDonell, A., Burgess, S., Williams, B. From academia to clinical practice. In: O’Meara P., Grbich C., eds. Paramedics in Australia: Contemporary Challenges of Practice. Sydney: Pearson Education, 2009. McLean, S., Preston, J., Flapan, A. D. Belching: an unusual clinical presentation of coronary ischaemia. Scottish Medical Journal. 2008; 53(4):10. Norman, G. R., Eva, K. W., Brooks, L. R., Hamstra, S. Expertise in medicine and surgery. In: Ericsson K.A., Charness N., Feltovic P.J., Hoffman R.R., eds. The Cambridge Handbook of Expertise and Expert Performance. New York: Cambridge University Press, 2006. O’Meara, P. Searching for paramedic academics: vital for our future, but nowhere to be seen!. Journal of Emergency Primary Health Care. 4(4), 2006. O’Meara, P. The maturation of the paramedic profession through international scholarship. International Journal of Paramedic Practice. 2011; 1(2):2–3. O’Meara, P. Professional and community expectations of rural ambulance services in Australia. Prehospital Immediate Care. 2001; 5(1):27–30. Pammenter, A. The new training programme. Ambulance World. 1(4), 1978. Pearson, L.Submission: regulation of unregistered health practitioners. Adelaide: Council of Ambulance Authorities, 2011. Reynolds, L. Contextualising paramedic culture. In: O’Meara P., Grbich C., eds. Paramedics in Australia: Contemporary Challenges of Practice. Sydney: Pearson Education, 2009. Sheather, R. Professionalisation. In: O’Meara P., Grbich C., eds. Paramedics in Australia: Contemporary Challenges of Practice. Sydney: Pearson Education, 2009. Smith, J., Carley, S. Belching as a symptom of myocardial ischaemia. Emergency Medicine Journal. 2001; 18:467.

Speake, D., Terry, P. The first ECG has a low sensitivity for myocardial infarction in patients with chest pain. Retrieved February 2012 from http://bestbets.org/bets/bet.php?id=75, 2001. Steketee, C., & Adrian, B. (2007). Augmenting the clinical apprenticeship model. Paper presented at the International Educational Research Conference, Fremantle. Stirling, C. Paramedic practice in rural and regional Australia. In: O’Meara P., Grbich C., eds. Paramedics in Australia: Contemporary Challenges of Practice. Sydney: Pearson Education, 2009. Wilde, S.From Driver to Paramedic: A History of the Training of Ambulance Officers in Victoria. Melbourne: Ambulance Officers’ Training Centre, 1999. Willis, E., McCarthy, L. From first aid to paramedical: ambulance officers in the health division of labour. Community Health Studies. 1986; 10:57–67. Willis, E., Williams, B., Brightwell, R., et al. Road-ready paramedics and the supporting sciences curriculum. Focus on Health Professional Education. 2010; 11(2):1–13.

SECTION 5

LEGAL AND ETHICAL CONSIDERATIONS O U TL I N E CHAPTER 10: Legal and ethical considerations in clinical decision making

CHAP TER 10

Legal and ethical considerations in clinical decision making By Brian Stoffell, Ruth Townsend and Hugh Grantham

OVERVIEW • Clinical reasoning is primarily focused on the ‘clinical’: developing a safe and accurate differential diagnosis on the basis of the patient history and vital signs. But the legal and ethical implications of assessing and treating patients can impact on the clinical decision-making process. • The ethical and legal principles of healthcare are well-established and apply to paramedic practice. • The unique nature of paramedic practice can also create ethical and legal challenges that impact on clinical decision making and patient management. • Understanding the ethical principles for healthcare will help paramedics to integrate ethical and legal standards of care into their clinical decision making.

Introduction In Chapters 1–9 we described the process of clinical decision making that occurs when clinicians are confronted with patients, particularly the clinical reasoning challenges that paramedics face. We described the paramedic workplace as an environment characterised by an excess of stimuli and a lack of clinical information; and where the clinical problems are multiple and ill-defined, but definitive diagnostic tools are almost entirely absent. Understandably, much of this discussion focused on how novice paramedics accumulate, contextualise and use their knowledge of disease processes. But we also outlined how our knowledge is error-prone and that even our clinical experiences can be misleading. And we identified that failing to address the patient’s illness (how the disease affects the patient) can make them resistant to treatment. While we have detailed the steps from assessment to confirmation, it was only briefly considered that the patient might actually refuse to allow the paramedic to assess them or initiate treatment, or that there might be ethical and legal implications of assessing and treating the patient. So far we have described that a decision-making process that starts with the patient, is considerate of the patient’s wishes and incorporates both the clinical picture and the wider environment of factors is far more complex than a simple protocol-driven treatment plan. How legal and ethical values need to be integrated with clinical understanding is the focus of this chapter. We concentrate on two areas of health law and their impact in clinical decision making: the emergency treatment of a non-competent adult; and standard consent or refusal of treatment by a competent adult.

Ethics and the law Faced with the diagnostic uncertainty that exists in most paramedic cases, it not unusual for novice clinicians to seek the certainty that ‘laws’ or ‘rules’ might provide in their decision-making process. In this chapter we demonstrate that, for the most part, making good clinical decisions is inherently consistent with the ‘rules’ prescribed by medical ethics and medical law.

Ethics Ethics can be considered as a set of principles that describe appropriate or good behaviour; ethics applies to many fields as well as medicine (Herring 2012; Paul & Elder, 2006). For centuries doctors have used an ethical framework, such as the Hippocratic Oath (Oath of Hippocrates, 1910), to support their decision making, but in the last century frameworks such as this have been increasingly formalised and transformed into codes of conduct that are tied to particular professions (see Box 10.1). In turn, practising in accordance with a code of conduct has become a requirement for continuing employment for most health vocations as they assume the status of a profession. B O X 1 0 . 1P

a r a m e dic s Austr a la sia Co de o f

Co nduc t A code of conduct may be defined as the standard of ethical and professional behaviour determined by a professional group in the form of a publicly accessible document. A publicly available code is a form of declaration setting out the standard of behaviour that the public expects of that professional group. Paramedics are required to work in accordance with their employers’ professional code of conduct. With respect to cases such as those involving illicit drug use and alterations of conscious state, it is necessary to consider what the code says about patient autonomy, choice, clinical presentation and consent for care. For our purposes we focus on the code of conduct released by Paramedics Australasia, but you should also consider the code that relates to your own state or territory and country.

Paramedics Australasia Code of Conduct • Integrity. In carrying out their professional duties, Members must be honest, sincere and trustworthy, acting in a manner that does not bring discredit to their profession. • Respect. Members must ensure their actions and treatment demonstrate respect for the client as a person and that care is provided at the highest professional standard. • Responsibility/accountability. Members must remain personally responsible and accountable for the professional decisions they make. • Competence. Members shall maintain and improve the necessary skills and

knowledge in their areas of professional practice. They shall further accept the responsibility to work as mentors for students in their areas of professional practice. • Consent for patient care. Wherever possible Members shall be committed to ensuring that they receive informed consent from their clients prior to instigating and providing treatment at the highest standard of contemporary care. • Confidentiality. Members must maintain confidentiality of any information they obtain in the course of their work. They must not disclose any such information to a third party unless there is a legal or professional duty to do so. • Research. Members shall promote, support and where possible participate in research of pre-hospital care practices and ambulance service management and technical service support systems. • Ethical review. Members shall participate in the ethical review of their actions resulting from the provision of pre-hospital care and conduct in their professional role, whether that role is of a clinical, managerial, educational or technical support system nature. (Paramedics Australasia, 2012) The three most relevant elements of this code with respect to case study 1 are: • Respect for the client as a person. This provision is met by ensuring that the care provided is at the highest professional standard and that potential courses of action are motivated by concern for the patient. • Consent for care. This becomes an issue once the patient has returned to consciousness. From that point forwards, and on the presumption of capacity, all treatment requires consent and any refusal is definitive. • Ethical review. The ethical review of your actions in the provision of prehospital care encompasses critical reflection on the elements in the Code of Conduct, but in particular the ramifications of respect and consent, both of which are central in this case.

CA SE ST U DY 1 Case 10504, 2250 hrs. Dispatch details: An unconscious young male at a domestic address. The caller identifies that the patient may have been using heroin. Initial presentation: On arrival the crew find the male patient unconscious, with a central cyanosis, a respiratory rate of 4, decreased tidal volume but a clear airway. He has a pulse that is palpable at the wrist at a rate of 130. The patient’s two housemates state that the three of them injected heroin shortly

before the patient fell unconscious. The crew support the patient’s respiration by bag-mask ventilation and he becomes less cyanosed. As one crew member draws draw up the naloxone, one of the patient’s friends says: ‘I’m pretty sure he wouldn’t want to be treated with that stuff. Isn’t there anything else you can do?’ Despite these concerns, the crew administer 0.4 mg of naloxone IM and 6 minutes later the patient is alert and oriented to place and time. He refuses all offers of further care or transport.

Regardless of the behaviours described in a specific medical profession’s code of conduct, there are four moral principles upon which medical ethics are built (Beauchamp & Childress, 2009; see Fig 10.1):

FIGURE 10.1 Despite the varying complexity and urgency of cases that paramedics attend, the same four moral principles that guide other medical practitioners apply to emergency health events that happen in the community setting. However, the urgency required, the limited diagnostic tools and a lack of patient privacy can make it difficult to integrate these four factors into your clinical decision making and how they can be applied will vary with almost every case. Source: Top image: courtesy of the Government of South Australia/SA Health.

1. Autonomy: the right of the patient to decide on treatment. 2. Non-maleficence: above all, do not harm. 3. Beneficence: decisions must be made in the best interest of the patient. 4. Justice: patients should receive equal care and access regardless of status. While these may appear to be statements of basic, widely-accepted moral principles that apply across most societies (Herring, 2012), the complexity of medical decision making can quickly reveal the uncertainty and subjective nature of these principles. For example, a doctor, aware that reducing hypertension significantly lowers the risk of stroke, recommends that a patient who has tried all other measures to reduce his blood pressure commence on a well-established medication (beneficence). The patient refuses (autonomy). Given the cost of caring for stroke patients for the general community, should the doctor be able to ‘force’ the patient to comply with the prescription? (See Box 10.2.) Although they do not explicitly prescribe an order of importance to the four principles, Beauchamp and Childress’ placement of autonomy at the top of the list is commonly interpreted as meaning that the patient’s autonomy is of primary importance.

Autonomy Self-determination, self-direction and self-control all have strong psychological connotations for us and we often employ these terms when explaining the relationship between a person and their choices in life. Personal development from childhood to adulthood seems to suggest that we acquire these abilities by degrees and not instantaneously. However, the capacity for self-direction can be diminished or lost, either temporarily after being rendered unconscious for example, or permanently when a person enters a persistent vegetative state. In case study 1, the patient’s ability to self-determine was lost when the overdose affected his brain and he lost consciousness. The ‘self ’ in self-determination, self-control and self-direction reminds us that an action is framed by an awareness of the situation and is expressed in an intentional response to it. You can make a big impact on your environment by accidentally losing your balance while on a tall ladder and catapulting yourself into the middle of your next-door neighbour ’s outdoor lunch, but that is not a self-determined action. While taking the heroin was a conscious decision, the patient didn’t take it with the intent of doing himself harm with an overdose. The history of ideas is littered with odd entities that were once said to be the source of a person’s actions: the soul, the will, the free will, the faculty of reason and so on. In this chapter our focus is not on some deep and mysterious seat of action but rather on people’s actions that express their intentions and the implications this has on how we assess a patient and decide on a treatment plan.

Non-maleficence Primum non nocere (above all, do no harm) appears at first well-defined and to impose specific behaviours on clinicians, but in fact it could be questioned on a daily basis: for example, paramedics routinely inflict short-term pain (inserting an IV) to administer a drug (say, adenosine to revert a cardiac arrhythmia) that will avoid more significant harm (see Box 10.2). In reality, ‘harm’ can be defined widely—pain, disability, disfigurement, embarrassment, regret—but medico-legal history is dotted with cases where harm was defined purely from a clinical perspective by the clinician. In this sense there is a close

connection to autonomy, with some commentators suggesting that the patient’s view of harm must be considered and others suggesting that a societal definition is more appropriate (Herring, 2012). B O X 1 0 . 2C o

nsequentialism and deo nto lo g y

Although there is wide acceptance of Beauchamp and Childress’ (2009) four ethical principles, this acceptance is by no means universal, and how clinical decisions and actions should be interpreted and implemented remains a point of contention for many. As an example of just how open the notion of ‘ethical decisions’ actually is, consider the divide between consequentialism and deontology. Consequentialists assess the morality of a clinician’s decision or action on the basis of its consequences: it the outcome is ‘good’, the decision is ‘right’, regardless of how unethical it might appear. Conversely, deontological absolutism insists that the outcome must not be considered and that a decision is morally right or wrong regardless of the outcome. Questions of how to decide on a ‘good’ outcome and for whom (the individual or society) remain unanswered and while these approaches may appear extreme, these notions have been used to defend or attack medical practices in recent history, from the ‘medical experiments’ conducted by Nazi doctors during World War II, to the unknowing inoculations of Indigenous populations and, most recently, proposals for mass screenings and genetic testing.

Beneficence Clinically, beneficence is closely related to non-maleficence (doing good surely reduces harm), but the inference here is that clinicians will put the patient’s good before their own. Interestingly, this principle can be used to contrast the roles of ethics and law in medicine. It is wrong both ethically and legally to harm an individual, but there is no law that compels citizens to help each other. Ethically, however, clinicians are bound to help, even if it involves a degree of discomfort or inconvenience to the clinician.

REF LECT ION If a reduced dose of naloxone would wake the patient but retain the euphoric effects of the narcotic, should it be considered? Or should you provide a dose of naloxone that completely reverses the condition?

This principle can also be used to guide a particular course of treatment. Long before the concept of evidence-based practice, the Hippocratic Oath obliged doctors to ‘follow that system which, according to my ability and judgment, I consider for the benefit of the

patient’ (Oath of Hippocrates, 1910).

Justice The simplest of the four ethical principles (‘treat all equally’) is actually impossible for any health system to provide. Responding to every case with the maximum possible resources and investigations would paralyse most health services within hours and quickly restrict access for later patients. Some degree of triage and resource allocation has to occur for health systems to function effectively. Of particular relevance to case study 1 is the clinician’s perception of the patient’s worth. Attribution bias (blaming the patient for their condition; see Ch 5) has been identified as a source of error in clinical decision making among emergency doctors (Croskerry et al., 2009) and, given the exposure paramedics have to accidental overdoses on illicit substances, they will regularly be faced with patients they may consider less deserving of an equal allocation of resources than those whose illness is not self-inflicted. Failing to conduct a thorough assessment and exclude other causes of unconsciousness in this patient (because he is a drug user) could cause harm to the patient. While you may not agree with the patient’s lifestyle choices, he has just as much right to your care and consideration as anybody else.

The law The law is a system of rules that regulate our society and many facets of our life. Laws are established by an authority (parliaments and courts) and are enforceable. Unlike the areas of family law or criminal law, there is no specific set of laws describing health. ‘Health law’ is in fact a combination of common law principles, various legislative provisions and professional guidelines, all of which combine to regulate the manner in which health services are delivered and the obligations of health providers in this regard. While professional codes of conduct may attach sanctions to behaving unethically, the distinction between ethics and the law can be simplified as ‘what you should do’ and ‘what you must do’. The context in which this is judged, however, is changing over time and as the traditional view of the doctor–patient relationship (Parsons, 1951) is challenged. The eroding of the paternalistic nature of medicine (‘the patient will do what the doctor says’) has created a view where patients now have the ‘right’ to adequate medical care. The legal notion of the patient’s rights in healthcare is greatest where it details the ethical notion of autonomy and the patient’s right to refuse treatment. Legally, this is referred to as ‘consent’. (The right to dignity and the right to life are other areas where the law might prescribe the actions and decisions of healthcare professionals.)

Consent Consent (or more accurately, the ability to withhold it) is where the ethical concept of autonomy is enshrined in law. In reality, the ‘right of autonomy’ is better described as the ‘right to choose treatment’. This right includes both the right to select a treatment and the right to refuse a treatment. Where the patient is conscious and aware, this needs to be considered by the healthcare professional. As noted above, however, the patient’s loss of autonomy due to an inability to respond as a self-determining agent does not impose any restrictions on the paramedic initiating treatment (see Fig 10.2).

FIGURE 10.2 The ‘right of autonomy’ is better described as the ‘right to refuse treatment’. Where the patient is conscious and aware this needs to be considered by the paramedic, but it does not prevent the paramedic from treating an unconscious patient. Source: Courtesy of the Government of South Australia/SA Health. The conflict between the ‘need to treat’ and the ‘right of autonomy’ can occur when paramedics are faced with an Advance Directive for Care (see Fig 10.3). This is a written

statement regarding a person’s wishes for their healthcare if, at some point in the future, they become incapable of making healthcare decisions for themselves. Advance Directives for Care embody the right of autonomy and can restrict clinicians from initiating certain treatments. There are, however, significant variations in Advance Directives (or orders) between states and territories in Australia and New Zealand as well as local variations in terms of ambulance service guidelines and policies in this area (Betts, 2013). This inconsistency makes it impossible to summarise all the implications in this text. The reader is recommended to consider the local law, policies and procedures relating to patients with anticipatory directions or end-of-life wishes.

FIGURE 10.3 Emergency care of the patient isn’t always straightforward, as some patients who are elderly, disabled or terminally ill may have Advance Directives, where appointed third parties may be empowered to provide consent or reject treatment. Source: Courtesy of the Government of South Australia/SA Health.

Providing emergency care without consent: the legal justification In case study 1 the patient was unconscious when the crew arrived so his active autonomy was not in operation. Respecting the person’s dignity and life therefore took the

form of doing everything possible to protect and preserve his capacities for selfdetermination. It follows then that the ethical and legal imperatives were to provide active treatment and avoid doing harm. The facts in the case make it abundantly clear that emergency treatment must be provided to safeguard the patient by avoiding any further threat to his physical or mental wellbeing. The doctrine of emergency is a common law creation that provides healthcare personnel with a justification to intervene without the patient’s prior consent. In Marion’s case, Justice McHugh said: Consent is not necessary … where a surgical procedure or medical treatment must be performed in an emergency and the patient does not have the capacity to consent and no legally authorised representative is available to give consent on his or her behalf. NT v JWB (Marion’s Care) (1992) 175 CLR 218, 310. The justification for emergency treatment rests on a clinical assessment that the patient is incapable of consent and faces an imminent risk to their life and health. Since in the initial presentation in case study 1 the patient was unconscious and in need of urgent and necessary treatment, the doctrine of emergency/necessity applies, providing the paramedic with legal authority to administer the life-saving naloxone. This course of action is also ethically sound as it will benefit the patient (beneficence) and prevent further harm (non-maleficence). Once the patient has regained consciousness his capacity to make decisions regarding further treatment would need to be reassessed. So you and your partner acted ethically as well as legally in treating the patient with naloxone because you have good evidence that without it he was at risk. Consider a situation in which a patient was initially conscious and able to consent to treatment but then subsequently deteriorated. In this situation the paramedic might consider that the patient’s changing condition necessitates the administration of additional treatments that were not previously anticipated and thus not discussed with the patient. The scope of the original consent does not extend to include these additional treatments unless it can be demonstrated that they were provided out of necessity as an emergency intervention in order to protect the life and health of the person, and it was not possible or practical to discuss the additional procedures with the patient, and obtain their consent, before the procedures were performed (Hunter and New England Area Health Services v A (2009) 74 NSWLR 88[31–33] C.F.R.).

P RACT ICE T IP If a conscious patient you are treating for, say, chest pain has a cardiac arrest and you are treating them for something that they understood and consented to, you don’t have to stop and obtain their consent before defibrillating.

Although the patient in case study 1 might have lost his capacity to demonstrate his autonomy or self-determination when he was unconscious, avoiding harm would seem to apply to reversing his overdose and stopping him from aspirating or dying from respiratory

arrest. When you decided to reverse his overdose you did it in his interests, not yours, as you honestly thought that it would be bad to leave him like that. This course of action was also consistent with the recommended treatment guidelines in the jurisdiction in which you and your partner were operating. Of the four principles, the two that seemed to be important at that moment were beneficence and avoiding harm.

Refusal of treatment The clinical reasoning process employed in the management of the patient in case study 1 is relatively straightforward: the patient self-administered an accidental overdose of an opioid narcotic. Non-invasive management of the patient’s airway and ventilation removed an immediate life-threat and evidence-based practice supported the use of intramuscular naloxone. Once the patient has regained consciousness, however, the justification of imposing your judgement of what should occur becomes more complex. Upholding the principle of self-determination requires us not only to seek and uphold the patient’s right to give consent for treatment, but equally importantly to recognise the patient’s right to refuse consent for further treatment. Chief Justice Martin of the Western Australian Supreme Court described it thus: The corollary of [self-determination] is that an individual of full capacity is not obliged to give consent to medical treatment, nor is a medical practitioner or other service provider under any obligation to provide such treatment without consent, even if the failure to treat will result in the loss of the patient’s life … the principle is applied without regard to the reasons for the patient’s choice, and irrespective of whether the reasons are rational, irrational, unknown or even non-existent … Brightwater Care Group (Inc) v Rossiter (2009) WASC 229 (20 August 2009) at 24–27. The key point here is the notion of competence or capacity (these terms are used interchangeably) and paramedics therefore need an understanding of how competence is assessed. Transport is a form of treatment and a patient who is deemed to be competent needs to consent to transport as they would any form of treatment. So, in case study 1, once the patient has woken up and asked you not to treat him any further, you are ethically and legally bound to follow that instruction, provided you think he is competent to make the decision. This applies even if it is not the decision that you think the person should make. You must therefore assess the validity of the patient’s decision.

Elements of consent Consent is one of the most difficult concepts to apply in the paramedic setting (see Fig 10.4). There are four elements of consent and each must be satisfied for consent to be deemed valid or lawful.

FIGURE 10.4 Patients who are confused after suffering a minor head injury may refuse treatment, but do they have the capacity to make that decision? Similarly, patients who have overdosed on drugs and require ongoing treatment may refuse transport for fear of legal consequences. Where does this leave the paramedic legally? Source: Image supplied by St John Ambulance WA. The elements are: 1. The consent is voluntary. 2. The patient has been provided with sufficient information. 3. The consent covers the treatment that is to be provided.

4. The patient has the capacity to make the decision about the treatment.

Voluntary decision We have discussed the right of individuals to make decisions for themselves regarding their own healthcare and this extends to include the notion that the patient must not be coerced into making decisions. Coercion takes away the necessary requirement of voluntariness implicit in self-determination. In situations where a third party may be influencing the patient’s decision, the paramedic should give consideration to, and take note of, the nature of the relationship that this person has with the patient, and the patient’s vulnerability to undue influence by the third party (e.g. husband or wife). It is particularly important that paramedics do not engage in coercive behaviour by persuading a patient to do what is convenient or expeditious for the paramedic but not in the best interests of the patient (Re T (Adult: Refusal of Medical Treatment) (1992) 4 All ER 649).

P RACT ICE T IP ‘If you don’t come to hospital with us, I’ll call the police and tell them you have illicit drugs here’ is an example of coercion and hence is unacceptable.

Sufficient information It is both an ethical and a legal requirement that paramedics provide their patients with information regarding their condition, the options for treatment, the broad nature and effects of that treatment and the risks associated with the treatment. This includes risks identified specifically by the patient that may be highly unlikely to occur but that the patient has a particular concern about (Rogers v Whittaker (1992) 175 CLR 479, 490). The Court has said that medical service providers should, where it is perfectly feasible to do so, ensure that the competent patient is ‘given full information as to the consequences of any decision to discontinue treatment before [the patient] makes that decision’ and indeed reiterated that they have a legal duty to do so (Brightwater Care Group (inc) v Rossiter (2009) 40 WAR 84 at 30–32). It is also important to note that while it is expected that health professionals will make every effort to provide comprehensive information where it is feasible to do so, the patient can still make a valid decision refusing treatment in the absence of this information.

P RACT ICE T IP ‘If you don’t come with us you’re certainly going to die’ probably isn’t a fair and balanced view of the information. You need to explain all the possible risks and how likely they are.

Consent given specific to treatment offered After the patient has been advised of the nature and effect of the proposed treatment (including the risks and benefits) and the patient has given consent, that consent only applies to the treatment described. The emergent nature of paramedic work is such that further treatment that has not been specifically consented to may be required to be administered to the patient if, for example, their condition deteriorates and they are no longer able to consent to the new treatment. In this case, provided the treatment is administered out of necessity in order to protect the patient’s life and health and it is not practicable to obtain consent from a surrogate decision maker, the paramedic may administer the treatment. This treatment can be given only if it is in the patient’s best interests.

P RACT ICE T IP If a patient voluntarily consents to transport, having understood all the risks of not going to hospital versus going, you have consent only for those things you explained—that is, the transport. You can put a dressing on the graze on his leg but you haven’t got the authority to do much more than that unless you get consent from the patient. If, however, the patient collapses in cardiac arrest, you can treat this event because he is unable to provide consent and it is a lifethreatening emergency.

Competence/capacity The validity of the patient’s consent to or refusal of treatment is dependent on the patient’s capacity: that is, their ability to understand the nature and effect of their decision. The issue in case study 1 is whether the patient actually has the capacity to make the decision to refuse transport. This involves a legal test. There is a presumption at law in Australia that every person over the age of 18 is competent (Re C (Adult: Refusal of Medical Treatment) (1994) 1 All ER 819, 822). The presumption is also embodied in the New Zealand Code of Health and Disability Services Consumers’ Rights, Right 7(2). The onus to disprove the presumption is on the healthcare practitioner (Re MB (Medical Treatment) (1997) 2 FCR 426). There are several factors that can erode a person’s decision-making capacity, either on a temporary or on a permanent basis. For example, a person with an intellectual disability may not be able to understand the nature and effect of proposed treatment or the risks and benefits of consenting or refusing consent for it. Conditions that could leave a patient with a temporary loss of capacity include conditions that result in hypoxia; drug or alcohol intoxication can also impact on a person’s decision-making capacity (Re B (Adult: Refusal of Medical Treatment) (2002) 2 All ER 449; Re T (Adult: Refusal of Medical Treatment) (1992) 4 All ER 649). However, the responsibility to demonstrate that this impairs the patient’s decision-making capacity remains with the paramedic. The evidence of the condition itself is not enough to prove the patient’s lack of competence: the paramedic must make an assessment of the patient’s capacity.

In case study 1, even though you don’t think the patient is demonstrating competence after his near respiratory arrest, you cannot just presume that he is incompetent: you have to check.

Assessment of competence The legal test of competence (Re C (Adult: Refusal of Medical Treatment)) requires the health practitioner to assess whether the patient is able to: 1. take in, retain and comprehend the treatment information 2. believe that information and then 3. weigh up the risks and benefits of the treatment before communicating their decision to consent or refuse consent for the treatment proposed. Retention and understanding of the treatment information: this could be assessed by asking the patient to repeat, in their own words, the treatment information that has been given to them by the paramedic. Believe the information: it is difficult to imagine that a patient might disbelieve a paramedic’s explanation of proposed treatment, but there are several mental health conditions where the patient disbelieving that they are unwell is an element of the condition. For example, many patients who suffer from anorexia simply don’t believe that they are unwell and so would disbelieve any health practitioner who suggested that a course of treatment would involve feeding of some sort. Weighing up the risks and benefits: again, it is possible to ask the patient to explain, in their own words, what they believe are the risks and benefits of the proposed treatment. The test is merely to check that the patient has noted the risks and benefits. There is no requirement for the patient’s ultimate choice to match the choice that the paramedic would make were they to be faced with the same scenario. The paramedic may believe that the patient’s choice is illogical or irrational, but this is not relevant in determining whether or not the patient has demonstrated that they are capable of weighing up the risks and benefits. For example, you may have told a patient that without a particular treatment they are certain to die. The patient may say, ‘OK, I understand that without this treatment I will die, but I choose not to have the treatment anyway.’ This demonstrates the patient’s capacity to refuse the life-saving treatment knowing that to do so will result in their death.

The importance of the decision A patient’s competence also needs to be considered on a sliding scale that is commensurate with the seriousness of the potential consequences of the decision being made. In other words, a patient’s capacity to make decisions may alter with the seriousness of the decision to be made. For example, if you were to offer a patient pain relief and they refused, it is unlikely that this will result in any long-term serious harm to the patient. Therefore, even though the patient may not believe that the medicine will help them and this causes the paramedic to doubt the patient’s competence, the harm to the patient in refusing the pain relief is such that the patient’s autonomy should be upheld. However, when a patient refuses life-sustaining treatment and the same doubt as to the patient’s competence arises, the potential consequences of the refusal are so much greater that the paramedic must

carefully consider their decisions and actions. In the case Hunter and New England Area Health Services v A, Justice McDougall said: it is necessary to bear in mind that there is no sharp dichotomy between capacity on the one hand and want of capacity on the other. There is a scale, running from capacity at one end through reduced capacity to lack of capacity at the other. In assessing whether a person has capacity to make a decision, the sufficiency of the capacity must take into account the importance of the decision (as Lord Donaldson pointed out in Re T). The capacity required to make a contract to buy a cup of coffee may be present where the capacity to decide to give away one’s fortune is not. (2009) 74 NSWLR 88, [24] In case study 1, the patient needs to be competent to make an informed decision about a very significant issue because there is a substantial risk that harm may come to him when the naloxone wears off if he does not go to hospital for observation.

Clinical cases are not legal cases In case study 1, the legal position is that there is an underlying presumption that the patient is competent to refuse consent for transport. However, the patient’s clinical history of a narcotic overdose and resultant period of unconsciousness could undermine this presumption if—in hindsight—he suffers harms from the refusal. The paramedic therefore needs to determine whether the patient is capable of making a decision to consent or reject the treatment that the paramedic has recommended and this requires not only an assessment of the patient’s orientation to time and place but also his level of understanding of the nature and effect of his decision again (Re T (Adult: Refusal of Medical Treatment) (1992) 4 All ER 649, 641). While assessment of competence is a legal test, it is the paramedic who is required to make the assessment and take into consideration the gravity of risk involved. In considering this situation the paramedic has to weigh the relative legal and physical risks of transporting the patient against his will versus the clinical risk of nontransport.

P RACT ICE T IP A repeated and consistent instruction to the paramedics to go away does not necessarily constitute evidence of competence. The patient needs to demonstrate competence associated with the refusal of care. An extreme example is a patient with a significant head injury. It is worth noting that a patient who has lost two points on the Glasgow Coma Scale may still be capable of saying ‘yes’, ‘no’ and expletives.

The lack of clarity provided by the law in this situation is a common problem for paramedics and there is no simple answer that covers all circumstances. Being aware that

a ‘scale of capacity’ exists and that a lack of capacity may only be demonstrated after the patient has suffered places paramedics in a difficult position. Trying to apply other forms of legislation to the circumstance may not clarify the situation either. The mental health Acts in some jurisdictions provide a mechanism by which paramedics can transport a patient who has refused treatment and transport—however, the patient must be suffering from a mental illness as defined in the Act and meet strict criteria before the relevant mechanism can be invoked. In reality, if the paramedic feels that the clinical risks of not transporting the patient are too significant, it falls to the paramedic to convince the patient to agree to transport. The legalities and logistics of involuntary transport are simply too complicated and lengthy to be effective in the field in most acute cases, and the ability to communicate with the patient and engage them in your treatment plan will be more effective than relying on the legalities of the situation. A third party who is willing and competent to supervise the patient is commonly seen as a means of mitigating some of the risks of non-transport, but this should be done only after the paramedic has decided that the patient has the requisite decision-making capacity to refuse transport. Only when it has been decided that the patient is not being transported because of a valid refusal and the patient’s consent to inform a third party of the paramedic’s suspected diagnosis is obtained is it allowable to involve a third party. Once these criteria have been met, the third party must be effectively informed as to the clinical risks, signs and symptoms to watch for and the proposed action plan in the case of the patient’s deterioration. In case study 1, although there are others present who could constitute a third party, they have by their own admission been using heroin, which may influence their ability to perform a useful function. The clinical question is whether you are sure on reasonable grounds that the patient is competent to refuse transport or whether he is not in a fit state to demonstrate competence. Therefore, he is either competent or: • incompetent secondary to the effects of hypoxia precipitated by his near respiratory arrest • incompetent secondary to the effects of hypercarbia precipitated by his near respiratory arrest • incompetent secondary to the effects of the original drug overdose • incompetent secondary to another factor (e.g. hypoglycaemia, electrolyte disturbance, infection) If the patient is deemed to be incompetent, then the duration of effect of the causative agent comes into question. In other words, could he reasonably be expected to regain his capacity to demonstrate competence in the near future? Hypoxia and hypercarbia rapidly correct with the restoration of normal ventilation, and their metabolic consequences rapidly correct too. The original overdose may still impair the patient’s ability to make a competent decision: although the naloxone has improved his conscious state it does not necessarily mean that it has improved to a point where he is capable of demonstrating competency. Hypoglycaemia, infection, electrolyte imbalance or other unrelated conditions could also be coexisting. Obtaining a blood glucose level will exclude hypoglycaemia, but the ability to assess electrolyte levels is not readily available in the field.

Legal consequences for the paramedic The legal consequence associated with such decisions impact on both the individual paramedic and the employing ambulance service. The paramedic has a duty to conduct a thorough clinical assessment that is reasonable in the circumstances and must inform the patient of the assessment findings and recommendations for treatment and transport. If the patient refuses the recommendation, the paramedic informs them of the associated risks and determines that the patient’s decision is valid, and the patient then suffers harm, it is unlikely that the paramedic would be liable for the harm provided there is sufficient documented evidence that the paramedic acted reasonably, in terms of both the assessments undertaken and the decisions reached on the basis of those assessments, and it is not their failure to act that has damaged the patient (Neal v Ambulance Service of New South Wales (2008) NSWCA 346, 24). However, if the paramedic assesses a patient as requiring further treatment but does not offer to transport the patient for further treatment and the patient experiences an adverse outcome as a result, it is possible that the paramedic may be found to have been negligent. In case study 1, you have made a thorough assessment, including an assessment of the patient’s competence. You have documented this assessment and clearly communicated the risk to the patient. You, your partner and the bystanders have witnessed the thorough professional briefing.

Case study 1 evaluation Having considered the ethics and legal requirements in the case, the crew need to make a decision about how to support a course of action when confronted with a patient who rejects any further treatment. Consider the two actions listed in Table 10.1. They are based solely on an ethical stance taken in tandem with a code provision. TABLE 10.1 Possible paramedic actions when a patient refuses transport to hospital

The case facts advise only that following treatment with naloxone the patient is alert and aggressively refusing all offers of further care and transport. In dealing with this patient’s refusal to be transported, subsequent actions will hinge entirely on the paramedic’s evaluation of the patient’s competence. Either: • It has been determined that the patient is competent and therefore able to make decisions regarding further treatment and transport. Or • It has been determined that the patient is not capable of understanding the nature and consequences of his decision about further treatment and transport. Currently, the paramedics don’t have enough information to make a decision regarding further treatment or transport, but they will be able to assess his level of understanding and evaluate his competence with more questioning and interaction. There are many clinical benefits to be gained for this patient in going to hospital. For example, access to withdrawal support can be provided in addition to a full clinical review. Despite this, the paramedics cannot transport the patient against his will unless it has been determined that he is not able to make a competent decision.

Documentation One final legal requirement is to document the assessment and communication with the patient. It is essential that the case sheet is comprehensively completed with details about the patient’s assessment, including their competence, and your communication with the patient regarding any recommendations for further treatment. In the past a patient’s refusal of treatment or transport was something that paramedics may not have considered a significant issue. The presence of adequate documentation demonstrating a detailed and thorough assessment of both the clinical problem and the patient’s competence has proved extremely useful when assessing these cases.

CA SE ST U DY 2 Case 1563, 2327 hrs. Dispatch details: A 27-year-old female is said to have fallen down stairs and possibly fractured her ankle. Initial presentation: The paramedics arrive at a large two-storey house and are shown to the patient. She is a young woman who appears to have some bruising and abrasions to her face, forearms and her knees. She is sitting in a chair and her right ankle is obviously swollen. She tells them that she tripped and fell down stairs. She says that she was unable to walk on her ankle immediately afterwards and it is now swollen and displays a limited range of movement. There is point tenderness over the lateral malleolus and she is very reluctant to bear weight on the joint. Perfusion to the toes is good and her vital signs, including pulse, BP, oxygen saturation and respiratory rate, are all normal. The crew note a strong smell of liquor on her husband’s breath. He appears to have some abrasions to the knuckles of his right hand.

ASSESS The patient gives the history of her fall resulting in what sounds like a sprained ankle, but at this stage a fracture cannot be ruled out. The rest of her injuries are not consistent with her story, however, and the crew’s suspicions are further raised by the fact that her husband is very reluctant to leave the room

and she seems to be looking to him for confirmation before answering any questions about the injury. It seems possible that they are looking at the results of domestic violence.

CONFIRM Although the paramedics suspect that the patient’s story is not the truth and that she is a victim of domestic violence, they have no absolute evidence one way or the other. She is consistent in her story that she tripped on the stairs and does not need further assessment. She states that she still has crutches from a previous injury and will use them to go to the doctor if necessary.

DIF F ERENT IA L DIA GNOSIS Domestic violence with undisclosed injuries including contusions, abrasions and a sprained ankle Or • Injuries as above sustained by having tripped down the stairs

T REAT Ideally, the paramedics would like to transport the patient to hospital where her ankle can be fully assessed. This might also allow her other injuries to be explored and a safe environment arranged where she would have the opportunity to give a different history detailing the suspected domestic violence. Unfortunately, she is adamant that she does not wish to go to hospital and that she will be all right and will see her own doctor in the morning if her ankle remains sore.

Legal assessment of refusal: consent Each of the four elements of consent must be satisfied for the consent to be deemed valid or lawful. Competency The first test is to determine whether the patient is competent to refuse treatment. This requires the paramedics to determine if the patient: 1. can take in, retain and comprehend the treatment information 2. believes that information 3. has weighed up the risks and benefits of the treatment before communicating

their decision to refuse consent for the treatment proposed. Retention and understanding of the treatment information: the physical examination reveals no evidence of mental disability or drug use that could underpin the assessment of incompetence. The patient is oriented to time and place and states she can recall all the events of the day Believe the information: the patient does not refute the information and states she will go to her local medical clinic if needed. Weighing up the risks and benefits: the paramedics have explained the complications associated with an unstable fracture and the patient repeats that she will seek medical advice if the ankle does not improve. As a result, the patient has to be deemed competent and the paramedics have no legal authority not to acknowledge and adhere to her refusal with regard to consent. Sufficient information The paramedics have explained the need for an x-ray to rule out a fracture and have explained the complications associated with an unstable fracture, and the patient repeats that she will seek medical advice if the ankle does not improve. Consent is specific to treatment The patient has refused transport but has not refused any other form of treatment that may be available to the paramedics. Although the paramedics may disagree with the patient’s decision regarding transport, that does not preclude them from providing any other treatments available to them within their guidelines. Similarly, although the patient consents to treatment at the scene, this consent does not extend to transport. Coercion The paramedics clearly suspect that the patient is not free from coercion to make an informed decision to remain at home with her husband, so in declining transport it could be argued that it might not be a valid refusal. However, there is insufficient evidence that the patient has been coerced and therefore her decision to refuse is valid. Without further information, coercion remains just a suspicion. Ethically, the paramedics are faced with significant concerns for the patient’s wellbeing but they do not have her assistance to help her or even confirm their concerns. If they could arrange an opportunity for her to talk privately and safely they might gain a clear direction to help her. Otherwise, the patient remains an autonomous individual with self-determination.

EVALUAT E The paramedics need to evaluate not only their clinical treatment and the patient’s response to the treatment, but also their own ethical position and its potential influence on their decision making. Every situation is different and every individual’s evaluation will be different, so the first check should be to ascertain whether both clinicians assessed the situation as suspicious. If they

are of the same opinion, then the subsequent decision-making process will be complex, involving assessment of risk, urgency and a review of the legal and ethical situation. Consultation with an experienced senior mentor may be of great value but should occur while maintaining patient confidentiality. Unfortunately, as in most ethical dilemmas there is no single right answer. The best answer is the one that we can be satisfied with, even after critical reflection. The answer we arrive at today may well be different from the answer to a similar case tomorrow. It is unfortunately outside the scope of this book, or any book, to provide absolute answers to difficult questions like this. It is, however, appropriate to remind you that the first step to self-care is awareness and the ability to share (albeit within the bounds of patient privacy) difficult problems with your mentors and advisers.

Summary The ethical and legal principles of healthcare rarely impact on the process of clinical decision making: making good decisions inherently aligns clinical practice with ethical and legal behaviour. There are cases, however, where the decision-making process can be supported by referring to the ethical and legal principles that support paramedic practice. The widely-held assumptions that patients understand their condition and agree to the most appropriate clinical care are quickly tested in the pre-hospital environment where social factors, drug use, mental health and personal freedoms commonly interact with emergency healthcare. A clear understanding of the principles of autonomy, nonmaleficence, beneficence and justice will not only allow paramedics to understand why and how good clinical practice is supported by the law, but also act as a guide where the clinical situation is unclear or when the rights of the patient to refuse care are raised. Liberal societies espouse individual freedom or liberty as a preeminent value. In these societies self-determining individuals are presumed to exercise their capacities consistent with the equal exercise of capacities by others. Democracy advances this cause by giving equal weight to individual participation in the business of determining who will govern. The main idea here is the equal status of individuals. No-one has any prior claim to worth or value above anyone else.

References Beauchamp, T. L., Childress, J. F. Principles of Biomedical Ethics, 6th ed. Oxford: Oxford University Press, 2009. Betts, B. Consent and refusal of treatment. In: Townsend R., Luck M., eds. Applied Paramedic Law and Ethics: Australia and New Zealand. Sydney: Elsevier; 2013:92–129. Croskerry, P., Cosby, K. S., Schenkel, S. M., Wears, R. L.Patient Safety in Emergency Medicine. Philadelphia: Lippincott Williams & Wilkins, 2009. Herring, J. Medical Law and Ethics, 4th ed. Oxford: Oxford University Press, 2012. Oath of Hippocrates. Harvard Classics; Vol. 38. P. F. Collier & Son, Boston, 1910. Paramedics Australasia. Code of conduct. Retrieved January 2013, from www.paramedics.org.au/about-us/who-we-are/code-of-conduct, 2012. Parsons, T.The Social System. Glencoe, IL: The Free Press, 1951. Paul, R., Elder, L.The Miniature Guide to Understanding the Foundations of Ethical Reasoning. Dillon Beach, CA: Foundation for Critical Thinking Free Press, 2006.

SECTION 6

CLINICAL REASONING AND THE PARAMEDIC MODEL OF PRACTICE O U TL I N E CHAPTER 11: Developing a philosophy of practice

CHAP T ER 11

Developing a philosophy of practice By Stephen Burgess

OVERVIEW • Formal education and clinical placements create a model of practice that describes how each paramedic approaches their tasks. • This model of practice is also defined by the wider community’s expectations of the paramedic role in healthcare. • Clinicians are often unaware that they operate within a model of practice and how it shapes their practice. • The integration of your knowledge, clinical skills and attitudes is your model of practice. • Gaining an awareness of your model of practice and comparing it with your values and beliefs describe your philosophy of practice. • A philosophy of practice transitions your practice model from an unconscious and retrospective summary of how you work into a framework that will guide you to be the type of paramedic you want to be. • A philosophy of practice is always developing; it is never fully developed.

Introduction The words ‘paramedic’ and ‘practice’ frequently occupy the same line, but ‘paramedic’ and ‘philosophy’ are two words that are not usually found in the same conversation, let alone the same sentence. Indeed, they seem ill-suited: paramedics are typically pragmatic, result-oriented clinicians, whereas the term ‘philosophy’ conjures up images of academics in tweed jackets engaging in pointless discussions about impossibly difficult arcane theories. Yet in reality, every paramedic has a philosophy to their practice—why they do the job—and this irrevocably defines how they do the job. This connection exists even if the paramedic has never spared a moment to consider what their philosophy might be. Gaining an awareness of your model of practice and comparing it with your values and beliefs is what defines your philosophy of practice. This process can change your practice from an unconscious and unwitting process to a framework that will guide you to become the type of paramedic you imagined you would be when you started your career. This chapter provides a guide on how to develop an insight into your philosophy of practice, because even if you are a student yet to assess a single patient you already have a philosophy of practice. Gaining an insight into this philosophy will help you identify both its strengths and its weaknesses and how to develop it.

Models of practice In Chapter 1 we introduced a model of paramedic practice (see Fig 1.1) that placed the paramedic at the centre of a host of distracting and competing forces while trying to solve a clinical problem. While models of practice present a framework to describe how a profession operates (Trede & Higgs, 2008) they also depend largely on perspective, and the model described here is weighted towards how paramedics view their work. Taken from a patient’s or a manager ’s perspective, this model would almost certainly be drawn slightly differently.

CA SE ST U DY 1 Case 17399, 1335 hrs. Dispatch details: An 82-year-old female complaining of chest pain. Initial presentation: The patient, Jing, is recently widowed and lives alone. When the crew arrive she tells them that the door is open and they find her fully dressed, sitting upright in a lounge chair. She says she had some chest pain but her clinical examination is unremarkable and while she is cooperative, her history and description of her symptoms are vague and her answers often bear little relation to the questions put to her by the attending paramedic, Sarah. Feeling the pressure from her instructor, Sarah performs an exemplary clinical assessment, but everything she finds leads her down a clinical deadend. She feels frustrated and aware of the need to make a decision, but she says to Jing that as far as she is concerned there is nothing they can do for her because there appears to be nothing wrong. Jing bursts into tears. Background: Sarah decided that she wanted to become a paramedic at secondary school, and after years of hard work studying at university she recently completed her degree and gained employment with an ambulance service. She has spent the last few months working under the guidance of her clinical supervisor, David. Apart from ‘the job’, they have little in common. David is a middle-aged man and a 20-year veteran. He is a self-described dinosaur: when he started out they didn’t even carry sphygmomanometers. He was employed by his ambulance service in his mid-20s after almost a decade as a ‘jack of all trades’. Once employed, he completed an in-service diploma parttime, but most of his first few years were spent on the road, ‘learning what you really need to know to do this job’. Greying and carrying some extra weight, he has children not much younger than Sarah. While not unpleasant to his partner, Sarah feels he is slightly irritated by almost everything she says and does.

P RACT ICE T IP Cases of accidental heroin overdose can provide an interesting perspective on your model of practice. Early in your career you may approach these cases enthusiastically as an opportunity to practise your clinical skills and administer medications. As your clinical skills become established and no longer challenging, however, your attitude to illicit drug use and ambulance workload can become your most overt reaction to the case.

How important each of the factors described in the model are to the paramedic also changes with experience: novice paramedics are inherently less aware of the leadership role but are acutely aware of being assessed not only by the patient, but also by their instructor. In case study 1 the combination of Sarah’s heavy reliance on clinical knowledge early in her career and her perception of paramedics as diagnosing diseases has resulted in her declaring to the patient that there is ‘nothing wrong’—and from her perspective, she is correct. David, on the other hand, has learned through experience that isolated elderly people can easily become afraid when they feel relatively minor symptoms and the relief can produce an emotional response that seems excessive to a young medical professional searching for an acute disease. He is also aware that depression can exacerbate a person’s fear and, with no other resources available to them, they may call on the ambulance service to initiate some form of support. David’s model of practice recognises that his responsibility extends beyond the process of cardiovascular disease and his response to Jing would have taken the form: ‘Jing, your heart appears to be fine, but you still seem very worried. Is there anything else bothering you at the moment?’

Novice to expert As novice paramedics it is likely that most students will firstly adopt the model of practice as it appears to them when they encounter paramedics on clinical placements. This process of gaining a view of how to act and behave from the actions and views of those you work with is called professional socialisation and it is one of the more important aspects of clinical placements (Ajjawi & Higgs, 2008; Clouder, 2003). In fact, by the time students start their careers as paramedics they will not just have gained knowledge of how to be a paramedic but will also have assumed the professional identity of what they perceive to be a paramedic (Christensen et al., 2008). This cycle of experience leading to a revision of role identify will occur regularly as student paramedics progress through the stages of becoming an expert practitioner (see Fig 11.1).

FIGURE 11.1 As paramedics enter each new stage of progression from student to expert paramedic, the new role will test their existing role identity. Changes in the degree of authority, autonomy and scope of practice should lead them to adjust their model of practice according to their level of expertise. For most paramedics the model of practice is largely invisible: they could probably describe aspects of it if pressed but they are not aware of it as a framework by which they operate. Having an awareness of the model of practice that has evolved around you during your education is the first step in developing a philosophy of practice. Thinking about how you can shape that model to match how you perceive you should practise is the next step. Little has previously been written describing a philosophy of practice for paramedics, although we can gain some useful insights from cognate disciplines that have a more established body of professional literature (Bishop & Scudder, 1990; Clark et al., 1996; Eraut, 1994; Fagermoen, 1997; Fry, 1999; Gambrill, 2001; Ikiugu, 2004; Jensen et al., 2000; Kouw, 2000 (rev 2005); Long & Hollin, 1997; Mitchell & Audet, 2005; Rosen, 1988; van Strien, 1997; Walsh, 1992). Nevertheless many of these insights are necessarily discipline-and contextspecific which limits their applicability to our needs and our clinical context. Ambulance services in Australia and New Zealand, and the clinical practice guidelines they use, are by and large much alike. Yet despite the similar structures, paramedicine is practised in very different ways. This can be explained partly by the nature of the work. Paramedic practice is by definition broad in scope as it is completely defined by patients’ calls and is therefore impossible to predict. Paramedics attend people of all ages, from the very young to the very old, with every possible ailment, ranging from exacerbations of chronic medical conditions to acute medical emergencies, minor and major traumas, mental health crises, drug and alcohol problems, and major social emergencies. But aside from the breadth of practice, paramedics also manage the immediacy of the life threat, and it is the time-critical nature of crucial interventions that separates paramedics from most other health practitioners (Burgess et al., 2003).

Yet context and skills alone cannot explain paramedic practice and applying this ‘clinical capacity’ model is a source of frustration for many paramedics. If we define ourselves as responding only to life-threatening emergencies when the role is in fact so much broader, then most of our patients will fall outside of our model of practice and we will find ourselves wondering why they have called. While only a minority of our patients are in danger of dying, all of them are to some extent vulnerable. This vulnerability has many causes. Patients may be young children without a parent or guardian present, or people who are physically frail, suffering dementia or acutely confused. They may be acutely mentally ill or they may be suffering a serious or life-threatening medical or traumatic event. This clinical capacity model focuses almost solely on the clinician and the disease and fails to incorporate the patient and the concept of illness (see Ch 5). While we are busy trying to diagnose the disease, our patients are actually more concerned with their illness: how the disease makes them feel (see Fig 11.2). To ignore this aspect is to ignore most of why patients call and what they need us, as a profession, to do for them.

FIGURE 11.2 While we are busy trying to diagnose the disease, our patients are more concerned with their illness: how the disease makes them feel. Source: Courtesy of the Government of South Australia/SA Health. Individual paramedics approach similar cases and clinical situations with a wide variety of methods. Paramedics develop their own way of practice as they learn from their professional and personal experiences. The degree to which this development is a deliberate process of learning and reflective practice varies. For some paramedics, regardless of their years of clinical experience, their practice remains relatively immature: they habitually follow dominant practice approaches that are often determined through their education and training and the setting in which they practice (usually an ambulance service).

DISCU SSION P OINT 1. What are the attributes of a good paramedic? 2. What is the principle that guides your patient management? 3. How would you like people to describe you as a paramedic? Compare your answers with those of more experienced paramedics. How

your answers evolve and how successful you are in meeting your goals will be guided by your awareness of your own model of practice.

The ability to recognise how others perceive your behaviour is often an uncomfortable burden: being aware that you have appeared rude, arrogant or ignorant, even when that was not your intention, is usually a painful insight. It is somewhat ironic then that those who lack this degree of awareness are rarely discomforted. However, the knowledge that the world may not see you as you see yourself, or that your inherent personality may not be suitable for every occasion, is a key skill in developing as a professional. For such insightful paramedics, the development of their practice and their philosophy of practice is a deliberate and active process that continues throughout their career. For them, clinical development is inseparable from personal and professional development, and a process of active reflection underpins their career. Their philosophy of practice is a domain in which there are limitless challenges. For these paramedics, developing a philosophy of practice means that paramedicine remains fresh and rewarding, a sphere of unending opportunities for development and enrichment, even when clinical practice is mastered and few aspects of practice are particularly challenging.

Case 1 Leon loves life. He is a happy-go-lucky, knockabout type. He loves people, he loves a laugh and he loves being a paramedic—it is his ‘dream job’. A graduate paramedic is currently working with Leon and they are called to attend an elderly man who is generally unwell. On arrival at the patient’s pin-neat apartment, they are greeted by an elderly lady who shows them to the lounge room where the patient is seated. Leon: ’G’day mate, my name’s Leon. What’s yours?’ The patient looks slightly startled. He replies slowly and deliberately in perfect English, but with a hard-to-place European accent: ‘Oh, hello sir. My name is Dreyfus, Samuel Dreyfus.’

Leon: Patient: Patient’s wife: Leon:

’Pleased to meet you, Sam. Now what’s up? By the way, we’re all friends here, so no need to call me sir.’ ’My wife, she worries. It’s nothing, really nothing.’ ’He never makes a fuss—never. It’s been happening on and off for weeks, but he just won’t go to the doctor. There’s something wrong, I know it, and it could be serious.’ ’Worried about you after all these years, hey, Sam? How long have you two been married?’ ’What?’ ’He wants to know how long we have been married.’

Patient: Patient’s wife: Patient: ’Oh. Almost 59 years.’ Leon, ’59 years? You only get 14 years for murder, 12 with an early plea!’ laughing: Winking at the patient’s wife: ’I reckon my missus would have me knocked off tomorrow except my super isn’t worth it yet!’ Patient’s ’We have spent our lives together. We have been through everything. I wife: would never do that.’ Leon: ’No, of course you wouldn’t. Sorry, I missed your name.’ Patient’s ’My name? My name is Eve.’ wife: Leon: ’No worries, Eve. We’ll look after Sam for you.’ Patient’s ’We always look after each other.’ wife: Leon: ’Now, Sam, what’s the bother?’ Patient: ’Oh nothing. It has almost passed now; really, it’s nothing at all.’ Patient’s ’Take no notice. It is something. He has these terrible pains in the wife: stomach, and getting dressed earlier, when he was putting his trousers on he could hardly breathe.’ Leon, ’Normally I get short of breath when I’m taking my pants off! Anyway, laughing: Sam, let’s get this tie and suit coat off so we can have a good look at you.’ Patient’s ’Which hospital are you going to take him to?’ wife: Leon: ’We don’t know yet. He might be right to stay home. Let’s just have a quick look.’ With his wife’s help, the patient slowly removes his suit coat and tie.

Leon: Patient: Leon: Patient (becoming agitated): Leon: Patient (becoming more agitated):

’Right-o, Sam, let’s roll this sleeve up and we’ll check your blood pressure.’ ’Eve, come and help me with this cufflink. I can’t get it.’ ’No worries, mate, I’ll just take this one off for ya and do the left arm instead.’ ’No, really … Eve, can you come here and help?’ ’Don’t worry, I won’t knock it off. I’ll just take this left one off and do the BP on that arm instead.’ ’No. Eve, come and help me.’

The patient’s wife attends her husband and removes the cufflink. Patient’s wife: Leon (muttering to himself ): Speaking audibly:

’There. It’s off now.’ ’Gawd, with help like this…’ ’Ha! Lucky we’re getting paid by the hour, heh? Are we right now? All good? All right Sam, let’s see what we can find.’

The paramedics complete their examination of the patient and after speaking on the telephone with the patient’s GP, who was unable to make a house call, eventually arrange for a non-emergency transfer for the patient for later that day. As they depart, Leon turns to his partner and says: ‘I don’t know what it is with these patients. They’ve always been the same—always so bloody difficult to deal with.’

Building a philosophy of practice The transition to tertiary paramedic education has raised a number of challenges to building a model of practice. Compared to the vocational/apprenticeship model of training, graduates do not arrive with their theoretical knowledge supposedly complete. Rather, completion of an undergraduate education is just the first door to professional practice. Your degree is a licence to practise: it is not documentary evidence of your ability to practise. Developing clinical competence is a high priority for novice paramedics but paramedic practice is not simply a technical profession requiring the correct execution of particular procedures: it is an applied practice whose aim is to promote the health and wellbeing of patients. At its core paramedic practice involves interactions between people. How paramedics approach these interactions is shaped by the philosophy of practice they (knowingly or unknowingly) adopt. The great strength of deliberately developing a philosophy of practice is that it allows you to purposefully construct the answer to the questions ‘What sort of paramedic do I want to be?’ and, even more importantly, ‘What do I need to do to become that paramedic?’

Reflective practice Paramedicine in Australia is not yet a profession, although it is moving towards this position (Williams, Onsman & Brown, 2010). Members of a profession are responsible and accountable to society in general, their patients, the health system in which they work, their professional peers and themselves. Professional practice reflects an organised body of knowledge and expertise, statutory regulations, accountability and autonomy (Eraut, 1994). An important part of professionalism is the notion of developing reflective practice and making a professional habit of active reflection.

Gibbs’ reflective cycle The process of active reflection has been described in many ways (Ghaye & Lillyman, 1997). Two of the most well-known are Kolb’s experiential learning cycle and Gibbs’ reflective cycle (see Fig 11.3). Both are well regarded, but we look at Gibbs’ reflective cycle here as it more closely aligns with the processes of clinical decision making in paramedic practice. Gibbs’ reflective cycle provides a clear model for us to identify the steps involved in active reflective practice. It demonstrates the circular process by which our thoughts affect our actions, which in turn affect the situation we are dealing with, and that feedback from others involved can influence how we understand and think about the situation. This process allows us to align our initial expectations with our experience, which enables us to form new plans based on new insights. Our revised expectations, which are hopefully better matched to reality, will be realigned after further experience, enabling us to form new plans based on new insights. And so the cycle repeats until our revised expectations are closely aligned with our best understanding.

FIGURE 11.3

Gibbs’ reflective cycle.

This process of gradual steady clinical development also holds true for the development of our individual philosophy of practice. When we commence as paramedics, we often struggle to cope with all the aspects of even straightforward low-acuity cases. We are often overwhelmed with the many unfamiliar aspects of our new role, leaving us (at least to some extent) floundering. We might think of this process as an attempt to balance and align the foundations of our practice. These foundations are our knowledge, skills, behaviours, and attitudes and beliefs. These domains are represented in Figure 11.4.

FIGURE 11.4

The domains of the novice and the expert paramedic.

For novices these ‘practice domains’ tend to exist independently, as component pieces of a structure, with little overlap between them. We try to master the complexities and challenges that each presents as they arise. If we encounter a disease with which we are not familiar, we read about it; if we struggle with a clinical procedure or skill, we seek advice from more experienced colleagues and practise it, and so on. Over time, we develop greater mastery of each individual domain: our theoretical knowledge becomes consolidated and grounded in a clinical context, our skills become more finely honed with frequent application, our behaviours become more attuned to clinical practice and the clinical context of paramedicine, and our attitudes change with greater experience and exposure to a wide variety of patients, other paramedics and other health professions. With greater experience and the passage of time (almost) all paramedics will achieve greater proficiency and development in each of these domains. But greater proficiency in each domain is not sufficient to develop a philosophy of practice. How can this be? The answer lies in Gibbs’ reflective cycle. The essential missing ingredient for developing a philosophy of practice is reflection. To develop a philosophy of practice that integrates the separate domains of clinical practice into a coherent, closely aligned whole requires reflection about each of the key components not only individually, but also collectively. We need to reflect on these components as a coherent whole. Active, deliberate reflection is the catalyst for the process of integrating our domains, which leads us to develop a philosophy of practice. In this context, immersing our domains of practice in active, deliberate reflection is a kind of marinade that permeates our practice.

Overcoming the pitfalls However, there are some pitfalls that lie in store for the novice or the unwary. One of the major problems with developing a philosophy of practice based on Gibbs’ reflective cycle is that it needs to be done well. If we do it poorly we run the risk that we engage with the process in a superficial way, which mistakenly rationalises existing practice or

retrospectively justifies our actions. When we are busy and reflect while on-the-run we run the risk of believing we are reflecting, when we may actually be simply going through the motions of reflection: appearing to reflect rather than truly engaging with the process. Like most things, developing genuine reflection doesn’t just happen: it requires deliberate practice. Reflective practice cannot happen if it occurs simplistically. So developing this mindset requires time and effort. For the novice it may be challenging to step back from difficult or unpleasant experiences (whether clinical, operational, interpersonal or personal) and seek to be analytical about them. We already know that the process itself isn’t automatic. When a deliberate process requires us to honestly reflect on ourselves, we may find shortcomings that we prefer not to acknowledge or that we find difficult to resolve. Such potential discomfort may deter some from making the attempt at all. This is particularly relevant for high achievers, who tend towards perfectionism. The impact of reflection as a constant quest for self-improvement may lead to feelings of inadequacy and dejection, especially if the reflector takes critical reflection to mean finding the negatives rather than to fairly evaluate the strengths and weaknesses of performance. Rather than attempting solitary introspection, newer clinicians may find it useful to engage in critical dialogue with a thoughtful and experienced colleague—a trusted professional mentor. Mentors need to be alert to the problems noted above and remain sensitive to their role. For those undertaking the role (either informally or as part of their work) it is important to clearly establish and maintain professional boundaries, especially if the people they mentor are performing poorly or reveal matters that are personal in nature.

Active reflection Reflection is a different and unique form of thinking. One of the first people who thought about reflection in practice was an educator named John Dewey (Dewey, 1933). His way of thinking about reflection was based around teaching, but it is very useful for new paramedics because it aligns closely with their daily experience in clinical practice. Dewey suggested that reflection stems from doubt, confusion or hesitation arising from a situation that we have experienced directly. Episodes of doubt, confusion or hesitation arise daily for novice paramedics. This discomfort prompts us to move from routine action and thinking (often influenced by customary practice or sources of authority) towards reflective practice. Dewey argued that we need to think the problem through, develop new ideas, plan how we will use them and test them in real life to see if they work (or at least work better than what we did previously). Intuitively, this seems to be a reasonable way to approach reflection. Others have since developed Dewey’s ideas. One influential writer is Schon (1983), who developed the idea of two types of reflection: reflection-on-action (thinking after the ‘event’) and reflection-in-action (thinking while undertaking the event). Realistically, reflection-in-action is likely to be beyond novice paramedics because they are likely to be so fully engaged with simply managing the case at the time: they lack the level of clinical mastery required to undertake reflection-in-action. So novices are more likely to use reflection-on-action, taking some time away from the immediate demands of clinical practice to describe, review, analyse and assess past practice to gain insights that will guide improvement in future practice.

Although you may not know it, as a novice paramedic you do this already. You have developed clinical strategies that you apply or will apply when the situation demands: you may not yet have managed a cardiac arrest but you have a well-developed plan for what you will do, and after the first case is over you will reflect on it to gain insights that will help you next time. If you apply this idea of clinical strategy and reflection-on-action from the clinical domain and start to develop a reflective habit about all aspects of your practice you are well on the way to developing a true philosophy of practice. The concept of active reflection is not fanciful navel-gazing. It is fundamentally important to other aspects that are central to good paramedic practice that are discussed in the preceding chapters: patient safety, communication, clinical reasoning and fundamental knowledge. Each of these domains forms the essential components that when integrated become part of your philosophy of practice. When your knowledge, skills, behaviours, and attitudes and beliefs become consistent, congruent and aligned it is no accident. It happens when you actively reflect on your practice (see Fig 11.5). To the extent that this happens, you develop not just your philosophy of practice, but also your professional integrity. You can answer the question ‘What sort of paramedic do I want to be?’ When you then ask the question ‘What do I need to do to become that paramedic?’, you know the answer: I reflect on action and act on my reflection to develop an integrated philosophy of practice.

FIGURE 11.5

Developing your philosophy of practice.

Summary Clinicians from all areas of healthcare are often unaware that they operate within a model of practice, despite how it shapes their everyday practice. Each clinician’s model of practice is influenced by their knowledge, skills, attitudes and experiences. The model describes how they approach their tasks and patients and is always developing: responding to patients, colleagues and circumstances. The model starts to form during the formal education process but the components are not really tested until the novice enters clinical placements and is required to integrate them instinctively. Students’ models of practice are largely defined by the wider community’s expectations of the paramedic role in healthcare and this perspective of how ‘others’ (i.e. patients, carers, other health professionals) view paramedic practice is often lost as paramedics become embedded in their own community of practice. Gaining an awareness of your model of practice and comparing it with your own values and beliefs transitions your practice model from an unconscious and retrospective summary of how you work into a framework that will guide you to being the type of paramedic you want to be.

References Ajjawi, R., Higgs, J. Learning to reason: a journey of professional socialisation. Advances in Health Sciences Education. 13(2), 2008. Bishop, A. H., Scudder, J. R.The Practical, Moral and Personal Sense of Nursing: A Phenomenological Philosophy of Practice. Albany: State University of New York Press, 1990. Burgess, S., Boyle, M., Chilton, M., Ellis, B., Fallows, B., Lord, B., et al. Monash University Centre for Ambulance and Paramedic Studies (MUCAPS) Submission to the Department of Human Services (DHS), in response to the DHS Discussion Paper examining the regulation of the health professions in Victoria. Journal of Emergency Primary Health Care. 1(3–4), 2003. Christensen, N., Jones, M. A., Edwards, I., Higgs, J. Helping physiotherapy students develop clinical reasoning capability. In Higgs J., Jones M.A., Loftus S., Christensen N., eds.: Clinical Reasoning in the Health Professions, 3rd ed., Sydney: Elsevier, 2008. Clark, J. M., et alProject 2000: Perceptions of the Philosophy of Practice of Nursing. London: English National Board of Nursing, Midwifery and Health Visiting Publications Department, 1996. Clouder, L. Becoming professional: exploring the complexities of professional socialisation in health and social care. Learning in Health and Social Care. 2(4), 2003. Dewey, J.How We Think: A Restatement of the Relation of Reflective Thinking to the Educative Process. Chicago: Henry Regnery, 1933. Eraut, M.Developing Professional Knowledge and Competence. London: Falmer, 1994. Fagermoen, M. S. Professional identity: values embedded in meaningful nursing practice. Journal of Advanced Nursing. 1997; 25(3):434–441. Fry, S. T. The philosophy of nursing. Research and Theory for Nursing Practice. 1999; 13(1):5–15. Gambrill, E. Social work: an authority-based profession. Research on Social Work Practice. 2001; 11(2):166–175.

Ghaye, T., Lillyman, S.Learning Journals and Critical Incidents: Reflective Practice for Health Care Professionals. Dinton: Quay, 1997. Ikiugu, M. N. Instrumentalism in occupational therapy: an argument for a pragmatic conceptual model of practice. International Journal of Psychosocial Rehabilitation. 2004; 8:109– 117. Jensen, G. M., Gwyer, J., Shepard, K. F., Hack, L. M. Expert practice in physical therapy. Physical Therapy. 2000; 80(1):28–43. Kouw, W. A. (2000 [rev 2005]). Toward a philosophy of clinical practice. Paper presented at the 58th Annual Meeting of the International Council of Psychologists, Padua, Italy. Long, C. G., Hollin, C. R. The scientist–practitioner model in clinical psychology: a critique. Clinical Psychology & Psychotherapy. 1997; 4(2):75–83. Mitchell, P. R., Audet, L. R. Development of a clinical philosophy by graduate students in speech-language pathology. Contemporary Issues in Communication Science and Disorders. 2005; 32(Fall):134–141. Rosen, H. Evolving a personal philosophy of practice: toward eclecticism. In: Dorfman R.A., ed. Paradigms of Clinical Social Work. New York: Brunner/Mazel Inc, 1988. Schon, D. A.The Reflective Practitioner. New York: Basic Books, 1983. Trede, F., Higgs, J. Clinical reasoning and models of practice. In Higgs J., Jones M.A., Loftus S., Christensen N., eds.: Clinical Reasoning in the Health Professions, 3rd ed., Sydney: Elsevier, 2008. van Strien, P. J. Towards a methodology of psychological practice. Theory & Psychology. 1997; 7(5):683–700. Walsh, K. Some gnomes worth knowing. Clinical Neuropsychologist. 1992; 6(2):119–133. Williams, B., Onsman, A., Brown, T. Is the Australian paramedic discipline a full profession? Journal of Emergency Primary Health Care. 8(1), 2010.

PART 2 PARAMEDIC PRACTICE O U TL I N E INTRODUCTION TO THE PARAMEDIC APPROACH TO THE PATIENT IN AN ALTERED CONSCIOUS STATE CHAPTER 12: Hypoglycaemia CHAPTER 13: Cerebrovascular accidents CHAPTER 14: Overdose CHAPTER 15: Seizures INTRODUCTION TO THE PARAMEDIC APPROACH TO THE PATIENT IN RESPIRATORY DISTRESS CHAPTER 16: Airway obstruction CHAPTER 17: Asthma CHAPTER 18: Acute pulmonary oedema CHAPTER 19: Chronic obstructive pulmonary disease CHAPTER 20: Pneumothorax CHAPTER 21: Pulmonary embolism CHAPTER 22: Pleural effusion CHAPTER 23: The paediatric patient with a noisy airway INTRODUCTION TO THE PARAMEDIC APPROACH TO THE PATIENT SUFFERING A CARDIAC EMERGENCY CHAPTER 24: Chest pain CHAPTER 25: Arrhythmias CHAPTER 26: Cardiac arrest INTRODUCTION TO THE PARAMEDIC APPROACH TO THE PATIENT WITH A SEVERE ALLERGIC REACTION CHAPTER 27: Anaphylaxis INTRODUCTION TO THE PARAMEDIC APPROACH TO THE PATIENT PRESENTING WITH PAIN CHAPTER 28: Pain CHAPTER 29: Lower back pain CHAPTER 30: Renal colic INTRODUCTION TO THE PARAMEDIC APPROACH TO THE TRAUMA PATIENT CHAPTER 31: The structured clinical approach to trauma patients CHAPTER 32: Head injuries

CHAPTER 33: Chest injuries CHAPTER 34: Musculoskeletal injuries CHAPTER 35: Traumatic spinal injuries CHAPTER 36: Burns INTRODUCTION TO THE PARAMEDIC APPROACH TO THE PATIENT PRESENTING WITH ENVIRONMENTAL INJURY CHAPTER 37: Hypothermia CHAPTER 38: Hyperthermia CHAPTER 39: Decompression injuries CHAPTER 40: Snake bites CHAPTER 41: Spider bites CHAPTER 42: Marine envenomation INTRODUCTION TO THE PARAMEDIC APPROACH TO THE UNWELL PATIENT: SPECIFIC CHALLENGES TO PARAMEDIC REASONING CHAPTER 43: Acute abdominal pain CHAPTER 44: Sepsis CHAPTER 45: Bleeding from the gastrointestinal or urinary tract INTRODUCTION TO THE PARAMEDIC APPROACH TO COMPLEX CASES: SPECIFIC CHALLENGES TO PARAMEDIC REASONING AND MANAGEMENT CHAPTER 46: The socially isolated patient CHAPTER 47: The dying patient CHAPTER 48: The patient on out-of-hospital dialysis CHAPTER 49: Indigenous Australian patients CHAPTER 50: Māori patients INTRODUCTION TO THE PARAMEDIC APPROACH TO THE PATIENT DISPLAYING ABNORMAL BEHAVIOUR CHAPTER 51: The patient displaying abnormal behaviour CHAPTER 52: De-escalation in the pre-hospital environment INTRODUCTION TO THE PARAMEDIC APPROACH TO OBSTETRIC AND NEONATAL EMERGENCIES CHAPTER 53: Imminent birth CHAPTER 54: Neonatal resuscitation

SECTION 7

THE PARAMEDIC APPROACH TO THE PATIENT IN AN ALTERED CONSCIOUS STATE O U TL I N E INTRODUCTION TO THE PARAMEDIC APPROACH TO THE PATIENT IN AN ALTERED CONSCIOUS STATE CHAPTER 12: Hypoglycaemia CHAPTER 13: Cerebrovascular accidents CHAPTER 14: Overdose CHAPTER 15: Seizures

INTRODUCTION TO THE PARAMEDIC APPROACH TO THE PATIENT IN AN ALTERED CONSCIOUS STATE IN THIS SECTION CHAPTER 12 Hypoglycaemia CHAPTER 13 Cerebrovascular accidents CHAPTER 14 Overdose CHAPTER 15 Seizures

AT THE COMPLETION OF THIS SECTION YOU SHOULD BE ABLE TO • Describe the common causes of alterations of conscious state that present to paramedics. • Describe a succinct and effective assessment of these conditions to determine the most likely cause. • Discuss the principles of management of patients in an altered conscious state and the specific management for causes that are treatable in the pre-hospital environment. The first-aid principles of supporting airway, breathing and circulation continue to be the pillars of emergency medical care regardless of the level of training or skillset of the responder. For the paramedic, airway compromise is intrinsically linked to the patient’s conscious state and any patient unable to protect their own airway—regardless of how benign the cause—is at threat of airway occlusion and death from hypoxia. Paramedics may carry a number of airway support tools such as oropharyngeal airways, laryngeal masks and endotracheal tubes. While these may seem harmless, each device carries significant risks. Far more effective than trying to mechanically maintain a patient’s airway is to raise the patient’s conscious state so that they can protect it themselves. Dispatches to patients in an altered conscious state make up a significant proportion of paramedic cases. In order to manage these patients effectively you will need to quickly differentiate between the causes of unconsciousness and know which can be corrected in the field. This section reviews common causes of alterations in conscious state, steps you through the clinical reasoning process to provide a differential diagnosis and links the pathophysiology to the paramedic management of these common conditions.

CHAP TER 12

Hypoglycaemia By Jason Bendall, Janelle White and Paul Middleton

C O N C E P TS U S E D I N TH I S C H A P TE R • The paramedic’s clinical approach: Section 2 • Perfusion: Chapter 55 • The autonomic response: Chapter 56

O V E RV IE W • Glucose is the preferred energy source for the brain, which is highly sensitive to reduced blood levels. • Hypoglycaemia is a reduction in the plasma glucose concentration that may induce symptoms or signs such as altered mental status and sympathetic nervous system stimulation. • Hypoglycaemia is common in diabetics treated with either insulin or oral hypoglycaemic agents but may also occur rarely in non-diabetics. • Diagnosis of hypoglycaemia involves a simple blood glucose test; treatment varies according to severity and aetiology. • Simple oral administration of glucose can be effective in reversing the symptoms of hypoglycaemia. • Special patient groups such as neonates, the elderly and alcoholics provide additional challenges for paramedics. • Hypoglycaemia should always be considered as a potential cause of an altered conscious state in a patient. • Paramedic treatment of hypoglycaemia can resolve the symptoms but does not correct the underlying pathology. Some patients may require transport to hospital while others can stay

safely at home. • There are five common insulin preparations and five common oral hypoglycaemic medications used in Australia. • In the event that a patient who is suffering from hypoglycaemia is not a diabetic, rare causes of hypoglycaemia must be considered and transport to hospital is always required regardless of how well the patient responds to emergency treatment.

Introduction An estimated 275 Australians develop diabetes every day and by 2031 it is estimated that 3.3 million Australians will have type 2 (T2) diabetes. While the disease causes a number of severe long-term effects, its main disruption is to the regulation of blood glucose levels. Blood glucose levels are usually well-controlled by ingestion of food and the subsequent release of insulin and glucagon from the pancreas and liver, respectively (see Fig 12.1).

FIGURE 12.1

Regulation of insulin and glucagon secretion. FFA = free fatty acids; GLP-1 = glucagon-like peptide-1; GIP = gastric inhibitory peptide. Sympathetic stimulation and decreasing concentrations of glucose increase the secretion of glucagon, which acts primarily on liver cells to increase the rate of glycogen breakdown and the secretion of glucose from the liver. The release of glucose from the liver helps maintain blood glucose levels. Increasing blood glucose levels has an inhibitory effect on glucagon secretion. Increasing concentrations of glucose and amino acids stimulate the beta cells of the islets to secrete insulin. In addition, parasympathetic stimulation causes insulin secretion. Insulin acts on most tissues to increase the uptake of glucose and amino acids. As the blood levels of glucose and amino acids

decrease, the rate of insulin secretion also decreases. Source: Kleinridders, Könner & Brüning (2009). Although most health providers recommend immediate treatment if a patient’s blood glucose drops below a certain level, the clinical definition of hypoglycaemia should be more complex than merely stating the blood glucose level (BGL). The minimum BGL that a person can tolerate without becoming symptomatic differs between individuals. Therefore, clinical hypoglycaemia is best-defined using Whipple’s triad (see Fig 12.2).

FIGURE 12.2 W hipple’s triad. Three components indicate a diagnosis of hypoglycaemia and should be documented in all cases of hypoglycaemia. This is especially important in patients who are not diagnosed diabetics, as hypoglycaemic disorders are rare and this will assist specialists when initiating further investigations. A low BGL may be defined as one that is sufficient to cause signs and symptoms, including impaired brain function. While it is widely accepted among pre-hospital providers that a BGL 100 ms), and there will usually be a large R wave in aVR (see Fig 14.2). The widening QRS is reflective of the degree of fast sodium channel blockade and the onset of other life-threatening symptoms:

FIGURE 14.2 Sodium channel blockade along with other toxic effects from TCA agents. A Sinus tachycardia, primarily resulting from anticholinergic properties of the drug class. B Wide QRS complex tachycardia. C Prolonged QT interval. D Large S wave in lead I and prominent R wave in lead aVR, an indication of impending sodium channel blocker toxicity. This ECG finding is indicative of a far rightward axis deviation. Source: Delk, Holstege & Brady (2007). • QRS > 100 ms is prognostic of seizures • QRS > 160 ms is prognostic of ventricular tachycardia (VT) (Parkinson et al., 2011). Other potential ECG abnormalities in TCA overdose include a Brugada ECG pattern, which occurs in approximately 20% of TCA overdose presentations. This pattern is seen in a condition known as Brugada syndrome, a rare genetic phenomenon characterised by non-ischaemic ST segment elevation in the right praecordial leads V1–V3, coupled with a right bundle branch block and linked to sudden cardiac death (Pierog et al., 2009). A Brugada ECG pattern can also be caused by acute myocardial infarction (AMI), myocarditis, pulmonary embolism and cocaine use (Pierog et al., 2009).

Continuous monitoring of physical status and clinical and cardiac monitoring are required until there is full reversal of toxicity.

CA SE ST U DY 1 Case 12492, 2225 hrs. Dispatch details: A 21-year-old male who is unconscious; query intoxicated. Initial presentation: The ambulance crew find the patient at his 21st birthday party with approximately 100 other people in attendance. There are about 20 guests gathered around the patient who is lying on the grass. He has been placed in the recovery position by his friends following advice from the emergency call-taker. He responds only by withdrawing to pain. He is making snoring sounds and his breathing is slightly shallow (there is a strong odour of metabolites of alcohol). He is also pale and diaphoretic and is dry retching. He is covered in vomit and has been incontinent of urine.

ASSESS Patient history Estimating the amount of alcohol that the patient has consumed and over what time period can assist in determining whether alcohol is consistent with the patient’s condition, but it is rare to get a detailed and accurate answer. Nonetheless, it could indicate that alcohol poisoning is a factor beyond simple intoxication. The phone numbers of Poison Information Centres are a vital addition to any paramedic toolkit (see Box 14.4). B O X 1 4 . 4P

o iso n I nf o r m atio n Centr es

Poison Information Centres operate 24 hours a day in Australia and New Zealand. Paramedics use them regularly, particularly when a patient has ingested a medication, chemical or plant that is unknown to them. The numbers are: • Australia: 131126

• New Zealand: 0800 764 766 (0800 POISON)

Gaining a past medical history may reveal prescription medications or conditions that are exacerbated by alcohol (epilepsy, diabetes). Events immediately preceding the patient’s collapse are also worth examining: for example, did the patient suffer any head trauma prior to falling or as a result of falling that could explain their altered conscious state? This case study reveals a fairly typical presentation of severe alcohol (ethanol) intoxication/poisoning. The patient is at a party and alcohol is freely available. He presents with signs and symptoms that are classic of severe intoxication, including severe CNS depression, and has no significant past medical history of recent trauma.

Airway Alcohol presents a dual-pronged challenge to airway patency. As a CNS depressant alcohol suppresses all of the protective reflexes of the airway including coughing, swallowing and the gag reflex. The metabolites of alcohol can also trigger vomiting and when this is combined with a loss of airway reflexes the risk of aspiration is significant. Predicting the likelihood of vomiting is difficult as it depends on both the volume of alcohol (and other fluids/food) consumed and the period of time over which it has been consumed.

HIST ORY Ask! • Past medical history (including medications, pre-existing conditions and allergies)? • Has the patient eaten anything that evening? • Can anyone show you the alcohol bottles that the patient consumed? • Was the alcohol made in cocktails or was it from commercial bottles/cans? • Were there any other drugs, prescription or otherwise, available at the party? • Could the patient have sustained any traumatic injury? • When did people last see the patient conscious?

This patient’s snoring sounds suggest a significant degree of CNS depression and he should be placed in the lateral position as soon as possible. This should resolve the snoring but a small amount of manual jaw lift/support may be needed. A visual inspection of the upper airway should be sufficient to identify

any major obstructions. Persistent airway noises and an increased work of breathing are indicative of airway obstruction and need to be managed if present. Otherwise, the insertion of oropharyngeal airways into the mouth of an intoxicated patient should be avoided at this stage, as it is likely to precipitate vomiting.

Breathing This patient’s alcohol level is potentially quite high and it is therefore possible that depression of the medulla and the respiratory centre is occurring. His respiration rate is currently 10 and provided the tidal volume is sufficient this should be adequate (and can be checked against his SpO2). Absorption of alcohol is probably still occurring, however, and both the rate and the depth of his breathing could deteriorate.

Circulation Alcohol is both a mild vasodilator and a diuretic, meaning that it can lead to poor perfusion. It has less cardiovascular effects than benzodiazepines, so profound hypotension should raise suspicions of other drugs. Alcohol’s vasodilatory effects direct blood to the skin, so heat loss can develop quickly in cold environments and further depress the patient’s conscious state and vital signs.

Gastrointestinal/urinary systems Toxic levels of ethanol (and its metabolites) can trigger the chemoreceptor trigger zone (CTZ) and the vomiting centre. Urinary incontinence is also common due to CNS depression and alcohol affecting the pituitary gland inhibiting antidiuretic hormone (ADH) (Mental Health, Drug and Alcohol Office, 2007).

Physical examination Physical examination and assessment should be undertaken with an open mind. The tendency to reach premature diagnostic decisions is one of the main causes of diagnostic error: this patient has been drinking in excess; drinking in excess leads to unconsciousness—therefore, this patient is intoxicated. Intoxication increases risk-taking behaviour and the likelihood of falls. Close examination of the patient’s face and skull for wounds could reveal injuries from an earlier fall that was possibly unwitnessed.

Initial assessment summary

Problem Unconscious, possibly intoxicated Conscious GCS = 7 (E1, V2, M4) state Position Lying on his side on the grass Heart rate 98 BPM, weak Blood 105/78 mmHg pressure Skin Pale, cool appearance Speech Incomprehensible sounds pattern Respiratory 10 BPM rate Respiratory Even cycles rhythm Respiratory Normal but decreased tidal volume effort Chest Clear chest auscultation Pulse 97% on room air oximetry Temperature 36.3°C History The patient is covered in vomit and has been incontinent of urine. His friends state that he started drinking at 6.30 pm and has consumed a 750-mL bottle of bourbon and at least 8 or 9 stubbies of beer. They say he is at university full-time and works part-time at a fast-food outlet; he regularly gets drunk at parties but they have never seen him this bad. They assure you that it would be unusual for him to take anything else. There is no evidence of traumatic injury. BGL 4.7 mmol/L D: There are no immediate dangers to the patient or crew. A: The patient is unconscious and his airway is clear. B: Respiratory function is slightly depressed but SpO2 is normal. C: Heart rate and blood pressure are approaching normal limits. The patient smells of alcohol, has been seen drinking at his party and has a social history of binge drinking. A physical examination reveals no obvious injuries.

CONFIRM The essential part of the clinical reasoning process is to seek to confirm your initial hypothesis by finding clinical signs that should occur with your

provisional diagnosis. You should also seek to challenge your diagnosis by exploring findings that do not fit your hypothesis: don’t just ignore them because they don’t fit.

What else could it be? Hypoglycaemia Hypoglycaemic patients can present in a similar way to patients with acute alcohol intoxication. A simple BGL check will allow the paramedic to either detect and correct or rule out hypoglycaemia. A BGL should always be recorded for patients with an altered conscious state. A BGL check would also detect the presence of a condition known alcoholic ketoacidosis (see Box 14.5). B O X 1 4 . 5A l c

o ho lic keto ac ido sis

Alcoholic ketoacidosis (AKA) is found in those with a history of chronic alcohol abuse and recent rapid/excessive intake. The toxidrome includes the history coupled with the following symptoms: • severe nausea with hyperemesis • severe abdominal pain • tachycardia • hypotension • increased respiratory rate. In rare cases it can present in less-experienced drinkers who have consumed alcohol rapidly/excessively. People are at increased risk if they have a recent history of consuming a large amount of alcohol rapidly with a decreased food intake (malnourished) and are vomiting profusely (Vonghia et al., 2008; Saunders et al., 1993).

DIF F ERENT IA L DIA GNOSIS Acute alcohol (ethanol) poisoning Or • Hypoglycaemia • Hypothermia • Acute hypoxia/hypercapnia • Hypotension • Effects of other drugs or toxins • Effects of other toxic alcohols • Head injury

Hypothermia

Hypothermic patients can present in a similar way to patients with acute alcohol intoxication. A simple check of the patient’s temperature will allow the paramedic to either detect and correct or rule out hypothermia. This patient’s temperature is slightly low but not enough to explain his condition. Hypoxia Hypoxia is another condition that can be readily detected and corrected with oxygen, basic airway management and assisted ventilation. Correction of airway compromise, breathing assistance and oxygen should quickly rule out hypoxia as the cause of a decreased GCS. With oxygen saturations of 97% it is highly unlikely that this patient is hypoxic. Hypotension Insufficient cerebral perfusion will cause alterations of consciousness. This patient’s blood pressure is slightly low but not enough to explain his condition. Effects of other drugs or toxins Alcohol is commonly consumed along with other medications and/or drugs that may interact with it in negative ways. These include: • antihistamines, antidepressants, opioids, antianxiety medications and antipsychotics (these all increase the CNS depressant effects of alcohol) • disulfiram (this drug is used specifically for treating alcohol dependence but causes severe side effects including nausea, vomiting, hypotension, flushing, stomach cramps, tachycardia and headache) • oral hypoglycaemics (these may place the patient at risk of hypoglycaemia) • anticonvulsants and anticoagulants (in chronic alcohol abuse where there is impaired liver metabolism these may cause elevated serum levels) • non-steroidal anti-inflammatory drugs (NSAIDs; these may increase gastric irritability) • nitrates (these may increase the risk of hypotension and syncope due to excess vasodilation) • anticholinergics and antispasmodics (these may slow gastrointestinal function, which in turn slows absorption of alcohol) • metoclopramide (this may increase the absorption of alcohol) • paracetamol (increases the risk of liver damage and toxicity) (Smith & Quan, 2011). Other toxidromes can be considered as part of the differential diagnoses. One drug in particular that can present in a similar way is an opioid overdose, but this patient’s pupils are normal and his respiratory depression is not severe. Combined with the lack of any recent IV marks found on physical examination, this is not suggestive of an opioid overdose. Effects of other toxic alcohols (methanol, ethylene glycol) Methanol leads to the same alcohol-type odour, tachycardia and hypotension exhibited by this patient but it is not readily available in Australia and New Zealand. It is therefore unlikely that this patient was consuming methanol. Ethanol is the antidote for methanol poisoning (given in hospital only) and a positive outcome is more likely if given early. If methanol poisoning is suspected, early hospital management may have a significant impact upon outcome.

Ethylene glycol is an odourless liquid and therefore would be less likely to cause a strong alcohol-type odour on the patient’s breath. The hallmark signs of ethylene glycol poisoning are CNS depression, metabolic acidosis and renal failure. The main source of ethylene glycol in Australia and New Zealand is radiator antifreeze/coolant. Although it is unlikely that the patient has ingested ethylene glycol, it cannot be ruled out confidently in the field without a clear history of what was actually ingested. Head injury Questioning bystanders regarding the patient’s activities prior to the paramedics’ arrival is essential. There must also be consideration of a possible mechanism of head injury, so a survey of the scene and where the patient is found is important. The next important step is the secondary survey: a full head-to-toe examination is necessary to ascertain if there is any evidence of trauma or any injuries. No injuries are found in this patient.

T REAT Emergency management The principles of management for the unconscious patient are outlined in Box 14.6. B O X 1 4 . 6P

rinc iples o f manag ement

T he unconscious patient There are five key questions that can be applied to all cases of overdose: 1. What is the agent/s? 2. What was the dose? 3. How long since ingestion? 4. Is there an obvious toxidrome? 5. What are the patient’s age, weight and comorbidities? (Murray et al., 2007)

Safety Negative consequences of alcohol consumption include antisocial and aggressive behaviour, violence, assault and crime. Paramedics should always consider their safety when approaching a scene where one or several people may be intoxicated. It may be necessary to contact the police and have them attend the scene to assist in crowd control. In many cases it is the police that

call the ambulance. Wearing personal protective equipment (PPE) including gloves and eyewear is essential due to the high possibility of bodily fluids being present and the fact that antisocial behaviour can include spitting. Fix the fixable! Drugs and trauma are obvious causes of an altered conscious state but there are a number of other (largely) reversible causes that should always be addressed prior to managing specific overdoses or injuries. Before commencing specific management of overdose always ensure that any abnormalities of the following have been corrected: • Hypoxia: ensure adequate rate and depth of ventilation and FiO2. • Hypercapnia: ensure adequate rate and depth of ventilation. • Hypoglycaemia: ensure BGL >4.0 mmol/L. • Hypothermia: ensure temperature >35°C. • Hypotension: ensure adequate heart rate and blood pressure.

P RACT ICE T IP It is important to approach all patients equally and not to judge or negatively stereotype people just because they have a problem with alcohol. All patients should be treated with dignity and respect regardless of their choices or lifestyle. If paramedics approach patients in an open, honest and non-judgemental way, patients are more likely to respond by being open and honest in return.

Airway Posture (lateral) and jaw support are likely to be sufficient in this patient. Suctioning of excess saliva should be done with care in order not to provoke the gag reflex and vomiting. There is an increased risk of morbidity and mortality if an intoxicated patient aspirates vomit into the lungs, but the risks associated with intubation outweigh the benefits if the airway can be controlled by position and support (see Box 14.7). B O X 1 4 . 7A d v a n c

e d a ir wa y m a n a g e m e n t

in patients who are into xic ated Patients who are intoxicated or have been poisoned often present with both a decreased conscious state and decreased aspiration. In these circumstances it is worth considering the need (or otherwise) to manage the patient’s airway and ventilation with an endotracheal tube. While endotracheal intubation provides control of ventilation and FiO2 there are a number of risks and drawbacks that should be considered. For example, the sedative drugs used to enable intubation

can exacerbate the respiratory and cardiovascular impacts of the drugs already in the patient’s system. These will need to be managed if the intubation is successful, but if it is unsuccessful the crew will be faced with a worse situation than they currently have. Even intoxicated patients may require significant sedation to enable the endotracheal tube to pass through the vocal cords and this is likely to impact on blood pressure and cerebral perfusion. Intubation also limits the ability to conduct a physical neurological assessment when the patient arrives at hospital. Other issues that should be considered with every intubation include: • the consequences of a failed intubation • the consequences of an unrecognised oesophageal intubation. While these variables can appear confusing and vague, the solution is relatively simple. Where the oxygen saturation cannot be kept above 90–92% using oxygen and noninvasive airway support, the potential harm of widespread cerebral hypoxia outweighs the risks associated with advanced airway management. In case study 1 the patient is not hypoxic and provided his airway can be maintained with positioning he is unlikely to be intubated at hospital. If the patient is hypoxic, refractory to noninvasive means of intubation should be considered.

Breathing Once the airway has been secured it is necessary to ensure adequate breathing/ventilation. This patient’s breathing is shallow so the tidal volume may be insufficient. His alcohol levels may be sufficiently high to cause CNS depression at the level of the medulla and the respiratory centres. It would be unwise to assume that the cause of this patient’s decreased GCS score is due to alcohol only. The normal breathing rate for an adult male is approximately 12–15 BPM. While this patient’s rate is just below that, some would still consider it within the normal range. The depth of his respirations is a concern. It is essential that the paramedic assess for signs and symptoms of hypoxia including: • central cyanosis of the buccal mucosa, tongue and lips • altered conscious state, leading to a loss of consciousness. Given the decrease in tidal volume it would be worth commencing this patient on oxygen via a rebreather mask at 8 L/minute, despite his SpO2 being relatively normal. This is unlikely to improve his conscious state but it will prevent rapid desaturation if the crew choose to intubate him. Gently assisting the depth of each ventilation using a bag valve mask (BVM) would also be recommended if hypoxia is suspected to be developing. Circulation This patient is borderline with regard to perfusion; IV fluids should be made ready but are not needed at this point. A bolus of 10 mL/kg would not be

harmful and will provide a buffer should the patient need to be sedated for intubation. Other An antiemetic such as ondansetron can be considered and given either IV or IM as part of treatment, especially if the patient has already vomited and is dry retching. Metoclopramide is a less desirable option as it may actually increase absorption of alcohol. Glucose 10% IV can be considered and administered if the patient’s BGL is low and requires correcting. If you give glucose (oral or IV) to a patient who has consumed alcohol it is recommended that you notify the staff at triage about this so that they can include thiamine in their treatment.

EVALUAT E Evaluating the effect of any clinical management intervention can provide clues to the accuracy of the initial diagnosis. Some conditions respond rapidly to treatment so patients should be expected to improve if the diagnosis and treatment were appropriate. A failure to improve in this situation should trigger the clinician to reconsider the diagnosis. The aim of pre-hospital management of the acutely intoxicated patient is generally supportive and fits in the standard primary survey ABCDE of patient assessment. The patient with mild acute alcohol intoxication provides a dilemma. It is difficult to ascertain whether the patient’s condition is going to worsen or not, as there is no way of knowing if their BAC is continuing to rise. If the patient refuses transport, this raises issues of autonomy and competence (see Ch 10). It is important to remember that this condition does not fall under the scope of mental health legislation, which allows involuntary admission of patients. The opportunity to engage such a patient in the health system relies on the paramedic’s ability to convince the patient to accompany them to hospital. The patient in this case has severe alcohol intoxication and requires significant intervention and supportive care, and operating with implied consent is sufficient. For more severe cases of intoxication where the conscious level is profoundly altered the focus becomes protection of the airway from vomit/secretions, especially in patients with severe CNS depression. Circulation may be compromised due to the vasodilation effects of alcohol and should be monitored and treated if necessary. Investigations and a thorough secondary survey should include searching for and treating other causes of a decreased GCS, such as hypoglycaemia, head injury or other types of overdose. All patients with severe CNS depression must be supervised at hospital. Mildly intoxicated patients may be supervised by a responsible adult who is not intoxicated if the patient is to remain at home.

Ongoing treatment Treatment at hospital remains primarily supportive with repeated monitoring. Endotracheal intubation is avoided if possible as the patient’s conscious state will start to improve within hours. Hypoglycaemia can develop but is usually responsive to treatment. A new drug used in the treatment of acute alcohol intoxication is metadoxine. A single IV dose of 900 mg has been shown to significantly decrease the half-life of ethanol in the blood and increase the rate of ethanol elimination, leading to faster recovery from intoxication (Ali & Kopf, 2010). All patients admitted to the ED for acute alcohol intoxication should be assessed for the risk of alcohol misuse or evidence of alcohol abuse or dependence. To assist in identifying risk, screening tools are generally used, such as AUDIT or CAGE—a tool to assess alcohol dependence (see Box 14.8). A positive test result warrants further investigation and follow-up for an alcohol-related problem (Roxburgh & Burns, 2012; Paech, Bloor & Schug, 2012). If the results are negative, the patient is often counselled at the ED and advised regarding safe alcohol use and the risk of alcohol-related problems. Patients who have been consuming excessive amounts of alcohol over a long period are also likely to have comorbidities as a consequence of the abuse (see Box 14.9). These can complicate the shortterm management but assessment at hospital can provide an opportunity for health workers to engage in management of these chronic conditions. B O X 1 4 . 8C A G E

assessm ent

CAGE is a tool for the detection of alcoholism. It takes less than 1 minute to administer. Two or more affirmative responses to the following questions suggest that the patient has a problem with alcohol: 1. Have you felt the need to Cut down on your drinking? 2. Do you feel Annoyed when people complain about your drinking? 3. Do you ever feel Guilty about your drinking? 4. Do you ever drink an Eye-opener in the morning to feel good?

B O X 1 4 . 9T

h e c u m u l a t i ve e ff e c t s o f a l c o h o l

c o nsum ptio n There are many negative long-term effects associated with chronic heavy alcohol consumption, including the following: • Cardiovascular—hypertension, arrhythmias, cardiac failure, haemorrhagic stroke, hyperlipidaemia and mild anticoagulation. • Cancers—oral, pharynx, larynx, oesophagus, liver, colorectal and female breast cancer. • Diabetes—there may be a relationship between alcohol consumption and

insulin sensitivity, T2 diabetes and metabolic syndrome. Alcohol negatively affects the management of diabetes. • Nutritional—alcohol consumption is linked with malnutrition, in particular thiamine (Wernicke’s encephalopathy), vitamin A and folate deficiency. • Overweight/obesity—alcohol is energy-dense and contains 27 kJ/g compared with 16 kJ/g for carbohydrates. • Risk to unborn babies—alcohol crosses the placenta and can also be found in breast milk. Fetal alcohol spectrum disorder causes mental and physical abnormalities in babies. • Liver—alcohol is the most common cause of liver cirrhosis and disease. This is exacerbated by diseases such as hepatitis B and C. • Mental health—alcohol increases the risk of depression and anxiety. Alcohol use disorders increases the risk of violent and suicidal behaviours. • Tolerance—alcohol tolerance develops early and occurs partly because the liver becomes more efficient at metabolising alcohol. People with greater tolerance will have a higher BAC more frequently. • Dependence—alcohol is both psychologically and physically addictive. Dependence ranges from mild to severe. People with severe dependence will experience a progression of life-threatening withdrawal symptoms including anxiety, tremors and seizures within a few hours of ceasing to drink. • Cognitive impairment—long-term alcohol consumption is associated with structural and metabolic changes to the brain and increases the risk of dementia (Haber et al., 2009).

Investigations If the patient is able to perform the test, the BAC is measured using a breathalyser; otherwise, it forms part of a blood analysis. Liver enzyme tests may be considered to assess chronic disease.

Hospital management Provided the investigations do not reveal underlying disease and that the intoxication was not a deliberate attempt at self-harm, most patients will be discharged from the ED once they have achieved a GCS score of 15 and are cooperative, ambulant, eating and drinking fluids, and passing urine.

CA SE ST U DY 2 Case 13423, 1030 hrs. Dispatch details: A 66-year-old female who is unresponsive; caller states ‘not breathing properly’. Initial presentation: The crew find a 66-year-old female propped up in bed on several pillows. She has slow, shallow breathing.

ASSESS 1039 hrs Primary survey: The patient is in an altered conscious state. Her airway is clear with slow, shallow ventilations. 1041 hrs Vital signs survey: Perfusion status: HR 64 BPM, sinus; BP 105/80 mmHg; skin pale with cyanosed lips. Respiratory status: RR 6 BPM, chest difficult to auscultate due to shallow ventilations; SpO2 88%. Conscious state: GCS = 5 (E1, V1, M3), pupils 1 mm in size, unresponsive to light. 1045 hrs Pertinent hx: The patient’s husband is present. He states that she has cancer and woke in a lot of pain this morning so took some of her medication, Ordine (oral morphine solution), for when she has breakthrough pain. She then went back to sleep. He came in to see if she wanted a cup of tea and couldn’t wake her. He noticed that her breathing was very slow and shallow. The patient wears a fentanyl patch (Durogesic 100) that delivers 100 mcg/hour of fentanyl over 72 hours transdermally. She also takes a 10-mL oral dose of liquid morphine (Ordine 1 mg/mL) when she has breakthrough pain (see Box 14.10). The husband shows the bottle to the paramedics and they

discover that it is a new prescription and she has potentially taken 100 mg of morphine instead of the 10 mg she usually takes. The paramedics ask whether the patient has an intrathecal pump (see Box 14.11) but the husband states she doesn’t. B O X 1 4 . 1 0B r e a k t h r o

ug h pain

Breakthrough pain is an acute episode of severe pain that also has an underlying pathology causing persistent pain (usually wellcontrolled by medication). It is common in cancer patients, who often establish a pain-relief plan with their specialists for when they experience breakthrough pain. They generally have a high tolerance for opioid medication and require large doses for adequate pain relief. Other terms for breakthrough pain include episodic pain, transient pain, exacerbation, acute on chronic (Koneru, Satyanarayana & Rizwan, 2009).

B O X 1 4 . 1 1I n t r a t h e c

al pump (‘ pain

pump’) An intrathecal pump is a medical device that is used to deliver medications to treat pain and spasticity. The pump stores and delivers medication to a catheter inserted into the intrathecal space (the drug enters the spinal fluid). The pump must be surgically implanted and can either be programmed via a computer or deliver constant medication. Morphine can be delivered in this way, with the advantages that doses are very small and there are fewer side effects. Patients with persistent pain may have a pump in situ and a possible malfunction (although rare) should be considered if the patient remains unresponsive to naloxone. If possible, contact the treating doctor and provide urgent transport to hospital for definitive care (Buykx & Dietze, 2012; Phillips, 2013).

Ask! • What medications is the patient taking? • Does the patient have a particular specialist? • Does the patient have a particular hospital they attend? • Why is the patient taking the opioid (is it for pain)?

Consider! • What naloxone dose should be used? It would be an error to completely reverse the patient’s analgesia with naloxone; if naloxone is used, the smallest dose possible to achieve adequate respiration is all that is needed. • Is there a possibility of opioid dependence and induction of withdrawal syndrome? • Is the overdose clinical or non-clinical? • Is the drug prescribed to the patient?

CONFIRM In many cases paramedics are presented with a collection of signs and symptoms that do not appear to describe a particular condition. A critical step in determining a treatment plan in this situation is to consider what other conditions could explain the patient’s presentation.

What else could it be? Other drug overdose For details regarding alcohol, see above. In this case there is no characteristic odour of alcohol, nor is there evidence of alcohol on the scene or from questioning the husband. The key to ruling out whether opioids are the cause of this patient’s signs and symptoms is to give a challenge of naloxone and monitor for a response. As naloxone is a competitive antagonist at opioid receptors, it will cease the action of opioids in the patient’s system and her signs and symptoms will improve. If the patient does not respond to naloxone, then other drugs or causes for her symptoms must be considered.

DIF F ERENT IA L DIA GNOSIS Opioid overdose Or • Other drug overdose • Hypoglycaemia • Hypoxia • Head injury • CVA • Sepsis

Hypoglycaemia Hypoglycaemic patients can present in a similar way to patients with an opioid overdose (see Ch 12). A simple BGL check will allow the paramedic to either detect and correct or rule it out. A BGL should always be recorded for patients with an altered conscious state. Hypoxia Hypoxia (see Ch 55) is another condition that can be readily detected and corrected with oxygen therapy. This patient is definitely hypoxic as a result of respiratory depression. Correction of airway compromise, breathing assistance and oxygen should eventually rule out if hypoxia is the underlying cause of her decreased GCS but it may take several minutes before any improvement is noted. In this case it is unlikely that reversing the hypoxia will return the conscious state to normal but it must be provided immediately to reduce ongoing harm. Head injury In this case the patient is in bed so a recent head injury or trauma seems highly unlikely. However, the signs and symptoms may be the result of an injury sustained days earlier, so careful examination and questioning of the husband regarding what the patient was doing prior to the paramedics’ arrival and in the days preceding are essential. It is important to ascertain the last time the patient was seen behaving in her normal manner. A full secondary survey should be conducted. CVA There is no way to perform a stroke assessment on this patient due to her low GCS. A quick look at the pupils will indicate whether they are equal in size and pinpoint. In severe CVA they may vary in size and may not react to light. If naloxone does not produce a response, then CVA could be an option, as patients who are less mobile and on chemotherapy have an increased risk of CVA. Sepsis Patients on chemotherapy have a high risk of sepsis and this could be a consideration in this case. Careful questioning about the patient’s condition in the days leading up to the incident may give clues. It is possible that a patient with sepsis will either have a lower than normal temperature or be febrile. This patient’s temperature is normal, as is her blood pressure—and a patient with severe sepsis resulting in a GCS of 5 would probably be hypotensive with a systolic blood pressure of 100 ms (see Fig 14.2). Sodium bicarbonate is considered an antidote for TCA overdose (Pierog et al., 2009). The mode of action may simply be the sodium load or it may change the plasma pH and affect the protein binding of the drug. 1446 hrs: The crew treat with 100 mL of sodium bicarbonate 8.4% administered IV over 3 minutes. Normal saline of 10 mL/kg is also administered. Generalised seizures are not uncommon in TCA overdose and multiple seizures are reported in up to 30% of cases, but they are usually brief. Preparation of benzodiazepines should be made up but not administered prophylactically.

EVALUAT E Evaluating the effect of any clinical management intervention can provide clues to the accuracy of the initial diagnosis. Some conditions respond rapidly to treatment so patients should be expected to improve if the diagnosis and treatment were appropriate. A failure to improve in this situation should trigger the clinician to reconsider the diagnosis. A failure to improve in patients who have overdosed is not unexpected as their condition is often complicated by the drugs ingested during the overdose attempt. The crew must now balance the complications of attempting endotracheal intubation in the field against the benefits of airway protection and control of ventilation. This will depend on the patient’s anatomy, the likely presence of other drugs, the time to hospital and the ability to control hyperventilation using noninvasive means.

Future research Studies have been conducted into intranasal and nebulised administration of naloxone in the pre-hospital setting but investigations are ongoing as there is a need to clarify the dose regimen and time of onset via these routes. Both routes could prove useful in the prehospital setting due to their safety and noninvasive nature.

Summary Overdose can be accidental or intentional and psychiatric assessment is required for all patients who intentionally overdose. Poisons information centres operate 24/7 and can be a good source of information in overdoses. Certain types of overdose have specific antidotes that can be considered in the pre-hospital setting. The main roles for the paramedic are recognition, supportive care, monitoring and managing, while ensuring transport to hospital for definitive care.

References Ali, G., Kopf, A., Breakthrough pain, the pain emergency, and incident pain (Chapter 36). In IASP Guide to Pain Management in Low-Resource Settings 2010; . Retrieved December 2012 from www.iasp-pain.org/AM/Template.cfm? Section=Home&Template=/CM/ContentDisplay.cfm&ContentID=12199 Anderson, K., Alsina, M., Bensinger, W., Biermann, S., Cohen, A., Devine, S., et al. Multiple myeloma, NCNN Guidelines Version 1. Journal of the National Cancer Comprehensive Network. 11(1), 2013. Body, R., Bartram, T., Azam, F., Mackway-Jones, K. Guidelines in Emergency Medicine Network (GEMNet): guideline for the management of tricyclic antidepressant overdose. Emergency Medicine Journal. 2011; 28:347–368. Briatburg, G., Kerr, F. Central nervous system drugs. In Cameron P., Jelinek G., Kelly A., Murray L., Brown A., eds.: Textbook of Adult Emergency Medicine, 3rd ed., Sydney: Elsevier, 2009. Bryant, B., Knights, K. Pharmacology for Health Professionals, 3rd ed. Sydney: Elsevier, 2011. Buykx, P., Dietze, P. Medication overdose, depression and their management by first responders: exploring Melbourne’s hidden epidemic. A research project funded by Beyond Blue. Retrieved December 2012 from www.beyondblue.org.au/index.aspx? link_id=6.806&tmp, 2012. Cartwright, M., Hajja, W., Al-Khatib, S., Hazeghazam, M., Sreedhar, D., Na Li, R., WongMcKinstry, E., Carlson, R. Toxigenic and metabolic causes of ketosis and ketoacidotic syndromes. Critical Care Clinics. 2012; 28:601–631. Daly, F. Drugs of abuse. In Cameron P., Jelinek G., Kelly A., Murray L., Brown A., eds.: Textbook of Adult Emergency Medicine, 3rd ed., Sydney: Elsevier, 2009. de Crespigny, C., Elliot, J., Athanasos, P. Alcohol, tobacco and other drug use. In: Curtis K., Ramsden C., Lord B., eds. Emergency and Trauma Care for Nurses and Paramedics. Sydney: Elsevier, 2011.

Delk, C., Holstege, C. P., Brady, W. J. Electrocardiographic abnormalities associated with poisoning. American Journal of Emergency Medicine. 2007; 25(6):672–687. Doyon, S. Opioids. In Tintinalli J., Stapczynski S., Ma J., Cline D., Cydulka R., Meckler G., eds.: Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7th ed., Sydney: McGrawHill, 2011. Graudins, A., Gunja, N. Antihistamine and anticholinergic poisoning. In Cameron P., Jelinek G., Kelly A., Murray L., Brown A., eds.: Textbook of Adult Emergency Medicine, 3rd ed., Sydney: Elsevier, 2009. Haber, P., Lintzeris, N., Proude, E., Lopatko, O.Guidelines for the Treatment of Alcohol Problems. Canberra: Australian Government Department of Health and Ageing, 2009. Koneru, A., Satyanarayana, S., Rizwan, S. Endogenous opioids: their physiological role and receptors. Global Journal of Pharmacology. 2009; 3(3):149–153. Lee, M., Silverman, S., Hansen, H., Patel, V., Manchikanti, L. A comprehensive review of opioid-induced hyperalgesia. Pain Physician. 2011; 14:145–161. Marx, J. A., Hockberger, R. S., Walls, R. M. Rosen’s Emergency Medicine, 8th ed. Elsevier, 2014. McCoubrie, D. Ethanol and other alcohols. In Cameron P., Jelinek G., Kelly A., Murray L., Brown A., eds.: Textbook of Adult Emergency Medicine, 3rd ed., Sydney: Elsevier, 2009. McGuire, L., Cruickshank, A., Munro, P. Alcoholic ketoacidosis. Review. Emergency Medicine Journal. 2006; 23:417–420. Mental Health, Drug and Alcohol Office. NSW Mental Health Act. Retrieved December 2012 from www0.health.nsw.gov.au/policies/ib/2007/ib2007_053.html, 2007. Monteban-Kooistra, W., van den Berg, M., Tulleken, J., Ligtenberg, J., Meertens, J., Zijlstra, J. Brugada electrocardiographic pattern elicited by cyclic antidepressants overdose. Intensive Care Medicine. 2006; 32:281–285. Murray, L., Daly, F., Little, M., Cadogan, M.Toxicology Handbook. Sydney: Elsevier, 2007. National Drug and Alcohol Research Centre. Retrieved December 2012 from

http://ndarc.med.unsw.edu.au, 2012 National Health and Medical Research Council (NHMRC) Australian Guidelines to Reduce Health Risks from Drinking Alcohol. Commonwealth of Australia, 2009. Retrieved December 2012 from www.nhmrc.gov.au/your-health/alcohol-guidelines/alcohol-faq Osborn, M., Horvath, N., Bik To, L. New drugs for multiple myeloma. Australian Prescriber. 2009; 32:95–98. Paech, M. J., Bloor, M., Schug, S. A. New formulations of fentanyl for acute pain management. Drugs Today (Barc). 2012; 48(2):119–132. Parkinson, S., Cadogan, M., Armstrong, J., Nickson, C. Toxicological emergencies. In: Curtis K., Ramsden C., Lord B., eds. Emergency and Trauma Care for Nurses and Paramedics. Sydney: Elsevier, 2011. Phillips, J. Prescription drug abuse: problem, policies, and implications. Nursing Outlook. 2013; 61(2):78–84. Pierog, J., Kane, K., Kane, B., Donovan, J., Helmick, T. Case report: tricyclic antidepressant toxicity treated with massive sodium bicarbonate. American Journal of Emergency Medicine. 2009; 27:1168.

Roxburgh, A., Burns, L. Accidental drug-induced deaths due to opioids in Australia, 2008. National Drug and Alcohol Research Centre, Sydney, 2012. Retrieved December 2012 from http://ndarc.med.unsw.edu.au/sites/ndarc.cms.med.unsw.edu.au/files/ndarc/resources/NID %20opioid%20induced%20deaths%20in%20Australia%202008.pdf Saunders, J., Aasland, O., Babor, T., de la Fuente, J., Grant, M. Development of the Alcohol Use Disorders Identification Test (AUDIT): WHO Collaborative Project on Early Detection of Persons with Harmful Alcohol Consumption II. Addiction. 1993; 88:791–804. Smith, J., Quan, D., AlcoholsTintinalli J., Stapczynski S., Ma J., Cline D., Cydulka R., Meckler G., eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 7th ed. McGraw-Hill, Sydney, 2011. Thomas, K., Malheiro, M., Barbara, M., Crouch, I., Porucznik, C. Buprenorphine prescribing practices and exposures reported to a poison centre from 2002–2011. Morbidity and Mortality Weekly Report. 61(49), 2012.

Veris-van Dieren, J., Valk, L., van Geijlswijk, I., Tjan, D., van Zanten, A. Coma with ECG abnormalities: consider tricyclic antidepressant intoxication. The Netherlands Journal of Medicine. 65(4), 2007. Vonghia, L., Leggio, L., Ferrulli, A., Bertini, M., Gasbarrini, G., Addolorato, G. Acute alcohol intoxication: a review article. European Journal of Internal Medicine. 2008; 19:561–567.

CHAP TER 15

Seizures By Alan Morrison, Pip Lyndon-James and Paul Middleton

C O N C E P TS U S E D I N TH I S C H A P TE R • The paramedic’s clinical approach: Section 2 • Perfusion: Chapter 55 • The autonomic response: Chapter 56 • The inflammatory response: Chapter 57

O V E RV IE W • Seizures are a symptom of underlying instability of neuronal cell membranes. • Seizures can represent the full extent of a disease, or develop as a result of infection, injury, cerebral ischaemia or lesions. • Partial seizures produce neurological symptoms localised to discrete regions of the brain. • Generalised seizures involve the whole brain and are associated with unconsciousness. • New seizures and changes in seizure patterns are indicative of changes in the physiological environment, or in the use or effectiveness of medications, and require investigation. • Emergency management of seizures is aimed at maintaining oxygenation and terminating the seizures, usually with benzodiazepines. • Failure to terminate a seizure with benzodiazepines requires advanced airway management and circulatory support.

Introduction A seizure is a transient alteration of brain function due to uncontrolled depolarisation of cerebral neurons (Huff & Fountain, 2011). Clinical signs may include alterations to sensation, movement, awareness or consciousness, behaviour and perception. Depending on the location of the seizure in the brain, seizures can produce clearly observable neurological symptoms, but in some cases the presentation can be subtle and may be missed by both the patient and observers. The spectrum of seizure presentation extends from collapse with tonic–clonic movements (sometimes referred to as convulsions or fits) through to involuntary twitching of a particular muscle group while retaining full consciousness, to absences and visual disturbances. In general, seizure activity can occur in any individual in whom the normal neuronal depolarisation threshold is altered, but this usually requires either disease or injury to be present. Seizures are generally self-resolving but some generalised seizures need intervention in the community setting; the use of benzodiazepines by paramedics has been shown to be safe and effective. In some instances a seizure may not resolve either spontaneously or with treatment and the condition is described as status epilepticus. In this case a seizure may represent a life-threatening emergency requiring further intervention that may not be available in the pre-hospital setting. Epilepsy is a condition encompassing a broad range of seizure disorders and is diagnosed in patients suffering recurrent seizures (Huff & Fountain, 2011). Epilepsy is one of the most common serious neurological dysfunctions (see Box 15.1). The incidence peaks in childhood, falls in the teenage age group and increases again in the over-60s. It is the third most common neurological disorder in older people after dementia and stroke (Epilepsy Australia, 2012). B O X 1 5 . 1E p i l e p s y

fac ts and fig ures

• Up to 5% of the world’s population may have a seizure at some time in their life. • Approximately 50 million people in the world have epilepsy. • The incidence in developing countries is double that in developed countries. • 70% of people gain full control over the disease • 15% of people are diagnosed with epilepsy but actually do not have the disorder. • 10% of Australians will have a seizure during their lifetime, while 3–4% will be diagnosed with epilepsy. • Epilepsy is more common in children and those over the age of 65. Source: Epilepsy Australia (2012); Joint Epilepsy Council Australia (2009).

Pathophysiology Seizure activity is the result of abnormal or uncontrolled neuronal depolarisation. Normal neuronal depolarisation occurs when positive ions (usually sodium) enter the neuron via channels in the cell membrane. These channels open (and close) according to the actions of neurotransmitters and adjacent cells, and the influx of positive sodium ions (Na+) raises the resting membrane potential to a point where a threshold potential is reached. At this point further voltage-activated sodium channels open and allow more positive sodium ions to enter the cell and complete the depolarisation process. Repolarisation is achieved when positive potassium ions (K+) leave the cell through voltage-regulated potassium channels following an ion gradient (see Fig 15.1). The ion gradient is constantly maintained through the action of the sodium potassium ATP/ADP (adenosine triphosphate/adenosine diphosphate) pump (Guyton & Hall, 2006).

FIGURE 15.1 The action potential changes in membrane potential in a local area of a neuron’s membrane result from changes in membrane permeability. RMP = resting membrane potential. Source: Patton & Thibodeau (2010). Individual neurons will depolarise once their threshold potential has been reached. A balance between excitatory neurotransmitters (allowing positive ions to enter the cell) and inhibitory neurotransmitters (allowing negative ions such as chloride to enter the cell) determines whether a neuron will depolarise. In the case of the brain it is the balance between excitatory and inhibitory that determines the level of brain function and it is closely related to consciousness (see Fig 15.2).

FIGURE 15.2 The spectrum of brain activity and consciousness. Neuronal activity is complex and subject to various mechanisms that control the level of electrical activation. These mechanisms can act inside the cell, between the cells, in neighbouring cells or in the extracellular space. The neurotransmitter glutamate is the primary extracellular excitatory mechanism, while GABA is an inhibitory neurotransmitter that makes the cell interior more negative and less likely to reach threshold potential and depolarise. Both are intrinsically linked to seizure generation. Source: Adapted from CC-BY, Arseny Khakhalin, http://khakhalin.blogspot.com.au/2012/08/excitationinhibition-balance.html. There are many neurotransmitters involved in the signalling and regulation of neuronal function, including acetylcholine, noradrenaline, dopamine, serotonin, histamine and various amino acids such as glutamate and gamma-aminobutyric acid (GABA). While most of these are excitatory, an important neurotransmitter responsible for inhibition is GABA, which binds to GABAA receptors allowing movement of chloride ions into the cell. This is an inhibitory process because it results in a decrease of the membrane potential, away from the threshold potential, preventing depolarisation. Increased release of excitatory neurotransmitters or decreased availability of GABA is associated with seizure activity, whereas increased GABA activity may result in sedation or coma. In the context of seizures, GABA chloride channels are important in the termination of seizure activity with benzodiazepines, which bind to the GABA chloride channel at a separate site, allowing negative chloride irons into the cell and lowering the resting membrane potential (Guyton & Hall, 2006). Disruption to neuronal excitation-inhibition equilibrium or to normal ion homeostasis gives rise to a seizure if the resting membrane potential is too close to the threshold potential (see Table 15.1). Discharge of this neuron recruits surrounding susceptible neurons. In focal seizures the discharge is limited to a specific area, but in generalised seizures this discharge continues to spread across both hemispheres and subcortical structures such as the basal ganglia, thalamus and brainstem. Involvement of subcortical

structures is responsible for alterations of consciousness. Disruption of neuronal excitationinhibition equilibrium can occur as a result of changes to ions, neuronal cell receptors, neurotransmitters, cell networks or whole brain regions, with ictogenic (seizure-causing) neurons particularly susceptible to the effects of hypoxia, hypoglycaemia, hyperthermia, hyponatraemia and sensory stimulation (Guyton & Hall, 2006). Seizures are generally selflimiting due to the loss of synchronous discharge and the impact of synaptic transmission fatigue, which occurs as excitatory neurotransmitters’ supplies are exhausted, allowing the inhibitory effects of GABA to prevail (Chang & Lowenstein, 2003). TABLE 15.1 Seizure generation Excitation Inward flow of sodium (+) and calcium (+) ions Triggered by glutamate Raises cell towards threshold potential Needs smaller stimulus to reach threshold

Inhibition Inward flow of chloride (−) and outward flow of potassium (+) ions Triggered by GABA Makes the cell more negative, moving it away from threshold potential Needs larger stimulus to reach threshold

Seizure activity uses large amounts of ATP, the body’s energy storage substrate, thus increasing oxygen and glucose consumption. The reflexive increase in cerebral blood flow, if accompanied by normal ventilation, will generally compensate for these changes with little lasting impact on brain function. Tachypnoea, tachycardia, hypertension and hyperglycaemia are normal clinical signs found in patients suffering seizures. In the absence of adequate ventilation, generally due to airway compromise, these people are at risk of hypoxia, hypercarbia and respiratory acidosis. Prolonged seizures can result in lactic acidosis, hyperthermia, hyperkalaemia and, rarely, rhabdomyolysis, and prolonged cerebral hypoxaemia may lead to permanent brain injury (Guyton & Hall, 2006). Status epilepticus is a medical emergency requiring prompt intervention by paramedics in the field in order to avoid permanent brain injury. Status epilepticus is technically defined by the Epilepsy Foundation (2012) as: ‘More than 30 minutes of continuous seizure activity or two or more sequential seizures without full recovery of consciousness between seizures.’ However, waiting this long to make a diagnosis can negatively impact on both morbidity and mortality. To support early recognition and intervention a seizure lasting longer than 5 minutes, or repeated seizures in the absence of an intervening lucid interval, is usually considered indicative of status epilepticus (Lowenstein, Bleck & McDonald, 1999). Excessive neuronal excitation, a failure of inhibition or a combination of the two have been suggested as reasons why a seizure does not self-terminate. Irreversible neuronal injury is thought to commence some time between 30 and 60 minutes after the start of the seizure due to excitotoxic cell injury, with further insult occurring due to the mismatch between the greatly increased metabolism of the seizing brain cell and declining blood flow and nutrient availability (Huff & Fountain, 2011).

P RACT ICE T IP • New seizures or changes in seizure pattern are significant. • Seizure is a symptom of unstable neurons. • Look for the cause of instability.

Seizure classification Ae ti ol ogy Seizures occurring as a result of an identifiable cause can be referred to as provoked, reactive, secondary or acute symptomatic seizures. They can be due to a wide variety of causes (see Table 15.2) and do not recur once the cause is removed. The cause may be static (e.g. anatomical scarring), progressive (e.g. degenerative cortical disorders) or transient (e.g. acute electrolyte derangement). TABLE 15.2 Common causes of provoked seizures

Source: Slattery & Pollack (2010). Febrile convulsions are the most common seizure type in young children. Febrile

convulsions are defined as those occurring in children aged between 6 months and 5 years with a febrile illness (Joint Epilepsy Council Australia, 2009). The peak incidence is between 18 and 24 months of age. Fever is believed to lower the seizure threshold in susceptible children, but the exact pathophysiology of this lowered threshold is unknown; it may be related to either the peak temperature or the rate of temperature rise (Joint Epilepsy Council Australia, 2009). These seizures may be categorised as simple or complex: Simple febrile seizures are generalised, last less than 15 minutes and occur no more than once in 24 hours. They represent the majority of febrile seizures and carry few risks.

Ask! • What is the patient’s history? (ask a bystander/relative) • How did the seizure start? • For how long has it been going on? • Has it happened before? • Is the patient on any regular treatment for it? • Is there a known predisposing cause?

Look for! • Airway: is it clear? • Breathing: is it adequate? What is the respiratory rate and SpO2? Is the patient cyanosed? • Circulation: is there evidence of perfusion?

Complex febrile seizures last longer than 15 minutes, occur more than once within 24 hours and may display a focal component. Generally the child will be in a post-ictal state or have returned to a normal state prior to the paramedic arriving, but if the seizure is still occurring, treatment is the same as for other seizure types. There is no evidence that active cooling has a clinical impact on the risk of further seizures. Transport to ED for a first-time febrile seizure or a complex seizure is advised for comprehensive evaluation. Identifying the source of the fever is an important consideration even though the risk of bacterial infection in these children is the same as in children who present with seizure alone (Blumstein & Friedman 2007). Derangements of metabolism such as ischaemia, hypoxia and hypoglycaemia increase the concentrations of excitatory neurotransmitters such as glutamate, leading to an increased potential for seizure activity.

Seizure type Seizures are commonly described in terms of their type based on an international classification system (see Box 15.2). The basic distinction is whether the seizure is partial or generalised:

B O X 1 5 . 2C l a s s i fi c

atio n o f c linic al seizur es

Partial seizures Simple partial seizures Motor symptoms Sensory symptoms Special sensory symptoms Autonomic symptoms Psychic symptoms

Complex partial seizures Simple partial onset followed by impaired consciousness Impairment of consciousness at onset

Partial seizure evolving into generalised seizure  

Generalised seizures Absence seizures Myoclonic seizures Clonic seizures Tonic seizures Tonic–clonic seizures Atonic seizures

Unclassifiable seizure types   Source: Huff & Fountain (2011).

• Partial seizures generally involve only one hemisphere of the brain and originate from a particular cortical area of the brain. Simple partial seizures affect one part of the brain with no impact on consciousness, whereas complex partial seizures affect more than one part of the brain and may result in impairment or clouding of consciousness. Partial seizures can progress to generalised seizures. • Generalised seizures involve both hemispheres of the brain and do not originate from one cortical area. Generalised seizures always result in an alteration to consciousness. An example of the unique electrical activity associated with each type of seizure can be seen in Figure 15.3.

FIGURE 15.3 Electroencephalograms in different types of epilepsy. Source: Hall (2010).

Management Emergency management of seizures can be assisted by a classification system based on the clinical presentation (see Fig 15.4). This system considers whether the seizure involves an impairment of consciousness, whether it was provoked and whether it is simple or complex. The key operational decision is whether the patient requires active management with benzodiazepines now or may require it imminently. All patients having a seizure for the first time and those who have an unusual seizure (in either frequency or nature) require hospital evaluation (Warden et al., 2003). Patients who are still having a generalised seizure when the ambulance arrives warrant intervention to reduce the chance of brain injury due to hypoxia.

FIGURE 15.4

Basic treatment flowchart.

P RACT ICE T IP What is the nature of the observable external signs of the seizure? • Tonic • Atonic • Tonic/clonic • Focal or other neurological presentation

CA SE ST U DY 1 Case 10994, 1006 hrs. Dispatch details: A 42-year-old male was sitting at his office desk, when his

colleague reports he heard a shrill cry and looked over to see the patient shaking violently on the floor. This lasted for 8 minutes and then the patient was unresponsive. His colleague placed him in the recovery position and called the ambulance. Initial presentation: The paramedics find the patient in a lateral position. There is evidence of urinary incontinence. He is flushed and sweaty. He is responsive to pain, but appears confused and disoriented. There is evidence of haemorrhage around the corners of his mouth and a small laceration to his tongue.

ASSESS Patient history The overt presentation of a seizure makes diagnosis less challenging than other conditions but an understanding of the history can assist in determining the probable response to treatment and whether the patient is likely to resist transport to hospital. In most cases bystanders can provide vital information in terms of: • the events leading up to the seizure • the duration and appearance of the seizure before the paramedics arrived • the patient’s personal and medical history • whether this event is similar to past events. Bystanders are the ‘eyes’ for the event and if not used to their full capacity, correct diagnosis and subsequent management can become difficult. It is important to realise that while seizures may be a familiar presentation for paramedics to manage, bystanders can be stressed by such an event and every effort should be made to take a calm and reassuring approach when asking questions. Table 15.3 provides a series of questions as a framework for systematically soliciting information from bystanders to assist in the identification of the seizure type. The responses pertaining to the opening case study are noted. In this case the paramedics also find a packet of valproate in the patient’s belongings (see Box 15.3). B O X 1 5 . 3C o

mmo n antiepileptic drug s

Patients may have their chronic epilepsy controlled with drugs whose role is to stabilise the neuron cell membrane. • Some work on sodium channels or sodium efflux: 〉 Phenytoin

〉 Lamotrigine 〉 Valproate 〉 Carbenazepam 〉 Oxcarbenazepine • Some work on GABA (or like GABA) either on the channel or on the bioavailability of GABA: 〉 Valproate 〉 Gabapentin 〉 Tiagabine 〉 Pregabalin 〉 Phenobarbitone 〉 Clonazepam 〉 Vigabatrin 〉 Topiramate Note that valproate appears in both lists.

TABLE 15.3 A framework for systematically soliciting information from bystanders

AVPU = alert, voice, pain, unresponsive.

P RACT ICE T IP Some patients experience an aura prior to a seizure. This is a subjective symptom or sensation such as a smell or taste and represents a focal fit. The aura may provide information indicating

where the generalised seizure began (Huff & Fountain, 2011).

Airway The snoring suggests obstruction: consider either a foreign substance or the patient’s tongue. Trismus (clenching of the jaw) and movement of the head and limbs can make it difficult to perform basic airway manoeuvres and the patient’s jaw should not be forced open. The airway should be managed as circumstances allow without using invasive techniques. Vomiting is not common with seizures but excessive build-up of saliva may occur.

Breathing Seizure-induced hypoxia can produce an elevated respiratory rate but spasm of the chest and abdominal muscles can concurrently reduce the patient’s tidal volume. Aspiration of stomach contents into the lungs is possible and auscultation should occur once the seizure has resolved.

Cardiovascular Seizure-induced hypoxia and the contraction of major muscles typically generate an elevated heart rate. Resolution of the acidosis caused by the seizure activity can take several minutes during which the respiratory rate and heart rate will remain elevated.

Initial assessment summary

D: The patient is now post-ictal and safe on the floor. A: The patient is in an altered conscious state and is currently exhibiting signs of a partial airway obstruction (through the snoring). B: Respiratory function is currently normal but needs frequent reassessment. The respiratory rate is elevated but ventilation is normal. C: Heart rate is normal and there is sufficient blood pressure. The patient appears to have suffered a generalised seizure that has resolved spontaneously and the patient is now presenting in a post-ictal state. The seizure is the first in several years and is not typical of previous episodes.

CONFIRM The essential part of the clinical reasoning process is to seek to confirm your initial hypothesis by finding clinical signs that should occur with your provisional diagnosis. You should also seek to challenge your diagnosis by exploring findings that do not fit your hypothesis: don’t just ignore them because they don’t fit.

What else could it be? Syncope A sudden fall in blood pressure can cause temporary cerebral hypoxia, which in turn can cause a seizure, but this tends to be short-lived and the patient tends to either recover as perfusion returns or cease to have a seizure and become flaccid if this is the start of a cardiac arrest. In this case the seizure has been sustained so syncope is unlikely (see Table 15.4). Benign causes of hypotension

are usually secondary to vasodilation from a hot environment and are common in elderly patients where their sympathetic response is not sufficient to maintain a cardiac output that supports cerebral perfusion. Hot showers, prolonged hot weather and newly prescribed drugs such as beta blockers, calcium channel blockers or ACE inhibitors are all potential causes of benign transient hypotension. More sinister causes are listed in Box 15.4. B O X 1 5 . 4S i n i s t e r

c a u se s o f h yp o te n sio n

and seizur es • Arrhythmias • Atrial fibrillation • Ventricular tachycardia • Supraventricular tachycardia • Third-degree heart block • Sepsis • Cardiogenic shock • Hypovolaemia • Acute coronary syndromes • Anaphylaxis

TABLE 15.4 Differentiation between cardiogenic syncope and generalised tonic-clonic seizure

Stroke/cerebrovascular accident A cerebrovascular accident may well present with either focal or generalised seizure activity, but it would be unlikely to leave the patient with no obvious neurological deficit once the seizure had ceased.

DIF F ERENT IA L DIA GNOSIS A seizure in the setting of long-term epilepsy Or • Syncope (neurocardiogenic, vasovagal, orthostatic, cardiac) • Stroke/cerebrovascular accident • Traumatic head injury • Migraine with aura • Movement disorder (e.g. dystonia, Parkinson’s disease) • Toxic or metabolic encephalopathy (hypoglycaemia, renal or liver dysfunction, recreational drug use) • Sleep disorders • Psychogenic

Traumatic head injury Post-traumatic seizures (PTS) are a sequel to acute brain injury, and if occurring within 24 hours of injury are termed immediate PTS, but PTS may also occur later. The incidence of PTS is 2–2.5% in the civilian population, and increases with severe head injury (GCS 40 years old) is not uncommon: it may occur in up to 10% of lifetime non-smokers (GOLD, 2010) and is often associated with gastro-oesophageal reflux disease (GORD; Bersten & Soni, 2003). Although the aetiologies are different, first-line management of acute exacerbations of both diseases in the prehospital setting is similar.

DIF F ERENT IA L DIA GNOSIS Exacerbation of COPD Or • Asthma • Congestive heart failure • Pneumonia • Pleural effusion • Pneumothorax • Pulmonary embolism • Cardiac ischaemia or arrhythmia

However, even though these two diseases may be difficult to differentiate, and initial management interventions are comparable, it is important to elicit a sound medical history and identify COPD patients, because ongoing management, particularly in relation to continuing oxygen administration and ideal SpO2 levels, may differ considerably. Congestive heart failure It can be difficult to distinguish heart failure, particularly left-sided failure, from an acute exacerbation of COPD (Shujaat et al., 2007). This difficulty is compounded as approximately one-third of heart failure patients have concurrent COPD (Hawkins et al., 2011). Both conditions are common to smokers, with the prevalence of COPD greater in patients with heart failure than the general population. The systemic inflammation associated with COPD may contribute to atherosclerosis, leading to adverse cardiac events (Hawkins et al., 2011; Le Jemtel, Padeletti & Jelic, 2007). This presents a dilemma, as the management of dyspnoea with β 2 agonists may be detrimental to patients with heart failure or myocardial ischaemia (Maak, Tabas & McClintock, 2011). Delineating between an acute exacerbation of COPD and acute heart failure requires the paramedic to be diligent and thorough in the history and physical examination. Indications that heart failure is the more likely underlying cause include: • a history of atrial fibrillation (Bersten & Soni, 2003; Wang et al., 2005) • a history of coronary artery bypass graft (CABG) surgery or ischaemic heart disease (IHD) (Bersten & Soni, 2003; Wang et al., 2005) • elevated JVP, peripheral pitting oedema • coarse breath sounds, particularly crackles above the lung bases (Shujaat et al., 2007) • atrial fibrillation and ischaemic ST-T wave changes on ECG (Wang et al., 2005) • chest pain suggestive of an acute coronary syndrome. Pneumonia The signs of dyspnoea, cough and sputum production are also common to patients with pneumonia. Differentiating between the two may be possible only with x-ray imaging. Pneumonia patients have been found to have higher fevers and a more acute onset of illness (Shujaat et al., 2007). Pleural effusion Pleural effusion may exacerbate dyspnoea in COPD. It may also be secondary to other exacerbating pathologies such as pneumonia. Auscultation may reveal decreased or absent breath sounds (Cameron et al., 2000; Shujaat et al., 2007). Pneumothorax Pneumothorax can occur in patients with COPD. Lung diseases with chronic airflow limitation, such as bronchitis and asthma, are associated with the majority of secondary spontaneous pneumothorax cases (Cameron et al., 2000). Pneumothorax should be suspected if there is a decrease in air entry to one side, although this can be difficult to identify (Shujaat et al., 2007). Pulmonary embolism Pulmonary embolism can be difficult to distinguish from an exacerbation of

COPD (GOLD, 2010). The prevalence of PE in patients with COPD who have been admitted to hospital with dyspnoea of unknown origin has been reported to be as high as 25% (Tillie-Leblond et al., 2006). Clinical factors associated with an increased risk of PE in patients with COPD are a history of thromboembolic disease, malignancy and PaCO2 decrease of ≤ 5 mmHg (Shujaat et al., 2007; Tillie-Leblond et al., 2006). The clinical history should investigate any recent onset of dyspnoea and/or chest pain, symptoms commonly associated with PE (Cameron et al., 2000). A low systolic blood pressure and a persistently low SpO2 despite adequate oxygen therapy may suggest PE (Shujaat et al., 2007). Cardiac ischaemia or arrhythmia The nature of any cardiac pain should be explored. The ECG may assist in identifying any ischaemia or arrhythmia (GOLD, 2010; Shujaat et al., 2007). This patient has obvious worsening dyspnoea beyond his normal daily variations. He has had a recent cold, a precipitant of an exacerbation and an indication of a potentially more severe episode (Hurst & Wedzicha, 2004). His elevated temperature is also suggestive of an underlying infection. His dyspnoea is still present despite treatment with his usual medications and oxygen.

HIST ORY Ask! • Do you have an asthma/COPD management plan?

Chest auscultation has revealed a wheeze, which may not respond as effectively to bronchodilators in COPD as in asthma. His oxygen saturations at 88% are on the low end of the target range for patients on home oxygen—the target range is an SpO2 between 88 and 92% (McKenzie et al., 2011). He has no cardiac history, but given that he is on home oxygen therapy, he may have underlying pulmonary hypertension and right heart failure (McKenzie et al., 2011). The ECG may also assist in identifying signs of heart failure.

How severe is the exacerbation? Clinically the patient is tachypnoeic, tachycardic and pale with an SpO2 of 88% on 3 L/min, which would indicate moderate respiratory distress (Barnes, 2009). However, he is most likely to have severe COPD, being on home oxygen therapy, where exacerbations may be life-threatening (GOLD, 2010). This may potentially lead to worsening respiratory failure, with subsequent respiratory acidosis, hypoxaemia and hypercapnia, where prognosis is poorer (McKenzie et al., 2011). There is no peripheral oedema or elevated JVP, nor are there signs of crackles consistent with heart failure on chest auscultation. He has not

described any chest pain. The severity of the exacerbation must also take account of the work of breathing, speech, accessory respiratory muscle use, retractive breathing and signs of an extreme severe exacerbation with imminent respiratory failure, fatigue and paradoxical respirations.

T REAT Emergency management Management of an acute exacerbation is directed at the symptoms, while identifying a cause of the exacerbation such as an infection, where the appropriate therapy can be initiated (Hurst & Wedzicha, 2004). In the prehospital setting this involves correcting hypoxia, treating airflow limitation (bronchospasm, inflammation) and supporting ventilation. Position The patient with an acute exacerbation of COPD will most likely adopt an upright sitting or tripod position—elbows or hands resting on knees or other surface (Cameron et al., 2000). This assists with the use of accessory muscles and the work of breathing. The patient should be encouraged into this position if not already in it. It is unlikely that hypotension will be present unless there is another cause of the exacerbation or acidosis and respiratory failure are imminent. If this is the case a recumbent position may be possible but it will most likely depend on the patient’s respiratory function. It is important to note that when transferring a patient with COPD who is in severe respiratory distress onto an ambulance stretcher, this alters the sitting position they have adopted to maximise their ventilation. The patient may experience a worsening of their condition during or after they have moved; if necessary, allow them to assume a more physiologically favourable position when feasible and safe to do so. This can include allowing them to sit with their feet off the stretcher once they are in the ambulance. Oxygen therapy The role that oxygen therapy plays differs depending on the stage and severity of COPD, and the guidelines for one aspect are often mistakenly transposed to other areas of treatment. Although oxygen is often avoided in mild episodes of COPD-related dyspnoea, it remains the cornerstone of treatment in patients with an acute exacerbation of COPD who are profoundly hypoxaemic and with increased dyspnoea. What separates oxygen therapy delivered to COPD patients compared with other patients is that it should be titrated to an appropriate SpO2 reading (GOLD, 2010; McCrory et al., 2001). In the acutely and profoundly hypoxaemic patient oxygen therapy facilitates essential metabolic reactions and prevents complications from hypoxaemia (Bersten & Soni, 2003). In an acute COPD exacerbation, oxygen therapy relieves pulmonary vasoconstriction and right heart strain. Cardiac output is improved, as is oxygen delivery to the central nervous system and other organs (McCrory

et al., 2001). It is not without potential complications, however, and needs to be used appropriately. Potentially oxygen therapy may cause a significant increase in CO2 even while it is improving arterial oxygen tension (Wedzicha, 2009). This counterintuitive effect of hypercapnia, acidosis and respiratory failure (McCrory et al., 2001) is related to an increase in morbidity and mortality (Joosten et al., 2007) and is caused by a range of factors. The physiology of the patient with COPD is altered by their normal hypercarbia and hypoxaemia. Providing them with excessive levels of oxygen can reverse the hypoxic vasoconstriction that normally restricts blood supply to poorly ventilated areas of their lungs, effectively resulting in increased dead space and decreasing CO2 elimination. COPD patients also have a diminished sensitivity to hypoxia and rely on hypercarbia to simulate their respiratory drive. These are important factors in the chronic management of the disease but are unlikely to manifest themselves as problematic in the severely hypoxaemic patient suffering an infective exacerbation. Maintaining oxygen saturation within the recommended range (SpO2 88– 92%) has been shown to reduce mortality, respiratory acidosis and hypercapnia (Austin et al., 2010). A number of studies point to the uncontrolled nature of oxygen delivery by prehospital and emergency practitioners in the belief that more oxygen is better for patients experiencing severe dyspnoea (Austin et al., 2010; Joosten et al., 2007; Wijesinghe et al., 2011). This is in spite of the evidence of worse outcomes in COPD patients. Delivery is preferably by nasal cannula at 2–4 L/minute. However, the administration of bronchodilators in the prehospital setting may require the use of an oxygen-driven nebuliser. In these situations, when the nebuliser has delivered the therapy, treatment should revert to nasal cannula as above. If there is persistent hypoxia (SpO2 < 85%), oxygen therapy should be continued, but the patient should be monitored for signs of deterioration. Persistently low SpO2 (90% and there has been a favourable response to initial bronchodilator therapy, commence O2 therapy via a nasal cannula at 2–4 L/min. • Deteriorating after initial treatment? 〉 Look for and eliminate possible cause of deterioration.

〉 Check O2 therapy: if SpO2 is high, trial O2 at a lower concentration. 〉 Consider other causes of respiratory distress: acute pulmonary oedema, pulmonary embolism, pneumonia, pneumothorax (tension) and cardiac arrhythmia. Findings such as cardiac arrhythmias may be secondary to β 2 agonists or hypoxia. Be diligent in monitoring the patient who has cardiac disease. 〉 Check for hypotension. Determine the cause and manage according to local guidelines. 〉 Does the patient have profound airflow limitation and bronchospasm? Consider IV bronchodilators (salbutamol). There is no evidence to support their use in exacerbation of COPD and they should be reserved for patients who are in immediate life-threat. 〉 If non-invasive ventilation is available (BiPAP) and patient is still conscious and breathing, consider this. • Now unconscious? 〉 Start primary survey. 〉 Monitor for respiratory arrest, decreasing conscious state, exhaustion and fatigue. Provide assisted ventilation ± lateral chest pressure to assist with expiration. Provide a ventilation rate of 5–8 L/min with a long expiratory pause to allow for expiration and prevent worsening hyperinflation. 〉 Consider intubation. • Now pulseless? 〉 Check monitor. 〉 Not ventricular tachycardia or ventricular fibrillation? 〉 If APPV initiated and patient loses output with PEA, allow 1 minute of apnoea. 〉 If a carotid pulse is present but no BP, adrenaline and fluid should be administered according to local guidelines (adrenaline 50 mcg IV, NaCl 20 mL/kg). 〉 Commence CPR.

Hospital admission COPD is an irreversible disease with exacerbations and presentations to hospital a reflection of the deterioration of a patient’s lung function (Cameron et al., 2000). Patients in acute respiratory failure that is refractory to NIV or where NIV is contraindicated may be admitted to ICU. This decision will take into account quality of life and likely outcomes for patients who have end-stage COPD, where poor outcomes may not justify mechanical ventilation (Bersten & Soni, 2003). Antibiotics are recommended for exacerbations with clinical signs of infection, particularly purulent sputum, increased sputum amount or change in sputum colour (Bersten & Soni, 2003; GOLD, 2010; McKenzie et al., 2011; Wedzicha, 2009). Patients with a higher severity exacerbation are likely to experience a greater benefit from antibiotics than those with a milder form (McCrory et al., 2001). Additional hospital treatments include: fluid therapy, as patients can be dehydrated—or conversely diuretic therapy where cardiac impairment is evident (Hurst & Wedzicha, 2004); nutritional supplements for patients with a low body mass index; prophylaxis for DVT; and sputum clearance therapy (GOLD, 2010). There is limited clinical data available to determine the optimal hospital duration (GOLD, 2010). In general patients will be admitted for 1 or 2 days. They may be discharged from the ED, but this depends on conditions at home and support being in place (Cameron et al., 2000). The patient will be discharged when they have been clinically stable for 12–24 hours and the patient, doctor and family or carers are confident they can manage competently at home and have a full understanding of the correct use of their medications. Criteria for clinical stability include inhaled β 2 therapy is required no more frequently that every 4 hours and arterial blood gases (ABGs) have been stable for 12–24 hours. If the patient was previously ambulant, they should be able to walk across a room; and they should be able to sleep without frequently being awoken by dyspnoea. Discharge should include appropriate follow-up arrangements for outpatient or home visits, medication effectiveness, spirometry and smoking cessation therapy as required (GOLD, 2010).

Investigations In hospital, investigations are further aimed at evaluating the severity of the exacerbation and identifying alternative diagnoses and the causative nature of this episode (GOLD, 2010). Spirometric measurement may be undertaken depending on the degree of respiratory distress. An FEV1 93% on room air, but given the underlying diagnosis and dyspnoea in this case, increasing the fraction of inspired oxygen (FiO2) via a rebreather mask is recommended, especially prior to the exertion associated with being transferred to a stretcher for transport. The increase in alveolar partial pressure may offset the hypoxaemia caused by the V/Q mismatch and oxygen at 6–8 L/minute would most likely be adequate to achieve the required effect, but a higher dose may be needed. There is no evidence that continuous positive airway pressure (CPAP) is effective in PE as alveolar collapse is not widespread or significant. Similarly, endotracheal intubation should be reserved for the patient with severe hypoxaemia and an altered conscious state who has proved refractory to noninvasive oxygen therapy. Analgesia Analgesia can be useful in both reducing the patient’s anxiety (and subsequent sympathetic nervous system stimulation) and increasing their tidal volume by reducing the pain occurring with ventilation. The patient may have a small reduction in tachycardia and dyspnoea in association with a decrease in pain and any anxiolytic properties the analgesia may possess. Haemodynamic support The use of fluids and inotrope infusions to support blood pressure in patients suffering a PE is not uncommon when their perfusion is extremely poor, but it should be remembered that this does not treat the underlying cause. If the patient is extremely poorly perfused or deteriorating rapidly, local guidelines will most likely support these agents in an attempt to maintain perfusion and enable the administration of anticoagulants.

EVALUAT E Evaluating the effect of any clinical management intervention can provide clues to the accuracy of the initial diagnosis. Some conditions respond rapidly to treatment so patients should be expected to improve if the diagnosis and treatment were appropriate. A failure to improve in this situation should trigger the clinician to reconsider the diagnosis. The aim of pre-hospital management is to ensure that the patient receives the appropriate treatment in the appropriate location in as comfortable a condition as possible. Evaluation of the success of this treatment is therefore driven by evaluation of the patient’s shortness of breath and pain, and is confirmed by objective observations including respiratory rate and depth, pulse oximetry and cardiovascular observations. Maintaining adequate oxygen saturation with comfortable breathing and no cardiovascular collapse while travelling to an appropriate hospital would be seen as successful treatment.

Ongoing management The aim of ongoing management is to dissolve the clot by the use of anticoagulants. Subcutaneous low-molecular-weight heparin (LMWH) or IV unfractionated heparin is most commonly used, and therapy often continues for up to 3 months after symptoms resolve. Patients who are haemodynamically unstable are increasingly being treated with anti-thrombolytic agents, but the risk–benefit profile for this treatment is yet to be firmly established. Unstable patients who are contraindicated to receive a thrombolytic medication may receive a catheter or surgical embolectomy.

Investigations Bl ood te sts While there is no blood test that specifically diagnoses PE, a coagulation screen is usually undertaken to identify the risk factor. If the presentation is consistent with PE but the probability assessment (e.g. Wells score) suggests PE is unlikely, a D-dimer test is usually performed. D-dimer is a fibrin degradation product—a small fragment of protein present in the blood after a blood clot has been degraded by fibrinolysis: a negative result rules out PE, but because the test is not specific to PE a positive result is not definitive that PE is present. Patients with a low probability and a negative D-dimer test do not have PE, but patients with a positive D-dimer test are directed into the same diagnostic stream as those patients who scored >4 on the Wells score and will require computed tomography pulmonary angiography (CTPA; see below). Cardiac enzymes are also routinely assessed where chest pain has formed part of the presentation.

Imaging Chest x-ray is not especially sensitive to detecting PE but it is quick to perform and is often taken to exclude other pathologies while access to CTPA is being arranged. CTPA is the gold standard for PE diagnosis (Estrada-Y-Martin & Oldham, 2011) and uses computed tomography to obtain an image of the pulmonary arteries and map the extent and location of any emboli. It will also reveal other pathologies, but it may not be available in all areas and a V/Q scan (see Fig 21.4) is still considered sufficiently sensitive to exclude PE (McRae, 2010). Ultrasound of the lower limbs is routinely performed if there are symptoms of a DVT and a positive result can be sufficient to commence anticoagulant therapy if other tests are not available.

Other tests The 12-lead ECG will identify classic ECG signs indicative of PE but their absence does not exclude PE. The 12-lead ECG may also reveal ischaemic changes to the heart.

Hospital admission Duration of stay in hospital will be determined by the underlying condition, the severity and size of the pulmonary embolism and the management plan. A patient with a small PE without ongoing underlying pathology will often be treated as an outpatient, with the patient’s GP providing medication and monitoring.

Follow-up Follow-up involves assessment of anticoagulation and determination of the optimal period for anticoagulation. An uncomplicated PE may be anticoagulated for up to 3 months if there are no underlying risks to manage, but the anticoagulation period can extend for 6 months. Ongoing management is required for any underlying medical condition, such as radiotherapy or chemotherapy in the setting of metastatic disease. In the presence of defects in the clotting cascade, anticoagulation may be continued for a substantially longer period.

CA SE ST U DY 2 Case 11009, 0835 hrs. Dispatch details: A 24-year-old pregnant female complaining of a history of shortness of breath since last night. She has chest pain whenever she breathes deeply, and complains of nausea. Initial presentation: On arrival the crew are let into the patient’s house by her mother.

ASSESS 0855 hrs Primary survey: The patient is conscious and talking. 0855 hrs Chief complaint: ‘I was feeling fine until last night, when I got woken up in bed by this sudden pain in my chest. It goes all across from the left to the right, and is really bad when I breathe. I’ve had a dry cough since it came on, and I’m worried about my baby because I’m 35 weeks pregnant.’ 0857 hrs Vital signs survey: Perfusion status: HR 118 BPM; sinus tachycardia; BP 90/50 mmHg; skin pale, warm centrally and cool peripherally; capillary refill of 4 seconds; ECG demonstrates sinus tachycardia with S waves in lead I and inverted T waves in lead III. Respiratory status: Anxious, RR 35 BPM, clear air entry, L = R, slightly increased work of breathing, speaking in 2–3 word phrases, SpO2 85% on room air. Conscious state: GCS = 15.

0903 hrs Pertinent hx: The patient is normally well and takes no medications. Her pregnancy has been normal with no complications. She has varicose veins in both legs, with some ankle swelling.

CONFIRM In many cases paramedics are presented with a collection of signs and symptoms that do not appear to describe a particular condition. A critical step in determining a treatment plan in this situation is to consider what other conditions could explain the patient’s presentation.

What else could it be? Many elements of the presentation of an acute pulmonary embolism are similar to the elements of other common diseases. It is known that specific symptoms are not in themselves diagnostically helpful as they often present in patients without acute pulmonary embolism. In this case alterations to the patient’s vital signs are clearly abnormal; in particular, the oxygen saturations are very low and must be considered severely altered. Pneumonia This patient has a short history of cough, but this came on after the chest pain and shortness of breath, which would not be expected in an infective cause. The cough is not productive of sputum and she presents with no features of infection such as high temperature, rigors or coryzal (cold) symptoms. Given the severity of the pain and alterations to her vital signs, this diagnosis does not correlate with her symptoms.

U SING T HE MNEMONIC DENT Define: • What is the patient’s main presenting problem? Explore: • What else could it be? 〉 Pneumonia/bronchitis 〉 Pneumothorax 〉 Pericarditis 〉 Acute coronary syndrome/acute myocardial infarction Narrow: • Is this pulmonary embolism? • Does it fit the definition?

Pneumothorax The onset of pneumothorax may be similar to PE, with a sudden onset of

pleuritic pain and dyspnoea: there is no way to diagnose this or, perhaps more importantly, to rule it out in the pre-hospital setting. The signs of pneumothorax are similar, with tachypnoea, tachycardia and dyspnoea predominating, and patients are often not clearly hypoxic until a pneumothorax is very large. Examination findings may include decreased breath sounds, but subtle differences between left and right lungs are difficult to appreciate outside hospital, and detecting hyperresonance is not a typical paramedic skill. This patient’s vital signs are so altered that if a pneumothorax were present it would have to be very large or progressing to a tension pneumothorax (see Ch 20). In this circumstance the diagnosis should be more obvious, but even if the diagnosis of a tension pneumothorax is discarded here it should be regularly revisited to see if it has become clear. Pericarditis Inflammation of the pericardial sac around the heart can cause some of the above symptoms (pain, tachycardia) but it does not explain the dyspnoea or the altered oxygen saturations. Pericarditis also produces a typical ECG pattern with PR segment depression and global concave ST segment elevation. This anatomically inconsistent ST elevation often helps to differentiate pericarditis from acute myocardial infarction. In this case the ECG is actually typical of PE (see Box 21.2). Acute coronary syndrome/acute myocardial infarction ACS can present with pleuritic-type pain and with early ECGs lacking sensitivity for AMI, this will be a difficult diagnosis to exclude entirely. Even though this patient is not especially high risk for ACS, treating with anticoagulants (aspirin, clopidogrel) and pain relief as per local guidelines would be prudent and would not harm the patient. The administration of nitrates is precluded due to the patient’s poor perfusion. Typical of a PE presentation there is nothing definitive in this case on which to make a diagnosis: PE is simply the ‘best fit’ and is consistent with the patient’s presentation. A risk assessment for PE is also positive (pregnancy), the ECG is consistent with PE, but the ankle swelling is bilateral and could be considered a side effect of the pregnancy. Even so, her Wells score is greater than 4.

T REAT This patient is pregnant, so her blood pressure is expected to be slightly lower than in a non-pregnant patient due to normal hormone-induced vasodilation. Some local guidelines recommend fluid administration in the setting of tachycardia regardless of blood pressure. In this case the patient’s symptoms should be viewed in the context of the diagnosis: she is both hypoxic and poorly perfused. The obstruction in her lung is significant and her body is not able to compensate completely for the alteration: her BP is low despite the tachycardia and her oxygen saturations are poor despite the tachypnoea. A small amount of IV fluid may assist in

improving her blood pressure but it will not resolve the underlying problems, so transport should not be delayed in order to administer it. A number of guidelines correctly recommend the administration of inotropes to poorly perfused patients who have not responded to fluid, but inotropes can disproportionately restrict fetal blood supply. While this patient’s perfusion is poor, it is not critical and such an aggressive measure would not be recommended without consultation with the receiving hospital. 0905 hrs: The patient is administered supplemental oxygen in an attempt to restore her oxygen saturations above 94%. This is effective, with the SpO2 rising to 97% on a non-rebreather mask at 8 L/min. The respiratory rate remains unchanged. 0906 hrs: IV access is gained, suitable for analgesia and fluid administration. 0909 hrs: 250 mL of crystalloid fluid is administered to observe any change in the blood pressure, tachycardia and peripheral perfusion while the patient is prepared for transport.

EVALUAT E Evaluating the effect of any clinical management intervention can provide clues to the accuracy of the initial diagnosis. Some conditions respond rapidly to treatment so patients should be expected to improve if the diagnosis and treatment were appropriate. A failure to improve in this situation should trigger the clinician to reconsider the diagnosis. IV analgesia has reduced the patient’s pain but the fluid has had no effect. The dyspnoea has been only marginally relieved and there is slight but significant change in the pulse oximetry. This lack of dramatic improvement is not unexpected as the volume of fluid given probably won’t be sufficient to overcome the obstruction created by the embolus. Fluid alone will rarely resolve poor perfusion secondary to a PE and a lack of further deterioration is an acceptable outcome. Adding an inotrope such as adrenaline would be the next line of therapy if perfusion worsened. The improvements in dyspnoea and oxygen saturation are a positive sign and indicate that there is no need to consider endotracheal intubation at this stage. Perfusion status: HR 114; sinus tachycardia; BP 90/50 mmHg; skin pale, warm centrally and cool peripherally; capillary refill of 4 seconds; ECG demonstrates sinus tachycardia with S waves in lead I and inverted T waves in lead III. Respiratory status: anxious, RR 35, clear air entry, L = R, increased work of breathing, speaking in 2–3 word phrases, SpO2 97% on oxygen at 8 L/min. Conscious state: GCS = 15. A further 250 mL of crystalloid fluid challenge is administered en route to hospital. The patient remains stable and unchanged.

Research A review in 2008 ( Jimenez & Yusen) described a number of prognostic prediction rules for PE and showed that rules such as the Pulmonary Embolism Severity Index and the more conservative Home Management Exclusion Criteria could identify patients with acute symptomatic PE who were at low risk of fatal or nonfatal adverse outcomes. It suggested that clinicians should incorporate such predictive models into treatment algorithms for patients with acute symptomatic PE diagnosed in the ED. The utility of these tools is yet to be validated in the pre-hospital setting. A more recent study (Zondag et al., 2012) compared the performance of two clinical decision rules—the Hestia criteria and the simplified Pulmonary Embolism Severity Index (sPESI)—to select patients with acute PE for outpatient treatment. It concluded that although both rules classified different patients as eligible for outpatient treatment, with similar low risks for 30-day mortality, they could both select patients at low and high risk.

Summary Pulmonary embolism is a potentially fatal disease that often presents in the community setting but is characterised by a set of nonspecific symptoms, which makes diagnosis difficult. The unintuitive combination of respiratory distress despite normal ventilation and lack of abnormal lung sounds is a strong clue that PE may be present. The inclusion of a risk assessment and probability assessment score can guide the diagnostic process. Prehospital management is relatively simple and involves appropriate assessment, positioning and administration of oxygen and analgesia. Sometimes, however, the PE will be severe enough to cause marked respiratory distress, impaired cardiac return and shock, which should prompt an increase in the urgency of transport.

References American Heart Association (AHA). Guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. International Consensus on Science. Circulation. 2000; 102(8):237. Carroll, R. G. Elsevier ’s Integrated Physiology, 1st ed. St Louis: Mosby, 2007. Cross, S. S. Underwood’s Pathology: A Clinical Approach, 6th ed. Edinburgh: Churchill Livingstone, 2013. Estrada-Y-Martin, R., Oldham, S. CTPA as the gold standard for the diagnosis of pulmonary embolism. International Journal of Computer Assisted Radiology and Surgery. 2011; 6(4):557–563. Jiménez, D., Yusen, R. D. Prognostic models for selecting patients with acute pulmonary embolism for initial outpatient therapy. Current Opinion in Pulmonary Medicine. 2008; 14(5):414–421. Klatt, E. C. Robbins and Cotran Atlas of Pathology, 3rd ed. Philadelphia: Saunders, 2015. Kuipers, S., Cannegieter, S. C., Middeldorp, S., et al. The absolute risk of venous thrombosis after air travel: a cohort study of 8755 employees of international organisations. PLOS Med. 2007; 4:e290. Lee, C., Hankey, G., Ho, W., Eikelboom, J. Venous thromboembolism: diagnosis and management of pulmonary embolism. Medical Journal of Australia. 2005; 182(11):569–574. McCance, K., Huether, S. Pathophysiology: The Biologic Basis for Disease in Adults and Children, 6th ed. St Louis: Mosby, 2010. McRae, S. Pulmonary embolism. Australian Family Physician. 2010; 39(7):462–466. Næss, I. A., Christiansen, S. C., Romundstad, P., Cannegieter, S. C., Rosendaal, F. R., Hammerstrøm, J. Incidence and mortality of venous thrombosis: a population–based study. Journal of Thrombosis and Haemostasis. 2007; 5:692–699. Nordenholz, K., Ryan, J., Atwood, B., Heard, K. Pulmonary embolism risk stratification: pulse oximetry and pulmonary embolism severity index. Journal of Emergency Medicine. 2011; 40(1):95–102.

Ouellette, D., Setnik, G., Beeson, M. S., Garg, K., Amorosa, J., Kamangar, N., Sutherland, S., Harrington, A., Tino, G., Talavera, F., O’Connor, R., Lin, E., Mosenifar, Z., Stern, E., Pulmonary embolism. eMedicine 2012; . Accessed 12 November 2012 from http://emedicine.medscape.com/article/300901-overview Stein, P., Terrin, M., Hales, C., Palevsky, H., Saltzman, H., Thompson, B., Weg, J. Clinical, laboratory, roentgenographic and electrocardiographic findings in patients with acute pulmonary embolism and no pre-existing cardiac or pulmonary disease. Chest. 1991; 100:598–603. Wells, P., Anderson, D., Rodger, M., Stiell, I., Dreyer, J., Barnes, D., Forgie, M., Kovacs, G., Ward, J., Kovacs, M. Excluding pulmonary embolism at the bedside without diagnostic imaging: management of patients with suspected pulmonary embolism presenting to the emergency department by using a simple clinical model and D-dimer. Annals of Internal Medicine. 2001; 135:98–107. Zondag, W., den Exter, P. L., Crobach, M. J., Dolsma, A., Donker, M. L., Eijsvogel, M., Faber, L. M., Hofstee, H. M., Kaasjager, K. A., Kruip, M. J., Labots, G., Melissant, C. F., Sikkens, M. S., Huisman, M. V., on behalf of The Hestia Study Investigators. Comparison of two methods for selection of out of hospital treatment in patients with acute pulmonary embolism. Journal of Thrombosis and Haemostasis. 109(1), 2012.

CHAP TER 22

Pleural effusion By Phillipa Gent, David Anderson, Jason Bendall and Paul Middleton

C O N C E P TS U S E D I N TH I S C H A P TE R • The paramedic’s clinical approach: Section 2 • Perfusion: Chapter 55 • The autonomic response: Chapter 56 • The inflammatory response: Chapter 57

O V E RV IE W • Pleural effusion is not a disease entity by itself, but is usually a complication of another underlying condition. • The parietal pleura is responsible for the formation and reabsorption of pleural fluid. • For an effusion to form there is usually an increase in the formation of pleural fluid and a concurrent decrease in reabsorption. • The ability of patients to compensate for the effects of an effusion by increasing their respiratory rate can make the onset appear sudden when in fact it has been insidious and occurring over days or weeks. • Hypoxaemia occurs frequently, but hypotension is less common. • Pleural effusion is difficult to diagnose conclusively in the field but needs to be considered in order for paramedics to make appropriate management decisions. • The underlying condition may be terminal and will need to be considered when making decisions regarding treatment and transport.

Introduction The paramedic assessment and management of dyspnoea is almost entirely focused on acute causes. The sudden onset of shortness of breath from asthma, acute pulmonary oedema (APO) or acute infections generally defines the scope of respiratory pathologies that paramedics are equipped to detect and treat. As detailed in Chapters 20 and 21, however, there are a number of disease processes that can cause relatively acute dyspnoea but lack the abnormal chest sounds that usually guide paramedic treatment. While immediate paramedic treatment of this group of conditions can be limited, the ability to accurately diagnose their presence will avoid patients receiving unnecessary (and ineffective) treatments and direct patients to appropriate resources. A pleural effusion is a pathological accumulation of fluid between the visceral pleura and the parietal pleura (see Fig 22.1). The condition is capable of disrupting pulmonary function and causing shortness of breath, but most commonly it is a symptom of another underlying disease that may be pulmonary, pleural or extrapulmonary (Maskell & Butland, 2003).

FIGURE 22.1 The anatomy of the pleura. The parietal pleura lines the thoracic cavity and forms a physical boundary between the mediastinum and the lungs. It is connected to the ribs and intercostal muscle by the endothoracic fascia and continues across the surface of the diaphragm. The visceral pleura covers the external surface of the lungs and invaginates into each of the lobes. Source: Patton & Thibodeau (2013).

Pathophysiology As discussed in Chapter 20, there is a space between the external surface of the lungs and the internal surface of the chest wall. This space is always under ‘tension’ as the elasticity of the lungs pulls inwards while the structures of the chest wall try to expand. If a disruption occurs to either the wall of the chest or the lung, air and/or blood can be drawn into the negative pressure of this space and allow the lung to collapse away from the chest wall. In the healthy individual neither air nor blood has access to the pleural space and the equilibrium that exists between the lungs and the chest wall is often referred to as a ‘potential’ space. In reality, the space actually exists and is filled with between 10 and 50 mL of pleural fluid (Shuey, 2005). The fluid acts as a lubricant to allow the lungs and chest wall to glide past each other during ventilation (up to 25,000 km covered in a lifetime) and although small in volume the fluid is in a constant process of formation and absorption. Pleural fluid enters the pleural space at a rate of about 0.01 mL/kg per hour (Shuey, 2005) and the parietal pleura is responsible for almost all of the fluid movement into and out of the pleural space (Sahn, 1990; see Fig 22.2). The fluid forms from the normal movement of fluid across the capillary walls. Under hydrostatic pressure, fluid escapes from the capillaries that line the parietal pleura and is drawn into the negative pressure that is present in the pleural space. In normal circumstances, the fluid does not accumulate because it is reabsorbed through small openings in the partial pleura (stomata) that connect the pleural space to the network of lymphatic vessels that drain back into the systemic circulation.

FIGURE 22.2 Fluid movement in the pleural space. Hydrostatic pressure within the parietal pleura capillaries forces protein-free fluid into the space at about the rate of 0.01 mL/kg per hour. Small openings in the pleura on the costal, diaphragmatic and mediastinal portions reabsorb the fluid, keeping the volume constant. Source: Cardoso (2012). CC BY 3.0 license.

Mechanism of pleural effusions This cycle of filtration and reabsorption reveals the process behind the most common causes of fluid accumulation in the pleural space: either an increase in the rate of filtration or a decrease in reabsorption (or both). An increase in the hydrostatic pressure of the parietal capillaries will force more fluid across the capillary membrane. Pulmonary hypertension is a common cause, in particular pulmonary hypertension (PH) with isolated right heart failure (Brixey & Light, 2011).

Other causes of pulmonary hypertension that regularly cause pleural effusions are connective tissue disorders such as pulmonary fibrosis and liver disease. A decrease in the oncotic pressure within the capillaries will allow fluid to escape at a greater rate than normal from the parietal capillaries, so any disease that leads to a reduction in plasma proteins may result in pleural fluid accumulation as there is less opposition to hydrostatic pressures. A reduction in plasma proteins is commonly seen in patients with severe malnutrition or liver failure, often due to cirrhosis, leading to inadequate protein production. It is also observed in patients with conditions such as nephritic syndrome, where excessive excretion of protein molecules is seen in urine (proteinuria). Patients with pleural effusions secondary to hypoalbuminaemia commonly have evidence of fluid collections in other extracellular compartments such as abdominal ascites and peripheral oedema. The final mechanism by which the rate of fluid movement into the pleural space can increase is due to damage to the capillary wall. Injury and inflammation can both increase the permeability of the capillary wall, allowing increased rates of fluid movement. Of particular concern is that the capillary membrane can become so porous that proteins can escape the intravascular space and accumulate in the pleural fluid. This creates an oncotic pressure within the pleural fluid that attracts more fluid into the space by osmosis. An isolated increase in the rate that fluid enters the space is unlikely to cause the sudden development of a pleural effusion as the system of lymphatic drainage has a significant excess capacity to remove fluid from the space. It is worth noting that an isolated reduction in fluid absorption due to fibrosis or tumours in the lymphatic system is not sufficient to cause the sudden development of an effusion. For example, a normal fluid entry rate of 0.01 mL/kg per hour would generate a total of nearly 15 mL/day in a 60kg woman; at this rate of entry (without any exit of fluid) it would take more than a month for 500 mL to accumulate in the pleural space. In most cases an effusion develops because there is a change to both filtration and absorption that favours accumulation.

Categorisation of pleural effusions Pleural effusions may be categorised into two broad groups based on the type of fluid that accumulates (see Table 22.1). These types of fluid are known as either exudates or transudates, and are defined by the concentration of protein in the fluid.

TABLE 22.1 Mechanisms of pleural fluid accumulation Type of fluid/effusion Transudate (hydrothorax): clear fluid in the pleural space

Source of accumulation

Primary or associated disorder

Watery fluid that diffuses out of capillaries beneath the pleura (i.e. capillaries in the lungs or chest wall)

Cardiovascular disease that causes high pulmonary capillary pressures; liver or kidney disease that disrupts plasma protein production, causing hypoproteinaemia (decreased oncotic pressure in the blood vessels) Exudate: highly Fluid rich in cells and Infection, inflammation or malignancy of proteinproteins (leucocytes, the pleura that stimulates mast cells to concentrated fluid plasma proteins of all release biochemical mediators that increase in the pleural kinds) that migrates out of capillary permeability space the capillaries Empyema: pus in Debris of infection Pulmonary infections, such as pneumonia; the pleural space (microorganisms, lung abscesses; infected wounds leucocytes, cellular debris) dumped into the pleural space by blocked lymphatic vessels Haemothorax: Haemorrhage into the Traumatic injury, surgery, rupture or blood in the pleural space malignancy that damages blood vessels pleural space Chylothorax Chyle that is dumped by Traumatic injury, infection or disorder that (chyle): collection lymphatic vessels into the disrupts lymphatic transport of fluid-containing pleural space instead of lymph and fat passing from the droplets in the gastrointestinal tract to the pleural space thoracic duct Source: Craft, Gordon & Tiziani (2011). The fluid that normally enters the pleural spaces is very low in protein as these molecules are too large to cross the capillary membrane. Effusions where the pleural fluid protein levels resemble normal pleural fluid are described as transudate effusions. This indicates the capillaries are normal but the flow rates into or out of the space are affected. When the fluid that comprises a pleural effusion has a high protein concentration it is termed an exudate and is usually the result of a breakdown in the normal vascular mechanisms that retain protein in the capillaries. Exudative pleural effusions usually contain high concentrations of white blood cells and are normally the result of an inflammatory process involving the pleura or the lungs. They are often seen in patients with pneumonia, malignancies or a pre-existing pulmonary embolism (see Box 22.1).

B O X 2 2 . 1C o

m m o n c auses o f pleur al eff usio n

Exudate (high protein) • Pneumonia • Malignancy • Tuberculosis • Heart surgery • Pulmonary embolism (can be exudate or transudate)

Transudate (low protein) • Chronic heart failure • Liver failure • Renal failure

Pleural effusions caused by a tumour within the pleural space or associated with any tumour that impairs fluid distribution in the pleural cavity are almost always exudative (Shuey, 2005). Leading causes of malignant pleural effusions are leukaemia, lymphoma, lung or breast cancer (Shuey, 2005). A mesothelioma is a rare tumour that occurs near the surface of the lung and affects the pleura, commonly resulting in a pleural effusion. This type of cancer is often associated with asbestos exposure. Less commonly are pleural effusions characterised by the presence of pus (empyema), blood (haemothorax) or chyle (chylothorax).

Presentation Regardless of the type of effusion, the direct respiratory consequences of the effusion are shared. The fluid allows a portion of the lung to move away from the chest wall. The portion is unlikely to ventilate normally and the impact on gas transport is directly proportional to the volume of fluid in the pleural space. Small pleural effusions tend not to cause dyspnoea at rest because the portion of the lung that is affected does not lead to alterations in the amount of oxygen and carbon dioxide in the blood. The physiological effect of the effusion may manifest, however, when the patient attempts physical activity and the limitations on ventilation imposed by the pleural effusion become more apparent. Very large pleural effusions that continue to accumulate can act like a tension pneumothorax and lead to a mediastinal shift away from the side where the effusion started. These effusions typically have a significant impact on both ventilation and perfusion and can consequently impair both cardiac function and venous return. The lower limit of the pleura is at the 10th intercostal space posteriorly but it is much higher anteriorly, extending only to the 6th intercostal space. This means fluid will tend to accumulate posterior to the lung until there is a significant volume. This is significant when trying to detect an effusion on x-ray but also during auscultation and percussion of the lungs.

CA SE ST U DY 1 Case 12048, 1242 hrs. Dispatch details: A 61-year-old female with severe respiratory distress. Initial presentation: On arrival, the paramedics find the patient with her husband in attendance. She is seated on a kitchen chair and is clearly dyspnoeic and anxious.

ASSESS Patient history The absence of adventitious sounds and a previously diagnosed respiratory history can present paramedics with a significant clinical reasoning challenge when confronted with the dyspnoeic patient. While the lack of abnormal sounds doesn’t provide an early hypothesis to test, it does place more emphasis on gaining an accurate history to develop a differential diagnosis. Questions regarding when the symptoms commenced, whether they appeared gradually or suddenly, whether they were associated with an activity (cough, exercise, etc), any pain and other symptoms all become especially important in building a clinical picture. Pleural effusions are usually manifestations of an underlying medical condition, so obtaining an accurate history of conditions that have the potential to alter fluid distribution in the pleural space should be explored if an effusion is one of the differential diagnoses. Specifically, any history of malignancy, excessive alcohol intake or liver disease should be elicited, along with medication use and occupation, as malignant pleural effusions may occur distant from the primary site years after the original disease. In this case the patient states she is postmenopausal and has no medical history or allergies. She and her husband have spent the last week away on an interstate holiday. She says that she felt well initially but noticed a dry cough during the week and thought she might be getting a chest infection. She did not have any other symptoms of an upper respiratory tract infection but did notice she was lacking her ‘normal energy’. She felt a little short of breath (SOB)

on the one-hour flight home this morning but passed it off as a lack of air on the flight, but over the past 4 hours has become increasingly short of breath. She denies any pain, nausea, palpations or other symptoms.

HIST ORY Ask! • Do you have any past medical history? • When did the shortness of breath start? • Did it start suddenly or gradually get worse? • What were you doing when you first noticed it? • Is it getting worse, remaining constant of improving?

RE SP I RAT ORY A SSE SSM E NT Look for! • Tachypnoea • Decreased oxygen saturations • Decreased air entry on auscultation (see Box 22.2) B O X 2 2 . 2S k i l l s :

ausc ultatio n and

per c ussio n Auscultation Learning the subtleties of chest auscultation is a difficult skill to acquire and often is not suited to the noisy prehospital environment. Nonetheless, it is an essential diagnostic skill that guides diagnosis in the dyspnoeic patient more than any other tool. The common description of a pleural effusion is of decreased breath sounds in the lower regions of the lungs if the patient is sitting upright. Because the pleura extend further posteriorly, the changes should occur there first. The vesicular breath sounds are decreased over the area of the perfusion since the ventilation to that hemithorax is decreased. But fluid is a good conductor of sound, so bronchial breathing can often be heard over the effusion. The key message is that volume and nature are both important.

When auscultating a patient’s chest, the patient should be in a sitting position where possible, which will help the paramedic to recognise the level on the chest wall where the reduction in breath sounds occurs. It is very important when examining a patient’s chest to expose the chest and back rather than just opening their clothing to provide some access, as clinical signs over the lower areas of the chest are frequently missed in this situation, particularly those gravity-dependent pathologies such as pleural effusion. Maintaining the patient’s dignity during this process can be difficult, but asking for privacy can assist.

Percussion Percussion is not commonly practised by paramedics despite how sensitive it can be to conditions such as an effusion. By tapping on the chest wall percussion produces vibrations and the presence of air in the lungs of a normal chest will produce a resonant note on percussion, just like tapping a drum. In contrast, a dull sound is heard when the lung tissue is filled with fluid or a solid mass (like tapping on stone). In an effusion the affected area is dull and flat to percussion. In an erect position the paramedic should hear the change in note from a normal, resonant percussion note in the upper chest (above the effusion) to a stony dull percussion note in the lower chest (over the effusion). If a large effusion has occurred the entire hemithorax may be filled with fluid, revealing a dull percussion note over the entire side of the chest with the effusion. Percussion should be performed on the back of the chest in similar positions to auscultation. • Dullness on percussion (see Box 22.2) • Increased respiratory rate and effort • Signs of infection • Dullness to percussion and decreased breath sounds • Evidence of other pathology (malignancy, failure etc)

Airway As the fluid accumulates between the lungs and the chest wall, pleural effusions do not usually compromise the airway. The presence of upper airway noises is suggestive of other disease processes.

Breathing The patient may present with an increased respiratory rate and minute volume in an attempt to normalise their blood gases; this is exacerbated as the size of

the effusion increases. In severe cases the fluid can affect ventilatory workload and unequal excursion of the chest wall and the use of accessory muscles may be apparent.

Cardiovascular In this patient’s case the tachycardia is consistent with the degree of hypoxaemia and her blood pressure is well within normal limits. Her ECG reveals only a sinus tachycardia.

Initial assessment summary Problem Mild SOB for 5 days, severe SOB for 4-5 hours Conscious state GCS = 15 Position Sitting Heart rate 110 BPM Blood pressure 120/70 mmHg Skin appearance Pale, warm, dry Speech pattern Speaks in phrases Respiratory rate 28 BPM Respiratory rhythm Even cycles Respiratory effort Slightly increased Chest auscultation Decreased breath sounds on the lower right side Pulse oximetry 91% on room air Temperature 37.0°C D: The there is no danger to the crew or patient. A: The patient is conscious with no airway obstruction, B: Respiratory function is elevated but there are no adventitious sounds. Tidal volume is normal. C: Heart rate is elevated; blood pressure is within normal limits The patient is presenting with dyspnoea at rest after 5 days of possibly increasing exertional dyspnoea. Her tidal volume is normal but her SpO2 is 93% on room air but given the underlying diagnosis and SpO2 level in this case, increasing the fraction of inspired oxygen (FiO2) via a rebreather mask is strongly recommended. The increase in alveolar partial pressure may offset the hypoxaemia caused by the non-ventilated portion of the lungs and oxygen at 6–8 L/min would most likely be adequate to achieve the required effect, but a higher dose may be needed. There is no evidence that continuous positive airway pressure (CPAP) is effective in effusions as alveolar collapse is not widespread or significant. Similarly, endotracheal intubation should be reserved for the patient with severe hypoxaemia and an altered conscious state who has proved refractory to non-invasive oxygen therapy. Analgesia In patients with both dyspnoea and pain, analgesia can be useful in reducing anxiety (and subsequent sympathetic nervous system stimulation) and may also increase their tidal volume by reducing the pain that is occurring with ventilation. The patient may have a small reduction in the tachycardia and dyspnoea in association with a decrease in pain and any anxiolytic properties the analgesia may possess. In this case the patient has no pain so there is no need for analgesia. Haemodynamic support

The use of fluids and inotrope infusions to support blood pressure in patients suffering a PE is not uncommon when their perfusion is extremely poor, but it should be remembered that it does not treat the underlying cause. If the patient is extremely poorly perfused or deteriorating rapidly, local guidelines will most likely support these agents in an attempt to maintain perfusion and enable the administration of anticoagulants. IV access should be established in this patient in case of sudden cardiovascular deterioration (remember, pneumothorax or PE hasn’t been conclusively ruled out) but the skin and BP both suggest that she is adequately perfused and does not urgently need fluid support.

EVALUAT E Evaluating the effect of any clinical management intervention can provide clues to the accuracy of the initial diagnosis. Some conditions respond rapidly to treatment so patients should be expected to improve if the diagnosis and treatment were appropriate. A failure to improve in this situation should trigger the clinician to reconsider the diagnosis. The aim of pre-hospital management is to ensure that the patient receives the appropriate treatment in the appropriate location in as comfortable a condition as possible. Evaluation of the success of this treatment is therefore driven by evaluation of the patient’s shortness of breath and pain, and confirmed by objective observations including respiratory rate and depth, pulse oximetry and cardiovascular observations. Maintaining adequate oxygen saturation with comfortable breathing and no cardiovascular collapse while travelling to an appropriate hospital, or while consulting with an appropriate palliative care clinician, would be seen as successful treatment.

Ongoing management Ongoing management is performed in the ED and will be focused on diagnosis and management of the pleural effusion and underlying cause.

Investigations I m a gi ng Depending on the resources available, a chest x-ray or ultrasound (or both) will be used to explore the presence and extent of an effusion, as well as any other diseases (see Fig 22.3). Imaging cannot reliably differentiate exudate from transudate effusions. Computed tomography (CT) may be also performed, both to assess the size and potential choices for drainage of the effusion, and to image the potential underlying causes. A significant pleural effusion may be an incidental finding on CT scanning of the chest or abdomen.

FIGURE 22.3

Chest X-ray of a right-sided pleural effusion. Note the arrows highlighting the extent of the effusion. This angle should be sharp and this blunting is due to fluid formation. Source: Craft, Gordon & Tiziani (2011).

Blood tests Blood tests may aid in the identification of the underlying cause of a pleural effusion, but no blood test specifically diagnoses an effusion. Blood tests may indicate if an infection or malignancy is likely or if there is evidence of organ failure (e.g. hepatic/renal).

Thoracentesis Also known as a pleural tap or pleural aspiration, this involves the insertion of a needle through the chest wall (usually under ultrasound guidance) and aspiration of some of the pleural fluid for laboratory analysis. Thoracentesis is also performed to drain the pleural effusion and produces immediate relief; it is considered an excellent option for palliated patients with metastatic pleural effusions (Shuey, 2005). Nearly all patients with a malignant pleural effusion will have a reoccurrence of the effusion within 30 days of undergoing thoracentesis (Shuey, 2005).

Percutaneous thoracostomy This procedure involves the construction of an artificial opening in the chest and typically the insertion of a drain (e.g. chest tube or pigtail catheter).

Laboratory analysis of pleural fluid Laboratory analysis of pleural fluid will enable the treating doctor to decide if the effusion is an exudate or a transudate. It will also allow the doctor to determine whether there are any bacteria or malignant cells in the aspirated fluid that would help to identify the underlying cause.

Thoracoscopy Thoracoscopy is performed if the fluid analysis does not allow the treating doctor to determine the cause of the effusion. It involves the use of an endoscope to view the pleura and is almost always conclusive (Shuey, 2005).

Hospital admission Duration of admission to hospital will be determined by the underlying condition, the size of the effusion and the management plan. A simple effusion may not require drainage and the patient may return home under the care of their local GP.

Follow-up Follow-up involves repeat imaging, such as chest x-ray, and ongoing management of the underlying medical condition, such as with radiotherapy or chemotherapy in the setting of metastatic pleural effusion, or antibiotic therapy if bacterial pneumonia was the underlying cause.

CA SE ST U DY 2 Case 12049, 0830 hrs. Dispatch details: A 64-year-old male complaining of a 4-day history of shortness of breath. The patient is palliated with stage IV liver cancer. Initial presentation: On arrival the crew are greeted by the patient’s wife and led to the patient’s bedroom.

ASSESS 0843 hrs Chief complaint: ‘I’ve had increased shortness of breath over the past 4 days. It’s worse on exertion.’ 0845 hrs Primary survey: The patient is conscious but very jaundiced. 0847 hrs Vital signs survey: Perfusion status: HR 112 BPM; sinus tachycardia; BP 100/70 mmHg; skin pink, warm, dry; cool peripheries. Respiratory status: RR 34 BPM, decreased breath sounds bilaterally to both lower zones (bases), SpO2 90%. Conscious state: GCS = 15. 0850 hrs Secondary survey: On percussion there is bilateral basal dullness. The patient is jaundiced and has spider angiomas on his chest and upper abdomen. 0850 hrs Pertinent hx: The patient was palliated 6 weeks ago due to his advanced metastatic cancer; he has primary liver cancer with known lung and pancreatic metastases. ‘When did the shortness of breath start?’ ‘It started 4 days ago but has been bearable. Now I can’t even walk to the fridge without having to rest.’

‘Have you ever experienced this before?’ ‘Yes, I’ve had this before and the fluid was removed via a needle.’

CONFIRM In many cases paramedics are presented with a collection of signs and symptoms that do not appear to describe a particular condition. A critical step in determining a treatment plan in this situation is to consider what other conditions could explain the patient’s presentation.

U SING T HE MNEMONIC DENT Define: • What is the patient’s main presenting problem? Explore: • What else could it be? 〉 Pneumonia 〉 Pulmonary embolism 〉 Acute pulmonary oedema 〉 Normal progressive deterioration of his cancer Narrow: • Is this pleural effusion? • Does it fit the definition?

What else could it be? Pneumonia While there is almost certainly a bilateral effusion, which makes pneumonia less likely, this does not rule it out as a cause. A patient who is very sick and debilitated from cancer may not mount a sufficient immune response to generate the typical signs and symptoms of pneumonia, and his underlying disease process (cancer) also makes him more susceptible to infection. Pulmonary embolism Patients with cancer are at very high risk of developing pulmonary embolism due to alterations in their coagulation and to venous stasis secondary to bed rest (see Ch 21). While a pleural effusion can develop secondary to a pulmonary embolism and a pulmonary embolism may cause some of the clinical symptoms seen with this patient, such as tachypnoea, hypoxia and tachycardia, the bilateral decreased air entry is not consistent, nor is the relatively good perfusion compared with the severity of the dyspnoea. A pulmonary embolism large enough and centrally located to cause marked reduction in breath sounds bilaterally would probably cause inadequate perfusion, sudden loss of

consciousness or even death. Acute pulmonary oedema While acute pulmonary oedema would cause tachypnoea, dyspnoea, hypoxia and tachycardia, the absence of fine end inspiratory crackles on auscultation makes this differential less likely. Severe pulmonary oedema, particularly in chronic conditions, can lead to bilateral effusions and the associated poor air entry and frequent patient exhaustion mean that sometimes fine crepitations are not heard. Normal progressive deterioration of his cancer Pulmonary hypertension can cause increased pleural fluid production and this patient has a number of factors that indicate pulmonary hypertension is present. The spider angiomas certainly suggest higher than normal pressures but the liver disease is most likely the cause. Portopulmonary hypertension describes the syndrome that occurs when occlusion of the portal vein (most often by a mechanical obstruction) shunts blood from the portal circulation to the systemic circulation. This exposes the lungs to a number of unmetabolised substances that eventually lead to vascular changes in the pulmonary circuit and the development of pulmonary hypertension. It is therefore not surprising that patients with liver metastases have an increased likelihood of developing a bilateral effusion (Shuey, 2005). In some unusual cases the effusion can also develop due to ascites in the abdomen forcing fluid through the lymph system into the pleural space. The most likely diagnosis is a pleural effusion but chest radiography and blood tests will be needed to confirm this.

T REAT This patient is receiving palliative care so contact with his oncologist or palliative care team should be initiated before any conclusive decisions are made. There are two parts to the management of this patient that need to be considered. One is the pleural effusion, which is developing but reversible, and the other is his underlying condition, which is terminal. The specialist, in consultation with the patient and his family, may elect to manage the pleural effusion at home via the palliative care team. Alternatively, the specialist may recommend that the patient be taken to the nearest ED to manage the effusion. It is important to remember that while a patient is palliated, management of reversible symptoms should still be initiated to ensure that the patient is comfortable and to allow a dignified death. If the paramedics cannot contact the patient’s specialist they should transport the patient to the nearest ED to treat the reversible condition unless the patient or his family resolutely refuse and are considered capable of withholding consent. The patient should be transported in a position of comfort, ideally semi-recumbent or sitting to assist the mechanics of ventilation. 0855 hrs: The paramedics administer supplemental oxygen via a non-

rebreather mask at 8 L/min and minimise the amount of work for the patient by loading him onto the stretcher inside the house. Although the patient has decreased peripheral perfusion he has good cognitive function, so there is no need to administer fluids or inotropes at this time. Opiates could be used to decrease the patient’s anxiety, but higher-thanusual doses may be required if the patient is already on a high-dose regimen to manage his cancer pain. The paramedics decide to wait and evaluate the effect that oxygen has on reducing the patient’s hypoxia and thus his distress.

EVALUAT E Evaluating the effect of any clinical management intervention can provide clues to the accuracy of the initial diagnosis. Some conditions respond rapidly to treatment so patients should be expected to improve if the diagnosis and treatment were appropriate. A failure to improve in this situation should trigger the clinician to reconsider the diagnosis. Perfusion status: HR 112 BPM; sinus tachycardia; BP 100/70 mmHg; skin pink, warm and dry; cool peripheries. Respiratory status: RR 32 BPM, decreased breath sounds bilaterally to both lower zones (bases), SpO2 94%. Conscious state: GCS = 15. The patient appears less distressed. This lack of dramatic improvement is not unexpected as the paramedics are not able to manage the underlying problem. The improvements in dyspnoea and oxygen saturation are positive signs and indicate that there is no need to consider further interventions at this stage.

Summary Pleural effusion is a condition that paramedics will encounter occasionally, often while a patient is being evaluated for a cause of dyspnoea. Pre-hospital management of the effusion itself is relatively simple and involves appropriate assessment, positioning and administration of oxygen and analgesia. Sometimes, however, the effusion will be large enough to cause respiratory distress, tracheal deviation and impaired cardiac return, which may prompt an increase in the urgency of transport. Other emergency management may be required to manage the underlying disease that caused the effusion.

References Brixey, A. G., Light, R. W. Pleural effusions occurring with right heart failure. Current Opinions in Pulmonary Medicine. 2011; 17(4):226–231. Cardoso, P., Pathophysiology of Extravascular Water in the Pleural Cavity and in the Lung Interstitium After Lung Thoracic Surgery. Topics in Thoracic Surgery 2012; . Retrieved from http://www.intechopen.com/books/topics-in-thoracic-surgery/pathophysiology-ofextravascular-water-in-the-pleural-cavity-and-in-the-lung-interstitium-after-lung Craft, J., Gordon, C., Tiziani, A.Understanding Pathophysiology. Sydney: Elsevier, 2011. Maskell, N., Butland, R. BTS guidelines for the investigation of a unilateral pleural effusion in adults. Thorax. 2003; 58(11):ii8–ii17. Patton, K. T., Thibodeau, G. A. Anatomy & Physiology, 8th ed. St Louis: Mosby, 2013. Sahn, S. The pathophysiology of pleural effusions. Annual Review of Medicine. 1990; 41:7–13. Shuey, K. Malignant pleural effusions. Clinical Journal of Oncology Nursing. 2005; 9(5):529– 532.

CHAP TER 23

The paediatric patient with a noisy airway By Joe Acker

C O N C E P TS U S E D I N TH I S C H A P TE R • The paramedic’s clinical approach: Section 2 • Perfusion: Chapter 55 • The autonomic response: Chapter 56 • The inflammatory response: Chapter 57

O V E RV IE W • A noisy airway in the paediatric patient can potentially indicate a serious and/or life-threatening problem. • Respiratory symptoms are one of the most common reasons parents seek medical attention for their child. • Croup is a common childhood problem with a peak incidence in those aged between 1 and 3 years (Cameron et al., 2006). • Stridor is not a reliable indicator of the severity of airway obstruction. • An inhaled foreign body can present as a life-threatening emergency, but symptoms can vary; asymptomatic cases do occur. • Identifying the cause of respiratory distress in children can be particularly difficult due to their smaller anatomy as well as the inability of very young children to describe their symptoms. • A compromised but functioning airway should never be made worse by upsetting the child.

• Children with an inhaled foreign body are managed with basic care, followed by advanced life support procedures for removal of the foreign body. Emergency needle cricothyroidotomy is reserved for those who cannot be intubated or ventilated. Emergency surgical cricothyroidotomy is reserved for the older child.

Introduction A range of airway conditions are common to children. The reason these conditions are thought of as childhood conditions is generally due to the differences in airway anatomy found in children (see Fig 23.1). Other reasons include children’s immunity and susceptibility to disease (which in some cases have now been addressed by childhood vaccinations).

FIGURE 23.1 Anatomical airway differences in children. The paediatric airway is anatomically distinct from the adult airway and this makes it more prone to occlusion. The tongue is larger in proportion to the mouth, while the pharynx is smaller. The paediatric epiglottis is larger and less cartilaginous and the larynx is more anterior: together this can make it more difficult to intubate the child. Significantly, the narrowest point of the paediatric airway is at the cricoid and as such obstructions can occur below the vocal cords and out of site during laryngoscopy. Source: EMT-NationalTraining.com.

Pathophysiology A noisy airway in the paediatric patient generally indicates some degree of upper airway obstruction. The upper airway can be fully or partially obstructed by the tongue, blood or fluids, food or emesis, inhaled foreign bodies or inflamed and swollen tissues. Three of the most critical causes of a noisy airway in the paediatric patient are croup, epiglottitis and foreign body inhalation (see Table 23.1). TABLE 23.1 Characteristics of upper airway obstruction in children

Source: Gregory & Ward (2010); Cameron et al., (2006). The Australian Institute for Health and Welfare reported that in 2010 more children were vaccinated against major preventable childhood diseases, with 91% being fully vaccinated at 2 years of age—in contrast, only 82% of 5-year-olds are fully covered (AIHW, 2010).

Croup Croup, sometimes called laryngotracheobronchitis or acute viral laryngotracheitis, is an infection that affects the subglottic tissues of the upper airway in infants and children younger than 6 years of age. It is the most common form of upper airway obstruction in children under 3 years, with a peak incidence between the ages of 7 and 36 months. Interestingly, croup affects boys about 1.5 times more than girls (Cherry, 2008). Croup is most commonly caused by a viral infection with inflammation of the laryngeal area of the upper airway (De Bueck, 1995). The viruses that most commonly cause croup include parainfluenza types 1, 2 and 3, rhinovirus, enterovirus and respiratory syncytial virus (RSV). In acute croup, the patient develops oedema of the walls of the trachea, below the vocal cords. The upper airway of a small child is narrowest at the level of the cricoid ring; the inflammatory process involves the larynx and trachea and may in some cases extend to the smaller airways causing wheezing (see Fig 23.2). Swelling causes a

progressive narrowing of the airway and increasing respiratory distress (Bjornson & Johnson, 2008). The inflammation is especially dangerous in children under 3, whose airway diameters are much smaller than those of older children or adults (see Fig 23.3). A small amount of swelling can cause complete obstruction in these narrower airways.

FIGURE 23.2 Management of croup. Croup presents with varying degrees of severity. Children with mild croup characterised by no stridor or increased work of breathing at rest can be treated with oral steroids and observation by health professionals or informed carers; they do not require adrenaline or oxygen. Any child presenting with croup should undergo minimal examination and does not require throat or mouth examination. Children will assume the best position to support ventilatory efficiency and where possible they should be left in this position during assessment and treatment.

FIGURE 23.3 Progression of croup. In 85% of cases croup is caused by a virus that swells the airway. In the subglottic region of the trachea, just below the vocal cords, the airway is at its narrowest. Contributory factors include mucosal oedema and in children the mucous membrane in this region can be both softer and more vascular than in adults. Narrowing of the airway in this area causes turbulent airflow and a subsequent stridor. Source:

Craft, Gordon & Tiziani (2011). The typical presentation of croup is an acute onset of a distinctive ‘seal-like’ barking hoarse cough often associated with stridor. The patient often has a short history (12–48 hours) of upper respiratory tract infection with rhinorrhoea that the parents may describe as ‘a cold’. The respiratory symptoms will nearly always be worse at night.

Epiglottitis Epiglottitis is a rapidly progressing infection of the upper airway that in the past was primarily associated with the Haemophilus influenzae bacteria. With the introduction of routine Haemophilus influenzae immunisation the frequency of epiglottitis has changed dramatically. Epiglottitis is now much rarer in developed countries and infecting organisms tend to be other bacteria. The infection causes oedema of the epiglottis and supraglottic structures (pharynx, aryepiglottic folds and arytenoid cartilage; MD Consult, 2013b). Epiglottitis is characterised by having a very rapid onset and the cardinal features are sore throat, dysphagia and drooling in a patient who tends to be systemically unwell with a high temperature (Wood, Menzies & McIntyre, 2005). In severe cases there may be a soft expiratory noise described as a purring sound. This relatively uncommon condition typically affects children between the ages of 3 and 7 years, although it can occur at any age and is now more often seen in adults who have not been immunised. A patient with epiglottitis usually presents sitting upright, leaning forwards, tongue protruding, with their head hyperextended to aid breathing (see Fig 23.4). A key feature is that the child will be unable to swallow their saliva and will therefore be drooling. This postural position uses gravity to help draw the swollen tissues away from obstructing the airway. Typically these children will not be crying or struggling because they are focusing on maintaining their airway. It is important that the child should be allowed to maintain their own position of comfort. Furthermore, stimulation of the oropharynx by examination should be avoided until the child is in a situation where intubation or definitive surgical airway manoeuvres can be rapidly performed—in practice, this means an operating theatre or equivalent setting.

FIGURE 23.4 The classic presentation of epiglottis has the patient sitting upright with the head and neck extended and the upper body leaning forwards. These attempts to maintain the airway can include protruding the tongue. Movement and speaking are often absent as the child is

entirely focused on breathing. Source: Lissauer, Clayden & Craft (2012).

Foreign body inhalation Inhalation of a foreign body into the upper or lower airway may cause a partial or complete obstruction. Due to their inquisitive nature and inability to grind food objects (lack of molar teeth), toddlers younger than 3 years old are most at risk of foreign body inhalation. Foreign bodies may lodge at any place along the airway from the hypopharynx to the segmental bronchus (Cameron et al., 2006). Upper airway obstruction due to foreign bodies causes several deaths in Australia each year (Cameron et al., 2006). Obstruction is most often caused by food materials (peanuts, carrot, apple, hard lollies) or small objects (coins, toys, parts of balloons). Paramedics should suspect inhalation of a foreign body in all cases where a healthy child has a sudden onset of respiratory distress, coughing or stridor. A child who has inhaled a foreign body will present with an acute onset of respiratory distress or airway obstruction. The signs and symptoms of upper or lower partial airway obstruction include panic, stridor, muffled or hoarse voice, drooling (inability to swallow), pain in the throat, decreased breath sounds, wheeze and holding the hands to the throat. Incomplete airway obstruction does not always require pre-hospital intervention. Complete airway obstruction requires intervention as it will ultimately lead to respiratory and cardiac arrest if left untreated.

Management of a complete airw ay obstruction in paediatrics If the patient’s airway is completely obstructed it is recommended that five back blows and five chest thrusts be administered in conscious patients. If the patient is unconscious, they should receive the five chest compressions in the same rate and ratio as CPR. The Australian Resuscitation Council (ARC) no longer recommends abdominal thrusts due to the life-threatening complications of this procedure, especially in paediatric patients. Blind finger sweeps are never indicated in children. Always visualise the airway to remove a suspected foreign body (ARC, 2013). Direct visualisation of the pharynx and larynx can be performed with a laryngoscope if the patient is unconscious. If the foreign body is identified it can be retrieved with Magill’s forceps or a suction catheter (Cameron et al., 2006). In adults, an inhaled foreign body that passes the vocal cords is rarely immediately life-threatening because the narrowest part of the adult upper airway is the cords. In children, the narrowest part of the upper airway is just beyond the cords at the level of the cricoid ring and objects lodged here may not be removable with laryngoscopy and Magill’s forceps. Positive pressure ventilation with a bag-valve mask may be considered in an emergent situation. By providing positive pressure the pharynx is distended, which allows gas to move around the obstructing object and may free the object. Attempting to blow the obstruction down the airway using a bag and mask will not work and will simply result in gastric dilation. In a rare, life-threatening situation the paramedic may manage an obstruction below the level of the cords by pushing the object into one main bronchus with an endotracheal tube. This will allow only one lung to be ventilated, but it is much better

than a complete obstruction with no ventilation (MD Consult, 2013c). If these techniques fail, the paramedic should consider a needle cricothyroidotomy. This procedure requires the insertion of a large intravenous catheter (12–14 gauge) through the cricothyroid membrane into the trachea. The patient is then ventilated using highpressure oxygen connected to the cannula (simply cover the end of the cannula for 1 second) for a short period of time in jet insufflation: classically on for 1 second, off for 3 seconds.

CA SE ST U DY 1 Case 10064, 2332 hrs. Dispatch details: A 14-month-old child short of breath with noisy breathing. Initial presentation: The paramedics find the child sitting on his mother ’s lap wearing only a nappy. When they approach him they hear a brassy, barking cough and notice that his breathing is stridorous when he becomes more anxious.

ASSESS Patient history Determining the underlying cause of the patient’s presentation is not difficult in this case due to the presence of the classic signs and symptoms of croup. However, the paramedic must remain vigilant because other serious diseases can present with a noisy airway and respiratory distress. When assessing a child with respiratory distress it is important to make the child feel as comfortable as possible. The paramedic should take special care during assessment and treatment not to frighten or agitate the child because anxiety can substantially worsen the symptoms. Positioning the child sitting in the lap of a parent or caregiver is one way to reduce agitation. Furthermore, the paramedic should avoid being overly aggressive by using invasive treatments unless absolutely required.

HIST ORY

Ask! • What was the speed of onset of the symptoms? • Has the child had any cold-like symptoms recently? • Does the child have a cough? If so, what does it sound like? • Has the child had a fever? • Are other children in the home sick? • Are the child’s vaccinations up to date? • Does the child have asthma? • Is the child allergic to anything? • Was the child eating when the symptoms started? Was the child playing with small toys?

Airway Caution should be used when assessing a paediatric patient’s airway because an invasive inspection of the airway could potentially change a partial obstruction into a complete obstruction. In a responsive patient, listening to the air movement and observing the child’s colour and general condition are often sufficient to make a preliminary diagnosis. A clear airway is one that is free from obstruction, allows for the free movement of air, is maintainable by the patient and is therefore generally quiet. Abnormal airway sounds such as snoring (which indicates that the tongue or other tissue is obstructing the posterior pharynx), gurgling (which indicates fluid accumulation in the upper airway) or stridor (which indicates a significant narrowing of the upper airway) may require intervention such as changing the patient’s posture or encouraging the patient to cough to ensure the airway is patent. In a non-responsive, non-breathing patient the paramedic must assume that airway patency is compromised and that intervention, even if it is only positional, is required.

Breathing The goal is to assess the effectiveness of oxygenation and ventilation. This can be assessed by determining whether the patient has an acceptable respiratory rate and adequate tidal volume. If tidal volume is restricted for any reason, the patient may compensate by increasing the respiratory rate. When assessing the infant or child’s respiratory status look for signs of increased work of breathing. This can be demonstrated through postural changes, engagement of accessory muscles of ventilation and increasing the rate of ventilation. The effectiveness of their increased work of breathing can be assessed through noting their skin appearance and measuring oxygen saturations. As a general rule, an oxygen saturation value of 91–93% indicates mild hypoxaemia and a value less than 90% indicates moderate to severe hypoxaemia.

P RACT ICE T IP Children with mild upper respiratory tract infections can often present with ‘gurgling’ breathing due to an accumulation of mucus from the chest infection. Encouraging the child to cough is usually enough to clear this extraneous airway sound.

Circulation Central and peripheral circulation should be assessed for all paediatric patients to determine adequate perfusion. This can be accomplished by comparing central versus peripheral skin temperature, colour and condition. Remember that paediatric patients may initially respond to hypoxia by increasing the heart rate and reducing peripheral circulation. Profound bradycardia is an end-stage response to hypoxia.

A SSESSMENT Listen for! • Sounds that indicate a partial airway obstruction such as stridor, snoring or gurgling.

Look for! • Signs of respiratory distress: tachypnoea, tachycardia, diaphoresis, nasal flaring, retractions, tripod position, head bobbing, paradoxical ventilation (abdominal breathing), decreased level of consciousness, pallor, cyanosis, poor oxygen saturations.

Neurological status The infant or child’s mental status should be assessed by observing the manner in which the patient interacts with the paramedic, the parents and the surroundings. Depending on the patient’s age, the paramedic may need to ask the parents if the patient appears to be acting ‘normally’ under the circumstances. The hypoxic patient may present as confused, restless, inconsolable or agitated. Continued hypoxia and hypercarbia may lead to lethargy and sleepiness, which may ultimately lead to unconsciousness.

Initial assessment summary

Problem Short of breath; barking cough Conscious Looks at paramedics when they squat down in front of him; is state looking around the room, noting changes in his environment Position Sitting on mother ’s lap Heart rate 148 BPM Blood Not taken to avoid distressing the child pressure Skin Pink, warm dry (therefore BP not indicated as perfusion is appearance sufficient) Speech Not applicable pattern Respiratory 24 BPM rate Respiratory Even cycles rhythm Respiratory Mild sternal retraction effort Chest Clear chest, barking cough; suprasternal auscultation: expiratory auscultation stridor Pulse 94% on room air oximetry Temperature 38.1°C Motor/sensory Patient is holding onto his mother, moving all limbs function History Recent runny nose and mild chest infection for 2 days. Normally healthy, no medical history, no medications. The patient sat with his mother in a steamy shower for 30 minutes, but the cough and respiratory distress did not improve. D: The paramedics have ascertained that there is no foreign object involved in the respiratory distress. A: The patient is conscious with minor airway obstruction. B: Respiratory function is currently slightly elevated. The respiratory rate is elevated but ventilation is normal. C: Heart rate is normal and there is a sufficient blood pressure as indicated by the skin signs. The patient is displaying respiratory symptoms consistent with croup.

F ROM A DIST A NCE Look for! • Is the child moving spontaneously or are they limp? • What is the child’s skin colour and condition? • Is the child interested in you? Is the child aware/alert to movement around them? • Is the child consolable by a parent?

• Are there signs of respiratory distress? (e.g. suprasternal, supraclavicular or intercostal retraction, or nasal flaring)

CONFIRM The essential part of the clinical reasoning process is to seek to confirm your initial hypothesis by finding clinical signs that should occur with your provisional diagnosis. You should also seek to challenge your diagnosis by exploring findings that do not fit your hypothesis: don’t just ignore them because they don’t fit. At this point the paramedics have a 14-month-old patient presenting with a barking cough and stridor, respiratory distress, fever and a recent history of upper respiratory tract infection. These are all typical symptoms of croup, but there are other causes of many of these symptoms. They must now consider the differential diagnosis for a noisy airway and rule out the other possible causes.

What else could it be? DIF F ERENT IA L DIA GNOSIS Croup Or • Epiglottitis • Foreign body obstruction • Anaphylaxis or allergic reaction • Abscess (peritonsillar, retropharyngeal) • Asthma • Bronchiolitis • Pneumonia

Epiglottitis The patient does not have the classic drooling of saliva caused by an inability to swallow. Foreign body obstruction The history does not seem to be strongly in line with this diagnosis. A foreign body does not normally produce the classic barking cough. Anaphylaxis or allergic reaction

Upper airway obstruction due to allergic reaction could be considered but there is no history of an allergen and it is usually associated with involvement of other body systems. Abscess An abscess in the peritonsillar or pharangeal region could cause respiratory obstruction. However, it will not cause a cough and tends to present with exquisite pain on swallowing, so is more likely to be confused with epiglottitis than croup. Asthma Respiratory distress from asthma has a very different respiratory pattern, with classically an extended expiratory phase and lower airway wheeze sounds as opposed to stridor. Bronchiolitis This is basically a lower airway obstruction and although a cough can be associated with it, it tends to be more moist and the noises are lower airway wheezes. Pneumonia This may present with temperature and respiratory distress associated with a cough as mucus is cleared from the lungs, but the cough is not the classic barking cough and a patient with pneumonia tends to have pleuritic pain.

T REAT Emergency management Safety When dealing with any patient exhibiting signs or symptoms of a bacterial or viral infection, the paramedics should be vigilant to ensure that they are wearing all personal protective equipment, including gloves, protective eyewear and in some cases a gown and mask. The first priority is to protect the patient’s airway. To do this the paramedic must treat the child gently so as to reduce their anxiety; avoid inspecting, stimulating or irritating the airway; and keep the child in a position that reduces the work of breathing. The next safety consideration is securing the patient for transport. The best way to reduce anxiety is to position the child in the parent’s arms on their lap. To secure the parent and child in the ambulance it may be necessary to take the child’s baby capsule or booster seat in the ambulance to ensure the patient is safely secured. Humidified air Many parents still place the child in a warm steamy atmosphere. Close contact with the parent undoubtedly reassures the child and inspiration of humidified air may slightly ease dyspnoea, thus reducing anxiety, but it does not impact on the pathophysiology of the condition. Despite its long history of being used,

humidified air is not effective in croup: a systematic review of three randomised controlled trials of the administration of humidified oxygen in the emergency setting concluded that there was no change in the patient’s condition (Bjornson & Johnson, 2008). Oxygen The treatment for croup is to reduce airway swelling by administering nebulised adrenaline and to re-establish normal tidal volumes. Hypoxaemia resulting from inadequate tidal volume is unlikely to be corrected by the administration of oxygen without the addition of adrenaline. If a mask is not tolerated, the parent can hold the mask near the child’s face to supplement the concentration of oxygen in the inspired air. Adrenaline Children with moderate to severe dyspnoea associated with croup should be treated with adrenaline via a nebuliser. The use of 3–5 mg of nebulised 1:1000 adrenaline for the treatment of croup has long been established as both safe and effective (Cherry, 2008). The actual dose of adrenaline received by the patient is determined by their respiratory function and not the dose of adrenaline in the nebuliser. Nebulised adrenaline is effective due to adrenergic stimulation, which causes constriction of the pre-capillary arterioles. This decreases capillary hydrostatic pressure and leads to fluid reabsorption. This reabsorption of fluid in the interstitium reduces laryngeal mucosal oedema. Furthermore, the β 2adrenergic effects of adrenaline cause bronchial smooth muscle relaxation and bronchodilation. Combined, these two main effects of adrenaline result in a reduction of the upper airway swelling and improvement in oxygenation and ventilation (Cherry, 2008). A single dose of nebulised adrenaline works for up to 2 hours, so patients should be routinely transported for monitoring to ensure that symptoms do not recur. The most common side effects of nebulised adrenaline are tachycardia and pallor (Bjornson & Johnson, 2008). It is recommended that all patients treated with nebulised adrenaline in the field should also be given corticosteroids (Cameron et al., 2006; see below) and should be observed for long enough to ensure that the corticosteroids are improving the inflammatory response and that there will be no recurrence of symptoms as the adrenaline wears off.

EVALUAT E Evaluating the effect of any clinical management intervention can provide clues to the accuracy of the initial diagnosis. Some conditions respond rapidly to treatment so patients should be expected to improve if the diagnosis and treatment were appropriate. A failure to improve in this situation should trigger the clinician to reconsider the diagnosis. Continuous reassessment of all patients with respiratory distress and partial

airway obstruction is essential. These patients can deteriorate quickly and the paramedic needs to be prepared to manage the patient’s airway if required. The side effects of being treated with nebulised adrenaline include pallor and tachycardia: the paramedic should constantly assess the patient’s circulatory and perfusion status to ensure they maintain adequate end-organ perfusion. Is the patient: • Protecting their airway and ventilating adequately? > Provide oxygen > Administer nebulised adrenaline > Consider intubation as a last resort to ensure airway protection and adequate ventilation • Improving after the nebulised adrenaline? > Consider IV or oral corticosteroids • Adequately perfused? > Ensure that the receiving hospital is notified of the arrival of a paediatric patient > Consider the need for cannulation and intravenous fluid

Ongoing management Corti coste roi ds The anti-inflammatory actions of corticosteroids like dexamethasone and prednisolone have been shown to reduce laryngeal mucosal oedema in croup. Children with severe croup and impending respiratory failure who are treated with corticosteroids have about a five-fold reduction in the rate of intubations (Bjornson & Johnson, 2008). A single oral dose of 0.15 mg/kg of dexamethasone or 1 mg/kg of prednisolone is an established treatment of choice due to its long duration of action, ease of administration and low cost (MD Consult, 2013a).

Fluids As a general rule, patients with croup should not require intravenous access or fluid administration in the pre-hospital setting. The treatment of choice for these patients includes oxygen, nebulised adrenaline and oral corticosteroids; therefore, vascular access is not a priority. Furthermore, attempts to attain vascular access may increase the patient’s anxiety, which would increase their respiratory distress and potentially lead to complete airway obstruction. The patient may receive fluid administration in the hospital setting to treat any pre-existing dehydration caused by the underlying illness.

Intubation In very rare cases of severe croup when the patient’s airway patency is insufficient to maintain adequate consciousness, the airway should be secured with endotracheal intubation. This is rarely performed in the pre-hospital environment. When planning to intubate a child, an endotracheal tube 0.5 to 1 smaller than the one normally selected should be used (Jenkins & Saunders, 2009).

Heliox Heliox is a low-density mixture of helium and oxygen gas. Helium has no inherent pharmacological or biological effects. Administration of heliox to children with respiratory distress can reduce their work of breathing because the helium is less dense than nitrogen and thus creates less airflow turbulence through the narrow airways. While there is good evidence to demonstrate that heliox is effective for improving the signs and symptoms of croup, it should be noted that a limitation of heliox is that it may have a lower fractional concentration of oxygen than is required to treat a child with profound hypoxia (Bjornson & Johnson, 2008). In practice, heliox is rarely used.

Hospital admission When a child arrives at the ED with signs and symptoms of croup, a doctor will calculate a ‘croup score’ based on assessment of inspiratory breath sounds, stridor, cough, retraction, nasal flaring and cyanosis. The 11-point score (between 0 and 10) determines the severity of croup, with 6 severe croup with potential for respiratory failure and 9–10 impending respiratory failure (MD Consult, 2013a). When treatment with corticosteroids and adrenaline has been administered, the patient should be observed for at least 4–6 hours. If the patient does not respond well to treatment, requires intubation, has coexisting medical problems or serious respiratory symptoms return after treatment, the patient may require admission to hospital and treatment until symptoms resolve (see Box 23.1). B O X 2 3 . 1C r o

up: indic atio ns f o r adm issio n to

ho spital • Severe respiratory distress or failure • Unusual symptoms (hypoxia, hyperpyrexia) • Dehydration • Persistence of stridor at rest after nebulised adrenaline and steroids • Persistence of tachycardia, tachypnoea • Complex past medical history (prematurity, pulmonary, cardiac disease) Source: Marx (2010).

Long-term impact The doctor may consider broad-spectrum antibiotics for a severely ill child when bacterial tracheitis or epiglottitis is suspected. Generally, intubation for croup can be avoided by aggressive management with corticosteroids and nebulised adrenaline. Deaths due to acute croup are rare and the prognosis for these children is excellent if they are managed appropriately in the acute phase of the disease.

CA SE ST U DY 2 Case 00318, 1233 hrs. Dispatch details: A 4-year-old female with fever and breathing difficulty. The child’s mother is very distressed. Initial presentation: The crew are met at the front door by the child’s mother. She is very upset and urges them to see her daughter, who is ‘very sick’.

ASSESS 1240 hrs Primary survey: The child is sitting on a sofa in the lounge room. She has rapid, laboured, noisy breathing, is drooling and is leaning forwards with her neck extended and tongue protruding. She watches the paramedics as they approach her. Her skin is pale centrally and peripherally. 1242 hrs Vital signs survey: Perfusion status: HR 144 BPM, radial pulse present. The blood pressure is not taken because the patient becomes anxious when the cuff is applied to her arm. Her skin is cool and pale, and her temperature 38.8°C. Respiratory status: RR 44 BPM, shallow breathing, inspiratory stridor and no apparent cough; the patient is drooling; upper respiratory stridor, no wheeze or other adventitious breath sounds; SpO2 92% on room air. Conscious state: The patient is conscious and alert. 1243 hrs Pertinent hx: The symptoms started this morning and have significantly worsened over the last several hours. The patient woke up with a sore throat and had difficulty speaking. She didn’t want to eat breakfast

because it hurt to swallow. Her breathing became worse about an hour ago and her temperature has not come down after her mother gave her a dose of paediatric paracetamol. There are no other family members with a recent history of a cold or flu. The mother says she doesn’t believe in vaccinations because her friend told her that there are too many side effects. The patient has no known allergies and no medical history.

CONFIRM In many cases paramedics are presented with a collection of signs and symptoms that do not appear to describe a particular condition. A critical step in determining a treatment plan in this situation is to consider what other conditions could explain the patient’s presentation. This patient, however, seems to have the classic presentation of acute epiglottitis. The fact that she has not had her immunisations makes her more likely than the average child of this age to have epiglottitis. The particularly significant clinical signs are the systemic infection with drooling and the upright position.

What else could it be? DIF F ERENT IA L DIA GNOSIS Acute epiglottitis Or • Croup • Foreign body inhalation • Asthma or bronchiolitis • Anaphylaxis or allergic reaction

Croup While the patient does have stridor and respiratory distress, the clinical presentation does not have the cardinal feature of croup: the barking cough. Furthermore, this onset is more rapid than the traditional presentation of croup and the patient does not have a history of recent upper respiratory tract infection. Croup is therefore unlikely, but it cannot be excluded. Foreign body inhalation The patient had a relatively rapid onset of respiratory distress, which is consistent with foreign body inhalation. However, the history of waking up with a sore throat and the presence of fever suggest that the airway

obstruction is more likely to be an infectious or inflammatory process than a foreign body. Asthma or bronchiolitis The signs of hypoxia and respiratory distress are consistent with asthma and bronchiolitis. However, there is no wheezing or other abnormal breath sounds on auscultation. The presence of fever, drooling and upper airway stridor are not typical of asthma or bronchiolitis. Anaphylaxis or allergic reaction Anaphylaxis is an almost immediate and rapidly progressive process that involves more than one body system. The poor perfusion and subglottic angiooedema that can result in stridor and hypoxia are typical of anaphylaxis. However, there is no history of exposure to a known allergen, and the presence of a fever is not typical of anaphylaxis. Although there is a strong suspicion that this is epiglottitis, it will not be possible to confirm this until the pharynx and epiglottis can be safely examined. The appropriate setting for examination is usually a theatre suite or resuscitation room where emergency airway procedures can be instituted if the examination precipitates complete obstruction.

T REAT This is a case where it may be difficult to confirm a diagnosis in the field. If epiglottitis cannot be ruled out treatment should be managed as if it is present. The paramedics should manage the patient symptomatically and address the basic issues of airway, breathing, hypoxia and perfusion before reassessing to see if the underlying cause has become clearer. Once epiglottitis is suspected, the patient should be immediately, and gently, transported to hospital for appropriate airway support.

P RACT ICE T IP Airway deterioration may occur rapidly: prepare to secure the airway if necessary and never leave the patient alone.

Keeping the child calm and administering supplemental oxygen, if possible (which might cause distress), are the main approaches to treatment. If the patient does not tolerate a mask, 6–8 L/min of oxygen near the child’s mouth and nose could be considered. The swollen tissue caused by epiglottitis makes it difficult for the patient to maintain an airway and they rely on holding their head, mouth and tongue in a particular position and using the accessory muscles of ventilation. Any additional distress or agitation can affect this and

the patient may suddenly become unable to ventilate effectively. Paramedics faced with acute epiglottitis should be prepared to manage the patient’s airway with endotracheal intubation or cricothyroidotomy if the patient becomes unconscious and cannot be effectively ventilated using non-invasive equipment.

P RACT ICE T IP If epiglottitis is confirmed, the patient’s family should be treated prophylactically with antibiotics to prevent the spread of Haemophilus influenzae type B, the bacteria that most likely caused the epiglottitis (Kline, 2003).

1246 hrs: The paramedics attempt to place a non-rebreather mask on the patient but she starts to resist. They ask her mother to hold the mask near her mouth but out of her line of sight and she tolerates this without further distress.

EVALUAT E Evaluating the effect of any clinical management intervention can provide clues to the accuracy of the initial diagnosis. Some conditions respond rapidly to treatment so patients should be expected to improve if the diagnosis and treatment were appropriate. A failure to improve in this situation should trigger the clinician to reconsider the diagnosis. 1248 hrs: Perfusion status: HR 130 BPM, BP not taken, capillary refill time is slightly delayed at 3 seconds, skin is cool and pale. Respiratory status: RR 40 BPM, shallow breathing, inspiratory stridor, no cough heard, still drooling and refusing to swallow, SpO2 92% on O2 (near to her face). Conscious state: The patient remains alert. This lack of dramatic improvement is not unexpected as the paramedics are not able to manage the underlying problem. The improvement in oxygen saturation is a positive sign and indicates that there is no need to consider further interventions at this stage.

Hospital management Nebulised adrenaline does not appear to have any utility in the treatment of epiglottitis. IV antibiotic therapy is the treatment of choice once the patient is in a safe and secure environment. IV access should not be attempted in the field in a conscious patient, and the type of antibiotic used will vary depending on the likely infecting agent. Some authors recommend the administration of corticosteroids, but this practice is not universal and does not appear to impact outcomes in terms of the duration of intubation or ICU stay (Faden, 2006). In most cases, patients with moderate to severe epiglottitis will go to the operating theatre to be intubated in a controlled setting. Endotracheal intubation will definitively secure the airway and prevent complete obstruction while the appropriate antibiotics are being administered (Acevedo et al., 2009). Blood cultures, a full blood count and a swab culture from the epiglottis may also be used to identify the pathogen and determine antibiotic susceptibility.

CA SE ST U DY 3 Case 42804, 0923 hrs. Dispatch details: A 3-year-old male with a sudden onset of severe respiratory distress at a day-care centre. Initial presentation: The crew are met at the front gate of the day-care centre by a distraught staff member who tells them that the child seems to be choking.

ASSESS 0930 hrs Primary survey: They find the child sitting by a small craft table with another staff member. He appears pale and anxious, and is coughing and rubbing his neck with his hands. They note that he has rapid, laboured, noisy breathing, is drooling and is leaning forwards with his neck extended. The child watches them as they approach him. 0932 hrs Vital signs survey: Perfusion status: HR 148 BPM, SpO2 88% on room air, skin colour pale with peripheral cyanosis, temperature 37.3°C, blood pressure not taken.

Respiratory status: RR 60 BPM, shallow breathing, inspiratory and expiratory stridor, harsh cough, drooling. Conscious state: The patient appears to be getting tired. He is focusing only on his breathing and does not answer questions or follow any commands. 0933 hrs Pertinent hx: One of the carers says that the patient’s symptoms started about 15 minutes ago while he was colouring. He has had a runny nose for a few days, but hasn’t had a fever, cough or any other symptoms. 0934 hrs Past medical hx: The patient’s file states that he has no allergies, takes no medications and has been fully immunised. A note in the file listing his medical history mentions an episode of croup 4 months ago. There are a number of pathologies that could explain the symptoms at this early stage but this presentation is also consistent with foreign body inhalation.

CONFIRM In many cases paramedics are presented with a collection of signs and symptoms that do not appear to describe a particular condition. A critical step in determining a treatment plan in this situation is to consider what other conditions could explain the patient’s presentation.

What else could it be? Croup While the patient does have stridor and respiratory distress, the clinical presentation does not have the cardinal feature of croup: the barking cough. Also, the onset of the patient’s symptoms was more rapid than the traditional presentation of croup. Therefore, croup can be excluded as a primary management pathway.

DIF F ERENT IA L DIA GNOSIS Foreign body inhalation Or • Croup • Asthma or bronchiolitis • Anaphylaxis or allergic reaction • Epiglottitis • Spontaneous pneumothorax

Asthma or bronchiolitis The signs of hypoxia and respiratory distress are consistent with asthma and

bronchiolitis. However, the paramedics did not detect wheezing upon auscultation and the absence of air entry over the right lung field is inconsistent with bronchospasm. The very sudden onset of the patient’s condition is not typical of asthma or bronchiolitis. Anaphylaxis or allergic reaction Anaphylaxis is an almost immediate and rapidly progressive process that involves more than one body system. Poor perfusion and subglottic angiooedema that can result in stridor and hypoxia is typical of anaphylaxis. There is no history of exposure to a known allergen, although in a day-care centre this cannot be ruled out. The absent air entry over the right lung field is also inconsistent with anaphylaxis.

Look for! • Is there anything on the scene that the child may have inhaled? Small toys? Food? Balloons? Buttons? Coins?

Epiglottitis The patient has rapid, laboured, noisy breathing, is drooling and is leaning forwards with his neck extended, which is consistent with the presentation of epiglottitis. However, the patient had a sudden onset of respiratory distress and does not have a fever, which is not consistent with epiglottitis.

P RACT ICE T IP One in three cases of inhaled foreign body in childhood has no definite history of inhalation of an object. Consider an inhaled foreign body in any case in which there is a sudden onset of wheezing or coughing (Cameron et al., 2006).

Spontaneous pneumothorax Sudden onset of severe respiratory distress raises the possibility of a pneumothorax. This is further supported by the presence of hypoxia and poor perfusion. However, a spontaneous pneumothorax in a child of this age is not typical, nor is the presence of coughing and upper airway stridor. Inhaled foreign body should be the focus of the paramedics’ management as there is a possibility of complete obstruction. The patient had a rapid onset of respiratory distress, which is consistent with foreign body inhalation. Based on the history and the fact that the child was unsupervised at a craft table at day care, the provisional diagnosis of inhaled foreign body would be acceptable.

T REAT The patient should be kept calm. Supplemental oxygen should be administered if possible, but therapy should not be forced on him. He can be encouraged to cough to clear the obstruction but the paramedics should be monitoring him to ensure his breathing does not deteriorate. 0950 hrs: As the patient is prepared for transport to hospital, he coughs very strongly and then becomes silent. He stops breathing and his skin becomes blue centrally. 0951 hrs: The paramedics attempt to ventilate with a bag-valve-mask but there is no chest rise due to resistance. The paramedics administer five back blows and the foreign body is expelled.

EVALUAT E Evaluating the effect of any clinical management intervention can provide clues to the accuracy of the initial diagnosis. Some conditions respond rapidly to treatment so patients should be expected to improve if the diagnosis and treatment were appropriate. A failure to improve in this situation should trigger the clinician to reconsider the diagnosis. 0952 hrs: Perfusion status: HR 160 BPM, skin colour initially cyanosed but improving. Respiratory status: RR 28 BPM, good tidal volume, normal work of breathing, no abnormal breath sounds. Conscious state: Alert, agitated, crying. Even though the foreign body (or most of it) has been ejected the patient still needs a period of careful observation in hospital and therefore requires transport. A steady improvement in his vital signs would be expected.

Future research Corticosteroids and adrenaline have been firmly established as the treatment of choice for children with croup. While adrenaline is commonly used by paramedics to treat croup, most ambulance services do not use corticosteroids for this application. Research is needed to determine the need to administer systemic or oral corticosteroids in the pre-hospital setting to paediatric patients with signs and symptoms of croup.

Summary A noisy airway in a paediatric patient indicates a serious and potentially life-threatening emergency. Determining the cause of partial upper airway obstruction and respiratory distress in children may take some detective work. Your ability to recognise and differentiate between foreign body inhalation, infection and inflammation of the upper airway will help guide your treatment to ultimately have a positive outcome for your patients.

References Acevedo, J. L., Lander, L., Choi, S., Shah, R. K. Airway management in pediatric epiglottitis: a national perspective. Otolaryngology: Head & Neck Surgery. 2009; 140(4):548– 551. Australian Institute for Health and Welfare (AIHW)Australia’s Health 2010. Canberra: AIHW, 2010. [Cat. no. AUS 122]. Australian Resuscitation Council (ARC). Airway. Accessed 10 February 2013 from www.resus.org.au, 2013. Bjornson, C. L., Johnson, D. W. Croup. Lancet. 2008; 371(9609):329–339. Cameron, P., Jelinek, G., Everitt, I., Brown, G., Raftos, J.Textbook of Paediatric Emergency Medicine. Sydney: Churchill Livingston, 2006. Cherry, J. D. Croup. New England Journal of Medicine. 2008; 358(4):384–391. Craft, J., Gordon, C., Tiziani, A.Understanding Pathophysiology. Sydney: Elsevier, 2011. De Bueck, K. Croup: a review. European Journal of Paediatrics. 1995; 154:432–436. Faden, H. The dramatic change in the epidemiology of pediatric epiglottitis. Pediatric Emergency Care. 2006; 22(6):443–444. Gregory, P., Ward, A.Sanders’ Paramedic Textbook. Sydney: Elsevier, 2010. Jenkins, I. A., Saunders, M. Infections of the airway. Pediatric Anesthesia. 2009; 19:118–130. Kline, A. Pinpointing the cause of pediatric respiratory distress. Nursing. 2003; 33(9):58–64. Lissauer, T., Clayden, G., Craft, A. Illustrated Textbook of Paediatrics, 4th ed. London: Mosby, 2012. Marx, J. A. Rosen’s Emergency Medicine: Concepts and Clinical Practice, 7th ed. Philadelphia: Elsevier, 2010. MD Consult, First Consult. Croup. Accessed 11 January 2013 from www.mdconsult.com/das/pdxmd/body/281393236–9/1204361465?type=med&eid=9-u1.0-

_1_mt_1014274, 2013. MD Consult, First Consult. Epiglottitis. Accessed 14 February 2013 from www.mdconsult.com/das/pdxmd/body/281393236–9/1204361465?type=med&eid=9-u1.0_1_mt_1014277, 2013. MD Consult, First Consult. Inhaled Foreign Body. Accessed 14 February 2013 from www.mdconsult.com/das/pdxmd/body/281393236–9/1204361465?type=med&eid=9-u1.0_1_mt_101719, 2013. Wood, N., Menzies, R., McIntyre, P. Epiglottitis in Sydney before and after the introduction of vaccination against Haemophilus influenzae type b disease. Internal Medicine Journal. 2005; 35(9):530–535.

SECTION 9

THE PARAMEDIC APPROACH TO THE PATIENT SUFFERING A CARDIAC EMERGENCY O U TL I N E INTRODUCTION TO THE PARAMEDIC APPROACH TO THE PATIENT SUFFERING A CARDIAC EMERGENCY CHAPTER 24: Chest pain CHAPTER 25: Arrhythmias CHAPTER 26: Cardiac arrest

INTRODUCTION TO THE PARAMEDIC APPROACH TO THE PATIENT SUFFERING A CARDIAC EMERGENCY IN THIS SECTION Chapter 24 Chest pain Chapter 25 Arrhythmias Chapter 26 Cardiac arrest

AT THE COMPLETION OF THIS SECTION YOU SHOULD BE ABLE TO • Describe the common causes of chest pain and differentiate between chest pain that is cardiac in origin from pain of other causes. • Describe a succinct and effective assessment strategy of chest pain to determine the most likely cause. • Discuss the principles of management of patients with chest pain and arrhythmias, and the specific management for causes that are treatable in the pre-hospital environment. • Describe a succinct and effective assessment strategy of cardiac arrest to determine the most likely cause. • Outline the principles of management of patients suffering cardiac arrest, and the specific management for causes that are treatable in the pre-hospital environment. • Describe the principles of management of patients who have regained cardiac output following a period of cardiac arrest and the specific management in the pre-hospital environment. Disease of the organs contained by the chest wall can produce a confusing spectrum of pain and symptoms. The chest wall itself can also be affected by injury and disease and, overlaying the organs within, it can add to the complexity of diagnosing chest pain in the field. The most serious cause of chest pain is generally considered to be a blockage to a coronary blood vessel (acute coronary syndrome). The subsequent damage to the myocardium (the muscle of the heart) can lead to arrhythmias and ultimately cardiac arrest. Differentiating the wide variations of cardiac chest pain from other sources of chest pain with equipment limited by portability is a challenging but essential paramedic skill. Over the past decade the ability of paramedics to directly intervene in managing myocardial ischaemia has progressed from providing cautious pain relief to direct intervention in dissolving clots in the affected vessels or bypassing emergency departments to direct patients to cardiac theatres where the clots are removed mechanically. The ability to determine which patients receive these expensive and potentially dangerous interventions reflects the growing complexity of paramedic practice and its integration into broader medical practice. The ability of paramedics to manage the arrhythmias and cardiac arrests that can evolve from cardiac disease has also become more complex and effective. While the electrocardiogram (ECG) plays an important role in identifying which patients can be administered drugs to dissolve coronary occlusions or directed to cardiac catheterisation, the ECG is least accurate early in the development of cardiac chest pain and therefore of less help to paramedics than other medical professionals. Determining the nature of chest pain in the emergency setting relies on a strong knowledge of anatomy, disease pathology and risk factors and the ability to gain a succinct history to identify which patients require management of acute coronary syndrome.

The chapters in this section take readers through the progression of acute coronary syndrome, from the onset of pain to the subsequent development of potentially like-threatening arrhythmias and into the cohort of patients who ultimately go into cardiac arrest. Chapter 24 steps readers through the clinical reasoning process to determine whether chest pain is related to the heart. Chapter 25 provides the links between myocardial ischaemia and disturbances of heart rhythm and why some rhythms are more dangerous than others. Finally, Chapter 26 reveals the causes, not just ischaemic, of cardiac arrest and how recent changes to management are improving patient outcomes.

CHAP TER 24

Chest pain By Hugh Grantham

C O N C E P TS U S E D I N TH I S C H A P TE R • The paramedic’s clinical approach: Section 2 • Perfusion: Chapter 55 • The autonomic response: Chapter 56 • The inflammatory response: Chapter 57

O V E RV IE W • Chest pain is a common presentation in ambulance practice but a final diagnosis of ischaemia occurs in fewer than 10% of cases. • The underlying pathology of a proportion of chest pain presentations is an acutely obstructed coronary artery that can lead to cardiac arrest. • Cases presenting as chest pain include many non-ischaemic causes of chest pain. • Distinguishing an obstructed coronary artery from other causes of chest pain in the out-ofhospital environment is difficult. • Features distinguishing myocardial infarction on an ECG are not always present. • The principles of management of acute coronary syndrome seek to resolve the imbalance between oxygen supply and oxygen demand in myocardial tissue. • Early identification and early access to reperfusion strategies are essential to positive outcomes. • The consequences of myocardial ischaemia include angina, arrhythmia, altered muscle function and infarction.

Introduction Coronary artery disease (CAD) is the leading cause of death in western societies (AIHW, 2011) and must be considered a possible cause of any adult presentation of chest pain. But while cardiac ischaemia can lead to cardiac arrest in a matter of minutes, chest pain caused by ischaemia actually makes up less than 10% of the final diagnoses of all patients who initially present with chest pain (Bhuiya, Pitts & McCaig, 2010). For the layperson, diagnosis of cardiac ischaemia appears to be highly supported by technology and, in the hospital setting, this assumption is reasonably valid. In the community setting, however, the technology is far less definitive than the general population appreciates, and the weight of diagnosis falls on the patient’s description of their own symptoms and the clinical presentation perceived by the paramedic. Distinguishing ischaemic chest pain from all other causes of chest pain requires a thorough understanding of the pathology of cardiac ischaemia but also the clinical reasoning process used to initiate safe and effective treatment. Although access to life-saving clinical interventions for cardiac ischaemia is growing, definitive interventions such as coronary arterial stenting and bypass remain limited and expensive. Despite the lack of definitive diagnostic tools available to them, paramedics play a vital role in providing early access to these treatments through their in-field diagnosis and selection of appropriate treatment pathways (Ducas et al., 2012). This chapter briefly describes the process by which ischaemic chest pain presents and what factors should be considered essential in making a safe diagnosis.

Pathophysiology The chest cavity contains organs that differ remarkably in their structure and function. Packed tightly together, these organs are subject to a wide array of potential diseases that can develop in isolation or as a syndrome across the entire body. Worryingly for the paramedic, innervation of sensory nerves to most of the organs of the chest cavity is poor and the pain produced by a disease can refer away from the site or present as belonging to another organ. In the emergency setting, the condition of greatest concern is the sudden occlusion of a coronary artery, as it can quickly lead to the development of fatal cardiac arrhythmias. But it can be difficult to differentiate ischaemic pain from pain caused by diseases of the lungs, the great vessels of the chest, the chest wall itself or even the organs of the upper abdomen. Myocardial cells require just 1.3 mL of oxygen per 100 mL of blood but are normally supplied with six times this amount (Hall, 2012). Anatomically, therefore, the heart has more than sufficient blood supply to meet its metabolic demands, but the processes of ageing and disease can narrow the arteries supplying blood to the myocardium and lead to an imbalance between myocardial oxygen supply and myocardial oxygen demand (see Fig 24.1 and Table 24.1). Less commonly (and usually combined with CAD) diseases can also lead to an increased myocardial metabolic demand. In either circumstance, the result is ischaemia of the myocardial cells. If the ischaemia is severe and prolonged, the myocardial cells can begin to dysfunction (causing arrhythmias; see Ch 25) or they can die and/or limit the effectiveness of the heart as a pump. TABLE 24.1 Factors determining myocardial oxygen supply and demand

Determinants of myocardial oxygen supply Blood pressure (higher blood pressure increases coronary perfusion pressure) Length of diastole Intraluminal coronary artery size Haemoglobin value Dissolved oxygen content of blood

Determinants of myocardial oxygen demand Blood pressure (higher blood pressure increases afterload) Heart rate Contractility Amount of myocardial tissue (increase in hypertrophy) Sympathetic tone

FIGURE 24.1 Myocardial ischaemia occurs when the tissue demand for oxygen exceeds supply. The principle behind the management of ischaemia is to reduce demand (lower blood pressure, reduce activity) while increasing oxygen supply (inspired oxygen, lysis of thrombus). Source: Fleisher (2012). Arteriosclerosis and stable atherosclerosis produce a fixed obstruction that limits supply. An increase in demand may then produce ischaemia. A dynamic coronary obstructive component also exists with clot formation (over unstable atherosclerotic plaques) and/or vasospasm suddenly reducing supply. Arteriosclerosis refers to the gradual stiffening of the walls of the arteries with age (see Box 24.1). This can occur due to the loss of elastic tissue or the growth of smooth muscle in the vessel walls. Although arteriosclerosis occurs naturally with age it can be accelerated by hypertension, diabetes and other diseases. Atherosclerosis is a particular form of arteriosclerosis where fatty lesions develop between the intima and media of the vessel walls (see Figs 24.2 and 24.3). These lesions can grow large enough to occlude blood flow, or they can rupture and cause the sudden development of a clot that occludes the blood vessel. Atheroma occurs when erosion, rupture or fissuring of an atherosclerotic plaque disrupts the endothelium and exposes platelets to the underlying connective tissue (Sanders, 2007). A localised blood clot can form and the reduction in blood flow may be sufficient to cause myocardial ischaemia, particularly when myocardial oxygen demand increases (Kumar & Cannon, 2009).

B O X 2 4 . 1D e fi n i t i o

ns

• Angina: Reversible myocardial hypoxia occurring with exertion and improving with rest is termed stable angina (McCance & Huether, 2010). Patients often live with stable angina for years treating it symptomatically with glyceryl trinitrate (GTN) when required. It should be considered a fixed and irreversible occlusion of the lumen that doesn’t present with symptoms at rest. • Unstable angina (UA): In patients with a history of angina, a pattern of increasing frequency of pain or pain occurring at rest is described as unstable angina (McCance & Huether, 2010). It should not be considered as simply the extension of the fixed stenosis of angina as it could be the result of a ruptured atherosclerotic plaque with a superimposed thrombus creating a dynamic stenosis (Daga, Kaul & Mansoor, 2011). Until the return of negative biomarkers is provided, in-field assessment and management of unstable angina should be equivalent to an NSTEMI (see below). • Acute myocardial infarction (AMI): AMI occurs when there is myocardial cell death secondary to obstruction of blood flow. Myocardial infarction may occur in the absence of ST elevation. This is known as a non-ST elevation myocardial infarction (NSTEMI). NSTEMI may have no ECG changes or may present with ST depression or T-wave changes (Aroney et al., 2006). A myocardial infarction associated with classic ECG changes of ST elevation is described as an ST elevation myocardial infarction or STEMI (see Fig 24.3 below). Although NSTEMIs may involve the death of less tissue compared with STEMIs, the sixmonth mortality of both is comparable (Daga, Kaul & Mansoor, 2011). • Acute coronary syndrome (ACS): This term describes the spectrum of ischaemic disease from unstable angina through to STEMI and was developed to encourage clinicians to recognise that the conditions share a common pathology (a disrupted atherosclerotic plaque with superimposed thrombus), the progression is unpredictable and the principles of management are common (Aroney et al., 2006).

FIGURE 24.2 Atherosclerosis causing a narrowing of the coronary arteries is present in the majority of cases of ischaemic heart disease. Atherosclerosis is an accumulation of cholesterol and triglycerides within the

vessel wall that leads to stiffening of the vessel wall and occlusion of the lumen (McCance & Huether, 2010). A Damaged endothelium. B Diagram of fatty streak and lipid core formation. C Diagram of fibrous plaque. Raised plaques are visible: some are yellow; others are white. D Diagram of complicated lesion; thrombus is red; collagen is blue. Plaque is complicated by red thrombus deposition. Source: Craft, Gordon & Tiziani (2011).

FIGURE 24.3 Coronary artery atherosclerosis. A Coronary artery with 60–70% occlusion (black outline and arrow demonstrate narrowing of lumen) due to atherosclerosis. This degree of occlusion may lead to angina. B Severe coronary artery disease and evidence of past thrombus (black arrow), with only three small lumens (*) providing blood flow to the myocardium. Source: Craft, Gordon & Tiziani (2011). As an indication of how oversupplied with blood the heart is, the vessels can become up to 70% occluded before symptoms of ischaemia may present (Hall, 2012). For decades, arteriosclerosis and atherosclerosis were considered somewhat separate diseases with distinct profiles and treatment pathways. The past decade has seen a growing recognition

that the pathophysiologies of arteriosclerosis and atherosclerosis overlap significantly and that the traditional terms may not accurately describe the underlying causes or specific risks. As a thrombus overlying a plaque can form and lyse many times before causing an infarct, the term acute coronary syndrome (ACS) has been introduced. For paramedics it should also reinforce the dynamic nature of ischaemic chest pain and the potential for symptoms to evolve and make a diagnosis more or less clear. In the past the development of arteriosclerosis was considered to be slow and linear with the disease progressing asymptomatically until the occlusion prevented sufficient blood flow to maintain myocardial perfusion at higher workloads. When the workload was removed the balance between oxygen supply and oxygen demand was re-sorted and symptoms would resolve. This ‘fixed stenosis’ created the typical picture of angina where reducing workload (by rest or medications) relieved symptoms effectively and there was no death of myocardial tissue. If a patient with known angina presented with pain of a different intensity, nature or form of relief it was usually referred to as unstable angina, with the inference that it was primarily arteriosclerotic in nature. Conversely, the sudden rupturing of an atherosclerotic plaque and the formation of a thrombus over the rupture causes a non-fixed stenosis and was considered the common cause of nearly complete vessel occlusion. This classically causes the sudden presentation of symptoms that do not resolve with rest or medications that lower myocardial oxygen demand. The most common mechanism for complete occlusion of the coronary artery is rupturing of the surface of the plaque. This allows a new focus for platelet aggregation, thus precipitating blood clotting at the site. Much of the acute management is aimed at retarding the progression of this clot. Another potential mechanism of occlusion is an unstable plaque that mechanically obstructs the blood vessel when the proximal end becomes free and the other is anchored, creating a flap that obstructs flow (Hall, 2012). Coronary artery spasm can also restrict the flow to the extent that it creates an acute coronary ischaemia or acute coronary syndrome. Notable causes of coronary artery spasm include the use of sympathomimetic stimulant drugs. For example, cocaine has been shown to cause coronary artery spasm in young people (Menyar, 2006). In addition, severe coronary artery spasm has been recognised in females under extreme emotional stress, presenting as myocardial ischaemia (Golabchi & Sarrafzadegan, 2011). Nitric oxide released from the endothelium of coronary arteries in response to stress (pulsatile distension with the pulse) is thought to produce vasodilation in the downstream vessels by activating the intracellular production of cyclic guanine monophosphate (CGMP), which controls the smooth-muscle tone by reducing the level of free intracellular calcium. Vessels that have become rigid due to extensive atherosclerosis will have not only a reduction in flow but also a reduction in distension and thus creation of nitric oxide. An upstream atherosclerotic lesion may therefore also cause downstream vasoconstriction, further reducing myocardial oxygen supply. This mechanism explains the ability of glyceryl trinitrate (GTN) to reverse coronary artery spasm by providing an alternative source of nitric oxide to distal coronary arteries that still have the ability to constrict and dilate (Bryant & Knights, 2011). Restriction of coronary artery flow due to either obstruction associated with atherosclerosis or spasm results in a decrease in myocardial perfusion, creating myocardial hypoxia.

Myocardial perfusion and myocardial workload Normal perfusion of the myocardium occurs in diastole. Blood is delivered to the myocardium via the right and left coronary arteries, which originate from the aorta just above the aortic valve. During systole, the entry points into the coronary arteries are partially occluded by the open aortic valve leaflets. During diastole, the backward movement of blood towards the heart down the pressure gradient results in an increased supply of blood to the coronary arteries. The pressure in the coronary arteries is a reflection of the pressure in the aorta. The terminal branches of the coronary arteries and the myocardial capillary bed are subject to external pressure as the myocardium contracts. The perfusion pressure within the myocardial capillary bed allows perfusion of the myocardium only when the external pressure drops in diastole. As the heart is perfused in diastole, the diastolic pressure is effectively the perfusion pressure of the coronary circulation. Reduction in diastolic pressure and increase in heart rate, which reduces the relative diastolic period, reduce the myocardial blood flow (McCance & Huether, 2010). Myocardial ischaemia can alter the flow of electricity across the myocardium and this can be detected by an ECG in as many as 68% of cases (O’Connor et al., 2010) but also as few as 13%, depending on the type of ECG and the location of the occlusion. Death and rupture of myocardial cells due to lack of blood supply result in myocardial cell contents moving into the blood where they can be detected. Together, these two effects provide the diagnostic criteria for cardiac ischaemia: an abnormal ECG and a rise in cardiac enzymes. There is currently no ability to test for a rise in cardiac enzymes in the field. However, the enzymes can take hours to reach detectable levels in the blood after the onset of pain and their diagnostic utility to the paramedic is likely to always be limited. Similarly, the sensitivity of early ECGs is as low as 13%. The net effect of these two facts is that paramedics will never be able to solely rely on diagnostic tests to determine which patients are suffering a myocardial infarction and so will need to combine an accurate history with the clinical presentation. Determining the nature of chest pain is further complicated by the lack of any dedicated pain receptors in the heart. Pain is normally sensed by nociceptors responding to noxious stimuli and stimulating the transmission of an impulse to the brain that identifies the response as pain. In the case of myocardial ischaemia, the build-up of waste products is thought to be the stimuli, but the lack of dedicated pathways can lead to pain being interpreted as originating anywhere from the heart to the neck and arms. The reason for this distribution of pain is that both the heart and the arms originate in the neck during embryonic life; as a result they share the same spinal cord segments and the brain can misinterpret the stimuli (Hall, 2012). The lungs suffer a similar lack of direct sensory innervation but parts of the chest wall (especially the parietal pleura) are heavily supplied with nociceptors. Muscles, bones and joints are also well innervated and palpation or movement is generally able to replicate the pain. It is for these reasons that the location, nature and response to movement of chest pain can be key factors during in-field assessment. The pathophysiology of ACS reinforces both the uncertainty and the seriousness

involved in the assessment of chest pain (see Fig 24.4). Simultaneously, the relatively low frequency that chest pain is ischaemic in nature (1 in V1 or V2 is often considered diagnostic of a posterior STEMI.

Pain The location and nature of the pain, combined with other symptoms, will most often form the basis of the diagnosis (Kamali, Soderholm & Ekelund, 2014) and the use of a mnemonic to structure the patient interview can assist in gaining all the required information (see Ch 28). Caution is advised, however, as a number of factors can be inappropriately weighted in the assessment and there are many causes of chest pain other than ischaemia (see Table 24.2). TABLE 24.2 Potential causes of chest pain

*Can also cause myocardial ischaemia if it blocks main coronary arteries. Source: Adapted from Kumar & Cannon (2009).

Description ‘Heavy’, ‘crushing’, ‘dull’ and ‘pressure’ are typical terms used to describe ischaemic pain, while a ‘sharp’ or ‘stabbing’ pain that changes with ventilation is classically categorised as pleuritic or related to the chest wall. While any of the classic descriptors must be considered as positive predictors of ACS, atypical descriptions should be regarded as the rule rather than the exception. Up to 22% of AMI patients describe their pain as sharp, stabbing or pleuritic in nature, while up to half do not complain of chest pain at all (Green & Hill, 2012). Patients with diabetes and females are more prone to atypical presentations and must always be treated with a higher index of suspicion for ACS (Dorsch et al., 2001; Lefler & Bondy, 2004). A clenched fist held over the chest is known as Levine’s sign and was historically thought to be a strong indicator of ischaemic chest pain, but is in fact demonstrated in only 11% of cases and is not sensitive in more than 35% of cases. In fact, the palm sign (a flat palm over the chest) is more prevalent (35%) and shows equivalent sensitivity (Marcus et al., 2007). Physiologically, chest wall tenderness should be strongly suggestive of a musculoskeletal injury and not ischaemic pain, but it has been reported in up to 15% of patients who were subsequently diagnosed with AMI. This not only reinforces the difficulty of ruling out ACS using any single item, but should also remind clinicians that in their anxiety patients may report what they think the pain should be rather than what it actually is. Language, gender and cultural differences can also confuse the accuracy of the communication. Severity (usually on a scale of 0–10) can be a useful tool in measuring the effectiveness of analgesia, but a study of more than 2000 patients complaining of chest pain on arrival of the paramedics found severity is not useful in differentiating ischaemic pain from non-ischaemic pain (Galinski et al., 2014). Onset Pain that manifests suddenly is typically associated with plaque rupture and subsequent thrombus formation and as such is considered to be associated with ACS. In many cases, however, the plaque may become unstable over a period of days to weeks and the pain may rise and fall several times before patients call for an ambulance. Again, the sudden onset of pain and other symptoms should be considered consistent with ACS but other presentations should not be used as the sole basis to rule out ACS. Pain that increases with physical exertion such as walking is a positive predictor of ACS (Green & Hill, 2012) but conducting in-field stress tests is strongly discouraged. Similarly, a disrupted plaque can create a sufficient occlusion to cause pain at rest. Recent studies have revealed that there is no circaseptal (weekly) variation in the onset of ACS but there is a circadian variation: while the number of chest pain presentations to the ED was lowest between midnight and 9 am, this period had the highest proportion of chest pain patients who were diagnosed with ACS (Ekelund et al., 2012). Location Retrosternal pain is the ‘classic’ presentation but the area of pain and the ability

to accurately localise the pain are important predictors of ACS. Larger areas of pain are more predictive of ACS, while the ability to point to the pain with a finger has a high specificity for non-ischaemic pain (Marcus et al., 2007). Other signs and symptoms There are a number of other symptoms that can be predictors of ACS and paramedics should enquire specifically about each while remaining cognisant of their sensitively (true positive rate) and specificity (true negative rate). Likelihood ratios (LR) greater than 10 are considered to strongly indicate the presence of a disease, while LR 140/90 mmHg or on antihypertensives, current cigarette smoker, hypercholesterolaemia, diabetes mellitus, family history of premature CAD (CAD in male first-degree relative or father younger than 55, or female first-degree relative or mother younger than 65).

Score interpretation Percentage risk at 14 days of all-cause mortality, new or recurrent MI, or severe recurrent ischaemia requiring urgent revascularisation: • Score 0–1 = 4.7% risk • Score 2 = 8.3% risk • Score 3 = 13.2% risk • Score 4 = 19.9% risk • Score 5 = 26.2% risk • Score 6–7 = at least 40.9% risk

Beta-blockers Early administration of beta-blockers (within 24 hours of onset of pain) improves patient

outcomes for both STEMI and NSTEMI (Miller et al., 2007). Calcium channel blockers are an alternative if there is a sensitivity/allergy to beta-blockers.

Hospital admission Patients presenting with ischaemic pain but no ST changes will undergo a number of investigations while staff await the results of the cardiac enzyme test and will often be admitted on the basis of the nature of pain, even when all the tests are returned as negative. Exclusion of myocardial infarction involves a holistic process, which comprises the history, examination, serial ECGs, serial cardiac enzymes and further testing (e.g. exercise stress tests). This process can take some hours and in many cases is done in a chest pain assessment unit.

Follow-up Discharge planning and rehabilitation are now recognised as significant factors in reducing the rates of re-occlusion and progression of CAD (NICE, 2010). The era where large portions of myocardium were lost due to infarct has largely passed and patients without substantial occlusions who have been treated early can return to normal lifestyles. Without regular assessment and modification of risk factors, however, the likelihood of re-infarction is high. Multiple small infarcts also threaten long-term left ventricular failure and are a significant health burden for the individual and for the health system caring for them.

Acute coronary syndrome across the lifespan Although acute coronary syndrome is classically associated with older patients with relevant comorbidities, it is still possible for patients as young as 18 to experience the syndrome. Some cases of myocardial infarction in younger patients are due to either congenital abnormality or interactions with other factors such as drugs, while other cases have the same aetiology as older patients. The impact of early pre-hospital care for acute coronary syndrome is particularly relevant to the outcome of myocardial infarction, allowing better and earlier recovery if the coronary artery obstruction is identified and addressed quickly. Paramedics can have a very significant impact on patients’ quality and duration of life following an acute coronary episode. With improving approaches to management of coronary syndrome patients will live longer with more functioning myocardium, reducing the burden of chronic heart failure. A patient in this younger age demographic with an acute cardiac event may well put off calling an ambulance due to a combination of embarrassment and denial. Some patients may be reluctant to share information about their use of erectile dysfunction drugs unless questioned directly and in a supportive manner that explains the reason for the questioning.

CA SE ST U DY 2 Case 10940, 1505 hrs. Dispatch details: A 62-year-old woman with back pain. Initial presentation: The crew are led inside a private house and find the pale and sweaty patient sitting on a chair in the kitchen. A friend of the patient is in attendance.

ASSESS 1515 hrs Primary survey: The patient is conscious and talking. Chief complaint: ‘I’ve had back pain for an hour and it hasn’t gone away

with paracetamol.’ 1517 hrs Vital signs survey: Perfusion status: HR 108 BPM; sinus rhythm; BP 130/90 mmHg; skin cool, pale and sweaty. Respiratory status: RR 18 BPM; good normal air entry bilaterally; speaking in full sentences; denies SOB; oxygen saturations 98% on room air. Conscious state: GCS = 15. 1521 hrs Pertinent hx: The patient gives a history of upper back pain that has been coming and going for about a week. She hasn’t had it before. An hour ago, however, while having a coffee with her friend the pain suddenly returned, worse than ever. The pain has not changed since and has not responded to treatment with paracetamol or one of her friend’s indigestion tablets. There is no radiation of the pain and she is unable to accurately pinpoint its location. She describes the pain as a dull ache. 1524 hrs Past medical hx: She is a smoker and has a family history of ischaemic heart disease on her father ’s side. She takes no medications and ‘never goes to the doctor ’. 1525 hrs Physical exam: Taking a deep breath does not alter the pain, nor does movement of her arms or neck. Inspection of the area reveals no rash, bruising or swelling. She appears discomforted by the pain but not overly anxious. She rates the pain as 6/10. Her 12-lead ECG shows sinus rhythm with inverted T waves in leads I and V4–V6. BGL = 7.2 mmol. Females are more likely to develop atypical presentations of ischaemic chest pain and postmenopausal women do not have the protection against developing CAD that occurs with gender prior to menopause. A positive finding of ST elevation on the ECG would confirm the underlying cause but in this case the ECG is not so specific. While this pain is definitely not ‘classic’ for ischaemia, an inability to confidently attribute it to another cause means it has to be treated as such.

CONFIRM In many cases paramedics are presented with a collection of signs and symptoms that do not appear to describe a particular condition. A critical step in determining a treatment plan in this situation is to consider what other conditions could explain the patient’s presentation.

DIF F ERENT IA L DIA GNOSIS ACS Or • Musculoskeletal trauma • Dissecting aneurysm • Nonspecific ECG changes and nonspecific chest pain

What else could it be? Musculoskeletal trauma Osteoporosis is common among women in late middle age and fractures can occur from seemingly normal forces such as lifting and bending. Point tenderness is associated with almost all fractures and careful palpation of the spine should reveal any localised pain. The lack of response to ventilation or movement is not suggestive of musculoskeletal pain but a closer examination should be conducted. In this case, there is no localised tenderness. Dissecting aneurysm Sudden-onset chest pain radiating through to the back is typical of a dissecting thoracic aneurysm, although the pain is usually described as ‘tearing’ or ‘ripping’ and is worse at onset. The repeated nature of the pain does not rule an aneurysm in or out. Unequal brachial blood pressures can indicate a thoracic aneurysm, but that is not present in this case. Definitive diagnosis of a dissecting aneurysm requires a CT scan. Nonspecific ECG changes and nonspecific chest pain Sudden-onset, central, ‘crushing’ chest pain that radiates to one or both arms does occur, but more often paramedics are confronted with chest pain presentations (as in this case) that lack a conclusive cause. ECGs are similarly wide-ranging, and between the clear extreme of ST elevation and a normal ECG lies a host of changes that could be attributed to ischaemia or could just be normal variations. Changes to T wave shape and direction are among the early signs of ischaemia, with peaked and widened T waves usually preceding the development of ST elevation. T wave inversion is generally described as a sign of a fully resolved infarct, however, and widespread T wave inversion is also common in paediatrics, cardiomyopathy, pericarditis, left ventricular hypertrophy and bundle branch blocks. The key in this case is that the T wave inversion is occurring in only the lateral leads (I, V4, V5 and V6). Unlike widespread T wave inversion that is caused by structural changes (such as hypertrophy), this anatomical grouping suggests an (at least partial) occlusion to the vessel supplying this region of the heart. The narrow and symmetrical inverted T waves produced by myocardial ischaemia can also be distinguished from the deep and wide T waves of structural cause (Hayden et al., 2002). While neither the atypical chest pain nor the atypical ECG changes are definitive, the combined presentation adds weight to the diagnosis of ACS. Underpinning the diagnosis is the overt sympathetic response and change to the patient’s vital signs. While anxiety can cause these changes, the combination of altered vital signs (especially the changes to the skin), pain that could be ischaemic in nature and an abnormal ECG that is consistent with cardiac ischaemia make a strong case for ACS.

T REAT 1528 hrs: This patient has not been administered nitrates previously and is showing signs of poor perfusion. The crew wisely choose to place her on their stretcher prior to administering a conservative dose of GTN. If the GTN dose causes a significant drop in blood pressure, having the patient on the stretcher allows the crew to lay the patient flat. Aspirin and other anticoagulants are contraindicated in suspected cases of dissecting aneurysm, and while an aneurysm cannot be ruled out the symptoms are not definitive and the benefits of anticoagulation therapy in ACS outweigh the risks of worsening the aneurysm in this case. The patient is not hypoxic so receives no supplemental oxygen.

EVALUAT E Evaluating the effect of any clinical management intervention can provide clues to the accuracy of the initial diagnosis. Some conditions respond rapidly to treatment so patients should be expected to improve if the diagnosis and treatment were appropriate. A failure to improve in this situation should trigger the clinician to reconsider the diagnosis. The patient’s symptoms start to subside and within 2 minutes she is calmer and says the pain has partially resolved. She rates her pain 3/10. Pain relief from nitrates should not be considered diagnostic of ACS: one study of more than 400 patients initially managed for ACS found that patients ultimately diagnosed as not having ACS were more likely to report pain relief from nitrates compared with those ultimately found to have active ACS (41% compared with 39%; Hendrickson et al., 2003). 1530 hrs: Perfusion status: HR 92 BPM; sinus rhythm; BP 120/80 mmHg; skin cool, pale, dry. Respiratory status: RR 18 BPM; good normal air entry bilaterally; speaking in full sentences; patient denies shortness of breath; oxygen saturations 98% on room air. Conscious state: GCS = 15. Although this patient’s blood pressure has fallen significantly following her initial dose of nitrates, her perfusion has actually improved (heart rate lower, no longer sweaty). A repeated, conservative dose of nitrates is warranted and subsequent IV analgesia if required to achieve patient comfort. The paramedics should consider notifying the receiving hospital of the patient’s abnormal ECG finding to reduce triage delays.

CA SE ST U DY 3 Case 13914, 2340 hrs. Dispatch details: A 19-year-old male at a nightclub venue is complaining of chest pain and shortness of breath. Initial presentation: The crew find the patient sitting on the footpath outside the nightclub. He is distressed and sweaty.

ASSESS 2356 hrs Primary survey: The patient is conscious and talking. Chief complaint: ‘I had chest pain for a little while but now I feel like I can’t breathe.’ 2358 hrs Vital signs survey: Perfusion status: HR 190 BPM, narrow complex tachycardia, BP 120/90 mmHg, skin cool and pale. Respiratory status: RR 30 BPM; good air entry bilaterally; speaking in full sentences; patient denies shortness of breath but says his chest feels tight; oxygen saturations 100% on room air; normal work of breathing. Conscious state: GCS = 15. 0004 hrs Pertinent hx: The patient states that he developed chest pain inside the venue, went outside for fresh air but felt worse. The patient and his friends are adamant that he has taken nothing unusual or illegal. The patient holds a flat palm over his chest to indicate where he feels the discomfort. He describes the pain as a ‘tightness’ and says it extends up to his neck. The pain has not changed since it appeared suddenly and does not change with ventilation, palpation or movement. 0005 hrs Past medical hx: The patient has never had chest pain previously and has no significant medical history. 0007 hrs Physical examination: No obvious rashes, swelling or signs of trauma. Both pupils are dilated and sluggish. There are no obvious IV marks. On ECG, narrow complex junctional tachycardia (see Ch 25) with ST elevation of 2 mm is noted in leads V2 and V3. Although this is not the typical picture of ACS caused by the sudden occlusion of a coronary artery, the description of the pain is very typical of ACS. In this case the patient’s very high heart rate is likely to be the cause of the imbalance between myocardial oxygen supply and demand, but it raises the question of treating with both nitrates and aspirin.

CONFIRM In many cases paramedics are presented with a collection of signs and symptoms that do not appear to describe a particular condition. A critical step in determining a treatment plan in this situation is to consider what other conditions could explain the patient’s presentation.

DIF F ERENT IA L DIA GNOSIS ACS Or • Chest pain that is not associated with ACS

Such is the oversupply of blood to the myocardium that it takes a significant occlusion to a vessel to upset the balance between supply and demand. There are circumstances where a combination of a rise in demand and a mild reduction in supply are capable of producing myocardial ischaemia and subsequent chest pain. In this case the patient has developed a re-entry tachycardia that is causing a fixed, elevated heart rate (see Ch 25). At this rate the diastolic filling time is severely reduced while the myocardial demand is raised. This arrhythmia is neither uncommon nor especially dangerous in young people, and could be due to a minor structural abnormality within the heart. It could also have been triggered by use of stimulants such as caffeine, pseudoephedrine (cold and flu tablets), methamphetamine or cocaine. Denial of drug use is common when patients are confronted in public places but the ingestion could be accidental, and it is the clinical signs rather than an admission of guilt that should guide the clinician. While the speed of the arrhythmia has generated a supply–demand imbalance, methamphetamines and cocaine have both been shown to cause vasospasm of coronary arteries capable of producing a myocardial infarct (Jiao et al., 2009; Chen; 2007; Hung, Kuo & Cherng, 2003; Menyar, 2006; Waksman et al., 2001).

T REAT The description of the pain and the presentation fits concisely into the definition of acute coronary syndrome but there are a number of complicating factors that need to be considered prior to treatment.

Nitrates are routinely recommended for ACS in an effort to lower both preand afterload and to reduce myocardial workload. The ‘safety net’ for administering this drug, which lowers blood pressure, is that the patient can generate a higher heart rate if the GTN causes their blood pressure to fall too far. This patient’s heart rate is disengaged from normal sympathetic and parasympathetic feedback: it is fixed by an internal re-entry circuit and will not change if blood pressure rises or falls. Administering nitrates to this patient risks a catastrophic fall in blood pressure with no ability to compensate. The appropriate solution is to revert the arrhythmia (see Ch 25), allow the heart rate to return to normal and then reassess if the ischaemia has resolved. In most ambulance services this reversion of rate is restricted to paramedics trained in intensive care but it should be the first line of treatment rather than triggering the ACS guidelines (ARC, 2011). In areas where there is no ability to revert the arrhythmia in the field, urgent transport to hospital and judicious pain relief are the only options. 1540 hrs: The paramedics revert the arrhythmia according to local guidelines (see Ch 25).

EVALUAT E Evaluating the effect of any clinical management intervention can provide clues to the accuracy of the initial diagnosis. Some conditions respond rapidly to treatment so patients should be expected to improve if the diagnosis and treatment were appropriate. A failure to improve in this situation should trigger the clinician to reconsider the diagnosis. 1542 hrs: Perfusion status: HR 110 BPM, sinus tachycardia, BP 120/90 mmHg, skin normal. Respiratory status: RR 30 BPM, good air entry bilaterally, speaking in full sentences. The patient states he is no longer short of breath or has chest tightness. Oxygen saturations 100% on room air, normal work of breathing. Conscious state: GCS = 15. In most cases ischaemia due to grossly elevated heart rate will resolve once the arrhythmia has been reverted, but it is worth considering that in addition to producing vasospasm both cocaine and methamphetamine can cause a prothrombotic state and accelerated atherosclerosis (Jiao et al., 2009). A disrupted coronary plaque cannot be ruled out in any patient, regardless of age, and the benefits of aspirin are such that the combination of ischaemic pain and ECG changes should trigger administration provided there are no contraindications if symptoms persist once the arrhythmia has been reverted.

Future research Future research into the diagnosis and management of acute coronary syndrome includes research into the potentially harmful consequences of hyperoxaemia as opposed to targeted oxygen delivery (Nolan, 2011). Further systems-based research studying the effects of reduced time delay until reestablishment of perfusion is needed to fine-tune the response to acute coronary syndrome. In the past decade there have been a number of projects where hospitals have been notified about incoming STEMI patients to reduce ‘door to balloon time’. Although most of these studies have reduced this time by up to one-third there has been no corresponding improvement in patient mortality (Menees et al., 2013). The focus is now likely to shift to educating the public in order to reduce ‘pain to balloon time’. High-sensitivity biomarkers that are revealed within 30 minutes of infarct may allow the diagnosis of NSTEMI in the field. Heart-type fatty acid binding protein (hFABP) assays appear sensitive within 30 minutes and may provide a quick and portable test (McCann, 2008). The role that endothelial dysfunction and inflammatory mediators play in the development of unstable atherosclerotic plaques is also likely to be the target of new therapies and interventions. There is growing evidence that isolated ST elevation in aVR in patients who otherwise have no ST elevation (NSTEMI) is predictive of poor outcomes and this may become an indicator for early PCI in these patients (Barrabes, 2003).

Summary The management of acute coronary syndrome has undergone significant development, with early treatment options being available in the field. With the increasing treatment options comes an increasing level of clinical risk of iatrogenic effects. The assessment of clinical risk involves integration of the history and examination with a thorough working knowledge of interpreting 12-lead ECGs. Abnormal and unusual presentations of myocardial ischaemia necessitate keeping an open mind to the possibility of myocardial ischaemia. Conversely, there are a number of conditions that may mimic myocardial ischaemia, which necessitates careful evaluation before commencing on an invasive treatment pathway.

References Aroney, C., Aylward, P., Kelly, A., Chew, D., Clune, E., Acute Coronary Care Syndrome Guidelines Working Group. Guidelines for the management of acute coronary syndromes. Medical Journal of Australia. 2006; 8(8):S1–S30. Australian Institute of Health and Welfare (AIHW)Cardiovascular disease: Australian facts, 2011. Canberra: AIHW, 2011. [Cat. no. CVD 53]. Australian Resuscitation Council (ARC)Guidelines: Acute Coronary Syndrome. ARC, 2011. Barrabes, J. A., Figueras, J., Moure, C., Cortadellas, J., Soler-Soler, J. Prognostic value of lead aVR in patients with a first time non-ST elevation acute myocardial infarction. Circulation. 2003; 108:814–819. Bhuiya, F. A., Pitts, S. R., McCaig, L. F. Division of Health Care Statistics. Emergency department visits for chest pain and abdominal pain: United States, 1999–2008. NCHS Data Brief. 2010; 43:1–8. Brady, W. J. ST segment and T wave abnormalities not caused by acute coronary syndromes. Emergency Medicine Clinics of North America. 24(1), 2006. Burgess, S. Oxygen therapy for acute myocardial infarction. Australasian Journal of Paramedicine. 8(2), 2010. Bryant, B., Knights, K., Salerno, E.Pharmacology for Health Professionals. Sydney: Elsevier, 2011. Cabello, J. B., Burls, A., Emparanza, J. I., Bayliss, S., Quinn, T. Oxygen therapy for acute myocardial infarction. Cochrane Database of Systematic Reviews. 2010; 6. Chen, J. P. Methamphetamine-associated acute myocardial infarction and cardiogenic shock with normal coronary arteries: refractory global coronary microvascular spasm. Journal of Invasive Cardiology. 2007; 19:E89–E92. Collinson, P., et al. Very early diagnosis of chest pain by point-of-care testing comparison of the diagnostic efficiency of a panel of cardiac biomarkers compared with troponin measurement alone in the RATPAC Trial. Heart. 98(4), 2012.

Craft, J., Gordon, C., Tiziani, A.Understanding Pathophysiology. Sydney: Elsevier, 2011. Daga, L. C., Kaul, U., Mansoor, A. Approach to STEMI and NSTEMI. JAPI. 2011; 59:19–25. Diercks, D. B., Kontos, M. C., Chen, A. Y., Wiviott, S. D., et al. Utilization and impact of prehospital electrocardiograms for patients with acute ST-segment elevation myocardial infarction: data from the NCDR (National Cardiovascular Data Registry) ACTION (Acute Coronary Treatment and Intervention Outcomes Network) Registry. Journal of the American College of Cardiology. 2009; 53(2):161–166. Dörler, J., et al. Clopidogrel pretreatment is associated with reduced in-hospital mortality in primary percutaneous coronary intervention for acute ST-elevation myocardial infarction. European Heart Journal. 32, 2011. Dorsch, M. F., Lawrence, R. A., Sapsford, R. J., Durham, N., et al. Poor prognosis of patients with symptomatic myocardial infarction but without chest pain. Heart. 2001; 86(5):494– 498. Ducas, R. A., Wassef, A. W., Jassal, D. S., Weldon, E., Schmidt, C., Grierson, R., Tam, J. W. To transmit or not to transmit: how good are emergency medical personnel in detecting STEMI in patients with chest pain? Canadian Journal of Cardiology. 2012; 28(4):432–437. Dumaine, R., Borentain, M., et al. Intravenous low-molecular-weight heparins compared with unfractionated heparin in percutaneous coronary intervention: quantitative review of randomized trials. Archives of Internal Medicine. 167, 2007. Ekelund, U., Akbarzadeh, M., Khoshnood, A., Björk, J., Ohlsson, M. Likelihood of acute coronary syndrome in emergency department chest pain patients varies with time of presentation. BMC Research Notes. 8(5), 2012. Fleisher, L. A. Anesthesia and Uncommon Diseases, 6th ed., Philadelphia: Saunders; 2012:28–74. Galinski, M., Saget, D., Ruscev, M., et al. Chest pain in an out-of-hospital emergency setting: no relationship between pain severity and diagnosis of acute myocardial infarction. Pain Practice. 20, 2014. Goldman, L., Ausiello, D. A. Cecil Medicine, 23rd ed. Philadelphia: Saunders Elsevier, 2008.

Goodacre, S., Locker, T., Morris, F., Campbell, S. How useful are clinical factors in the diagnosis of acute, undifferentiated chest pain? Academic Emergency Medicine. 9(3), 2002. Green, G. B., Hill, P. B. Chest pain: cardiac or not. In Tintinalli J., ed.: Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7th ed., Sydney: McGraw-Hill, 2012. Golabchi, A., Sarrafzadegan, N. Takotsubo cardiomyopathy or broken heart syndrome: a review article. Journal of Research in Medical Sciences. 2011; 16(3):340–345. Hall, J. Guyton and Hall Textbook of Medical Physiology, 12th ed. St Louis: Saunders, 2012. Han, J. H., Lindsell, C. J., Storrow, A. S., Luber, S., Hoekstra, J. W., Hollander, J. E., Peacock, W. F., Pollack, C. V., Gibler, W. B., EMCREGi*trACS Investigators, The role of cardiac risk factor burden in diagnosing acute coronary syndromes in the emergency department setting. Annals of Emergency Medicine. 2007;49(2) Hayden, B. E., Brady, W. J., Perron, A. D., et al. Electrocardiographic T-wave inversion: differential diagnosis in the chest pain patient. American Journal of Emergency Medicine. 2002; 20(3):252–262. Henrikson, C. A., Howell, E. E., Bush, D. E., Miles, J. S., Meininger, G. R., Friedlander, T., et al. chest pain relief by nitroglycerin does not predict active coronary artery disease. Annals of Internal Medicine. 2003; 139:979–986. Hung, M. J., Kuo, L. T., Cherng, W. J. Amphetamine-related acute myocardial infarction due to coronary artery spasm. International Journal of Clinical Practice. 2003; 57:62–64. ISIS-2 (Second International Study of Infarct Survival) Collaborative Group. Randomized trial of intravenous streptokinase, oral aspirin, both, or neither among 17,187 cases of suspected acute myocardial infarction: ISIS-2. Journal of the American College of Cardiology. 12(6 supp A), 1988. Jiao, X., Velez, S., Ringstad, J., Eyma, V., Miller, D., Bleiberg, M. Myocardial infarction associated with Adderall XR and alcohol use in a young man. Journal of the American Board of Family Medicine. 2009; 22(2):197–201. Jneid, H., 2012 Writing Group Members, 2007 Writing Committee Members. ACCF/AHA Focused Update of the Guideline for the Management of Patients with Unstable Angina/Non–ST-Elevation Myocardial Infarction (Updating the 2007 Guideline and

Replacing the 2011 Focused Update). A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation. 126, 2012. Kamali, J., Soderholm, M., Ekelund, U. What decides the suspicion of acute coronary syndrome in acute chest pain patients? BMC Emergency Medicine. 2014; 14:9. Karnath, B., Holden, M., Hussain, N. Chest pain: differentiating cardiac from non-cardiac causes. Hospital Physician. April, 2004. Keller, K. B., Lemberg, L. Prinzmetal’s angina. American Journal of Critical Care. 2004; 13(4):350–354. Kumar, A., Cannon, C. P. Acute coronary syndromes: diagnosis and management, part I. Mayo Clinic Proceedings. 2009; 84(10):917–938. Lefler, L. L., Bondy, K. N. Women’s delay in seeking treatment with myocardial infarction: a meta-synthesis. Journal of Cardiovascular Nursing. 2004; 19(4):251–268. Løvlien, M., Johansson, I., Hole, T., Schei, B. Early warning signs of an acute myocardial infarction and their influence on symptoms during the acute phase, with comparisons by gender. Gender Medicine. 6(3), 2009. Marcus, G. M., Cohen, J., Varosy, P. D., Vessey, J., et al. The utility of gestures in patients with chest discomfort. American Journal of Medicine. 2007; 120(1):83–89. McCance, K. L., Huether, S. E. Pathophysiology: The Biologic Basis for Disease in Adults and Children, 7th ed. St Louis: Mosby, 2013. McCann, C. J., Glover, B. M., Menown, I. B.A., Moore, M. J., McEneny, J., Owens, C. G., Smith, B., Sharpe, P. C., Young, I. S., Adgey, J. A. Novel biomarkers in early diagnosis of acute myocardial infarction compared with cardiac troponin T. European Heart Journal. 29(23), 2008. McDonald, M. A., Fu, Y., Zeymer, U., Wagner, G., Goodman, S. G., Ross, A., et al. Adverse outcomes in fibrinolytic-based facilitated percutaneous coronary intervention: insights from the ASSENT-4 PCI electrocardiographic substudy. European Heart Journal. 2008; 29(7):871–879.

Mehta, S. R., Salim, Y., Peters, R. J.G., Bertrand, M. E., et al. Effects of pretreatment with clopidogrel and aspirin followed by long-term therapy in patients undergoing percutaneous coronary intervention: The PCI-CURE study. The Lancet. 2001; 358(9281):527–533. Menees, D., Menees, D. S., Peterson, E. D., Wang, Y., Curtis, J. P., Messenger, J. C., Rumsfeld, J. S., Gurm, H. S. Door-to-balloon time and mortality among patients undergoing primary PCI. New England Journal of Medicine. 369, 2013. Menyar, A. Drug-induced myocardial infarction secondary to coronary artery spasm in teenagers and young adults. Journal of Postgraduate Medicine. 2006; 52(1):51–56. Miller, C. D., Roe, M. T., Mulgund, J., Hoekstra, J. W., Santos, R., Pollack, C. V. Impact of acute beta-blocker therapy for patients with non–ST-segment elevation myocardial infarction. American Journal of Medicine. 120(8), 2007. NICE, National Clinical Guideline Centre (UK)Unstable Angina and NSTEMI: The Early Management of Unstable Angina and Non-ST-Segment-Elevation Myocardial Infarction. London: Royal College of Physicians, 2013. [(rev 2013). NICE Clinical Guidelines No. 94]. Nolan, J. P. Advances in post-resuscitation care. Clinical Medicine. 2011; 11(6):605–608. O’Connor, R. E., Bossaert, L., Arntz, H. R., Brooks, S. C., Diercks, D., Feitosa-Filho, G., et al. Part 9: Acute Coronary Syndromes 2010 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science with Treatment Recommendations. Circulation. 2010; 122(16, suppl 2):S422–S465. O’Gara, P. T., et al. 2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction. Journal of the American College of Cardiology. 2013; 61(4):e78–e140. Papadakis M.A., McPhee S.J., eds. Medical Diagnosis and Treatment, 51st ed., New York: McGraw-Hill, 2012. Pelter, M. M., Riegel, B., McKinley, S., Moser, D. K., Doering, L. V., et al. Are there symptom differences in patients with coronary artery disease presenting to the ED ultimately diagnosed with or without ACS? American Journal of Emergency Medicine. 30(9), 2012. Roongsritong, C., Warraich, I., Bradley, C. Common causes of troponin elevations in the absence of acute myocardial infarction: incidence and clinical significance. Chest. 2004;

125(5):1877–1884. Sabatine, M. S., Cannon, C. P., Gibson, C. M., Jose, L. L.-S., et al. Effect of clopidogrel pretreatment before percutaneous coronary intervention in patients with ST-elevation myocardial infarction treated with fibrinolytics: the PCI-CLARITY Study. JAMA. 2005; 294(10):1224–1232. Sanders, M. J. Mosby’s Paramedic Textbook, rev 3rd ed. St Louis: Mosby, 2007. Samad, Z., Hakeem, A., Mahmood, S. S. A meta-analysis and systematic review of computed tomography angiography as a diagnostic triage tool for patients with chest pain presenting to the emergency department. Journal of Nuclear Cardiology. 19, 2012. Sgarbossa, E. B. Value of the ECG in suspected acute myocardial infarction with left bundle branch block. Journal of Electrocardiology. 2000; 33:87–92. Stub, D., Smith, K., Bernard, S., Bray, J. E., Stephenson, M., Cameron, P., Meredith, I., Kaye, D. M. A randomized controlled trial of oxygen therapy in acute myocardial infarction: Air Versus Oxygen. In Myocardial Infarction Study (AVOID Study). American Heart Journal. 2012; 163:339–345. Van de Werf, F., Ross, A., Armstrong, P., Granger, C., et al. Primary versus tenecteplasefacilitated percutaneous coronary intervention in patients with ST-segment elevation acute myocardial infarction (ASSENT-4 PCI): randomised trial. The Lancet. 2006; 367(9510):569–578. Waksman, J., Taylor, R. N., Bodor, G. S., Daly, F. F.S., et al. Acute myocardial infarction associated with amphetamine use. Mayo Clinic Proceedings. 2001; 76(3):323–326. Zweier, J. L. The role of oxidants and free radicals in reperfusion injury. Cardiovascular Research. 2006; 70(2):181–190.

CHAP TER 25

Arrhythmias By Adam Rolley

C O N C E P TS U S E D I N TH I S C H A P TE R • The paramedic’s clinical approach: Section 2 • Perfusion: Chapter 55 • The autonomic response: Chapter 56 • The inflammatory response: Chapter 57

OVERVIEW • Cardiac arrhythmias are a common presentation and in 2010 were listed in the top 20 causes of death in Australia (ABS, 2010). • Arrhythmias may present with symptoms ranging from none through to respiratory distress, cardiovascular compromise and sudden cardiac death. • If at any time a patient presents with no signs of life, commence resuscitation as per the advanced life support guidelines. • The ECG must be interpreted in conjunction with the patient’s history and physical examination findings. • The key consideration is the presence or absence of compromised perfusion. • Wide-complex tachyarrhythmias should be considered to be ventricular tachycardia. • All antiarrhythmic medications can limit the effectiveness of emergency care. • Potential reversible causes should be considered and managed. • Understanding the principles of management of arrhythmias can assist primary responders when they are confronted by arrhythmias they cannot identify.

Introduction Cardiac arrhythmias are among the most complex cases facing any clinician. While the field appears well defined and structured, the range of possible arrhythmias, how they are identified and how they should be managed are open to infinite variations that challenge even experienced cardiologists. Arrhythmias that share the same name can present with vastly different ECGs and produce clinical presentations that range from asymptomatic to near cardiac arrest. Variations in cardiac structure, disease progression, medications and past history can all cloud the decision-making process in a field that requires expertise and experience simply to identify the classic presentations. For paramedics and other clinicians limited by diagnostic equipment and time, clear clinical pathways are described for many arrhythmias and reliable identification of arrhythmias is difficult but not impossible. Together, the definition of a particular arrhythmia and the subsequent guideline often leave little room for clinical reasoning. It is therefore not necessary for this chapter to list the values that describe the various arrhythmias and their usual course of management. Instead, we examine the relatively common group of patients who present in the pre-hospital environment and who do not fit the classic definition, presentation and pathway. It is for these patients that paramedics require their clinical reasoning skills. The term arrhythmia has been used for centuries to describe an abnormal rhythm and in 1978, following the rapid expansion of medical communication across borders, the World Health Organization and the International Society of Cardiology convened a taskforce to define terms related to cardiac rhythms (WHO ISC Task Force, 1987). The term ‘arrhythmia’ was given the broadest possible definition: any rhythm other than a sinus rhythm. Importantly, it was also suggested that the term should be used to describe the entire array of non-sinus rhythms, rather than an individual rhythm. The terms ‘arrhythmia’ and ‘dysrhythmia’ are often used interchangeably within the pre-hospital environment. This stems from discussion in the literature around the technical definition of the two terms, with some authors suggesting that arrhythmia means asystole (Royster, 1990). This is somewhat pedantic and inaccurate, and all clinicians are encouraged to use the term ‘arrhythmia’ when describing the collective group of non-sinus rhythms.

Pathophysiology Within the muscular structure of the heart there is a collection of cells that do not contract or play any direct mechanical role in the movement of blood. Rather, they are integral to cardiovascular function and it is these cells that generate and conduct the electrical impulses that stimulate the mechanical work of the heart. Cardiac myocytes (or contractile cells) are the most common cells of the heart and contract to generate the compressive force that moves blood out of each of the heart’s chambers. Autorhythmic cells propagate and conduct the impulses that trigger the mechanical action. They can be further divided into pacemaker cells (e.g. sinoatrial [SA] or atrioventricular [AV] node) that propagate the impulses, and specialised conduction cells that conduct the impulses to the myocardial cells. Over the past 50 years we have gained a greater understanding of how the contractile and pacemaker cells of the heart work and interact (Park & Fishman, 2011). Technological innovations have revealed how ion channels control the function of both groups of cells and this knowledge has given rise to medications that allow clinicians to manage an increasing number of arrhythmias.

Impulse formation and conduction Human cells generate some degree of electrochemical gradient between the contents within their cell walls and the environment outside the cell. This voltage difference across the cell membrane is known as the membrane potential and is maintained by the action of ion pumps, channels, transporters and exchangers (Park & Fishman, 2011). In addition to maintaining a resting membrane potential, muscle and nerve cells can, to varying degrees, generate an electrochemical wave known as an action potential to signal or activate other cells (Park & Fishman, 2011). For myocardial cells the receipt of an action potential primarily triggers the cell to contract, but the membranes of myocardial cells are also connected to allow the action potential to flow to other myocardial cells and thus spread the electrical wave (and mechanical contraction) throughout the myocardium (see Fig 25.1). As such, the heart effectively works as a single unit. This concept, called cardiac syncytium, occurs due to the presence of gap junctions, allowing the action potential to be propagated (transferred) from one cell to another through the movement of a small number of positively charged ions (property of conductivity).

FIGURE 25.1 The mechanical action of the heart is intrinsically linked to the ability of the cells to shift electrolytes against their concentration gradient across the cell membrane. Creating this chemical imbalance requires energy but creates an electrical difference across the cell membrane, with the inside of the cell more negatively charged than the outside (the cell is described as polarised). If the cell is triggered to open specific ion channels embedded in the membrane, the electrolytes will flow according to their chemical and electrical gradients and the cell will depolarise. The electricity generated will trigger the next cell to depolarise and trigger the movement of calcium into the cell to trigger contraction. Most antiarrhythmic medications act to alter the behaviour of one or more ion channels and thus make the cell less or more excitable, or less or more contractile. While myocardial cells are able to pass action potentials onto other myocardial cells, they are not able to generate action potentials spontaneously—that is, they do not normally possess ‘automaticity’. Automaticity is a property of the pacemaker cells. Being modified myocardial cells, these cells do not have the ability to contract but are able to move spontaneously from their resting membrane potential (RMP) to their threshold potential where the ion channels will open and trigger depolarisation (see Fig 25.2). The depolarisation of the pacemaker cells triggers the depolarisation of the surrounding myocardial cells and another wave of excitation–contraction will sweep across the heart. Action potentials allow rapid signal propagation across the cell membrane. In the heart, each type of cardiac cell (e.g. nodal, atrial, ventricular, Purkinje) has a characteristic action potential that is determined by the panel of ion channels expressed (see Fig 25.3).

FIGURE 25.2 A Myocardial cells wait at their RMP for an external stimulus to open sodium channels and allow the positive electrolytes to flow in and depolarise the cell. This

triggers the release of calcium, which causes the cell to contract and generate pressure to expel blood from the chambers of the heart. B By contrast, pacemaker cells do not contract but without stimulus move from RMP towards spontaneous depolarisation. This depolarisation triggers waiting myocardial cell to depolarise. Source: Craft, Gordon & Tiziani (2011); Patton & Thibodeau (2010); Boron & Boulpaep (2009).

FIGURE 25.3 Schematic of action potential waveforms and propagation at various points in the human heart. Source: Saksena & Camm (2011). During a normal cardiac cycle the pacemaker potential is generated within the sinoatrial node and conducted along the internodal conduction tracts to the atrioventricular junction, consisting of the atrioventricular node and the bundle of His (see Fig 25.4). After being held for a short period of time, the impulse travels through the bundle branches to the Purkinje network and finally to the ventricular myocardium.

FIGURE 25.4

The cardiac conduction system. Source: Hall (2012).

Cardiac myocytes rely on the autorhythmic cells to generate action potentials. Understanding the five phases of the action potential is important in the pathophysiology and management of arrhythmias. Figure 25.5 illustrates the five phases a myocyte transitions through during a depolarisation/repolarisation cycle. Sodium (Na+), calcium (Ca++) and potassium (K+) are the three key ions involved in the process. Each ion requires a specific voltage-gated channel to open, allowing movement of the relevant ion. In other words, the channel will not open until a specific voltage is reached. Importantly, once the cell has reached phase 1 it cannot create another action potential until approximately halfway through phase 3: this is referred to as the absolute refractory period. The action and pacemaker RMP and threshold potentials are also affected by the autonomic nervous system, hormones, drugs, electrolyte concentrations, ischaemia and hypoxia.

FIGURE 25.5 Ion movement during pacemaker and action potentials. Source: (Top image) Saksena & Camm (2011).

Arrhythmia mechanisms The primary bradyarrhythmia mechanisms include dysfunction or failure of the SA node to spontaneously propagate an action potential. Blocks within the AV node may also stop an action potential reaching the ventricles. Excessive parasympathetic activity, disease or a lack of blood supply to either the SA or the AV nodes can reduce their function (see Fig 25.6), as too will drugs that block the inward flow of sodium and calcium.

FIGURE 25.6 Autonomic innervation of the cardiovascular system. The sympathetic nervous system increases both heart rate and vasoconstriction, while the parasympathetic nervous system decreases heart rate. Source: Craft, Gordon & Tiziani (2011). The primary tachyarrhythmia mechanisms are excessive sympathetic activity or drugs that enhance the inward flow of sodium and calcium. Arrhythmias can also be generated when myocardial cells (usually through injury from ischaemia) develop automaticity and spontaneously trigger an action potential (see Table 25.1). If this occurs at a rate faster than the SA node, this activity will become the pacemaker that sets the rate of the heart. Reentry circuits within a small area of cells can also create tachycardias.

TABLE 25.1 Sources of arrhythmias

Source: Adapted from Ninio (2000). Under normal conditions, an impulse travels throughout the entire cardiac conduction system and, due to the absolute refractory period, dies out. In arrhythmias caused by a reentry mechanism, this does not occur: rather, as the impulse passes through the conduction system, it is delayed and/or blocked at one point, but conducted normally throughout the remainder of the system. This mechanism allows cells within the relative refractory period to again be depolarised and may occur on a macro or micro level. At a macro level, an accessory or anatomical pathway will typically be implicated, such as the bundle of Kent in Wolff-Parkinson-White syndrome. Usually a fibrous insulating barrier is present between the atria and the ventricles. In some patients, this fibrous barrier is not complete and so the impulse can pass between the ventricles and the atria via the alternative anatomical pathway. At a micro level, a functional circuit can be formed within the atria or the ventricles and is typically caused by ischaemia. These conditions slow the conduction of the impulse through the cell; if slowed enough it will re-excite cells that are in the relative refractory period. The enhanced automaticity mechanism occurs in autorhythmic cells due to an increase in the slope of phase 4 of the pacemaker potential through the influx of potassium. Increasing the slope causes the autorhythmic cell to reach its threshold potential sooner and is often caused by adrenergic stimulation. Abnormal automaticity occurs in cardiac myocytes that do not normally possess this property and is often caused by hypoxia, ischaemia or hypercarbia. Due to the less negative resting potential and influx of sodium

and calcium, the threshold potential is reached. Arrhythmias that arise due to triggered activity occur when a cardiac myocyte membrane potential is triggered more than once from a single impulse. It is termed afterrepolarisation and is further subdivided into early and delayed after-repolarisation. Early after-repolarisation occurs during phase 2 or 3 of the action potential and a classic example is torsades de pointes. Delayed after-repolarisation occurs after the completion of depolarisation and results in some ventricular tachycardias and digitalis-induced arrhythmias.

CA SE ST U DY 1 Case 13064, 2134 hrs. Dispatch details: A 55-year-old male has collapsed while walking in a local park. Bystanders indicate that the patient is pale, diaphoretic and complaining of difficulty breathing. Initial presentation: On arrival, the paramedics locate the patient lying under a tree in the local park. He acknowledges the paramedics’ arrival, but appears to be confused and presents with difficulty breathing. He is extremely pale and diaphoretic.

ASSESS Patient history Confusion is a common side effect of poor cerebral perfusion and it can make obtaining (or trusting) a history difficult. It is important to take note of other sources of information available, such as evidence of surgery, medications that the patient may be carrying, information from bystanders and/or persons who know the patient, medical alert necklace/bracelet/card and evidence of a pacemaker or implantable cardioverter-defibrillator (ICD).

HIST ORY Ask!

• When did the complaint start? • Has this happened before? • Do you have any significant previous medical history? • Do you smoke/drink/take drugs? What is your job? Where do you live and with whom? • Does your family have any significant illnesses (diabetes, for instance)? • Do you have any other symptoms in other body systems?

In addition to the standard goals of history taking and physical examination, the initial key question to resolve is whether the patient has compromised perfusion. Key signs and/or symptoms consistent with compromised perfusion include altered level of consciousness, shortness of breath or respiratory distress and the presence of shock or chest pain. These signs and symptoms principally result from poor cardiac output and, if left untreated, may result in cardiac arrest. After completing a patient history, the paramedics obtain the following information: • The patient was walking in the park when he was seen to hold his chest and collapse onto the grass. Prior to this, bystanders state that he appeared to be walking at a brisk pace and did not show any signs of distress. • At no point was the patient unconscious. • The patient cannot answer any questions due to his confusion. • He has no obvious surgical scars. • He has no medications with him. • Bystanders state that his condition appears to be deteriorating and after providing basic first aid, there was no improvement.

Airway Patients with an altered level of consciousness are at risk of airway obstruction and must receive ongoing assessment and active management. This patient is demonstrating a clear airway by his ability to talk normally.

Breathing The presence of respiratory distress, inadequate respiratory effort and pulmonary oedema require immediate intervention. This patient appears to have a raised respiratory rate that could be due to a metabolic (lactic) acidosis secondary to reduced perfusion. Respiratory compromise secondary to left ventricular failure is a possibility, but is unlikely to have developed this quickly.

B RE AT HI NG Look for! • Respiratory rate, rhythm and effort

Cardiovascular The cardiovascular assessment should seek to resolve the question of compromised perfusion (haemodynamic instability). Evidence of an altered level of consciousness, hypotension (BP 0.12 sec) (see Table 25.2). This simplified and stepped approach allows the clinician to quickly identify the tachyarrhythmia and instigate a management strategy, particularly when a patient is presenting with compromised perfusion. TABLE 25.2 Basic arrhythmia assessment

Neurological Patients with an arrhythmia who present with an altered level of consciousness require immediate management. The altered level of consciousness results from compromised cardiac output and increased myocardial demand. Although this patient appears to have some compromise to his cerebral perfusion he is not so badly affected that he is unconscious.

Initial assessment summary Problem Collapsed while walking in the park Conscious state GCS = 13 (E4, V4, M5) Position Lying under a tree Heart rate 170 weak, regular Blood pressure 85/50 mmHg Skin Extremely pale and sweaty appearance Speech pattern Phrases Respiratory rate 36 BPM Respiratory Even cycles rhythm Respiratory Elevated effort Chest Equal air entry bilaterally, no adventitious sounds auscultation Pulse oximetry 92% on room air Temperature 36.7°C Motor/sensory Normal function History Walking briskly in the park, seen to clutch his chest and collapse ECG Wide-complex regular tachycardia, which appears to be ventricular tachycardia (QRS 0.16 sec) D: The patient has been made safe by bystanders. A: The patient is conscious with no current airway obstruction, but needs frequent reassessment. B: The respiratory rate is elevated but ventilation appears normal. C: Heart rate is elevated and there is insufficient blood pressure to maintain adequate cerebral perfusion. The ECG indicates an arrhythmia that could be a possible cause. Considering the wider picture, this patient has a clinical appearance and history that is compatible with ventricular tachycardia, which is providing enough perfusion for him to remain conscious but not enough to maintain orientation.

CONFIRM The essential part of the clinical reasoning process is to seek to confirm your initial hypothesis by finding clinical signs that should occur with your provisional diagnosis. You should also seek to challenge your diagnosis by exploring findings that do not fit your hypothesis: don’t just ignore them because they don’t fit.

DIF F ERENT IA L DIA GNOSIS Ventricular tachycardia Or • Supraventricular tachycardia (SVT) with bundle branch block (BBB)

This patient is presenting with an arrhythmia that is greater than 100 BPM, regular and has a QRS complex of greater than 0.12 sec. Using Table 25.2, this would indicate that the patient could be presenting with one of two arrhythmias: ventricular tachycardia or supraventricular tachycardia with a bundle branch block (BBB).

What else could it be? SVT with BBB Distinguishing between ventricular tachycardia and supraventricular tachycardia with aberrancy (BBB) can be difficult and clinicians are strongly advised to manage the patient as if the arrhythmia were ventricular tachycardia, particularly if there is any uncertainty. Importantly, there is a significantly lower risk for the patient to manage supraventricular tachycardia with aberrancy as if it were ventricular tachycardia than to manage ventricular tachycardia as if it were supraventricular tachycardia with aberrancy. Primary cardiac causes of ventricular tachycardia include ischaemia, acute myocardial infarction and structural defects. Potential reversible causes may include electrolyte disturbances or medications/drugs.

P RACT ICE T IP Consider long QT as a cause of ventricular tachycardia/ventricular fibrillation. Selected causes of long QT include: • congenital (long QT syndrome) • electrolyte abnormalities (hypokalaemia, hypomagnesaemia, hypocalcaemia)

• medications (tricyclic antidepressants, antipsychotics, phenothiazines) • organophosphates.

Evidence of one or more of the following findings is associated with an increased likelihood of the arrhythmia being a ventricular tachycardia: • QRS complex width >0.14 sec • RS interval >0.1 sec (high specificity for ventricular tachycardia) • Negative concordance in praecordial leads (strongly favours ventricular tachycardia as this is evidence of a highly unusual axis of depolarisation) • Positive aVR likely to be due to significant axis deviation • Patient >35 years of age • Patient has a previous cardiac or ventricular tachycardia history • Evidence of P waves occurring independently of the QRS complexes seen as minor irregularities in the overriding ECG • Evidence of fusion beats where an atrial contraction initiates a ventricular contraction, which is then incorporated into the VT beat. This patient has a QRS complex width of >0.14 sec and is older than 35 years of age. This strongly supports the ECG interpretation of ventricular tachycardia.

T REAT Emergency management The management of all tachyarrhythmias is aimed at controlling the rate and/or rhythm. This allows for a reduction in the oxygen demand of the cardiac tissue and improved cardiac output. The increase in cardiac output leads to an increase in blood pressure and finally end-organ perfusion. This will be evidenced by improved mental status, a reduction in respiratory distress, increasing blood pressure and reduction of pale, diaphoretic skin. While developing a management plan, it is important to recognise the potential risks associated with each intervention. All interventions associated with the management of arrhythmias have the potential to adversely impact the patient. Principles of management for wide-complex tachycardias (with pulse) are outlined in Box 25.1. B O X 2 5 . 1P

rinc iples o f manag ement

Wide-complex tachycardias (with pulse) • Provide supportive care. • Identify and manage underlying cause. • If compromised perfusion, undertake synchronised cardioversion. • If cardioversion unsuccessful, consider amiodarone. • Transport patient to an appropriate facility.

Safety Management of patients presenting with arrhythmias may require the use of medications, defibrillation, synchronised cardioversion or pacing. At all times consideration should be given to the safety aspects of these skills and procedures, particularly in a moving vehicle. Position This patient is presenting with compromised perfusion and respiratory distress. He should be postured supine and receive supplemental oxygenation, and intravenous access should be gained. Posture and intravenous fluid can be used to increase central venous pressure and thus venous return to the heart. The improved filling pressure will increase ventricular stretch and force of contraction, producing increased cardiac output unless the heart is already overstretched and the patient already in failure. Optimising the patient’s preload will help reduce the possible haemodynamic risks that can be associated with sedation before cardioversion. Synchronised cardioversion Synchronised cardioversion, like a direct current countershock (defibrillation), involves passing an electrical current through the heart, forcing cardiac myocytes and autorhythmic cells to depolarise at one time. Cardioversion will then potentially allow one of the autorhythmic cells to resume pacemaker control of the heart. Unlike the unsynchronised delivery of a direct current countershock, the current delivered during cardioversion is synchronised with the R wave. This eliminates the risk of the current being delivered during the relative refractory period of the action potential and therefore the risk of ventricular fibrillation is also reduced. Initial biphasic energy settings for cardioversion will differ, depending on the arrhythmia present. This patient is presenting with monomorphic ventricular tachycardia, so an initial setting of 100 joules is appropriate. Should the initial attempt be unsuccessful, energy levels should be increased incrementally and attempted up to a maximum of three times before considering pharmacological intervention. If synchronised cardioversion is contemplated, sedation to the point of creating amnesia would be good patient care. Sedation of this patient presents a number of challenges if the patient is already haemodynamically compromised. While considering the use of sedating medication, the following questions must be considered:

• Does the patient have a predicted difficult airway for management? • What is the most appropriate pharmacological intervention, considering the compromised nature of the patient’s perfusion? • What are the potential risks? • If sedation is required, is waveform capnography available? • What is the plan to manage the patient’s airway, should it become compromised? • Is the pre-hospital team briefed and have individual roles been delineated? • Is all of the equipment prepared? Pharmacological intervention Patients who present with a wide complex tachycardia and compromised perfusion should, if cardioversion is unsuccessful, be administered amiodarone 300 mg intravenously over 10–20 minutes (a compromise between the urgency of the situation and the recommended rate of infusion in a controlled situation), followed by a second cardioversion attempt. Amiodarone is a class III Vaughan-Williams antiarrhythmic agent (see Box 25.2). B O X 2 5 . 2T

h e Va u g h a n -Willia m s

c la ssific a tio n o f a n tia r r h yth m ic d r u g s The Vaughan-Williams classification of antiarrhythmic medications was initially described as four distinct groupings (classes I–IV), based on their effect on the action potential. Later, due to the inability of the system to classify all antiarrhythmic medications, a fifth class was added. • Class I agents block fast sodium channels, decreasing the depolarisation rate of phase 0 of the action potential and increasing the refractory period. Class I agents are further subdivided into Ia (prolong the action potential), Ib (no change to the duration of the action potential) and Ic (slight prolonging of the action potential). • Class II agents include beta-adrenoceptor antagonists. These agents decrease the ability of the sympathetic nervous system and therefore slow impulse conduction, prolong the duration of the action potential and reduce automaticity. • Class III agents, including amiodarone, prolong the action potential (plateau phase) by blocking the efflux of potassium during repolarisation. • Class IV agents slow the voltage-gated calcium channels, decreasing the plateau phase and reducing contractility. • Class V is a mixture of antiarrhythmic medications and includes digoxin and adenosine. Note: amiodarone, although placed in class III, has actions that spread across classes I, II, III and IV.

EVALUAT E Any patient presenting with an arrhythmia requires continuous assessment, cardiac monitoring and the acquisition of a 12-lead ECG. Should the patient present with no signs of compromised perfusion (haemodynamically stable), they should be transported to an appropriate facility for further assessment and management. This patient requires sedation prior to cardioversion. The administration of sedation is likely to impact the patient’s central nervous, respiratory and cardiovascular systems. Optimising the central venous pressure and thus preload will mitigate some of the negative haemodynamic effects of sedation, but the patient will require close ongoing monitoring if the rhythm is not reverted by the interventions discussed above.

Ongoing management On arrival at the ED, if the patient is presenting with compromised perfusion, the initial priority will be to control the arrhythmia with synchronised cardioversion. Consideration will also be given to pharmacological intervention and management of reversible causes. If the patient is stable, additional assessment may be conducted, allowing for an exploration of potential causes of the arrhythmia. This may include: • 12-lead ECG to confirm the diagnosis of ventricular tachycardia • laboratory tests such as troponin, urea, creatinine, electrolytes and thyroid function; if the patient was prescribed medications such as digoxin, additional blood testing would be completed to exclude toxicity • chest x-ray to investigate structural defects • consultation with a cardiologist. If the aetiology of a regular, monomorphic, wide-complex tachycardia cannot be established and the patient is stable, consideration may be given to the use of adenosine as a treatment and/or diagnostic tool. For stable ventricular tachycardia the preferred management strategy is administration of antiarrhythmic medications (Vaughan-Williams class I [lignocaine] or class III [amiodarone]) or elective cardioversion.

Hospital admission Following acute management in the ED, the patient will be transferred for further evaluation. A 12-lead ECG completed at rest will assist in the diagnosis of congenital abnormalities, electrolyte disturbances or structural disease. Cardiac stress testing and ambulatory monitoring are often used for patients with ventricular arrhythmias and assist with diagnosis of myocardial ischaemia, structural disease/changes and diagnosis of arrhythmias. Where patients are believed to have structural heart disease, it is recommended they undergo an echocardiograph. Electrophysiological testing may also be recommended in patients with coronary heart disease. The primary goal of long-term management of arrhythmias is to reduce morbidity and mortality. Management may consist of a reduction in cardiac remodelling following myocardial infarction, ongoing management of electrolyte disturbance risks, antiplatelet and anticoagulant therapy, consideration of an implantable cardioverter-defibrillator in patients with low ejection fractions, radiofrequency catheter ablation or revascularisation of coronary arteries.

Arrhythmias across the lifespan Ne ona te s The normal heart rate for a neonate is 100–160 BPM. A rate less than 100 BPM requires intervention and a rate greater than 160 BPM should be investigated further. Arrhythmias are seen in approximately 1–5% of neonates and the most common symptomatic arrhythmia is supraventricular tachycardia (Dubbin, 2000). When managing arrhythmias in neonates, clinicians should use a similar approach to that used for all paediatric patients. Bradycardia in neonates is predominantly caused by hypoxia and requires appropriate airway and respiratory support. The bradycardia should resolve quickly following the instigation of effective airway and respiratory support. If effective management of the airway and ventilation does not resolve the bradycardia and further resuscitation is not required, consideration should be given to an assessment of the ECG and potential differential diagnoses (congenital, sepsis, acidosis, trauma, hypovolaemia etc). If unstable, consideration should be given to specific arrhythmia bradycardia management (atropine, pacing etc). Transportation to a tertiary facility specialising in neonatal services is key. Tachyarrhythmias may have an extremely rapid ventricular rate (240–300 BPM), increasing the difficulty of ECG diagnosis. Specialist medical support is required and clinicians should carefully consider the risks prior to initiating any interventions. As with other tachyarrhythmias, two classifications should be used: narrow complex and broad complex. Narrow complex are significantly more common than wide complex and both should be managed as per the paediatric treatment guidelines. As with bradycardia, transport to a facility with a specialist neonatal service is important. Pre-hospital clinicians generally have limited experience and knowledge relating to the management of neonates with arrhythmias. Due to this, consideration should be given to consultation with a specialist facility prior to the initiation of management outside of standard neonatal resuscitation.

During pregnancy Throughout pregnancy there are a number of compensatory alterations to the maternal anatomy and physiology. Specifically, the cardiac alterations include increased heart rate, increased cardiac output, alterations in the size and position of the heart, changes in systemic vascular resistance and alterations in blood pressure. Importantly, the criteria by which arrhythmias are diagnosed and the majority of management strategies are identical for pregnant and non-pregnant females. When assessing and managing a pregnant patient, follow the standard approach and management strategies, noting the following: • There is an increased risk of arrhythmia in patients with underlying cardiac disease. • Differential diagnoses should be considered, both related and unrelated to the pregnancy. • All medications used in the management of arrhythmias cross the placenta. • Patients who present as haemodynamically unstable require management. Remember that compromised maternal perfusion will result in fetal compromise. • Consideration should be given to the fetus when managing arrhythmias in this subgroup

of patients, but the mother ’s health should remain the primary consideration. • Transportation to a facility that has the appropriate specialist services should be considered. • Appropriate positioning of the mother should be considered to reduce the risk of supine hypotension syndrome, resulting from compression of the descending aorta by the fetus.

Athletes Athletes have an overall lower risk of adverse health events, but may present with arrhythmias and/or sudden cardiac death. The vast majority of young athletes (35 years of age) who die suddenly the majority are again male and are engaged in strenuous activity. Approximately half complain of symptoms preceding the collapse and all present with structural cardiac defects. The most common arrhythmia found in athletes is sinus bradycardia and this is strongly correlated with fitness. Despite this, other causes may be present and careful examination is recommended. When confronted with an athlete presenting with an arrhythmia or symptoms suggestive of an arrhythmia, the standard approach to assessment and management should be undertaken.

Wolff-Parkinson-White Wolff-Parkinson-White conduction occurs when an accessory conduction pathway is present between the atria and the ventricles. The additional pathways allow the electrical impulse to bypass the AV node and potentially cause a tachyarrhythmia. Wolff-ParkinsonWhite conduction presents with a shortened PR interval and delta wave. When the pathway is associated with a supraventricular tachycardia, it is known as Wolff-ParkinsonWhite syndrome. In athletes, there is no increased occurrence, but potentially increased risk due to high sympathetic drive.

Long QT syndrome Long QT syndrome can be either acquired (i.e. medications, AMI, electrolyte disturbances) or genetic and despite its origin it can result in polymorphic ventricular tachycardia (torsades de pointes; see Box 25.3). Management consists of direct current countershock and magnesium (in addition to standard advanced life support measures). Prevention includes the use of beta-blockers and, in a small subset of patients, an implantable cardioverter-defibrillator. Long QT syndrome is associated with cardiac arrest in young people and should be sought out in other family members once a case has been suspected. Other family members can be managed prophylactically to prevent further arrests. B O X 2 5 . 3P

o l ym o r p h i c ve n t r i c u l a r t a c h yc a r d i a

and to r sades de po intes Polymorphic ventricular tachycardia is easily distinguished from monomorphic ventricular tachycardia by assessing the morphology of the QRS complex. Monomorphic ventricular tachycardia presents with essentially similar-shaped QRS complexes, whereas in polymorphic ventricular tachycardia the complexes are irregular. Torsades de pointes (twisting of the points) is a polymorphic ventricular tachycardia and presents with a varying axis. Examination of the ECG will reveal a QRS complex that appears to be twisting around the isoelectric line. Torsades typically has a prolonged QT interval seen on the non-tachycardia baseline ECG and usually resolves spontaneously; however, patients are also at risk of ventricular fibrillation. Management of these arrhythmias consists of defibrillation as per ventricular fibrillation. Other management strategies are determined by the presence or absence of a prolonged QT interval. The QT interval is the time from the start of ventricular depolarisation to the end of repolarisation; increasing this interval is associated with an increased relative refractory period. Because the QT interval is affected by heart rate, a formula is used to correct for the rate when assessing for prolonged QT. The corrected QT interval (QTc) is calculated using Bazett’s formula: corrected QT = QT/square root of the R-R interval. The corrected values should be ≤0.44 sec in adult males and ≤0.46 sec in adult females. Management to prevent the recurrence of torsades consists of eliminating medications that prolong the QT interval, managing electrolyte disturbances or other underlying cause (if identifiable) and intravenous magnesium. Polymorphic ventricular tachycardia with a normal QTc (not always possible to examine in the pre-hospital setting as an ECG is required where the patient has a sinus rhythm) is predominantly caused by ischaemia and should be managed as per monomorphic ventricular tachycardia. Due to the mechanism, magnesium is unlikely to be effective. Intravenous amiodarone and betablockers should be considered.

Commotio cordis Commotio cordis is defined as sudden cardiac death in an individual with no structural cardiac disease following a blow to the chest. Factors that increase the risk of commotio cordis include male gender; small, hard and round objects striking the chest; a direct strike to the left side of the chest; and increased velocity of the strike. The object striking the chest causes a focal ventricular depolarisation during the upstroke of the T wave (relative refractory period), resulting in ventricular fibrillation. The majority of cases occur in individuals younger than 16 years of age and rarely occur in patients older than 21. It is probable that this is due to the increased compliance of the chest wall in younger patients, allowing the force to be more readily transferred through to the myocardium. Management is as per the standard advanced cardiac life support treatment guidelines.

CA SE ST U DY 2 Case 12487, 1850 hrs. Dispatch details: A 25-year-old male complaining of chest pain and palpitations. Initial presentation: The paramedics arrive outside a local gym and are taken inside by the patient’s friend. The patient is seated in the reception area.

ASSESS 1900 hrs Primary survey: The patient is conscious and alert. Chief complaint: ‘I have pain in my chest and my heart feels like it’s racing. The same thing happened a few days ago.’ 1903 hrs Vital signs survey: Perfusion status: HR 185 BPM, BP 110/70 mmHg, skin warm and pink, ECG (see Fig 25.8).

FIGURE 25.8 A Narrow-complex supraventricular tachycardia at a rate of 240 BPM with no retrograde or antegrade P wave visible in the R-R cycle. The tachycardia was subsequently confirmed to be type 1 atrioventricular nodal reentrant tachycardia on electrophysiological study. B Narrow-complex supraventricular tachycardia at a rate of 206 BPM with the retrograde P wave

clearly visible in the mid-R-R cycle, especially in lead V1. The tachycardia was subsequently confirmed to be atrioventricular re-entrant tachycardia with a retrograde posteroseptal accessory pathway on electrophysiological study. Source: Saksena & Camm (2011). Respiratory status: RR 16 normal effort, good air entry, L = R, SpO2 98% on room air. Conscious state: GCS = 15, dizzy. 1907 hrs Pertinent hx: The patient’s heart started racing during a workout. He describes it as ‘pounding’. He then had the onset of chest pain that he rates 1/10. A similar thing happened a week ago but he doesn’t recall what his doctor said it was. He was given medication that made him feel like he was going to die and he stresses that he doesn’t want it again. It did stop the pounding though. He has not followed up with his GP. He has no previous medical or family history, is generally fit and healthy and is currently not taking any medications.

CONFIRM In many cases paramedics are presented with a collection of signs and symptoms that do not appear to describe a particular condition. A critical step in determining a treatment plan in this situation is to consider what other conditions could explain the patient’s presentation. This patient is presenting with symptoms of, and an ECG consistent with, a paroxysmal atrial tachycardia otherwise known as an SVT. This could be due to a congenital extra conduction pathway.

What else could it be? Stimulants Stimulant drugs, such as amphetamines or cocaine, may lead to the presentation of arrhythmias and patients should be questioned in a respectful manner to investigate this possibility. Supporting evidence may include drug paraphernalia, changes in pupil size or intravenous injection marks. The actual arrhythmia may be a paroxysmal atrial tachycardia or simply a sinus tachycardia.

DIF F ERENT IA L DIA GNOSIS SVT Or

• Stimulants • Electrolyte or acid–base abnormalities • Psychological stress • Compensatory sinus tachycardia • Hyperthyroidism

Electrolyte or acid–base abnormalities Within the pre-hospital setting electrolyte or acid–base abnormalities may be difficult to confirm, but careful consideration of the patient’s medications, history and presentation may offer some insight. Electrolyte abnormalities may be responsible for instability of the cardiac cell membrane leading to increased automaticity and arrhythmias associated with both extra depolarisation and reentry. Psychological stress The history of the event and the patient’s presentation will assist in excluding this diagnosis. Increased automaticity affecting both the firing rate of the SA node (sinus tachycardia) and cell membrane stability across the whole myocardium can occur in response to raised catecholamine levels. Compensatory sinus tachycardia This may occur in the presence of trauma, hypoxia, infection or sepsis. The ECG should be reviewed, attempting to identify P waves, and the patient’s presentation and assessment should be considered in the light of the potential differentials. The approximate maximal sinus tachycardia rate for an adult can be calculated by subtracting the patient’s age from 220. Hyperthyroidism A rare but possible cause of tachycardia is increased automaticity associated with hyperthyroidism that can lead to arrhythmias including atrial fibrillation and supraventricular tachycardia. A history of weight loss, tachycardia and hyperreflexia might suggest hyperthyroidism, which could be confirmed with thyroid function tests in hospital. This case has a sudden onset of tachycardia in an otherwise fit individual. This is highly suggestive of supraventricular tachycardia. If the patient has a history of previous episodes with sudden onset and spontaneous resolution this would support the diagnosis of supraventricular tachycardia. In addition, he described the side effects of adenosine when stating he felt as though he was going to die following drug administration (see Box 25.4). B O X 2 5 . 4A d e n o

sine

Adenosine is a class V antiarrhythmic agent with a half-life of approximately 10 seconds. It works by hyperpolarising the pacemaker potential within the AV node, slowing the transit of impulses through the nodal tissues (negative dromotropic effect). Following

administration, patients may complain of an ‘impending doom’ and present with symptoms such as chest pain, respiratory distress, nausea or dizziness. Some patients require a small (0.5–1.5 mg) dose of midazolam before administration of adenosine. Due to its very short half-life, adenosine should be administered via a rapid intravenous push and flushed with at least 20 mL of saline: • First dose: 6 mg adenosine with saline flush (55–60% of patients will revert with a 6 mg dose). • Second dose: If arrhythmia does not revert after 1–2 minutes, 12 mg with saline flush will increase the reversion rate to 90%. • Third dose: If arrhythmia does not revert after 1–2 minutes, 12 mg with saline flush will increase the reversion rate to 96%.

T REAT 1910 hrs: The paramedics have the patient perform the Valsalva manoeuvre (see Box 25.5) but it is not successful in reverting the arrhythmia. B O X 2 5 . 5T

h e Va l s a l va m a n o e u vr e

The Valsalva manoeuvre is considered a first-line management strategy for regular, narrow-complex tachyarrhythmias. Successful reversion of a supraventricular tachycardia through the use of the Valsalva manoeuvre is approximately 15–25% (Mottram & Svenson, 2011). To perform the Valsalva manoeuvre, place the patient head down with their feet elevated for several minutes, then instruct them to blow into a 10-mL syringe (enough pressure to slowly move the plunger) for 15 seconds. This increases intrathoracic pressure, which reduces venous return to the heart and therefore reduces cardiac output. A sympathetic stimulation then occurs in response to the reduced cardiac output. When the Valsalva chest pressure is released, the increased venous return suddenly and dramatically increases cardiac output. It is the parasympathetic response to the rapidly increasing cardiac output in a situation where the sympathetic tone is increased that produces the vagal response. The vagal response causes a reduction in conduction velocity through the AV node. The possible outcomes from the Valsalva manoeuvre include successful reversion or a transient slowing of the rate, revealing a sinus rhythm or a flutter wave. If the Valsalva manoeuvre is unsuccessful, it should be repeated. A

carotid sinus massage may also be considered; however, it is painful if performed properly and it is not recommended in elderly patients (or in an unknown patient over the age of 50) because of the possibility of displacing an atheroma causing an embolic stroke.

1912 hrs: The paramedics gain IV access and administer adenosine. When administering adenosine the patient must be reassured that they are safe and that the feeling they are experiencing will pass. Midazolam may be considered prior to administration where local guidelines permit. If adenosine administration fails to revert the rhythm, or if the patient is rapidly deteriorating, synchronised cardioversion can be considered. 1915 hrs: After performing the Valsalva manoeuvre the patient’s ECG reverts to a sinus rhythm. He indicates that his chest discomfort is resolving. Perfusion status: HR 70 BPM; BP 125/85 mmHg; skin dry, warm and pink; ECG sinus rhythm. Respiratory status: RR 12 BPM, normal effort, good air entry, L = R, SpO2 97%. Conscious state: GCS = 15.

EVALUAT E Evaluating the effect of any clinical management intervention can provide clues to the accuracy of the initial diagnosis. Some conditions respond rapidly to treatment so patients should be expected to improve if the diagnosis and treatment were appropriate. A failure to improve in this situation should trigger the clinician to reconsider the diagnosis. This patient requires transport for a medical review. En route to hospital he should receive continuous cardiac monitoring, completion of a 12-lead ECG and regular vital signs assessment.

CA SE ST U DY 3 Case 18064, 2124 hrs. Dispatch details: A 75-year-old male has had a syncopal episode. He is at home and his wife advises that he is not alert and is pale and diaphoretic. Initial presentation: The crew are led inside a private house and find the patient sitting on the lounge.

ASSESS 2137 hrs Primary survey: The patient does not respond to their voices, but he does ‘groan’ following a painful stimuli. Chief complaint: The patient’s wife states that he had been complaining of feeling unwell for about 30 minutes and got up to go to bed. He then fainted. 2138 hrs Vital signs survey: Perfusion status: HR 32 BPM; sinus bradycardia; BP 80/50 mmHg; skin cool, pale, diaphoretic. Respiratory status: RR 28 BPM, good air entry, L = R, no adventitious sounds, SpO2 non-sensing. Conscious state: GCS = 8 (E2, V2, M4). Blood glucose level: 5.7 mmol/L. 2142 hrs Pertinent hx: The patient has a significant history of cardiac problems, based on his prescribed medications for hypertension, hyperlipidaemia, high cholesterol and diabetes mellitus type 2. ECG interpretation should follow the same structure as with any arrhythmia (see Table 25.3). Notwithstanding this, the ECG should be examined for P waves and if present, the P wave QRS complex ratio/relationship should be examined. TABLE 25.3 ECG interpretation for bradycardia

CONFIRM In many cases paramedics are presented with a collection of signs and symptoms that do not appear to describe a particular condition. A critical step in determining a treatment plan in this situation is to consider what other conditions could explain the patient’s presentation.

DIF F ERENT IA L DIA GNOSIS Sinus bradycardia Or • SA node hypoxia • Sinus bradycardia secondary to parasympathetic stimulation • Drug toxicity • Hypothermia

What else could it be? SA node hypoxia This patient is an elderly diabetic with a significant cardiac history and is on medication for hyperlipidaemia. It would not be surprising if he had ischaemic heart disease, particularly involving the right coronary artery, which is responsible for supplying the SA node. When an opportunity presents itself to perform an ECG (see Fig 25.9), evidence of acute ischaemia in the right coronary artery may confirm this.

FIGURE 25.9 Sinus bradycardia. Source: Saksena & Camm (2011). Sinus bradycardia secondary to parasympathetic stimulation A profound sinus bradycardia can be associated with excessive parasympathetic stimulation. Parasympathetic stimulation may be secondary to visceral innervation from urinary retention or bowel obstruction. Drug toxicity There are a number of drugs that could be responsible for bradycardia if they are present in too great a concentration. These include beta-blockers, calcium

channel blockers and digoxin. The drug concentration may be increased due to patient error or impaired drug clearance, often associated with renal failure. A detailed drug history may identify a possible drug. Renal function tests and levels of some drugs can be obtained at hospital. Hypothermia Elderly patients presenting with a decreased conscious state and bradycardia may actually be hypothermic. Clinical examination looking for hypothermia will exclude this, but note that many of the easily applied thermometers (i.e. tympanic membrane thermometer) may have a significant error, particularly at low temperatures.

T REAT The patient should be positioned supine to aid venous return to the heart. All patients should receive continuous cardiac monitoring and intravenous access should be gained. A fluid challenge to increase the central venous pressure (CVP) and preload may improve the patient’s perfusion and thus the perfusion of the SA node if positioning has been insufficient to restore adequate perfusion. However, fluid is unlikely to revert the bradycardia and in this case it makes no change to the patient’s vital signs. 2153 hrs: The crew administer 600 mcg of atropine IV. Atropine administration to block parasympathetic innovation to the SA node may allow for the sympathetic drive to increase the heart rate. In this case atropine is not effective (see Box 25.6). Adrenaline can be administered according to local guidelines if atropine is not effective. Adrenaline is a catecholamine and stimulates alpha, beta-1 and beta-2 receptors, resulting in peripheral vasoconstriction and increased inotropic and chronotropic effects. B O X 2 5 . 6T

r ansc utaneo us pac ing

Patients presenting with significant physiological derangement who are not responding to atropine or who have second-degree type II or third-degree AV block should have transcutaneous pacing pads placed anterior posterior and pacing initiated if they are significantly compromised (see Fig 25.10). In the pre-hospital setting fixed pacing mode will be used, as the pacing is not affected by movement artefact shutting off the demand pacing function. Once in a stable environment it is safer to employ demand pacing, which will cease when the patient’s own rate increases. Initiating transcutaneous pacing requires a number of considerations and ongoing assessments. The pacer rate should be set initially at 60–70 BPM and then adjusted to produce effective output, balancing rate and oxygen demand versus maintenance of

pressure. Electrical capture is evidenced by a pacing spike, followed by a broad QRS complex. The energy setting should be increased quickly until electrical capture is consistently achieved. Mechanical capture is evidenced by palpation of a pulse associated with every QRS complex. Ongoing monitoring is required to ensure that electrical capture and mechanical capture are maintained. Passing electrical currents through a patient’s chest may cause discomfort. This is typically managed with small aliquots of a narcotic analgesic and midazolam.

FIGURE 25.10 Transcutaneous pacemaker. Pacing electrodes are placed on the patient’s anterior A and posterior B chest walls and attached to an external pacing unit C. Source: Brown & Edwards (2012).

EVALUAT E Evaluating the effect of any clinical management intervention can provide clues to the accuracy of the initial diagnosis. Some conditions respond rapidly to treatment so patients should be expected to improve if the diagnosis and treatment were appropriate. A failure to improve in this situation should trigger the clinician to reconsider the diagnosis. This patient responds to the adrenaline infusion after several small increases in dose. At this point his heart rate has increased to 58 BPM and his blood pressure is 100/70 mmHg. Although technically still bradycardic, this response reflects a significant improvement and could be considered sufficient. Any further increases in inotrope infusions should be titrated against the onset of side effects such as ectopic beats.

Summary Arrhythmias are a leading cause of death in Australia and a common presentation within the pre-hospital environment. Irrespective of the type of arrhythmia, the central question to be answered is around the issue of compromised perfusion. End-organ dysfunction, resulting from compromised perfusion, commonly presents with syncope, altered level of consciousness, respiratory distress, hypotension, shock, chest pain and heart failure. A 12lead ECG is an important diagnostic tool for patients with an arrhythmia, but the clinician must weigh up the need for immediate management with the additional information provided by the ECG. When confronted with a patient with an arrhythmia, you should: complete a rapid but thorough assessment; consider and manage reversible causes; provide initial care including appropriate posturing, airway and ventilator support, oxygenation and intravenous access; consider and, if appropriate initiate, specific arrhythmia management; and provide ongoing assessment and transport to an appropriate facility.

References Australian Bureau of Statistics (ABS)Causes of Death in Australia. Canberra: ABS, 2010. [Cat. no. 3303.0]. Boron, W. F., Boulpaep, E. L. Medical Physiology, 2nd ed. Philadelphia: Saunders, 2009. Brown, D., Edwards, H. Lewis’s Medical-Surgical Nursing, 2nd ed. Sydney: Elsevier, 2012. Craft, J., Gordon, C., Tiziani, A.Understanding Pathophysiology. Sydney: Elsevier, 2011. Dubbin, A. M. Arrhythmias in the newborn. NeoReviews. 2000; 1(8):e146–e151. Hall, J. Guyton and Hall Textbook of Medical Physiology, 12th ed. St Louis: Saunders, 2012. Link, M. S., Estes, N. A. Athletes and arrhythmias. Journal of Cardiovascular Electrophysiology. 2010; 21(10):1184–1189. Mottram, A. R., Svenson, J. E. Rhythm disturbances. Emergency Medicine Clinics of North America. 2011; 29:729–746. Ninio, D. F. Contemporary management of atrial fibrillation. Australian Prescriber. 2000; 23:100–102. Park, D. S., Fishman, G. Basic electrophysiological procedures for the clinician. In Saksena I., Camm J., eds.: Electrophysiological Disorders of the Heart, 2nd ed., Philadelphia: Saunders, 2011. Patton, K. T., Thibodeau, G. A. Anatomy & Physiology, 7th ed. St Louis: Mosby, 2010. Royster, R. L. Arrhythmia or dysrhythmia. Anesthesia and analgesia. 1990; 70(1):125. Saksena, S., Camm, J. A. Electrophysiological Disorders of the Heart, 2nd ed. Philadelphia: Saunders, 2011. WHO ISC Task Force. Definition of terms related to cardiac rhythm. American Heart Journal. 1978; 95(6):796–806.

CHAP TER 26

Cardiac arrest By Andy Symons and Hugh Grantham

C O N C E P TS U S E D I N TH I S C H A P TE R • The paramedic’s clinical approach: Section 2 • Perfusion: Chapter 55 • The autonomic response: Chapter 56

OVERVIEW • Out-of-hospital cardiac arrest (OHCA) is common and has poor outcomes (Bernard, 2014). • Myocardial infarction and coronary heart disease are major risk factors for OHCA and significantly increase mortality risk. • Changes to cardiac arrest guidelines in the past decade have emphasised the importance of uninterrupted chest compression and have led to improved rates of return of spontaneous circulation (ROSC). • ROSC rates following cardiac arrest are now as high as 50% but survival with complete neurological recovery (CNR) remains around 2–3%. • Survival rates are linked to the underlying cause of cardiac arrest, comorbidities, arrest ‘downtime’, bystander CPR, time to first defibrillation and the type of presenting cardiac arrest arrhythmia (Nolan, 2011). • Cardiac arrest arrhythmias are divided into shockable rhythms and non-shockable rhythms. Shockable rhythms include ventricular fibrillation (VF) and pulseless ventricular tachycardia (VT); and the non-shockable rhythms are asystole and pulseless electrical activity (PEA). • The important factors in cardiac arrest management are non-interrupted cardiopulmonary resuscitation (CPR), effective chest compressions, adequate ventilation and non-delayed defibrillation of shockable rhythms. • There is no current evidence to suggest that the use of cardiac arrest drugs or advanced airway devices improves patient survival rates post cardiac arrest. • Paediatric cardiac arrest usually occurs as a result of hypoxia and/or hypovolaemia. The most common cardiac arrest arrhythmia is asystole. Shockable arrhythmias are uncommon and

usually result from underlying cardiac disease, poisoning or hypothermia. • Post-resuscitation care following ROSC is targeted at preserving normal cerebral, cardiac and haemodynamic function and is a rapidly developing field.

Introduction In Australia, in excess of 30,000 people die each year from cardiac arrest, with many victims having no previous symptoms (ABS, 2010). The leading underlying cause of death is ischaemic heart disease, which includes the spectrum of diseases found in acute coronary syndrome. Out-of-hospital cardiac arrest (OHCA) is common and, of those developing myocardial infarction, one-third will die before reaching hospital, with many dying within an hour of the onset of acute symptoms (ARC, 2011). Out-of-hospital cardiac arrests encapsulate most of the unique challenges that face paramedics: they occur in the public domain, unexpectedly and often in front of the patient’s friends and relatives. The possible causes are vast; the diagnostic tools are few. Equipment is limited by portability and the responding team members may never have even met each other beforehand. It is for these reasons that adhering to the evidencebased algorithms developed for cardiac arrest (see Fig 7.4) is so important (ARC, 2011). The structure, sequencing and standardisation that the algorithms provide have been demonstrated to improve patient outcomes and they allow people who are unfamiliar with each other to quickly form into a team that works cooperatively. The vast majority of cardiac arrests occur as a result of coronary artery disease (CAD; Modi & Krahn, 2011) and the standard Basic Life Support (BLS) and Advanced Life Support (ALS) algorithms support this pathology. In effect, they reduce the clinical reasoning required so that paramedics and other clinicians can deliver effective care without becoming overwhelmed by assessment and decision making. There are, however, a few forms of cardiac arrest that are unlikely to produce a positive outcome if some clinical reasoning is not applied and additional actions added to the procedure. The editors of this text fully endorse the BLS and ALS guidelines and stress they must be applied in all circumstances as every cardiac arrest requires a clear systematic approach. This chapter seeks to add to the understanding of cardiac arrest cases by exploring less typical causes and looking at firstly how they align with the standard algorithms and secondly how a deeper understanding can improve patient outcomes.

Chain of survival Successful outcomes following a cardiac arrest are influenced by a number of key interventions. These interventions are conceptualised in the chain of survival (Adgey & Johnston, 1998). The chain of survival is based on evidence that may help improve a person’s chances of surviving a cardiac arrest. Each link in the chain aims to improve survival outcomes in patients suffering from cardiac arrest through a number of connected actions. As with any chain, it is only as strong as its weakest link. The links are: early recognition and call for help; early commencement of cardiopulmonary resuscitation (CPR); early defibrillation of shockable cardiac arrest arrhythmias; and, where return of spontaneous circulation (ROSC) has occurred, appropriate post-resuscitation care (see Fig 26.1). All factors may play a vital role in increasing the patient’s chances of survival of a cardiac arrest.

FIGURE 26.1 The chain of survival illustrates the role and effectiveness of intervention in the patient who has suffered a ventricular fibrillation arrest. CPR effectively prolongs the period in which defibrillation is effective and minimises systemic ischaemia. Source: (Top image): Laerdal. (Bottom image) Adapted from Laerdal (2011).

Early recognition and call for help The first link in the chain acknowledges the importance of recognising a patient at risk of cardiac arrest. Identifying symptoms such as pain and poor perfusion by the victim, family or bystanders will hopefully initiate an early call to the ambulance service for an immediate response.

Early commencement of CPR The primary goal of CPR is directed at maintaining some supply of oxygenated blood to keep the brain, myocardium and vital organs alive (Mistovitch & Karren, 2010). A lack of effective CPR has been shown to predict negative outcomes in patients regardless of other interventions (Souchtchenko et al., 2013). For every minute that passes between collapse and attempted defibrillation, mortality increases by 10–12% if CPR is not conducted (Mistovitch & Karren, 2010). The aim of CPR is to produce blood flow through the body via compression of the chest and in turn the heart. Retrograde flow is inhibited due to valves in the heart and the veins (Jung et al., 2006; Rajab et al., 2011). Even when CPR is applied flawlessly, the effectiveness of this action produces blood flow approximate to only 20–30% of the normal heart (Artini, Nath & Bartholomew, 2011). The ability to generate flow requires constant compressions, with flow falling to zero almost instantly compressions are ceased and requiring 10–12 compressions to recommence (Kern, 2002). As such, minimising any interruptions to chest compression has been extensively investigated over the past decade (Souchtchenko et al., 2013) and the emphasis on ventilation during CPR has been reduced for both lay and expert providers. The primary reason is that ventilation interrupts the delivery of chest compressions. For many clinicians this is counterintuitive, as providing oxygen through ventilation was previously considered to be essential. Research indicates, however, that positive outcomes are linked to minimally interrupted chest compression and that constant blood flow with less-thanideal levels of oxygen is more beneficial than little or no flow of oxygenated blood. For lay providers, the complete removal of ventilation has led to more untrained providers commencing chest compressions and, as a result, better patient outcomes (Ogawa et al., 2011; Iwami, 2012). In addition to interrupting chest compressions, positive pressure ventilation increases intrathoracic pressures, decreasing venous return and limiting cardiac output during CPR (Berg, 2001). Some groups have even reported success rates that compare favourably with conventional approaches when CPR consists of no ventilation at all for the first few minutes (Bobrow & Ewy, 2009; Bobrow et al., 2010; Kellum, 2007; Nolan & Soar, 2008). The current recommendations of the Australian Resuscitation Council include ventilation at a ratio of 30:2 with a pause for ventilation prior to intubation and 15:1 with no pause after intubation. Importantly, the survival rate of cardiac arrest is more likely to be successful when CPR is initiated early by bystanders (Nolan, 2011). Unfortunately, the average proportion of cases of OHCA that receive bystander CPR is less than 30% (ARC, 2011). High-quality CPR with minimal interruptions to chest compressions (i.e. never more than 10 seconds ‘off the chest’) is the focus of this link.

Early defibrillation Numerous studies have advocated the benefit of early defibrillation in order to save lives. Ideally, OHCA patients should be defibrillated within 5 minutes of their cardiac arrest (Artini, Nath & Bartholomew, 2011). This may well be achieved in many areas by bystanders using public automatic external defibrillators (AEDs), as in most cases the arrival of an ambulance may take more than 5 minutes. The first monitored cardiac arrhythmia is ventricular fibrillation (VF) or pulseless

ventricular tachycardia (VT) in approximately 25% of all cardiac arrests (Adgey & Johnston, 1998). VF and VT occur not only in acute myocardial infarction and primary electrical disturbances, but also secondary to antiarrhythmic drugs, prolonged QT syndromes, re-excitation syndromes and systemic hypoxaemia (Mistovitch & Karren, 2010). Time to defibrillation is the single most important determinant of shockable cardiac arrests. However, as stated above, when attempting defibrillation, interruptions in CPR must be minimised.

Post-resuscitation care The final link is aimed at providing effective post-resuscitation care following return of spontaneous circulation. It is targeted at preserving normal cerebral, cardiac and haemodynamic function and providing an optimum environment for recovery to take place. This phase addresses the importance of restoring quality of life to the cardiac arrest survivor. With improved CPR performance, the number of patients achieving ROSC in the field is exceeding 50% in some ambulance services (VACAR, 2012) and this is driving research into treatments that minimise post-arrest brain and other organ damage during this phase.

Pathophysiology Cardiac arrest is the cessation of effective cardiac output as confirmed by unconsciousness, abnormal breathing and the absence of signs of circulation (ARC, 2011). The cessation of cardiac output can be divided into four major causes: the onset of cardiac arrhythmias that do not allow the chambers of the heart to fill and contract effectively; internal structural factors in the heart such as valve prolapse that do not produce blood flow despite normal mechanical contraction of the heart; poisoning of the heart and restriction of the ability of the cells to depolarise or contract; and external mechanical forces that either restrict blood flow to or from the heart, or restrict the heart from expansion and contraction. Common causes of cardiac arrest are outlined in Table 26.1. TABLE 26.1 Common causes of cardiac arrest

Source: Adapted from Handley (2010). The most common cause of cardiac arrest is the development of VT or VF as the result of a sudden coronary artery occlusion (Modi & Krahn, 2011). The combination of coronary artery disease (CAD) and a disrupted atherosclerotic plaque (see Ch 24) creates a thrombus that occludes blood supply to a portion of the myocardium. The subsequent ischaemia that develops downstream of the occlusion alters the resting and threshold membrane potentials of myocardial cells in the area (see Ch 25). Myocardial cells that normally do not demonstrate any automaticity can spontaneously depolarise and generate an action potential that spreads through the heart. Depending on the location and frequency of this new aberrant pacemaker, the ventricles may not relax and contract with any coordination and cardiac output will fall or cease. Although VT may generate a cardiac output, it is a rhythm that places a high oxygen demand on the heart while not generating a high perfusion pressure to the coronary vessels. Add this supply/demand imbalance to the already occluded vessel and the area of ischaemia can expand and more aberrant pacemakers will develop. With multiple pacemakers now generating action potentials, the electrical wave radiating outwards from each can encounter tissue in either relatively refractory or absolute refractory periods and re-entry circuits can develop. Electrically-inert tissue from previous infarcts can also contribute to the development of re-entry circuits. The deterioration of VT into the chaotic electrical activity of VF should be

considered the rule rather than the exception and is described in Box 26.1. B O X 2 6 . 1M e c

hanism o f fibr illatio n

Ventricular fibrillation is characterised by a multitude of aberrant pacemakers propagating action potentials across the left ventricles. Like pebbles thrown into a pond each pacemaker generates a wavefront of electricity that spreads and encounters other waves. From initially just a single central point (see heart A in Fig 26.2) the first wave emanating from an aberrant myocardial cell causes a depolarisation wave to spread in all directions, leaving all the muscle beneath the electrode in a refractory state. After about 0.25 seconds, part of this muscle begins to come out of the refractory state. Some portions come out of refractoriness before other portions. This state of events is depicted in Figure 26.2A by many lighter patches, which represent excitable cardiac muscle, and dark patches, which represent still refractory muscle. Now another stimulus from the aberrant cell can cause impulses to travel only in certain directions through the heart but not in all directions. Thus, in Figure 26.2A, certain impulses travel for short distances, until they reach refractory areas of the heart, and then are blocked. But other impulses pass between the refractory areas and continue to travel in the excitable areas. When a depolarisation wave reaches a refractory area in the heart, it travels to both sides around the refractory area. Thus, a single impulse becomes two impulses. Then, when each of these reaches another refractory area, it, too, divides to form two more impulses. In this way, many new wave fronts are continually being formed in the heart by progressive chain reactions until, finally, there are many small depolarisation waves travelling in many directions at the same time. More and more impulses are formed; these cause more and more patches of refractory muscle, and the refractory patches cause more and more division of the impulses. Therefore, any time a single area of cardiac muscle comes out of refractoriness, an impulse is close at hand to re-enter the area. Figure 26.2B demonstrates the final state of fibrillation: many impulses travelling in all directions, some dividing and increasing the number of impulses, others blocked by refractory areas. The lack of coordinated electrical flow leads to no effective muscular contraction and no cardiac output. With no effective supply to perfuse the myocardial cells the movement of electrolytes against their concentration gradient becomes limited and the voltage of each depolarisation weakens and asystole eventually develops.

FIGURE 26.2 Mechanism of fibrillation. A Initiation of fibrillation in a heart when patches of refractory musculature are present. B Continued propagation of fibrillatory impulses in the fibrillating ventricle. Source: Hall (2012).

P RACT ICE T IP CPR will maintain circulation, allowing for delivery of oxygen and nutrients to cells and removal of waste, but it does not offer an opportunity for arrhythmia reversion—the paramedic’s top priority. Defibrillation is a means by which the heart is given the opportunity to resume a rhythm conducive with cardiac output, which in turn will provide a circulation better than even the best CPR can produce. Therefore, if a defibrillator is readily available, it must be used at the earliest possible time.

In the cases of VF and VT, myocardial metabolism continues, exhausting oxygen and adenosine triphosphate (ATP) supplies. Metabolic acidosis results from increased anaerobic metabolism and the accumulation of CO2 in the tissues. Cardiovascular collapse causes release of catecholamines, adrenal corticosteroids, antidiuretic hormone and other

hormonal responses, which can all lead to hyperglycaemia, electrolyte imbalances, increased lactate levels and thus a tendency towards further arrhythmias (Mistovitch & Karren, 2010). It is postulated that there are three phases of cardiac arrest: electrical phase, circulatory phase and metabolic phase (Craft, Gordon & Tiziani, 2010; Vilke et al., 2004): • The electrical phase begins immediately following cardiac arrest and ends after 4 minutes. During the initial stage of cardiac arrest the myocardium still has a good supply of oxygen and glucose, so aerobic metabolism and energy production for cell function are maintained. Throughout this phase the heart is in a good state to respond to early effective CPR and defibrillation. It is during this phase that survival rates can be significant with prompt, effective cardiac arrest management (Bur et al., 2001). • The circulatory phase begins after 4 minutes of cardiac arrest and lasts approximately 10 minutes. Oxygen has been exhausted and the myocardial cells shift from aerobic to anaerobic metabolism. With the reduction in ATP production, cell function diminishes as large amounts of lactic acid accumulate. It is during this phase that the heart may not respond to early defibrillation. It has been suggested that a period of good-quality CPR preceding attempts to defibrillate would produce superior outcomes for patients in this phase, but subsequent studies have refuted this approach and CPR before defibrillation in this group is no longer recommended (Baker et al., 2008; Jacobs et al., 2005; Meier et al., 2010). • The metabolic phase begins approximately 10 minutes following cardiac arrest. The myocardium is now starved of oxygen and glucose, there is an accumulation of hydrogen ions and the tissues become ischaemic and begin to die. The sodium–potassium pump begins to fail, thus allowing sodium to enter the cells and potassium to leak out of the cells, resulting in profound metabolic acidosis and hyperkalaemia. During this phase, resuscitation is difficult and unlikely to respond to resuscitation attempts as the cells become unable to produce sufficient action potentials to initiate a viable rhythm. The spontaneous propagation of VT and the deterioration into VF are typical of an isolated area of ischaemia that develops due to an occluded coronary artery. This is by far the most common cause of cardiac arrest, but not the only cause. A profound increase in intrathoracic pressure (severe asthma, tension pneumothorax) can occlude any blood returning to the right atrium. With no input the heart cannot generate any output. In these cases the initial ECG may appear relatively normal, with sinus tachycardia the most common rhythm, but the patient presents in cardiac arrest. Eventually the heart itself will become hypoxic and bradycardia will typically develop. If there is an isolated area of poor myocardial perfusion VT may develop, but many of these cases will simply become more bradycardic with time and eventually fall into asystole. Profound hypovolaemia will cause a similar pattern. Similarly, conditions that cause profound hypoxia (airway occlusion, hanging, anaphylaxis) or a lack of ventilation (severe asthma, spinal injury) will progress from a narrow-complex tachycardia to a wide-complex bradycardia and eventually asystole. These groups of cardiac arrest where it appears that the initial rhythm should generate a pulse are described as pulseless electrical activity (PEA) or electromechanical dissociation (EMD). Unlike VT/VF arrest where the primary aim is to maintain cerebral perfusion (with CPR) while reverting the arrhythmia with defibrillation and medications, PEA/EMD requires the underlying cause to be reversed.

CA SE ST U DY 1 Case 22343, 0740 hrs. Dispatch details: A 50-year-old male motorcyclist has collided with a bus. He is now in cardiac arrest. Initial presentation: On arrival the paramedics find the patient lying supine on the road next to his motorcycle. His helmet has been removed and there are no immediately obvious injuries. Effective chest compressions are being performed by a bystander, who identifies herself as a nurse.

ASSESS Patient history For patients in cardiac arrest with a shockable rhythm the time to first defibrillation is a predictor of positive outcomes (ARC, 2011). Similarly, minimising downtime to effective CPR has been demonstrated to be associated with ROSC. There is nothing in either of these actions that requires or will be contraindicated by a detailed medical or social history. In almost every other type of case, the patient history forms the basis of clinical decision making, but when the patient is found to be in cardiac arrest there is nothing in the history that should stop treatment. Later, once the crew are performing their roles effectively, a history may assist in determining treatment after the patient regains a cardiac output, but it should never delay nor distract when a patient fails the primary survey.

Airway This patient is unconscious and is therefore unable to protect his airway. Patients who have arrested through a process of VT to VF may have maintained some cerebral perfusion after they had insufficient blood pressure to remain conscious and upright. Gag reflexes can therefore remain intact for a minute or two after arrest and trismus is not uncommon but both should no longer be in evidence within a minute of complete cardiac arrest. Jaw thrust and support should be adequate at this stage to inspect and maintain an airway. The inspection should not be so detailed (i.e. laryngoscopy) as to delay

initiation of CPR. For this reason, during the initial approach to a patient, only the oropharynx should be visually inspected.

Breathing This check should also occur quickly. If rise and fall of the chest cannot be easily detected, then it should be assumed that the patient is not ventilating. In previous adult resuscitation guidelines this point required that two breaths were administered to the patient. This has now been removed from the algorithm and paramedics should move on to assess for a pulse and then commence CPR or defibrillation before returning to reassess and manage both the airway and breathing. This patient is unconscious, cyanosed and nonventilating. The crew instruct the nurse to continue with CPR.

Cardiovascular The crew establish a baseline time on their monitor and attach the defibrillation pads while CPR continues. As 2 minutes approaches they organise who will take over compressions and who will control the monitor during the pulse/rhythm check. Establishing what electrical rhythm the patient is in will dictate the specifics of ongoing treatment. At the 2-minute mark they pause CPR and check the monitor and for a carotid pulse. The monitor displays a sinus tachycardia of 165 BPM but there is no pulse.

Initial assessment summary

Problem Conscious state Position Heart rate (monitor) Heart rate (pulse) Blood pressure Skin appearance Speech pattern Respiratory rate Respiratory rhythm Respiratory effort Chest auscultation Pulse oximetry Temperature Motor/sensory function History Visual inspection

EMD cardiac arrest GSC = 3 Supine 160 BPM, sinus tachycardia 0 0 Cyanosed, dry, cool N/A 0 N/A No effort Not yet performed Not yet performed Not yet performed N/A The patient was seen riding his motorcycle erratically before slowly colliding with a bus. No obvious long bone fractures, head injuries or bleeding.

D: The crew and patient are protected from traffic; there are no spills or other hazards. R: The patient is unconscious. S: The crew have requested another crew to assist. A: The patient is unconscious with no current airway obstruction. B: Respiratory function is currently absent. C: There is no cardiac output. H: There are no external haemorrhages. The patient was seen riding unsteadily but slowly before colliding with the side of a near-stationary bus. The bike is not severely damaged. The ECG reveals a normally perfusing rhythm but the patient is pulseless and unconscious. The mechanism and pattern of injury as assessed so far do not appear consistent with the presentation. The crew recommence CPR without delivering a shock and begin the next stage of the EMD resuscitation guideline.

CONFIRM The essential part of the clinical reasoning process is to seek to confirm your

initial hypothesis by finding clinical signs that should occur with your provisional diagnosis. You should also seek to challenge your diagnosis by exploring findings that do not fit your hypothesis: don’t just ignore them because they don’t fit.

What else could it be? Exsanguination Although there is no obvious haemorrhage and the mechanism of injury appears low, it is possible that the patient has ruptured a major vessel or organ (thoracic or abdominal) and is bleeding internally. Fractures of long bones can cause internal bleeding within limbs but it would be unusual for this to produce an EMD arrest so quickly. While CPR and intermittent positive-pressure ventilation (IPPV) are maintained, a member of the crew performs a moredetailed secondary survey but finds no obvious injuries. IV fluids as per the EMD guideline will assist in correcting any haemorrhage that is not able to be detected, but alone they will not lead to a resumption of cardiac output in a patient who has exsanguinated and where the site of bleeding is not controlled.

DIF F ERENT IA L DIA GNOSIS Cardiac arrest of ischaemic cause Or • Cardiac arrest from: > Exsanguination > Pericardial tamponade > Spinal injury > Drug effects > Upper airway obstruction > Asthma/anaphylaxis > Tension pneumothorax

Pericardial tamponade Blows to the chest can cause bleeding into the fibrous pericardial sac that surrounds the heart and this can ultimately restrict the heart from expanding to fill with blood. With nothing in the ventricles it is unable to produce any cardiac output but will maintain normal electrical activity for a period. Muffling of the heart sounds occurs as a tamponade develops but once blood is no longer travelling through the heart and causing the valves to open and close there are no sounds to detect. Very few paramedics are trained in pericardiocentesis (needle aspiration of a tamponade) and the procedure is potentially dangerous. If a pericardial tamponade develops in the field it is generally irreversible and the fluid and inotropes embedded in the EMD guideline are the only tools that may preserve some blood flow. Unable to

diagnose and unable to treat a tamponade if it is present, the paramedics continue with the EMD guideline. Spinal injury Injuries to the upper cervical area can paralyse the diaphragm and lead to a hypoxic cardiac arrest. However, these types of injuries also disrupt sympathetic innervation of the heart, and bradycardia and low blood pressure are the typical result. It doesn’t fit the clinical picture for this patient but neck stabilisation needs to be maintained. Drug effects Drugs that slow the heart and cause the development of blocks can ultimately lead to an EMD arrest. This patient’s tachycardia is inconsistent with a toxic level of these drugs. Tricyclic antidepressants do depress the level of consciousness and a sinus tachycardia that can trigger VT, but patients do not usually lose their cardiac output until VT develops. Upper airway obstruction Patients should be able to be effectively ventilated using normal volumes and pressures. After ensuring the patient is properly positioned and basic airway adjuncts (oropharyngeal or nasopharyngeal airway) have been introduced, higher-than-normal pressures should trigger a more detailed inspection of the airway. Asthma/anaphylaxis Hyperinflation of the chest increases intrathoracic pressure, decreasing venous return, and can produce an EMD arrest. Bronchospasm is central to asthma and is associated with high levels of mortality when it occurs from anaphylaxis. (Stings from flying insects are not uncommon for riders and drivers.) This patient shows no signs of a rash and his lips and face do not look overly swollen. A close assessment of the airway reveals higher-than-normal airway pressures and a decreased tidal volume. An inspection of his belongings reveals no medications to suggest either condition. Tension pneumothorax Blunt chest trauma (including CPR) is capable of producing a tension pneumothorax (see Ch 33) that will create sufficient intrathoracic pressure to restrict venous return and create an EMD arrest. Like pericardial tamponade, it is possible to detect a pneumothorax by distension of the jugular veins and changes to auscultated sounds, but once fully developed these discrimination signs become absent.

T REAT Emergency management Initiate CPR EMD arrests present a unique set of challenges as crews work through the

various reversible causes. While this reasoning process is performed, the EMD guideline must be maintained as it is possible that none of the easily reversible causes is present. Chest compressions at a rate of 100 compressions per minute with a 30:2 compression-to-ventilation ratio are required. Some guidelines suggest withholding any resuscitation for cardiac arrests that occur as a result of trauma and that such attempts are almost always futile (Hopson et al., 2003). In fact, research data suggests otherwise, with one study of nearly 170 patients suffering traumatic arrest revealing that 6.6% survived to make a complete neurological recovery (Leis, 2013), while another study found nearly 7% survived with 2% making a complete neurological recovery—a figure comparable with non-traumatic forms of arrest (Gräsner et al., 2011; see Fig 26.3). Of all the patients found to be in cardiac arrest following trauma, the majority in the studies were found to be in asystole (67–75%) on first assessment followed by EMD (13–26%) and VF (2–6%) (Leis, 2013; Deasy et al., 2012). Patients suffering hypovolaemia were the least likely to survive, while VF and EMD as the initial rhythms produced better outcomes than asystole (Lockey, Crewdson & Davies, 2006). Patients for whom an ALS crew arrived before a BLS were more likely to survive (Leis, 2013).

FIGURE 26.3 Summary of outcomes from the German Resuscitation Registry following traumatic cardiac arrest. The survivor rates are comparable with those of other forms of cardiac arrest. Source: Gräsner et al. (2011). During each 2-minute period of CPR it is essential that the crew plan ahead and manage resources to ensure effective cardiac arrest management. A number of elements need to be considered during this period: the paramedics swapping to alternate the CPR duties, gaining IV access and administering appropriate cardiac drugs, as well as continuing effective airway management. In most cases, cardiac arrest is managed initially by a two-person team, and in these instances one person should provide high-quality CPR while the other prepares the defibrillator, applies the pads and charges (ARC, 2011). The third link in the chain of survival emphasises early and immediate defibrillation of shockable arrhythmias. The aim of defibrillation is to cause global depolarisation of the myocardium with the hope that a pacemaker, preferably the SA node, will resume coordination of the myocardium. Consequently, following defibrillation, there will be a period of asystole before electrical coordination takes place, and the myocardium will have a short period of recovery before mechanical capture occurs. This is why it is important to immediately recommence chest compression following defibrillation unless there are obvious signs of life or active patient movement.

P RACT ICE T IP If a previously well (well-oxygenated) patient has a witnessed and monitored arrest, and the initial arrhythmia is VF/VT, then up to three successive stacked shocks can be given if the first shock can occur within 20 seconds. However, this is an extremely rare situation and in most pre-cardiac arrest situations the patient would not have a well-oxygenated heart.

Resolve reversible causes Although this patient has no obvious chest trauma, it is possible that he has suffered a tension pneumothorax as he is difficult to ventilate (see Table 26.2). If this is the case and it is not resolved, the outcome will be poor. With no breath sounds to assist in determining which side to decompress first, the crew choose to decompress the right side. This reduces the chance of damaging the heart or major vessels if a right-sided pneumothorax has pushed the heart to the left. The result of the decompression is negative, so the crew decompress the left side, but it too is negative. TABLE 26.2 Reversible causes of cardiac arrest (few are feasible in OHCA)

Fluid Hypovolaemia and raised intrathoracic pressures both reduce venous return and, subsequently, cardiac output. Isotonic fluid (crystalloid or colloid) can act as a volume expander and increase venous return. It should be administered according to local guidelines. Adrenaline The effectiveness of adrenaline in any form of cardiac arrest remains unclear, with some studies suggesting that it has little impact on ROSC, while others

report improved rates of ROSC but poorer long-term outcomes (Hagihara et al., 2012). The benefits of adrenaline in EMD arrests such as this case are most likely its effect on vessel tone and improving venous return. Adrenaline has both alpha-and beta-adrenergic effects. In arrest it is the alpha effects that are desirable as they cause systemic vasoconstriction, which increases coronary and cerebral perfusion pressures. Once adrenaline is given, it is repeated every 3 minutes (reflecting its half-life of 3–5 minutes): 1 mg is given via the IV or intraosseous (IO) route. Ventilation Overventilation of cardiac arrest patients in both rate and volume adversely affects the quality of CPR (Adgey & Johnston, 1998) and is common across all levels of clinical expertise (O’Neill & Deakin, 2007). In particular, excessive tidal volumes increase intrathoracic pressure and reduce venous return.

P RACT ICE T IP An initial EtCO2 25% from the initial reading are significantly associated with a failure to achieve ROSC in OHCA patients (Eckstein et al., 2011).

Endotracheal intubation during cardiac arrest remains a controversial topic, as some studies reveal the process of intubation can cause interruptions of CPR for more than 3 minutes, with a mean interruption of 46.5 seconds (Wang et al., 2009). Conversely, the ability to protect the airway of non-fasted patients, to deliver effective IPPV to the non-ventilating patient, to limit gastric insufflation and to allow effective management post-ROSC are all undeniable benefits of intubation. Intubation also allows accurate measuring of end-tidal CO2 (EtCO2) values, which are shown to both measure the effectiveness of CPR and predict negative outcomes (EtCO2 Continue with the highest level of available care • Deteriorating after IM adrenaline? > Continue with the highest level of available care • Unconscious? > Start the primary survey • Pulseless? > Check the monitor Not VT or VF? Commence CPR

Investigations Although hundreds of chemical markers are released during anaphylaxis, in-hospital investigation of anaphylaxis is limited in both scope and usefulness. Plasma histamine levels rise within 10 minutes of symptom onset but fall again within 60 minutes, and the blood needs to be specially handled if the histamine is to be detected (Estelle & Simons, 2009). Levels of tryptase (an enzyme released from mast cells during degranulation) stay elevated for up to 3 hours but are not always sensitive to food-induced anaphylaxis (Sampson, Mendelson & Rosen, 1992). Given that the symptoms demand instant treatment, testing for either histamine or tryptase is of limited clinical usefulness and, for the moment at least, anaphylaxis remains diagnosed from its clinical presentation.

Ongoing management Adrenaline is the drug of choice to manage anaphylaxis, but other interventions could include the following: • Steroids. Although there is a lack of research to support their inclusion in the acute management stage of anaphylaxis (Lieberman et al., 2005), steroids are traditionally given to suppress the production of inflammatory mediators at a cellular level. Their onset time (generally 4–6 hours) is too long to support patients in the short term, but their role in suppressing the inflammatory response may reduce biphasic reoccurrences or non-IgE reactions. • Fluids. Adrenaline should be given first to reduce the increased vascular permeability, otherwise the fluid will make the oedema worse when infused. Given patients’ profound vasodilation and increased capillary permeability, it is highly unlikely that those suffering shock secondary to anaphylaxis could be resuscitated with fluid alone, and some case studies have demonstrated hypotension refractory to very large fluid infusions (in excess of 60 mL/kg) (Lieberman et al., 2005). Colloids have shown no benefit over crystalloids and should be reserved for patients who remain hypotensive after adrenaline administration. • Bronchospasm. Asthmatic patients suffering anaphylaxis have been shown to exhibit bronchospasm and wheezing even after the majority of their symptoms have reduced. Nebulised salbutamol and ipratropium are recommended for these patients if bronchospasm persists after emergency management (Ellis & Day, 2003a). • Antihistamines. Antihistamines are routinely given during the non-emergency phase of management. Their effectiveness is still uncertain but the combination of a H 1 and a H 2 receptor blocker appears to be more effective than either one administered alone (Ellis & Day, 2003a). Both drugs can be given intravenously but as most patients have improved by this point they can be given orally.

Hospital admission Patients who remain unstable after treatment in ED will be admitted to ICU. Patients who return to normal are usually observed for at least 8 hours before discharge home but this is changing as the frequency of biphasic reactions becomes recognised. A recurrence of symptoms develops in about 20% of cases and can occur up to 10 hours after the initial event (Ellis & Day, 2003a). The severity of the initial presentation does not correspond to the severity of the second presentation, and the symptoms can appear quickly or slowly, together or individually (Limb et al., 2007). Some hospitals require overnight admission for paediatric patients, patients who have received more than one dose of adrenaline or any volume of fluid, patients who live alone or a significant distance from medical care, and those with comorbidities. Patients who have ingested their allergen tend to be kept in hospital longer than those whose contact was dermal or respiratory.

Follow-up It is important to attempt to identify the trigger and to desensitise patients who have had an anaphylactic reaction (Estelle & Simons, 2009). Patients who are deemed at significant risk of further episodes will be discharged with an EpiPen (adrenaline auto-injector) and instructions for its use. EpiPens are supplied in two fixed-dose forms: EpiPen Junior (0.15 mg adrenaline) for children 15–30 kg; and EpiPen Adult (0.3 mg adrenaline) for adults and children over 30 kg. Patients deemed at lower risk may be discharged with just a course of oral steroids and antihistamines. The association between fatal episodes and delayed administration of adrenaline has created a focus on developing anaphylaxis management plans (Estelle & Simons, 2009; Kemp, 2009). These emphasise the safety of IM administration of adrenaline via an EpiPen and, although there is no universally accepted management plan, the evidence supporting EpiPen use is growing (Nurmatov, Worth & Sheikh, 2008).

Long-term role The primary goal of paramedic management of anaphylaxis is to prevent morbidity and mortality. Since aggressive management of anaphylaxis with IM adrenaline has become routine, anaphylaxis fatalities have not increased, despite the increasing prevalence of the condition (Liew, Williamson & Tang, 2009). Continued education of patients, healthcare professionals and those people associated with anaphylaxis sufferers (see Fig 27.5) will hopefully see a drop in deaths from this condition.

FIGURE 27.5 Long-term management of anaphylaxis. Effective anaphylaxis management starts long before paramedics attend the scene, with the patient avoiding known triggers and optimally managing conditions such as asthma or cardiovascular disease. Patients should also activate their management plan (EpiPen or calling for an ambulance) at the first sign of symptoms. Educating patients and their carers is an essential role for paramedics. Source: Estelle & Simons (2009).

Anaphylaxis across the lifespan Estimating the prevalence and severity of anaphylaxis is complicated by the lack of consensus on a definition, the limited clinical tests to confirm a diagnosis and a reliance on hospital-based figures (Bohlke et al., 2004; Sicherer, 2011). Reactions to food represent the fastest growing category but even non-food reactions presenting to hospitals increased by an average of 8.5% per year in the period 1994–2005 (latest data available; Poulos et al., 2007). This aligns with the general consensus that allergic reactions are increasing in Western countries (Liew, Williamson & Tang, 2009; Tang, Osbourne & Allen, 2009). The number of hospital admissions for anaphylactic reactions in Australia is increasing at a similar rate to admissions in the United Kingdom and North America (Poulos et al., 2007). These presentations show specific age-related trends (see also Figs 27.6, 27.7 and 27.8).

FIGURE 27.6

Anaphylaxis admissions to hospital, 1994– 2005. Young children make up the majority of hospital admissions but fatal episodes occur more frequently in adults (see Fig 27.8). Source: Liew, Williamson & Tang (2009).

FIGURE 27.7 Anaphylaxis cause of deaths, 1994–2005. Anaphylactic reactions to medications and insect stings make up the majority of fatal episodes. This is most likely to be because these instances often involve antigens being injected directly into tissues or the bloodstream. Source: Liew, Williamson & Tang (2009).

FIGURE 27.8 Anaphylaxis fatalities in Australia, 1994– 2005. A Absolute number of anaphylaxis deaths by cause and age group. B Anaphylaxis death rates by cause and age group. All but 1 food-induced anaphylaxis death occurred in people aged 10–35 years (1 death at 8 years), most insect sting– induced anaphylaxis deaths occurred in people aged 35–84 years and most drug-induced anaphylaxis deaths occurred in people aged 60–85 years. Source: Liew, Williamson & Tang (2009).

A NA P HYL A X I S ON T HE R OA D

Anaphylactic patients can go from appearing fit and well to being profoundly unwell within a matter of minutes. Left unmonitored and untreated, these patients have a real risk of death. But assessed quickly and accurately and treated with adrenaline they generally stabilise within minutes. Like all health emergencies that occur in the community, paramedics have to balance a highly charged and emotional scene (remember, this person was probably in good health a few moments ago), which is often in a crowded place (anaphylaxis tends to occur in places where the patient isn’t in control of the cooking—restaurants, parties), with the priorities of clinical decision making. This is one of the cases where a standardised approach, good knowledge and good clinical skills will save a life.

• 0–4 years. Although hospitalisations for anaphylaxis increased across all age groups in the 12 years prior to 2004, the increase was greatest in children aged 0–4 years (Poulos et al., 2007), up from just over 4 per 100,000 population to slightly less than 20 per 100,000. This was mainly the result of food-induced reactions (Poulos et al., 2007). Allergies may appear in the toddler years and are usually associated with peanuts, eggs, milk and tree nuts (Liew, Williamson & Tang, 2009). Fatalities in this age range remain relatively rare. • 5–14 years. As children enter school they become exposed to a greater number of foods and other allergens: sensitivities to various nuts, fish and insects may emerge and presentations can be more serious. Risk of fatal episodes of anaphylaxis at this age is associated strongly with peanut allergies, asthma and previously unknown sensitivities. A study of 85 children who presented to ED found that cutaneous and respiratory manifestations were the most common symptoms (Bohlke et al., 2004). > Insect stings are a more common presentation in this age group; about 10% of all deaths occur in this age group despite it contributing more than half of all presentations. > Remember, it is difficult to predict with any accuracy the likely severity of a reaction based on a previous reaction. In this and the toddler age group, males are more likely to suffer from food-induced anaphylaxis, while females are at slightly higher risk of nonfood induced reactions (Poulos et al., 2007). Overall fatalities from food make up only a small proportion of deaths from anaphylaxis but it is important to remember that about 20% of deaths from anaphylaxis have no obvious trigger. • 15–35 years. This age group has fewer presentations than other age groups but has shown a similar growth rate in the number of presentations. This group—in particular 15– 29-year-olds—shows a second peak in hospital admissions for food-related reactions but the lowest for drug-induced reactions. Crustacean and fish allergies are added to the cohort of causes in this age group (Liew, Williamson & Tang, 2009). • 35–84 years. This group suffers the highest (85%) fatality rate from insect stings (Liew, Williamson & Tang, 2009) and medication-related reactions. This is of course potentiated by the increasing number of medications and procedures that are administered with age and with comorbidities limiting the body’s ability to resist the reaction. Angiotensin-converting enzyme (ACE) inhibitors are particularly known to cause profound angio-oedema (see case study 4) and this presentation has spiked since this class of drugs has become popular for the control of hypertension (Gabb et al., 1996). Whether this is truly an anaphylactic presentation is debatable. Aspirin has also been linked to anaphylactoid reactions,

particularly in asthmatics.

CA SE ST U DY 2 Case 11441, 1520 hrs. Dispatch details: A 21-year-old male with an allergic reaction to food. The patient has had a reaction to fish: he has a known allergy. Initial presentation: The crew are led inside a private house and find the patient sitting on a chair in the kitchen.

ASSESS 1529 hrs Primary survey: The patient is conscious and talking. Chief complaint: ‘I ate some fish and now my lips are tingling and I’m itchy all over. I haven’t eaten fish for years because I was allergic to it.’ (For more about fish allergies, see Box 27.3.) B O X 2 7 . 3F

ish aller g ies

Molluscs and crustaceans tend to cause more allergic reactions than fish with backbones. Nonetheless, allergies to fish do occur and, like other ingested allergens, reactions in the lips and mouth are especially common. There appears to be a cross-sensitivity between fish species (Hansen et al., 1997) but it varies according to how close the group is to the ‘sensitive’ group. Sensitivities between shellfish seem stronger but there doesn’t appear to be a strong cross-sensitivity between shellfish and fish. From an allergy point of view, fish may be divided into 6 groups: Group 1: Shark, flake Group 2: Sardines, anchovies Group 3: Salmon, pike, trout Group 4: Cod, hake, haddock Group 5: Tuna, mackerel, snapper, pink snapper, perch, barramundi, bream, flathead, whiting

Group 6: Sole, flounder, halibut. The closer one group is to another the more likely there will be an allergic reactivity. The fish parasite Anisakis simplex is also a major allergen and can masquerade as a fish allergy. Although it is killed by freezing or cooking, Anisakis can still trigger allergies.

1530 hrs Vital signs survey: Perfusion status: HR 146 BPM, sinus tachycardia, BP 140/90 mmHg, skin warm and pink. Respiratory status: RR 28 BPM, good air entry, L = R, mild expiratory wheeze across all fields, normal work of breathing, speaking in full sentences, denies shortness of breath. Conscious state: GCS = 15.

P RACT ICE T IP In the crowded and confusing world of emergency health in the community, the question ‘Of all your symptoms, which is distressing you the most?’ can be a great ‘cut to the bone’ question. Patients have many symptoms and they may want to explain them all to you. This lets you identify the most significant in the patient’s eyes and also conveys empathy towards the patient.

1531 hrs Pertinent hx: The patient is normally well and takes no medications. He hasn’t eaten fish since he was a child because of an allergic reaction, but he can’t remember how severe the reaction was. He took a bite of his friend’s fish burger just to see how it tasted; he didn’t think he was allergic anymore. It’s not uncommon for patients to think they no longer suffer from an illness because they have been good at avoiding triggers and maintaining treatments. The same can occur with patients with asthma and epilepsy. ‘How long after eating the fish did the symptoms start?’ ‘The tingling in my mouth and lips started within about a minute and then I could feel my heart suddenly racing. My mate called the ambulance straight away.’ ‘Does your voice sound normal?’ ‘Yeah, I think so.’ (To the patient’s friend) ‘Is his face normal or swollen?’ ‘He may be a little puffy around the eyes.’ ‘If there is one thing I could fix for you right now, what would it be?’ ‘My lips feel like they’re swelling but it’s the itching that’s driving me crazy. I’m itchy all over and I know if I start scratching I’ll never stop.’

CONFIRM In many cases paramedics are presented with a collection of signs and symptoms that do not appear to describe a particular condition. A critical step in determining a treatment plan in this situation is to consider what other conditions could explain the patient’s presentation.

What else could it be? Anxiety Anxiety rarely causes heart rates greater than 125 BPM and a sustained tachycardia of 143 BPM in a patient who is fit, sitting down, not short of breath and only mildly anxious is being driven by something significant. Tingling of the lips can be associated with the CO2 imbalance caused by hyperventilation. It is possible that the patient is simply anxious after realising he has eaten fish and this has caused him to hyperventilate, resulting in the tingling. Look for other signs of the chemical imbalance caused by hyperventilation—that is, tetany (carpal spasm) of the fingers and forearms—then look at the patient: is he really that anxious?

DIF F ERENT IA L DIA GNOSIS Food allergy/anaphylaxis Or • Anxiety • Asthma • Scombridae food poisoning

Asthma This patient has no history of asthma and it is unlikely that he has developed it at the same time as eating fish. The cutaneous signs are also inconsistent with asthma. Scombridae food poisoning Food poisoning rarely has such a sudden onset and this patient lacks the characteristic abdominal pain. One form of food poisoning should be considered however: fish flesh contains the protein histidine and, if stored improperly, bacteria can metabolise this protein into large amounts of histamine. Once produced, the histamine is not destroyed by cooking. Mistakenly known as Scombridae fish poisoning it also affects fish outside the Scombridae family. Because patients ingest high levels of histamine the presentation is difficult to separate from anaphylaxis and symptoms typically include erythema, hot

flushes, headache, nausea and vomiting (Smart, 1992). Definitive management is antihistamines but in the pre-hospital setting the differentiation is too dangerous to make and treatment should be consistent with anaphylaxis. The only exception to this might occur when a group of people who have shared the meal all present with typical Scombridae symptoms.

P RACT ICE T IP If it’s anaphylaxis, why isn’t the patient hypotensive? Hypotension is a classic characteristic of anaphylaxis so why isn’t this patient hypotensive? Paramedics tend to see patients early in their presentation when the full host of symptoms may not yet be present. Remember, hypotension is a late sign in all forms of shock.

T REAT This patient should be administered IM adrenaline 0.3–0.9 mg depending on local guidelines. IM (lateral thigh) is safe and the drug acts quickly by this route. Fear of increasing the heart rate and blood pressure are common barriers to the treatment of anaphylaxis by inexperienced paramedics. Remember, the cause of this patient’s symptoms is the widespread and uncontrolled release of histamine leading to small vessel vasodilation, increased capillary permeability and smooth-muscle contraction. Adrenaline will reduce the histamine release and assist with both alpha and beta effects. Because it reduces the cause, you can expect the patient’s heart rate to reduce after IM adrenaline. Similarly, you should not expect to see major changes in BP. 1535 hrs: The patient is given 0.3 mg of IM adrenaline into the right deltoid. Upon administering the adrenaline the crew notice the patient becoming flushed and increasingly anxious about the itching. 1537 hrs: The symptoms start to subside and with 2 minutes the patient is calmer and says the itching and tingling have almost gone. Perfusion status: HR 104 BPM, sinus tachycardia, BP 130/80 mmHg, skin warm and pink. Respiratory status: RR 24 BPM, good air entry, L = R, normal work of breathing, speaking in full sentences, denies shortness of breath. Conscious state: GCS = 15. 1541 hrs: The patient walks to the ambulance. He is talkative and calm. 1545 hrs: One of the crew notices that the patient is rubbing his arms and asks whether the itching is returning. The patient confirms that it is. The recurrence of symptoms after 10–15 minutes is typical of moderate anaphylaxis.

Perfusion status: HR 120, sinus tachycardia, BP 110/80 mmHg, skin warm and pink. Respiratory status: RR 28, good air entry, L = R, normal work of breathing, speaking in full sentences, denies shortness of breath. Conscious state: GCS = 15 1546 hrs: The paramedic administers another 0.3 mg IM bolus of adrenaline and the symptoms subside. 1559 hrs At hospital: Perfusion status: HR 104 BPM, sinus tachycardia, BP 130/80 mmHg, skin warm and pink. Respiratory status: RR 24 BPM, good air entry, L = R, normal work of breathing, speaking in full sentences, denies shortness of breath. Conscious state: GCS = 15.

EVALUAT E Evaluating the effect of any clinical management intervention can provide clues to the accuracy of the initial diagnosis. Some conditions respond rapidly to treatment so patients should be expected to improve if the diagnosis and treatment were appropriate. A failure to improve in this situation should trigger the clinician to reconsider the diagnosis. In this case, it is likely that the patient will continue to receive short-term relief from IM adrenaline, but with the recurrence of symptoms once the adrenaline is metabolised. If the transport time is significant, an IV adrenaline infusion might negate the need for regular IM injections.

CA SE ST U DY 3 Case 16532, 1940 hrs. Dispatch details: A 29-year-old female has collapsed while playing netball. She is in an altered conscious state. Initial presentation: The crew are met at the local netball stadium and led inside to find a female lying on her side. A doctor playing on the opposing team states that the patient was playing normally when she complained of ‘feeling funny’ to a team mate. She then collapsed, had a seizure that lasted a few seconds and vomited. She has remained on the ground since then.

ASSESS 1950 hrs Primary survey: The patient is semi-conscious and moaning. There is no obvious injury. 1951 hrs Vital signs survey: Perfusion status: HR 115 BPM; sinus rhythm; BP 70/P; skin warm, pink, clammy. Respiratory status: RR 18 BPM, good air entry, L = R, nil adventitious sounds, normal work of breathing, SpO2 = 97% on room air. Conscious state: GCS = 7; weak withdrawal, moans quietly (E = 1, M = 4, V = 2). 1953 hrs Pertinent hx: The patient’s medical history is not known to her team mates but they state she was playing normally until just before she collapsed. They say she did not strike her head when she collapsed. 1954 hrs Secondary survey: No obvious injuries. There is a small amount of vomit on the floor next to and under the patient’s head and in her hair. Her team mates say she vomited after she collapsed.

CONFIRM In many cases paramedics are presented with a collection of signs and symptoms that do not appear to describe a particular condition. A critical step in determining a treatment plan in this situation is to consider what other conditions could explain the patient’s presentation. Patients who present in the field can be extremely difficult to diagnose. Sometimes the picture is clear (as in case study 1) and it is easy to select and then confirm a hypothesis. But often the picture is incomplete and you need a method to help you sort the good information from the bad. The standardised clinical approach (see Ch 5) directs paramedics to ensure that the patient has a clear airway, is breathing and has circulation. It then sets out a path to obtain the relevant physiological information as quickly as possible. In this case the patient has an altered conscious state and is poorly perfused but has no obvious injuries. The cause is not clear and the crew need to contrast the information they have gained with their clinical knowledge. The DENT model is an effective problem-solving tool for difficult cases (see Ch 5).

Define In this case the crew define the problem as extremely poor perfusion. It could be argued that the patient’s altered conscious state is more significant, but whereas low blood pressure can cause an altered conscious state, an altered conscious state (a head injury) has no physiological mechanism to cause

hypotension.

Explore The crew need to quickly explore the conditions that can cause profound and prolonged hypotension in an otherwise fit young woman. Low blood glucose (diabetes) is a common cause of altered consciousness and the body tends to respond with an increased sympathetic output that causes tachycardia and clamminess but rarely hypotension. Nonetheless, it is worth considering.

Narrow 1956 hrs Blood glucose test: BGL 6.3 mmol/L. Hypoglycaemia is eliminated. A quick check of the monitor reveals no arrhythmia and the patient moves all her limbs (albeit weakly and with a moan) to painful stimuli. Cardiac and spinal causes can be reasonably eliminated. What can be gained from the scene? A young female is lying on the ground with her face and hair spattered with her own vomit. This is not a voluntary position or ‘place of comfort’. This patient is not well. With no obvious cause the crew can still only define the problem as profound hypotension. Sometimes the out-of-hospital environment will not allow paramedics to ‘pin’ a more specific label on a patient and they have to start fixing the problem. The crew request back-up from an intensive care unit.

T REAT 2000 hrs: The crew place some folded clothing under the patient’s legs to increase venous return. They keep the patient on her side in case she vomits again. 2001 hrs: The crew insert an IV cannula and commence an infusion of an isotonic crystalloid (normal saline). While they work to fix the defined problem they seek to further explore and narrow the cause of the patient’s persistent hypotension. What are the causes of poor perfusion? • Hypoxia: SaO2 is good, no respiratory distress, lungs clear. NO • Hypovolaemia: No external haemorrhage, lungs clear, abdomen soft. NO • Tension pneumothorax: Good air entry, L = R, SaO2 is good. NO • Spinal cord injury: No trauma, the patient doesn’t complain on spinal palpation, she is moving all limbs and is tachycardic. NO • Asthma: Good air entry, SaO2 is good, normal work of breathing. NO • Vasovagal: Uncommon in the young, tachycardic. NO • Anaphylaxis: By systematically analysing the presenting problem the crew have found a possible cause (anaphylaxis) they cannot eliminate. But can they confirm it? Is there evidence of a systematic hypersensitive immune response? The onset was rapid, the patient ‘felt funny’ before collapsing, she is extremely poorly perfused and has vomited. The lack of dermal symptoms is difficult to

assess and the patient was exercising and sweaty before she collapsed (see Box 27.4), but she is still tachycardic and flushed despite having been on the ground for more than 15 minutes. B O X 2 7 . 4E x e r c

i se - i n d u c e d a n a p h yl a x i s

Exercise-induced anaphylaxis is a relatively rare disorder in which anaphylaxis is triggered by physical activity (Lieberman et al., 2005). The condition appears in the literature as far back as the 1970s but it is not commonly associated with fatalities (Maulitz, Pratt & Schocket, 1979). The symptoms are typical of other forms of anaphylaxis and their severity appears to be related to the intensity of the exercise but there seems to be a summative effect (Brown, Mullins & Gold, 2006; Lieberman et al., 2005). This means that a combination of exercise along with certain foods and medications can create an anaphylactic response even when neither component causes symptoms in isolation. This has also been described as food-dependent exerciseinduced anaphylaxis. In this case a couple of hours before playing netball the patient ate a seafood pizza—a food she normally has no reaction to. A wide variety of foods have been linked to food-dependent exerciseinduced anaphylaxis, including the triggers normally associated with other forms of anaphylaxis (shellfish, nuts, NSAIDs). Exercising in cold temperatures may also predispose the reaction. As with other triggers the response can fall along a continuum from pruritus and urticaria at one end to anaphylactic shock at the other. Milder symptoms generally resolve as exercise levels are reduced but, once triggered, there may be no way of reducing the severity of a full anaphylactic reaction. The detailed pathophysiology of exercise-induced anaphylaxis and food-dependent exercise-induced anaphylaxis is not well understood. As with all forms of anaphylaxis, identifying a specific trigger is not required to diagnose the condition and the patient should be treated according to their clinical presentation.

2004 hrs: Perfusion status: HR 119 BPM; sinus tachycardia; BP 70/P; skin warm, pink, dry. Respiratory status: RR 18 BPM, good air entry, L = R, nil adventitious sounds, normal work of breathing. Conscious state: GCS = 7; weak withdrawal, moans quietly (E = 1, M = 4, V = 2). 2005 hrs: The patient is given 0.3 mg of IM adrenaline into the right vastus lateralis (lateral thigh). The fluid is continued. 2007 hrs: The patient’s conscious status improves. Initially confused, she sits

up and is horrified to find vomit in her hair. She recalls ‘tingling’ all over and feeling abdominal pain before collapsing. This has never happened before and she has no history of allergies. 2009 hrs: Perfusion status: HR 104 BPM, sinus tachycardia, BP 105/75 mmHg, skin warm and pink. Respiratory status: RR 18 BPM, good air entry, L = R, normal work of breathing, speaking in full sentences, denies shortness of breath. Conscious state: GCS = 15.

EVALUAT E Evaluating the effect of any clinical management intervention can provide clues to the accuracy of the initial diagnosis. Some conditions respond rapidly to treatment so patients should be expected to improve if the diagnosis and treatment were appropriate. A failure to improve in this situation should trigger the clinician to reconsider the diagnosis. The patient is assisted onto the stretcher for transport. She is talkative and calm. No further treatment is required and she is discharged from ED the next morning.

CA SE ST U DY 4 Case 14718, 0740 hrs. Dispatch details: A 79-year-old female is having an allergic reaction to an unknown substance. There is airway involvement. Initial presentation: The crew arrive at a nearby nursing home and are directed to the patient, who is sitting up beside her bed. A nurse tells them that she noticed the patient had gross facial swelling when she came to shower her this morning before breakfast.

ASSESS

0750 hrs Primary survey: The patient is conscious and sitting upright. She has obvious facial swelling including periorbital oedema, which is restricting her vision. Her tongue is so swollen she cannot speak easily and she is drooling due to difficulty swallowing. 0751 hrs Vital signs survey: Perfusion status: HR 75 BPM, sinus rhythm, BP 140/90 mmHg; skin warm, pink and dry. Respiratory status: RR 18 BPM, good air entry, L = R, no adventitious sounds, normal work of breathing, SpO2 = 97% on room air. Conscious state: GCS = 15. 0753 hrs Pertinent hx: The patient has a history of hypertension, angina, hyperlipidaemia, osteoporosis and bilateral knee replacements. She is normally well but requires assistance to shower and dress due to decreased mobility. 0754 hrs Secondary survey: Apart from the facial angio-oedema there are no other obvious signs or symptoms. Temperature: 36.8°C.

CONFIRM In many cases paramedics are presented with a collection of signs and symptoms that do not appear to describe a particular condition. A critical step in determining a treatment plan in this situation is to consider what other conditions could explain the patient’s presentation. The crew are faced with a patient where the underlying cause is unclear. They need to use the DENT model (see Ch 5) as a problem-solving tool.

Define A patient with no history of allergies is presenting with isolated angio-oedema without any obvious cause. The swelling is not producing hypoxia or a cardiovascular response.

Explore Because they share a common pathophysiological pathway, differentiating between a severe allergic reaction and an anaphylactic reaction is one of the more challenging diagnostic tasks. The usual distinction lies in the involvement of secondary systems (i.e. cardiovascular, respiratory and gastrointestinal systems). But when the isolated symptoms are severe enough to potentially block the upper airway it can easily trigger paramedics to make a diagnosis of anaphylaxis even when it isn’t supported by the data.

Narrow Isolated oedema to a single body part anywhere in the body but the airway would not meet the criteria for anaphylaxis given the patient has no cardiovascular, respiratory or gastrointestinal symptoms (see Box 27.5). Epiglottitis is a bacterial infection of the epiglottis that causes it to swell and occlude the airway. Although commonly perceived as a disease of children,

widespread vaccinations have virtually eradicated the disease in this cohort but it is not unusual to see it in elderly people who have migrated from overseas. It is usually associated with a sore throat and fever, but it does not cause swelling of the tongue or face. In this case the crew elect to treat for anaphylaxis despite the presentation not completely supporting this diagnosis. B O X 2 7 . 5I s o

lated ang io -o edema

Non-pitting oedema of the face and neck and around the eyes is referred to as angio-oedema and it can extend to include the tongue and the floor of the mouth (Agah, Bandi & Guntupalli, 1997). It may be caused by a hereditary gene mutation but it is increasingly seen as an allergic response to a particular group of medications. ACE inhibitors are a commonly prescribed antihypertensive medication that block the conversion of angiotensin I to angiotensin II and thus limit the amount of fluid reabsorbed by the kidneys. A side effect of this blocking action is an increase in an inflammatory mediator known as bradykinin. It is the same mediator that produces the chronic cough associated with ACE inhibitors. Although there is no direct evidence of the pathway, it is strongly suspected that this excess bradykinin invokes the localised reaction of angio-oedema in one to two patients per thousand taking ACE inhibitors (Vleeming et al., 1998). The bradykinin pathway may also explain reactions to nonsteroidal anti-inflammatory drugs (NSAIDs). Although the risk is low, patients taking ACE inhibitors account for around 40% of all angio-oedema patients presenting to hospital (Agah, Bandi & Guntupalli, 1997). While not an anaphylactic reaction, there is probably some form of hypersensitive allergic reaction in most of these cases and the crew in case study 4 were not irresponsible in administering IM adrenaline. The safe but mild response is typical of these cases. Nebulised adrenaline as per local guidelines could also be used. The action of adrenaline is localised and may reduce the swelling of the tongue and airway. In these cases adrenaline is not as effective at improving symptoms as in treating anaphylaxis, giving further evidence of a slightly different pathway. Patients who suffer from angio-oedema should cease receiving ACE inhibitors immediately and ACE inhibitors should not be recommended in the future. A new generation of this type of drug, angiotensin receptor blockers (ARBs), is considered less likely to produce angio-oedema but there have been instances of angiooedema with ARBs (Abdi et al., 2002).

T REAT 0800 hrs: The crew sit the patient upright to allow for better respiratory function. 0804 hrs: Concerned that the patient may occlude her airway the crew elect to treat with 0.3 mg of IM adrenaline into the right deltoid. They also request an intensive care crew in case intubation is required. 0808 hrs: Perfusion status: HR 78 BPM; sinus rhythm; BP 140/90 mmHg; skin warm, pink and dry. Respiratory status: RR 18 BPM, good air entry, L = R, no adventitious sounds, normal work of breathing, SpO2 97% on room air. Conscious state: GCS = 15. 0808 hrs: The patient nods when asked if she is feeling better and her angiooedema appears to have improved slightly. 0812 hrs: Perfusion status: HR 78 BPM; sinus rhythm; BP 140/90 mmHg; skin warm, pink and dry. Respiratory status: RR 18 BPM, good air entry, L = R, no adventitious sounds, normal work of breathing, SpO2 97% on room air. Conscious state: GCS = 15.

EVALUAT E Evaluating the effect of any clinical management intervention can provide clues to the accuracy of the initial diagnosis. Some conditions respond rapidly to treatment so patients should be expected to improve if the diagnosis and treatment were appropriate. A failure to improve in this situation should trigger the clinician to reconsider the diagnosis. The patient is assisted onto the stretcher for transport. She is calm and cooperative. The crew treat en route with a second dose of IM adrenaline but the patient shows no improvement or deterioration.

Future research Research into anaphylaxis is continuing, especially given its increased prevalence in society among young children. This research is primarily focused on determining why sensitivity to allergens is increasing and what the contribution of diet and modern lifestyles is. Immunological studies into desensitising anaphylactic patients to their allergens are also underway and genetic tests are being developed to determine risk factors. These studies have the potential to reduce fatal reactions, but have so far struggled to provide sufficient hard data to make recommendations for either preventative management or acute treatment (Sicherer, 2011).

Summary Anaphylaxis is a life-threatening medical emergency and paramedics are often the first healthcare professionals to assess these patients. Patients who exhibit the full gamut of manifestations of anaphylaxis may be readily diagnosed, but many patients present with only one or two features, thereby increasing diagnostic uncertainty and leading to delays in definitive treatment with adrenaline. Paramedics must be able to recognise anaphylaxis and implement treatment to prevent unnecessary and avoidable fatalities.

References Abdi, R., Dong, V. M., Lee, C. J., Ntoso, K. A. Angiotensin II receptor blocker–associated angioedema: on the heels of ACE inhibitor angioedema. Pharmacotherapy. 2002; 22:1173– 1175. Agah, R., Bandi, V., Guntupalli, K. K. Angioedema: the role of ACE inhibitors and factors associated with poor clinical outcome. Intensive Care Medicine. 1997; 23(7):793–796. Atkins, D., Bock, S. A. Fatal anaphylaxis to foods: epidemiology, recognition, and prevention. Current Allergy & Asthma Reports. 2009; 9(3):179–185. Bohlke, K., Davis, R. L., DeStefano, F., Marcy, S. M., Braun, M. M., Thompson, R. S. Epidemiology of anaphylaxis among children and adolescents enrolled in a health maintenance organization. Journal of Allergy and Clinical Immunology. 2004; 113(3):536–542. Brown, G. A. The pathophysiology of shock in anaphylaxis. Immunology and Allergy Clinics of North America. 2007; 27:165–175. Brown, G. A., Mullins, R. J., Gold, S. G. Anaphylaxis: diagnosis and management. Medical Journal of Australia. 2006; 185(5):283–286. Brown, S. Clinical features and severity grading of anaphylaxis. Journal of Allergy and Clinical Immunology. 2007; 114(2):371–376. Castro, M., Kraft, M.Clinical Asthma. Philadelphia: Mosby, 2008. Ellis, A. K., Day, J. H. Diagnosis and management of anaphylaxis. Canadian Medical Association Journal. 2003; 169(4):307–312. Ellis, A. K., Day, J. H. The role of epinephrine in the treatment of anaphylaxis. Current Allergy and Asthma Reports. 2003; 3(1):11–14. Ellis, A. K., Day, J. H. Incidence and characteristics of biphasic anaphylaxis: a prospective evaluation of 103 patients. Annals of Allergy, Asthma & Immunology. 2007; 98(1):64–69. Estelle, F., Simons, R. Anaphylaxis: recent advances in assessment and treatment. Journal of Allergy and Clinical Immunology. 2009; 124:625–636.

Gabb, G. M., Ryan, P., Wing, L. M.H., Hutchinson, K. A. Epidemiological study of angioedema and ACE inhibitors. Australian and New Zealand Journal of Medicine. 1996; 26:777–782. Greenberger, P. A., Rotskoff, B. D., Lifschultz, B. Fatal anaphylaxis: postmortem findings and associated comorbid diseases. Annals of Allergy, Asthma & Immunology. 2007; 98(3):252– 257. Hansen, T. K., Bindslev-Jensen, C., Stahl-Skov, P., Poulsen, L. K. Codfish allergy in adults: IgE cross-reactivity among fish species. Annals of Allergy, Asthma & Immunology. 1997; 78(2):187–194. Huether, S., McCance, K. Understanding Pathophysiology, 5th ed. St Louis: Mosby, 2012. Jirapongsananuruk, O., Bunsawansong, W., Piyaphanee, N., Visitsunthorn, N., Thongngarm, T., Vichyanond, P. Features of patients with anaphylaxis admitted to a university hospital. Annals of Allergy, Asthma & Immunology. 2007; 98(2):157–162. Kaufman, D. Risk of anaphylaxis in a hospital population in relation to the use of various drugs: an international study. Pharmacoepidemiology and Drug Safety. 2003; 12:195–202. Kemp, S., Lockey, R., Simons, F. Epinephrine: the drug of choice for anaphylaxis. A statement of the World Allergy Organization. Allergy. 2008; 63:1061–1070. Kemp, S. A. New action plans for the management of anaphylaxis. Australian Family Physician. 2009; 38(1/2):33–35. Lieberman, P., Kemp, S., Oppenheimer, J., Lang, D., Bernstein, L. The diagnosis and management of anaphylaxis: an updated practice parameter. Journal of Allergy and Clinical Immunology. 2005; 115(3, supp 2):S483–S523. Liew, W. K., Williamson, E., Tang, M. L. Anaphylaxis fatalities and admissions in Australia. Journal of Allergy and Clinical Immunology. 2009; 123(2):434–442. Limb, S. L., Strake, P. R., Lee, C. E., Chowdhury, B. A. Delayed onset and protracted progression of anaphylaxis after omalizumab administration in patients with asthma. Journal of Allergy and Clinical Immunology. 2007; 120(6):1378–1381. Male, D., et al. Immunology, 8th ed. St Louis: Mosby, 2013.

Maulitz, R. M., Pratt, D. S., Schocket, A. L. Exercise-induced anaphylactic reaction to shellfish. Journal of Allergy and Clinical Immunology. 1979; 63:433–434. McCance, K., Huether, S. Pathophysiology: The Biologic Basis for Disease in Adults and Children, 7th ed. St Louis: Mosby, 2014. Neugut, A. I., Ghatak, A. T., Miller, R. L. Anaphylaxis in the United States: an investigation into its epidemiology. Archives of Internal Medicine. 2001; 161(1):15–21. Nurmatov, U., Worth, A., Sheikh, A. Anaphylaxis management plans for the acute and long-term management of anaphylaxis: a systematic review. Journal of Allergy and Clinical Immunology. 2008; 122:353–361. Poulos, L. M., Waters, A.-M., Correll, P. K., Loblay, R. H., Marks, G. B., Trends in hospitalizations for anaphylaxis, angioedema, and urticaria in Australia, 1993–1994 to 2004– 2005. Journal of Allergy and Clinical Immunology. 2007;120(4):878–884 Pumphrey, R. S. Lessons for management of anaphylaxis from a study of fatal reactions. Clinical and Experimental Allergy. 2000; 30:1144–1150. Pumphrey, R. S. Anaphylaxis: can we tell who is at risk of a fatal reaction? Current Opinion in Allergy and Clinical Immunology. 2004; 4:285–290. Sampson, H. A., Mendelson, L., Rosen, J. P. Fatal and near-fatal anaphylactic reactions to food in children and adolescents. New England Journal of Medicine. 1992; 327:380–384. Sampson, M. A., Munoz-Furlong, A., Sicherer, S. H. Risk-taking and coping strategies of adolescents and young adults with food allergy. Journal of Allergy and Clinical Immunology. 2006; 117:1440–1445. Sanders, M. J. Mosby’s Paramedic Textbook, rev 3rd ed. St Louis: Mosby, 2007. Satish, R. R. Is cardiac output the key to vasovagal syncope? A re-evaluation of putative pathophysiology. Heart Rhythm. 2008; 5(12):1702–1703. Sheikh, A., Shehata, Y. A., Brown, S. G., Simons, F. Adrenaline for the treatment of anaphylaxis: Cochrane systematic review. Allergy. 2009; 64:204–212. Shen, Y., Li, L., Grant, J., Rubio, A., Zhao, Z., Zhang, X., et al. Anaphylactic deaths in

Maryland (United States) and Shanghai (China): a review of forensic autopsy cases from 2004 to 2006. Forensic Science International. 2009; 1(5):1–3. Sicherer, S. H. Epidemiology of food allergy. Journal of Allergy and Clinical Immunology. 2011; 127(3):594–602. Simons, F. First-aid treatment of anaphylaxis to food: focus on epinephrine. Journal of Allergy and Clinical Immunology. 2004; 113:837–844. Simons, F., Roberts, J. R., Gu, X., Simons, K. Epinephrine absorption in children with a history of anaphylaxis. Journal of Allergy and Clinical Immunology. 1998; 101:33–37. Smart, D. R. Scombroid poisoning. A report of seven cases involving the Western Australian salmon, Arripis truttaceus. Medical Journal of Australia. 1992; 7(21):748–751. Soar, J., Pumphrey, R., Cant, A., Clarke, S., Corbett, A., Dawson, P., et al. Emergency treatment of anaphylactic reactions—guidelines for healthcare providers. Resuscitation. 2008; 77:157–169. Tang, M., Osbourne, N., Allen, K. Epidemiology of anaphylaxis. Current Opinion in Allergy and Clinical Immunology. 2009; 9(4):351–356. Tole, J. W., Lieberman, P. Biphasic anaphylaxis: review of incidence, clinical predictors, and observation recommendations. Immunology and Allergy Clinics of North America. 2007; 27(2):309–326. Vleeming, W., van Amsterdam, J. G.C., Stricker, B. H.C., de Wildt, D. J. ACE inhibitorinduced angioedema: incidence, prevention and management. Drug Safety. 1998; 18(3):171–181. Vultaggioa, A., Matuccib, A., Del Pacec, S., Simonettic, I., Parronchia, P., Rossib, O., et al. Tako-Tsubo-like syndrome during anaphylactic reaction. European Journal of Heart Failure. 2007; 9(2):209–211. Westfall, T. C., Westfall, D. P. The Pharmacological Basis of Therapeutics, 11th ed. New York: McGraw-Hill, 2006.

S E C T I O N 11

THE PARAMEDIC APPROACH TO THE PATIENT PRESENTING WITH PAIN O U TL I N E INTRODUCTION TO THE PARAMEDIC APPROACH TO THE PATIENT PRESENTING WITH PAIN CHAPTER 28: Pain CHAPTER 29: Lower back pain CHAPTER 30: Renal colic

INTRODUCTION TO THE PARAMEDIC APPROACH TO THE PATIENT PRESENTING WITH PAIN IN THIS SECTION Chapter 28 Pain Chapter 29 Lower back pain Chapter 30 Renal colic

AT THE COMPLETION OF THIS SECTION YOU SHOULD BE ABLE TO • Describe the physiology and common types of pain. • Relate the structure of the spine to the common forms of back injury and back pain. • Describe the principles of management of both acute and chronic lower back pain. • Describe an assessment strategy for the patient presenting with acute lower back pain. • List possible causes of lower back pain that are not related to musculoskeletal spinal injury. Between 70% and 80% of patients presenting to Australian emergency departments report pain as their predominant complaint (NHMRC, 2011). Repeated studies have found that how patients express their pain and how clinicians repond to their complaints of pain are extremely variable and the overall experience is poorly perceived by both parties. To provide effective pain relief clinicians need a deep understanding of the pathology of pain and how it can be accurately assessed, as well as an understanding of the effectiveness of both pharmacological and non-pharmacological methods of pain relief. This section describes the basic physiology of pain and how it is typically expressed in the pre-hospital setting and uses the case studies to outline the role of paramedics in providing adequate pain relief—a practice that studies have demonstrated paramedics often struggle to achieve. The section then explores two very common presentations of pain that pose a challenge to clinical reasoning: lower back pain and renal colic. More than 80% of Australians will experience lower back pain at some time in their life but only a tiny fraction will call for an ambulance. The spine battles the contradictory tasks of providing support, mobility and protection. As a result the forces experienced by the joints during relatively normal activities such as bending over to brush the teeth can actually be extremely high and sudden damage to the lower spinal segment joints can place pressure on large nerve roots or the spinal cord itself. Without an understanding of the anatomy and mechanics of the spine, the innocuous nature of these injuries can lead clinicians to underestimate their seriousness and undertreat the associated pain. Back pain can also be an indication of other serious (non-spinal) conditions. The ability to identify chronic exacerbations of back pain or minor muscular (but still painful) injuries is essential in directing patients to appropriate treatment streams. A specific form of back pain that needs to be excluded from musculoskeletal causes and that requires aggressive pain management is renal colic. With paramedics increasingly being required to treat patients and direct them to agencies other than the emergency department, understanding which back complaints have the likelihood of complications is essential.

CHAP TER 28

Pain By Paul Jennings

C O N C E P TS U S E D I N TH I S C H A P TE R • The paramedic’s clinical approach: Section 2 • The autonomic response: Chapter 56 • The inflammatory response: Chapter 57

O V E RV IE W • Pain is a common presenting symptom for emergency patients but it often remains undertreated. Approximately one-third of patients presenting to ambulance services complain of pain (Jennings, Cameron & Bernard, 2011). • Early, effective pain management in both the prehospital and the ED setting is critical in reducing the likelihood of chronic pain syndromes and painrelated anxiety and distress following the acute phase. • The benefit of prehospital analgesia goes well beyond the prehospital phase of care. • Effective prehospital analgesia facilitates the in-hospital diagnostic and therapeutic process and increases the likelihood of timely ED analgesia.

Introduction Pain is defined as ‘an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such’ (Merskey & Bogduk, 1994). It is wellestablished as a ‘personal’ and ‘subjective’ phenomenon, comprising many physical, psychological and experiential dimensions. For this reason, quantifying pain continues to be a challenge to both clinician and patient. Acute pain is a common presentation to healthcare clinicians (Alonso-Serra et al., 2003; Cordell et al., 2002; Hennes, Kim & Pirrallo, 2005; McManus & Sallee, 2005), is often associated with injury (Castillo et al., 2006) and is a significant contributor to disability many months, or years, following an injury. A recent study of a large Australian urban and rural ambulance service found that approximately one-third of patients presented complaining of pain. Their median age was 56 years and just under half were males (46%). The majority of patients had pain of a traumatic or medical aetiology (40% and 39%, respectively), while pain of a cardiac nature accounted for only 17% of presentations. Approximately half of patients presenting with pain received analgesia in the prehospital setting, with opioid analgesics administered to 20% of patients reporting pain (Jennings, Cameron & Bernard, 2011). Patients presenting to ambulance services and the ED often do so with high-intensity pain. In one study 49% of patients complained of severe pain and 25% of these claimed the maximum possible pain intensity of 10 out of 10 (Todd et al., 2002). Another urban tertiary-care referral ED in North America found that 61% of presentations had a complaint of ‘any pain’ reported on their medical record: pain was documented as the patient’s chief complaint in 85% of cases (Cordell et al., 2002). A number of factors have been identified as predisposing people to clinically important pain reduction and these include age, pain aetiology and initial pain intensity (Jennings, Cameron & Bernard, 2010). Age is associated with clinically important pain relief, with the 45–69 year age group less likely to achieve clinically important pain reduction than all other age groups. Pain aetiology is statistically associated with clinically important pain severity reduction, in that people presenting with pain of a traumatic origin are most likely to achieve effective pain reduction compared with people presenting with pain of a cardiac or medical aetiology. Initial pain severity is also a strong predictor of the likelihood of a patient achieving clinically important pain reduction: patients with moderate or severe pain are much more likely to achieve clinically important pain reduction than those who present with mild pain (Jennings, Cameron & Bernard, 2010).

Pathophysiology Pain is broadly classified into two categories: nociceptive pain and neuropathic pain. Nociceptive pain is caused by stimulation of the peripheral sensory nerve fibres responding to noxious stimuli (see Fig 28.1). Neuropathic pain is caused by damage or disease to the peripheral or central nervous system and results in abnormal processing of sensory signals. As an example the pain associated with a cut finger is initially nociceptive pain, while that associated with an inflamed nerve in shingles is neuropathic pain.

FIGURE 28.1 The nociceptive pain pathway. Activation of peripheral pain receptors (nociceptors) by noxious stimuli generates signals that travel to the dorsal horn of the spinal cord via the dorsal root ganglion. From the dorsal horn, the signals are carried along the ascending pain pathway or the spinothalamic tract to the thalamus and the cortex. Pain can be controlled by pain-inhibiting and pain-facilitating neurons. Descending signals originating in supraspinal centres can modulate activity in the dorsal horn by controlling spinal pain transmission. Source: Bingham et al. (2009). Highly specialised sensory fibres provide information about injurious or potentially

injurious stimuli, as well as environmental conditions such as warmth, cold or touch. Nociceptors are specialised sensory receptors that respond preferentially to noxious stimuli, providing information to the central nervous system regarding the location and intensity of noxious stimuli (Meyer et al., 2006). Injury results in a number of inflammatory mediators being released locally, including bradykinin, prostaglandins, leukotrienes, histamine and cytokines. Some of these agents directly activate nociceptors. Many of the chemical mediators released during inflammation can have a synergistic effect in potentiating nociceptor responses and therefore pain (Meyer et al., 2006). Endogenous opioids released locally, triggered by inflammatory mediators, appear to be part of an ‘antinociceptive’ system that reduces this pain. Opioid receptors have been identified on peripheral terminals of afferent fibres (Meyer et al., 2006). Different cortical regions may be preferentially involved in the different aspects of the complex experience of pain. Somatosensory cortices are important for perception of sensory features. Limbic (emotional) regions are important for the emotional and motivational aspects of pain (Bushnell & Apkarian, 2006). Pain has useful functions. A painful sensation will alert an individual to a hazard, causing them to react—removing their hand from a hotplate, for instance. This fast response to pain using the fast pain fibres (A fibres) produces a subconscious withdrawal reflex. This reflex is faster because the nerves involved in fast transmission are generally larger in diameter and have a thicker myelin sheath. The impulse travels to the spinal cord, which responds with an impulse sent to the motor neurons to remove the hand from the damaging hotplate, as well as an impulse sent to the muscles on the other side of the body to prepare for the shift in body weight. This transmission and motor response are done without the requirement for the impulse to travel to the brain, be processed and responded to. The impulse is also transmitted to the brain, but the motor response removing the hand from the stimulus will already have occurred. These fast pain pathways are generally stimulated by mechanical and thermal stimuli and are very localised in their pain perception (Hall, 2010). There is also a slow pathway using C fibres. These fibres are small in diameter and are unmyelinated, producing a slow activation. They are stimulated by chemical, thermal and mechanical stimuli. Neurotransmitters involved in this pathway include substances that slowly build over time and linger, producing a delayed, less localised pain response. Because of the two types of pain transmission, the response to injury in this example is initially a sharp pain, provoking withdrawal, but then after a period of time with no further injury a pain remains. From a functional point of view the pain alerts the person to the danger and changes their behaviour. It was once thought that due to the immaturity of the peripheral and central nervous systems in children and infants, they did not feel pain and therefore did not require analgesia. It is now widely accepted that infants can be exposed to considerable pain as the result of disease or injury, and that the adverse effects of this pain are both immediate and potentially long term, affecting future sensation and behaviour (Baccei & Fitzgerald, 2006). Intravenous (IV) morphine has long been considered the gold standard for prehospital care in Australia (Rickard et al., 2007) and other emergency medical systems internationally (Bruns et al., 1992). Intravenous fentanyl has recently gained favour as an analgesic agent in the prehospital setting due to its rapid effect (even faster than morphine), shorter duration of effect and equivalent efficacy (Galinski et al., 2005). Opioids, or ‘drugs that

have morphine-like actions, naturally occurring or synthetic’ (MacIntyre & Schug, 2007), act as agonists on opioid receptors and are found in the central nervous system, urinary and gastrointestinal tracts, lungs and peripheral nerve endings. There are three types of opioid receptor: mu, delta and kappa. Different types of opioids produce different effects and analgesic efficacy as a result of their intrinsic activity (MacIntyre & Schug, 2007). The central effects of opiate receptors include analgesia and an alteration in both mood and the cognitive appreciation of pain. The peripheral effects allow opiates to imitate endogenous encephalins and endorphins, reducing the pain produced by the slow pain pathway. The analgesic effects of opioids are mediated predominantly by mu receptors, although delta and kappa receptors can also contribute to pain relief (see Table 28.1). Activation of opioid receptor sites and the subsequent effect on ion channel activities inhibit neuronal activity. Opioid receptor site activation, among other actions, opens potassium channels. This inhibits neurotransmitter release if the receptor is located on presynaptic terminals, and inhibits neuronal firing if the receptor is located postsynaptically on neural cell bodies (Dickenson & Kieffer, 2006). This therefore interrupts pain impulse transmission. TABLE 28.1 Receptor site, endogenous opioid and major effect of delta, kappa and mu receptors

Association of acute pain and persistent pain Early, effective pain management in both the prehospital and ED settings is likely to play a role in reducing the prospect of persistent pain and painrelated anxiety and distress following the acute phase (Buckenmaier et al., 2009; Thomas & Shewakramani, 2008; Turturro, 2002; Weisman, Bernstein & Schechter, 1998). Common types of pain presenting in the acute setting are outlined in Box 28.1. Pain lasting for more than 3 months (known

as persistent pain) can be debilitating (Williamson et al., 2009) and it is becoming clear that unrelieved acute traumatic pain is a risk factor for the progression to persistent pain (Shipton & Tait, 2005). The prevalence of persistent pain following injury has been reported to be between 11% and 62% (Andrew et al., 2008; Moore & Leonardi-Bee, 2008; Rivara et al., 2008; Williamson et al., 2009). Persistent pain has a substantial impact on people’s physical and mental health (Buckenmaier et al., 2009; Thomas & Shewakramani, 2008; Turturro, 2002; Weisman, Bernstein & Schechter, 1998) and can delay functional recovery following traumatic injury (Castillo et al., 2006; Mkandawire et al., 2002). This phenomenon is also seen in surgery, where there is evidence that some early, focused anaesthetic/analgesic strategies reduce the incidence of persistent pain following surgery (Shipton & Tait, 2005). B O X 2 8 . 1P

ainful c o nditio ns frequently

enc o unter ed in the pr eho spital se

ing

Abdominal pain • Provision of analgesia does not interfere with the diagnosis of acute abdominal pain (MacIntyre et al., 2010). • Acute abdominal pain may originate from visceral or somatic structures, may be referred or as a result of neuropathic pain states (MacIntyre et al., 2010). • Parenteral non-selective NSAIDs are as effective as parenteral opioids in the management of biliary colic (MacIntyre et al., 2010).

Back pain (acute) • Red flags that suggest a potentially serious condition include: > signs or symptoms of infection > history of trauma (including minor trauma in the elderly, patients with osteoporosis or those on corticosteroids) > history of malignancy or recent unexplained weight loss > neurological signs or cauda equina syndrome > age greater than 50 years (National Institute of Clinical Studies, 2011).

Burns • Acute burn pain can be nociceptive and/or neuropathic in nature (MacIntyre et al., 2010). • Opioids are effective in burn pain and will most likely require titrated boluses (MacIntyre et al., 2010). • Opioid requirements will typically be higher for burns than for other emergency presentations (National Institute of Clinical Studies, 2011). • Cool water is an effective analgesic if used for at least 20 minutes within 3 hours of the burn but hypothermia should be avoided (National Institute of Clinical Studies, 2011).

Cardiac pain

• Glyceryl trinitrate (GTN) is an effective and appropriate agent for the treatment of acute ischaemic chest pain (MacIntyre et al., 2010). • Morphine is an effective and appropriate analgesic for acute cardiac pain not responsive to GTN (MacIntyre et al., 2010).

Fractures • Immobilisation, ice and elevation of a suspected fracture are important in managing pain. • Femoral nerve block and parenteral opioids are more effective than parenteral opioids alone for managing pain associated with a fractured neck of the femur.

Migraine/tension headache • Acupuncture is effective in the treatment of tension-type headache (MacIntyre et al., 2010). • Simple analgesics (i.e. aspirin, paracetamol, NSAIDs) either alone or in combination are effective in the treatment of episodic tension-type headache (MacIntyre et al., 2010). • Aspirin with metoclopramide is effective in migraine with mild symptoms and is the treatment of first choice (National Institute of Clinical Studies, 2011). • Opioids are not recommended for the emergency treatment of migraine (British Association for the Study of Headache, 2010). • IV metoclopramide administered with a litre of IV fluid is often effective in the treatment of migraine (MacIntyre et al., 2010). • Triptans are effective in the management of severe migraine (MacIntyre et al., 2010). • IV prochlorperazine, chlorpromazine or droperidol is effective in the treatment of migraine, especially in the ED (MacIntyre et al., 2010), although IV metoclopramide and fluids is the gold standard in the ED. • IV triptans or oxygen therapy are effective treatment for cluster headache (MacIntyre et al., 2010).

Renal colic • There is no difference in effectiveness between morphine and pethidine (an older synthetic opioid rapidly disappearing from practice) for renal colic (MacIntyre et al., 2010). • Non-selective NSAIDs and opioids provide effective analgesics for renal colic (National Institute of Clinical Studies, 2011).

Barriers to optimal acute pain management Clinicians are often concerned with the legitimacy of a patient’s complaint of pain, especially when the source of the pain is not visible, and pain often remains undertreated (Alonso-Serra et al., 2003; Luger et al., 2003; McLean et al., 2003; McManus & Sallee, 2005; Todd et al., 2002). The phenomenon of undertreating pain was so pronounced that it led

to the term oligoanalgesia: ‘oligos’ from the Greek, meaning few or scanty; and ‘analgesia’ also from the Greek—‘an’, without, and ‘algesis’, sense of pain. There are many reasons for oligoanalgesia, most related to myths and biases held by healthcare providers brought about through education or culture (Hubert et al., 2009). Oligoanalgesia is a problem within the prehospital and hospital settings (Rupp & Delaney, 2004). The barriers to optimal acute pain management can be broken down into three main categories: (1) the caregiver ’s beliefs; (2) characteristics of pain management; and (3) systems barriers. The vast majority of these barriers to the provision of optimal analgesia in the prehospital setting are myths and are not supported by evidence. Education aimed at dispelling the myths of pain management, pain assessment and the importance of aggressive pain management regimens is critical to improving prehospital provider practice (Hennes & Kim, 2006; MacIntyre et al., 2010).

Caregiv er’s beliefs • Analgesics may interfere with assessment of mental status in the patient with a head injury (Thomas & Shewakramani, 2008). • Analgesics may interfere with general physical assessment (e.g. abdominal assessment) (Hubert et al., 2009; McManus & Sallee, 2005; Ricard-Hibon et al., 2008; Rupp & Delaney, 2004; Thomas & Shewakramani, 2008). • Analgesics can cause haemodynamic or respiratory suppression (Thomas & Shewakramani, 2008) or result in unwanted side effects (Hennes & Kim, 2006; Hubert et al., 2009; Ricard-Hibon et al., 2008; Rupp & Delaney, 2004). • Analgesics may preclude the ability to obtain informed consent for necessary procedures (Thomas & Shewakramani, 2008). • Pain is inevitable in emergency situations (Hubert et al., 2009; Ricard-Hibon et al., 2008). • Analgesia will be given immediately on arrival in ED (Hennes & Kim, 2006). • The use of opioids in acute pain leads to addiction (McManus & Sallee, 2005; Rupp & Delaney, 2004; Turturro, 2002). • Patients often overexaggerate pain (Hennes & Kim, 2006; McManus & Sallee, 2005; Rupp & Delaney, 2004).

Characteristics of pain management • Insertion of intravenous cannula/intramuscular injection is painful in itself (Watkins, 2006). • Children, females and those from lower socioeconomic groups are less likely to receive adequate analgesia (Hennes, Kim & Pirrallo, 2005; Swor et al., 2005; Michael, Sporer & Youngblood, 2007). • Patients are reluctant to report pain and to request analgesia (Duignan & Dunn, 2009; Thomas & Shewakramani, 2008).

Systems barriers • Lack of educational emphasis placed on pain management for healthcare professionals (Hennes & Kim, 2006; Rupp & Delaney, 2004). • Inadequate or non-existent clinical quality management programs (Rupp & Delaney, 2004).

• Some analgesics require intravenous access (Thomas & Shewakramani, 2008) and some crews are not trained in obtaining IV access. • Evaluation of pain intensity (Hennes & Kim, 2006; Ricard-Hibon et al., 2008).

Tolerance, dependence and addiction In considering analgesic agents and dosages, many clinicians are confused regarding the nature, identification and potential impact that tolerance, dependence and addiction can have on the management of acute pain. This can lead to inappropriate or suboptimal early management of pain (MacIntyre et al., 2010). Tolerance relates to a phenomenon whereby exposure to a drug results in a diminution of its effect or a larger dose is required in order to achieve an effect over time (Collett, 1998). Tolerance to a drug can occur as a result of pharmacokinetic or pharmacodynamic mechanisms, or it can be developed over time. Irrespective of the reason, tolerance, particularly relating to opioids, should be considered by the paramedic, especially in patients who have been receiving enteral or parenteral opioids on an ongoing basis, such as chronic cancer patients (Collett, 1998). Tolerance may be one explanation why some patients require larger doses of opioids than others with similar presentations. Physical dependence is defined as the potential for withdrawal symptoms (abstinence syndrome) following abrupt discontinuation or reversal of the drug (MacIntyre et al., 2010). The time it takes or the dose required to predispose a person to physical dependence is unknown (Collett, 1998). The prevention of unpleasant withdrawal symptoms is thought to be one motivation for people with physical dependence to seek drugs. Physical dependence should not influence clinical decision making surrounding the management of pain. Addiction is a type of physical dependence; it is a disease characterised by abnormal drugseeking or maladaptive drug-taking behaviours, which may include cravings and compulsive drug taking despite the risks of physical, social and psychological harm (MacIntyre et al., 2010). Identification of patients who are addicts or at risk of drug abuse can be difficult and effective treatment of the patient with an addiction disorder may be complex. Management of acute pain in this group should focus on the provision of effective analgesia, and this may require larger doses or administration of the drug for longer periods of time than for other patients. Pain management in patients with an addiction disorder can be challenging due to the patient’s fear of being stigmatised, fear of the provision of inadequate analgesia based on their higher tolerance and history, and past experiences and expectations (MacIntyre et al., 2010).

CA SE ST U DY 1 Case 50614, 1715 hrs. Dispatch details: A 25-year-old male cyclist has been struck by a car at low

speed. The patient was riding home from his inner-city office when he was Tboned at an intersection. Initial presentation: The paramedics find the patient lying on the ground supporting his right arm. His upper arm is obviously deformed and he is screaming in pain.

ASSESS Patient history The DOLOR or PQRST mnemonic can be used to elicit a thorough pain history from the patient (see Tables 28.2 and 28.3). Due to the subjective nature of pain, it can be very difficult for clinicians to quantify a patient’s pain intensity and measure the qualitative features of their pain experience. The pain severity perceived by the individual is dependent on a number of cognitive and experiential factors specific to the individual. For this reason, assessment of pain should be based on the patient’s perception of pain and not the clinician’s. TABLE 28.2 DOLOR pain assessment mnemonic

TABLE 28.3 PQRST pain assessment mnemonic

When a patient is complaining of acute pain as a result of a traumatic injury (as is this case), it is quite easy for the clinician to link the complaint of pain with a physical injury. It is harder for the clinician to gain a sense of the intensity of the pain when it is related to a less obvious cause, such as ischaemic chest pain or generalised abdominal pain as a result of gastritis. To assist the clinician in assessing the patient’s pain, it is important to gather some history of the patient’s prior experience of pain relating to intensity and nature. This can provide clues as to the cause of the pain (‘It’s just like the pain I had when I had my heart attack back in January’) or its relative intensity (‘It’s bad, really bad, even worse than when I had kidney stones last year ’). Heart rate, blood pressure and respiratory rate can be affected by a number of factors beyond pain intensity, such as fever, anxiety and medications. Several studies have found poor correlation between the patient’s reported pain intensity and vital signs including heart rate, blood pressure and respiratory rate (Bossart, Fosnocht & Swanson, 2007; Lord & Woollard, 2011; Marco et al., 2006). For this reason, vital signs cannot be used to validate pain intensity as reported by the patient (Lord & Woollard, 2011).

HIST ORY Ask! Use an open approach along the lines of: ‘I need to know if you have used or use morphine, heroin or other opiates regularly, so that I can increase your drug dose in order to get your pain under control.’ Once the patient understands that you are interested in an accurate history so that you can increase the dose you plan to give them, they will be reassured and honest in their reporting.

When gathering the patient history it is also important to establish any previous allergies, adverse experiences and exposure to potential analgesic agents. It is common for patients who have had unpleasant experiences or side effects to a drug—such as nausea, vomiting or disorientation—to describe these events as allergic reactions. In these situations the exact nature of the adverse event or side effect needs to be clarified and a distinction made between a side effect and a true drug allergy. This distinction is often important as it can limit the analgesic options available to the patient and risk suboptimal pain management in both the prehospital and the ED settings.

Quantifying acute pain intensity A reliable, objective pain measurement tool is particularly important as clinicians’ perceptions have been shown to be inaccurate when used to quantify the intensity of pain being experienced by patients. Clinicians have a tendency to underestimate pain (Duignan & Dunn, 2008) and this underestimation becomes more pronounced with increasing clinical experience (Solomon, 2001). Several multidimensional measures exist and these aim to explore and measure the physical, psychological, social, cultural and spiritual components of pain. However, they are complex to administer, require specific training in their use and interpretation, are time-consuming and rely on the availability of assessment forms. For these reasons, their utility in the prehospital setting is compromised. The three most commonly used self-reported, unidimensional rating scales used for adults in the prehospital setting are the verbal numerical rating scale (VNRS; Bijur, Latimer & Gallagher, 2003; Cork et al., 2004; McLean et al., 2003), the visual analogue scale (VAS; Bijur, Silver & Gallagher, 2001; Gallagher et al., 2002; Ho, Spence & Murphy, 1996; Lee, 2001; Price et al., 1994) and the adjective response scale (ARS; Maio et al., 2002). The two most commonly employed pain measurement tools for use in children are the faces pain scale and the Oucher scale. The verbal numerical rating scale The verbal numerical rating scale is commonly used in the prehospital setting as it is valid and easily applied. The patient is asked to rate the intensity of their pain on an 11-point scale, where 0 is considered no pain and 10 is the worst possible pain. The benefits of the VNRS are that it is quick to administer and provides a quantitative rating of the patient’s perceived pain intensity. It has been validated in patients aged 13 years and older (McLean et al., 2003; Gagliese et al., 2005). One potential barrier to its use is difficulty in translating instructions to patients if there is a language barrier (Bird, 2003). The visual analogue scale The visual analogue scale is commonly used for rapid assessment of pain severity and consists of a 100-millimetre horizontal or vertical line. The descriptors ‘no pain’ and ‘worst pain ever ’ are placed at either end of the line (see Fig 28.2) and the patient is asked to place a mark on the line representative of their pain severity. The clinician then measures from the ‘no pain’ mark to the intersection of the mark drawn by the patient to find the pain intensity. This provides a pain rating score out of 10. The validity and reliability of this

pain measure have been consistently demonstrated in a variety of settings (Bijur, Silver & Gallagher, 2001; Gallagher et al., 2002; Ho, Spence & Murphy, 1996; Lee, 2001; Price et al., 1994).

FIGURE 28.2 Visual analogue scale. Instruct the patient to point to the position on the line between the faces to indicate how much pain they are currently feeling. The far left end indicates ‘no pain’ and the far right end indicates ‘worst pain ever’. Given the visual nature of this measure, reliability may be reduced when used by patients who are visually impaired. Likewise, cognitive impairment, lack of understanding of the task and an inability to follow instructions can impact on the accuracy of the measure (Bird, 2003). The VAS has been found to be less accurate in the elderly (Jensen, Karoly & Braver, 1986) and young children (Shields et al., 2003). The measure relies on the immediate availability of the pain scale for patients to place their mark: Lord and Parsell (2003) reported that 26% of paramedics considered the VAS to be too cumbersome and said it was often lost or difficult to locate when required. The VNRS has been found to be comparable in accuracy to the VAS (Bijur, Latimer & Gallagher, 2003; Cork et al., 2004). Interestingly, while the VNRS has been found to perform as well as the VAS in assessing changes to pain, patients consistently score their pain higher on the VNRS (Holdgate et al., 2003). One of the clear benefits of the VNRS is that it does not require any associated equipment, which is particularly beneficial in the prehospital setting. The adjective response scale

The adjective response scale consists of between three and five ranked verbal pain descriptors: ‘none’, ‘slight’, ‘moderate’, ‘severe’ and ‘agonising’. The scale has been evaluated for its validity, reliability and ease of use, and strong correlations have been found between the ARS and the VAS. One of the limitations of the ARS is the relative lack of discrimination with a five-point scale. Also, like the VNRS, there are potential barriers around language and cross-cultural issues (Maio et al., 2002). The faces pain scale There are several versions of the faces pain scale that are predominantly used for assessing pain in children. Alternative measures are required as children have limited cognitive abilities and are unable to use most of the adult scales (McManus & Sallee, 2005). These scales use pictures of faces that illustrate steadily increasing intensities of pain or discomfort (see Fig 28.3).

FIGURE 28.3 The faces pain scale. Explain to the child that each face is for a person who feels happy because they have no pain (no hurt) or sad because they have some or a lot of pain. Face 0 is very happy because they don’t hurt at all. Face 1 hurts just a little bit. Face 2 hurts a little more. Face 3 hurts even more. Face 4 hurts a whole lot. Face 5 hurts as much as you can imagine, although you don’t have to be crying to feel this bad. Ask the child to choose the face that best describes how they are feeling. The rating scale is recommended for children aged 3 years and older. Source: Hockenberry & Wilson (2009). The Oucher scale The Oucher scale (see Fig 28.4) is another pain scale used to measure pain in children and it combines pictures much like the faces pain scale with a vertical VAS. It has been previously validated in children 3–12 years of age (Maio et al., 2002). Although not yet validated in the emergency or prehospital setting, the Oucher scale appears promising in the prehospital environment warranting further research (Maio et al., 2002).

FIGURE 28.4 The Oucher scale ‘This picture shows no hurt [point to first picture]; this picture shows just a little bit of hurt [point to the second picture]; this picture shows a little more hurt [point to the third picture]; this picture shows even more hurt (point to the fourth picture]; this picture shows a lot of hurt [point to the fifth picture); and this picture shows the biggest hurt you could ever have [point to the last picture]. Can you point to the picture that shows how much hurt you are having right now?’ The scale is available in various racial backgrounds. Source: © The Caucasian version of the OUCHER was developed and copyrighted by Judith E. Beyer, PhD, RN, USA, 1983.

Airway This patient is screaming in pain, indicating there is no problem with his airway.

Breathing The patient’s breathing appears to be sufficient, given he has the tidal volume to scream. However, as he has just been hit by a car, his breathing should be monitored continuously. Trauma to the thoracic wall or damage to internal structures is a possibility and could potentially hinder the patient’s breathing should it become worse.

Cardiovascular For this patient, internal and external haemorrhages are a possibility. Also, while we have established that vital signs are not a particularly reliable indicator of pain severity, trends in the patient’s condition can be tracked through cardiovascular vital signs.

Neurological There are three aspects that need to be considered when undertaking a neurological assessment. Firstly, were there any precipitating neurological

events that led to the event? For example, in this case did the patient become dizzy and swerve in front of the car? Secondly, are there any neurological deficits as a result of the accident indicating a head injury? And thirdly, are there any sensory deficits distal to the site of injury—in this case, on the patient’s arm? This patient had no precipitating neurological event before the accident and he has no neurological deficits following the accident, including those associated with injury to his arm.

Initial assessment summary Problem Injury to upper right arm Conscious GCS = 15; full recall of the event state Position Supine, holding right arm Heart rate 105 BPM Blood 120/80 mmHg pressure Skin Pink, warm, dry appearance Speech Sentences pattern Respiratory 24 BPM rate Respiratory Even cycles rhythm Chest Clear bilaterally auscultation Pulse 98% oximetry SpO2 Temperature 37.4°C Capillary refill 1 second (seconds) Pain score 10/10 Motor/sensory Normal sensory; patient can move fingers on right arm, but is function reluctant to try anything else due to pain Secondary Deformity and swelling to right upper arm survey History The patient was T-boned by a vehicle at low speed. He fell between his bicycle and the front of the car (i.e. he was not thrown onto the bonnet of the car). He was wearing a helmet. D: There is no danger to the ambulance crew or the patient. A: The patient is conscious with no airway obstruction. B: Respiratory rate is marginally elevated but this could be attributed to the pain. C: Heart rate is elevated, but again this could be attributed to the pain. Blood

pressure is within normal limits.

S I T U A T I O N A L A WA R E N E S S Individuals with drug tolerance and addiction may be influenced by prior contact with health service personnel who withheld opiates from them. Our sole focus as health professionals is improvement of our patients’ pain; do not be judgemental about a patient’s past use of opiates, whether prescribed or illegally obtained.

The patient is presenting with 10/10 pain and deformity and swelling to his upper right arm after being struck by a car while riding his bike. The secondary survey does not indicate any other injuries or involvement of other body systems.

CONFIRM The essential part of the clinical reasoning process is to seek to confirm your initial hypothesis by finding clinical signs that should occur with your provisional diagnosis. You should also seek to challenge your diagnosis by exploring findings that do not fit your hypothesis: don’t just ignore them because they don’t fit.

DIF F ERENT IA L DIA GNOSIS Pain related to a fractured arm Or • Referred cardiac chest pain • Drugseeking behaviour

What else could it be? Referred cardiac chest pain This scenario is unlikely in a patient of this age. However, when assessing patients involved in any sort of accident, it is important to determine any precipitating factors that may have led to the accident. For example, it is not uncommon for single-vehicle accidents to be caused by the driver losing consciousness due to experiencing a cardiac event. In this case, the patient is

young and presumably fit and has a clear deformity to his right upper arm, and the pain is well localised to the site of the deformity. Drugseeking behaviour The differential would be that the patient does not have pain, raising the possibility of drugseeking behaviour or some other reason to report pain when in fact it does not exist. In this situation, there is a very obvious injury associated with the pain.

T REAT Emergency management In planning a pain management regimen, you should consider the appropriateness of both pharmacological and non-pharmacological approaches. The likely effectiveness of many non-pharmacological interventions is often underestimated or overlooked. As a minimum, techniques such as immobilisation and splinting of injured body parts and reassurance and temperature control to prevent shivering should be employed as first-line management. Prehospital analgesic options Doses of analgesics should be based on locally approved clinical practice guidelines. Adjustments in dosing should be considered for the elderly, for those with diminished drug clearance such as renal or liver dysfunction (National Institute of Clinical Studies, 2011) and for those who may well have tolerance and thus potentially require much larger doses. Because a drug’s clinical effectiveness is proportional to the logarithm of the drug concentration, you should be prepared to increase the dose if an earlier dose does not have an effect. In practice this means that if 2.5 mg of morphine has no effect, you need to either give subsequent doses rapidly or be prepared to give a larger dose. Some clinical guidelines are consistent with this pharmacodynamic principle, while others just rely on repeating the same dose. Side effects and adverse events should be considered prior to administration and observed for following administration. A history of minor side effects may need to be weighed against the potential benefits of effective analgesia, and the incidence of adverse effects of opioids is commonly dose-related (MacIntyre et al., 2010). There is a need to have a range of analgesic agents that use various modes of administration. Table 28.4 summarises analgesic agents commonly available in the prehospital environment and their routes of administration. The oral route is often inappropriate to use due to poor absorption and gastric stasis in the critically ill (Borland, Jacobs & Rogers, 2002) and the IV route is not always ideal or achievable. The IM route is not advised in patients with reduced perfusion and rarely has a role in acute emergencies due to variations in absorption in shock states and the difficulty of accurately titrating a good analgesic effect.

TABLE 28.4 Analgesic agents commonly used in ambulance

P RACT ICE T IP The incidence of nausea and vomiting following the administration of intravenous morphine for acute pain is low despite common misconceptions (Bradshaw & Sen, 2006). Furthermore, there is little evidence that prophylactic metoclopramide following administration of intravenous morphine for acute pain is beneficial— and, in fact, it may cause harm (Simpson, Bendall & Middleton, 2001).

Inhalational agents have a rapid onset of action and are rapidly cleared via the lungs as soon as they are no longer applied. Nitrous oxide is still found in some ambulances around the world; however, studies have revealed that concentrations within this small confined space rise to many times the safety exposure limit unless a full scavenger system is operating. Methoxyflurane does not have this problem because it has a distinctive odour and so atmospheric concentrations are easy to detect. However, this odour can cause poor compliance among patients, so appropriate coaching is necessary for patients using methoxyflurane. The intranasal route is an important option for several prehospital analgesic agents (Carr et al., 2004; Christensen et al., 2007; Rickard et al., 2007) and is particularly useful in managing paediatric pain (Borland et al., 2007) and in ambulance services where personnel are restricted in gaining IV access. Non-pharmacological pain management options While pharmacological analgesics and anaesthesia are considered the gold standard of pain management, non-pharmacological interventions are effective and should be considered as an adjunct to pharmacological agents to enhance pain management. Non-pharmacological interventions are divided into three broad categories (McManus & Sallee, 2005): • cognitive: music, distraction, hypnosis, guided imagery • behavioural: relaxation techniques, biofeedback exercises, breathing control • physical: heat and cold (cryoanalgesia) application, massage or touch, position and comfort, temperature regulation, transcutaneous electrical nerve stimulation (TENS), acupuncture, chiropractic, immobilisation. Unfortunately, many of these options are not available or feasible within the prehospital environment. However, techniques such as talking and distraction, and parental presence for children, are easily implemented in the prehospital setting and have been shown to be effective in reducing pain intensity (Hennes & Kim, 2006). They should be implemented where appropriate whether or not the patient is receiving pharmacological analgesics (Thomas & Shewakramani, 2008). This patient will benefit from non-pharmacological measures of reassurance and splinting. An inhalational anaesthetic (methoxyflurane) may be very useful when preparing and applying the splint. Gaining IV access will allow the paramedics to administer opiates in small repeated doses, increasing as

necessary until analgesia is achieved. If the paramedics plan to use morphine, it is important to remember that the maximum clinical effect of morphine is felt some 15 minutes after it is administered IV. Therefore, they should give the patient opiates until he tells them that his pain is significantly reduced but stop short of a target of zero pain because the effect will continue to increase for 15 minutes.

EVALUAT E Evaluating the effect of any clinical management intervention can provide clues to the accuracy of the initial diagnosis. Some conditions respond rapidly to treatment so patients should be expected to improve if the diagnosis and treatment were appropriate. A failure to improve in this situation should trigger the clinician to reconsider the diagnosis. Regular reassessment of pain leads to improved acute pain management (MacIntyre et al., 2010) and is important for several reasons. Firstly it provides the clinician with a sense of the appropriateness of the analgesic choice based on the response of the individual to the chosen treatment regimen. One opioid is not superior to other opioids; however, some opioids have better effects in some patients than others (MacIntyre et al., 2010). Secondly it allows the clinician to observe the trend of pain intensity improvement or otherwise much like a clinician observes trends in blood pressure, conscious state and heart rate. Pain intensity should be reassessed and documented regularly and form part of the routine vital signs assessment.

P RACT ICE T IP Opiates are an antidote to pain and pain is an antidote to opiates. An increase in pain requires an increase in opiates; a decrease in pain will produce more sedation from the same dose of opiates.

Ongoing management Following the management of immediate life threats and the commencement of a pain management regimen, other injuries should be managed and other therapies initiated. It is important to remember that many interventions can increase the intensity of pain experienced by the patient. Pain associated with repositioning injured limbs, lifting and moving the patient and transporting them over rough terrain should be anticipated and taken into consideration when planning appropriate analgesia options and doses. Conversely, once a limb has been splinted and the pain sensation reduced, the opiate effect may be exaggerated and the patient may show signs of respiratory depression and sedation.

CA SE ST U DY 2 Case 11354, 0820 hrs. Dispatch details: A 26-year-old female with a severe headache, not relieved by paracetamol. Initial presentation: The paramedics are directed to the patient by her partner. She is lying in bed with her eyes closed.

ASSESS 0831 hrs Primary survey: The patient is conscious and talking. 0831 hrs Chief complaint: ‘I’ve had a headache all night. Paracetamol has done nothing, and I think it’s getting worse.’ 0832 hrs Vital signs survey: Perfusion status: HR 90, sinus rhythm, BP 130/75 mmHg, skin warm and pink. Respiratory status: RR 20 BPM, good air entry, L = R, normal work of breathing, speaking in full sentences, no complaint of dyspnoea. Conscious state: GCS = 14 (E3, V5, M6). 0834 hrs Pertinent hx: The patient is normally well and only takes the oral contraceptive pill. She says that she only occasionally gets headaches, generally thought to be due to ‘stress’, and they usually resolve within a few hours with paracetamol. She is nauseated, but doesn’t feel she is about to vomit. She rates

her pain as 5/10. The patient is presenting with a story of headache that is atypical for her and is not responding to simple analgesics. Although this could be a migraine it is not the classic presentation and is not following a wellestablished pattern and therefore needs formal evaluation and investigation in hospital. In the meantime, the paramedics should provide pain relief while they transport the patient.

CONFIRM In many cases paramedics are presented with a collection of signs and symptoms that do not appear to describe a particular condition. A critical step in determining a treatment plan in this situation is to consider what other conditions could explain the patient’s presentation. In this particular case, the fact that the patient has a headache is not in dispute. But the potential causes need to be considered. The issue here is how confident are the paramedics that this episode of pain is a benign headache?

What else could it be? Subarachnoid haemorrhage About 1–4% of patients who present to ED have subarachnoid haemorrhage (SAH). The incidence increases with age and is most common in the 40–60 year age group. Head trauma is the most common cause of SAH, while cerebral aneurysm is the most common non-traumatic cause. Headache is common in approximately 95% of SAH presentations and is typically sudden (within a few seconds in 75% of cases) and severe, often being the ‘worst ever ’ headache. Up to half of patients with SAH describe a mild headache in the hours or days leading up to the major bleed. Nausea and vomiting are common in 75% of cases and brief or permanent loss of consciousness is common.

DIF F ERENT IA L DIA GNOSIS Benign causes Or • Subarachnoid haemorrhage • Intracerebral haemorrhage • Ischaemic stroke • Systemic viral infection • Rhinosinusitis

Intracerebral haemorrhage Most commonly caused by chronic hypertension, intracerebral haemorrhage

(ICH) typically presents clinically as a sudden onset of neurological deficit with associated headache and collapse. Patients often have a transient loss of consciousness, are hypertensive and vomit. About 20% of all strokes are attributed to ICH.

P RACT ICE T IP Consider the following complaints when assessing a headache: • subacute and/or progressive headache over months • new or different headache • ‘worst headache ever ’ • any headache of maximum severity at onset • onset after the age of 50 years old • symptoms of systemic illness • seizures • any neurological signs.

Ischaemic stroke Ischaemic stroke is most commonly the result of thromboembolism arising from the cerebral vasculature, the heart or the aorta. Ischaemic stroke accounts for approximately 80% of all strokes. Signs and symptoms correspond to the area of the brain affected and imaging is performed to accurately identify whether the anterior or posterior circulation is affected and to definitively rule out haemorrhagic stroke. Systemic viral infection A number of systemic viral infections can cause headache. These are usually associated with other symptoms such as rhinitis, sinus congestion, cough, body aches and skin rash. Rhinosinusitis About half of the patients who present to ear, nose and throat specialists complain of severe headache. Headache is often present with rhinosinusitis, but may be aggravated with exertion, postural changes and coughing. Headaches associated with chronic sinusitis are usually mild and diffuse, becoming worse during the day.

T REAT For a simple primary (undiagnosed) headache, NSAIDs, paracetamol, prochlorperazine and opioids are all recommended. If the pain is severe, there is no contraindication to small doses of IV opiates. Some services restrict opioids for headaches due to the fear of generating an altered conscious state in the

patient that may make hospital assessment difficult. Provided the medications are titrated carefully, this should not occur. 0836 hrs: The paramedics offer reassurance and encourage the patient to take her own oral medications if she has them. 0837 hrs: The paramedics administer IV fluids and metoclopramide.

EVALUAT E Evaluating the effect of any clinical management intervention can provide clues to the accuracy of the initial diagnosis. Some conditions respond rapidly to treatment so patients should be expected to improve if the diagnosis and treatment were appropriate. A failure to improve in this situation should trigger the clinician to reconsider the diagnosis. This patient’s vital signs have not changed but the nausea has subsided slightly. The crew administer 250 mcg of fentanyl to reduce her pain and after 5 minutes she appears more comfortable. Small, titrated doses of opioids are suitable for undiagnosed headaches but large doses should be avoided. Any deterioration in the patient’s neurological status would suggest some form of intracranical haemorrhage and the paramedics will need to notify the hospital of the change in her condition.

CA SE ST U DY 3 Case 12067, 1020 hrs. Dispatch details: A 58-year-old male with abdominal pain. Initial presentation: The paramedics find the patient lying across the couch in his lounge room.

ASSESS 1041 hrs Chief complaint: ‘I’ve got a pain in my stomach.’ 1043 hrs Vital signs survey: Perfusion status: HR 80, sinus rhythm, BP 160/90 mmHg, skin warm and pink. Respiratory status: RR 20 BPM, good air entry, L = R, normal work of breathing, speaking in full sentences, no complaint of dyspnoea. Conscious state: GCS = 15 (E4, V5, M6). 1047 hrs Pertinent hx: The patient is moderately overweight and has a history of hypertension and hypercholesterolaemia. His current medications include an antihypertensive (ACE inhibitor) and lipid-lowering agent (statin). He states that he has not previously suffered from abdominal pain. He vomited three times this morning and is still nauseated. The pain is on his right side just under his ribs: it is intermittent and came on quickly about an hour ago. He rates the pain as 8/10.

CONFIRM In many cases paramedics are presented with a collection of signs and symptoms that do not appear to describe a particular condition. A critical step in determining a treatment plan in this situation is to consider what other conditions could explain the patient’s presentation. This patient has diffuse abdominal pain associated with vomiting. The colicky history could be consistent with gallstones and cholecystitis but at this stage it is impossible to discern without further investigations. The key issue is that he needs pain relief before and during transportation.

DIF F ERENT IA L DIA GNOSIS Gastroenteritis Or • Peptic ulcer • Abdominal aortic aneurysm • Mesenteric infarction • Acute myocardial infarction • Acute/chronic pancreatitis • Strangulated hernia • Appendicitis • Inflammatory bowel syndrome

What else could it be? Peptic ulcer Gastric or duodenal ulcer could present with pain. Usually the history is a little longer and often there is altered blood (‘coffee grounds’) in the vomit, which there is no history of in this case. Abdominal aortic aneurysm An aneurysm can present with diffuse abdominal pain, although classically one would expect more back pain and potentially groin pain. At this stage it remains a possibility, although unlikely. The absence of haemodynamic compromise is reassuring. Mesenteric infarction Mesenteric ischaemia or infarction can present with pain and vomiting but usually causes a metabolic acidosis that should be revealed because it causes a raised respiratory rate in an attempt to compensate. However, this may be difficult to differentiate in a patient with a raised sympathetic drive in response to pain. This raised sympathetic drive could also result in an increased respiratory rate. This is a possibility in this patient. Acute myocardial infarction Myocardial infarction can present with abdominal pain, particularly epigastric pain. Inferior myocardial infarction is more likely to present with nausea. This is certainly a diagnosis worth considering for this patient and he should be assessed using a 12-lead ECG. Acute/chronic pancreatitis Pancreatitis could present like this or it could present with the patient looking considerably sicker with signs of shock. Once again it is a diagnosis that will be considered and excluded with investigations in hospital. Strangulated hernia There is no history of a hernia but if there was and it had obstructed then a presentation with vomiting and pain is consistent. Appendicitis Appendicitis presents initially with nonspecific, non-localised pain. It can often occur with vomiting and as time passes the pain will localise to the right iliac fossa as the peritoneum becomes involved. Once again, although not the most likely diagnosis, it is possible in this case. Inflammatory bowel syndrome An exacerbation of an inflammatory bowel syndrome can present with pain, nausea and vomiting. The patient did not give a history that is consistent with this, but it is by no means excluded. All of these possible explanations for this patient’s abdominal pain could turn out to be correct; the issue at the moment is to arrange adequate analgesia. Confidently assessing the patient presenting with abdominal pain without the luxury of investigations or time to repeatedly observe the patient over a series of hours is extremely difficult and even the most experienced clinicians are often unable to make a confident diagnosis. The key is not to exclude any of the more serious diagnoses until proven otherwise.

T REAT The patient requires adequate analgesia before being transported to hospital, bearing in mind that movement will exacerbate his pain. This exacerbation is particularly relevant to pain associated with conditions such as peritoneal inflammation. Inhalational anaesthetics (methoxyflurane) are a good first step while also providing the patient with reassurance and undertaking further assessment. Once IV access has been established, IV opiates in repeated doses titrating the dose size to the effect will provide the best pain relief. 1050 hrs: The paramedics administer 250 mcg of fentanyl to reduce the patient’s pain and after 5 minutes he rates his pain as 5/10.

EVALUAT E Evaluating the effect of any clinical management intervention can provide clues to the accuracy of the initial diagnosis. Some conditions respond rapidly to treatment so patients should be expected to improve if the diagnosis and treatment were appropriate. A failure to improve in this situation should trigger the clinician to reconsider the diagnosis. This patient’s vital signs have not changed so the paramedics administer another 250 mcg of fentanyl. With a quick onset and peak time, titrating fentanyl every 5 minutes should provide effective pain relief. Any signs of respiratory depression, poor perfusion or deterioration in the patient’s conscious state indicate that the maximum safe dose has probably been exceeded.

Future research Future research should focus on age-and casespecific interventions and aim to identify individual interventions, or combinations of interventions, which favourably impact on both pain intensity and short-and long-term quality of life. Prehospital studies of all analgesic interventions, both pharmacological and non-pharmacological, should be of a rigorous experimental randomised design, include a control group and, where possible, be blinded to the patient and the paramedics. The emerging link between acute and persistent pain also requires further investigation, and given that emergency medical services are responsible for the earliest phase of care, they are integral to studies focused on the link between acute pain management and the likelihood of future persistent pain. Providers of early trauma care are well placed to engage in preventive medicine and to contribute to significant reductions in the burden associated with traumatic pain.

Summary Pain is a frequently encountered problem in the prehospital setting. It affects some people and conditions more than others, but can be substantially improved with appropriate pharmacological and non-pharmacological agents. Factors associated with the likelihood of clinically important pain reduction include the patient’s age, time criticality of the patient, pain aetiology, initial pain severity and the analgesic agent or combination administered to the patient. Knowledge of these characteristics associated with clinically important pain reduction is useful to clinicians, researchers, educators and policy makers and informs future practice.

References Alonso-Serra, H. M., Wesley, K., National Association of EMS Physicians. Prehospital pain management. Prehospital Emergency Care. 2003; 7(4):482–488. Andrew, N. E., Gabbe, B. J., Wolfe, R., Williamson, O. D., Richardson, M. D., Edwards, E. R., Cameron, P. A. Twelve-month outcomes of serious orthopaedic sport and active recreation-related injuries admitted to level 1 trauma centers in Melbourne, Australia. Clinical Journal of Sport Medicine. 2008; 18(5):387–393. Baccei, M., Fitzgerald, M. Development of pain pathways and mechanisms. In McMahon S., Koltzenburg M., eds.: Wall and Melzack’s Textbook of Pain, 5th ed., Philadelphia: Elsevier, 2006. Bijur, P. E., Latimer, C. T., Gallagher, E. J. Validation of a verbally administered numerical rating scale of acute pain for use in the emergency department. Pain. 2003; 10(4):390–392. Bijur, P. E., Silver, W., Gallagher, J. Reliability of the visual analogue scale for measurement of acute pain. Academic Emergency Medicine. 2001; 8(12):1153–1157. Bingham, B., Ajit, S. K., Blake, D. R., Samad, T. A. The molecular basis of pain and its clinical implications in rheumatology. Nature Clinical Practice Rheumatology. 2009; 5:28–37. Bird, J. Selection of pain measurement tools. Nursing Standard. 2003; 18(13):33–39. Borland, M., Jacobs, I., King, B., O’Brien, D. A randomized controlled trial comparing intranasal fentanyl to intravenous morphine for managing acute pain in children in the emergency department. Annals of Emergency Medicine. 2007; 49(3):335–340. Borland, M. L., Jacobs, I., Rogers, I. R. Options in prehospital analgesia. Emergency Medicine (Fremantle). 2002; 14(1):77–84. Bossart, P., Fosnocht, D., Swanson, E. Changes in heart rate do not correlate with changes in pain intensity in emergency department patients. Journal of Emergency Medicine. 2007; 32(1):19–22. Bradshaw, M., Sen, A. Use of a prophylactic antiemetic with morphine in acute pain: randomised controlled trial. Emergency Medicine Journal. 2006; 23(3):210–213.

British Association for the Study of Headache. Guidelines for all healthcare professionals in the diagnosis and management of migraine, tension-type headache, cluster headache and medication-overuse headache. Retrieved 10 October 2012 from www.bash.org.uk, 2010. Bruns, B. M., Dieckmann, R., Shagoury, C., Dingerson, A., Swartzell, C. Safety of prehospital therapy with morphine sulphate. American Journal of Emergency Medicine. 1992; 10(1):53–57. Buckenmaier, C. C., III., Rupprecht, C., McKnight, G., McMillan, B., White, R. L., Gallagher, R. M., Polomano, R. Pain following battlefield injury and evacuation: a survey of 110 casualties from the wars in Iraq and Afghanistan. Pain Medicine. 2009; 10(8):1487–1496. Bushnell, M., Apkarian, A. V. Representation of pain in the brain. In McMahon S., Koltzenburg M., eds.: Wall and Melzack’s Textbook of Pain, 5th ed., Philadelphia: Elsevier, 2006. Carr, D. B., Goudas, L. C., Denman, W. T., Brookoff, D., Staats, P. S., Brennen, L., et al. Safety and efficacy of intranasal ketamine for the treatment of breakthrough pain in patients with chronic pain: a randomized, double-blind, placebo-controlled, crossover study. Pain. 2004; 108:17–27. Castillo, R. C., MacKenzie, E. J., Wegener, S. T., Group, L. S., Castillo, R. C., Bosse, M. J. Prevalence of chronic pain seven years following limb-threatening lower extremity trauma. Pain. 2006; 124(3):321–329. Christensen, K., Rogers, E., Green, G. A., Hamilton, D. A., Mermelstein, F., Liao, E., et al. Safety and efficacy of intranasal ketamine for acute postoperative pain. Acute Pain. 2007; 9:183–192. Collett, B.-J. Opioid tolerance: the clinical perspective. British Journal of Anaesthesia. 1998; 81:58–68. Cordell, W. H., Keene, K. K., Giles, B. K., Jones, J. B., Jones, J. H., Brizendine, E. J. The high prevalence of pain in emergency medical care. American Journal of Emergency Medicine. 2002; 20:165–169. Cork, R. C., Isaac, I., Elsharydah, A., Saleemi, S., Zavisca, F., Alexander, L. A comparison of the verbal rating scale and the visual analogue scale for pain assessment. The Internet

Journal of Anesthesiology. 8(1), 2004. Dickenson, A. H., Kieffer, B. Opiates: basic mechanisms. In McMahon S., Koltzenburg M., eds.: Wall and Melzack’s Textbook of Pain, 5th ed., Philadelphia: Elsevier, 2006. Duignan, M., Dunn, V. Congruence of pain assessment between nurses and emergency department patients: a replication. International Emergency Nursing. 2008; 16:23–28. Duignan, M., Dunn, V. Perceived barriers to pain management. Emergency Nurse. 2009; 16(9):31. Gagliese, L., Weizblit, N., Ellis, W., Chan, V. W.S. The measurement of postoperative pain: a comparison of intensity scales in younger and older surgical patients. Pain. 2005; 117:412– 420. Galinski, M., Dolveck, F., Borron, S. W., Tual, L., Van Laer, V., Lardeur, J.-Y., et al. A randomized, double-blind study comparing morphine with fentanyl in prehospital analgesia. American Journal of Emergency Medicine. 2005; 23(2):114–119. Gallagher, E. J., Bijur, P. E., Latimer, C., Silver, W. Reliability and validity of a visual analog scale for acute abdominal pain in the ED. American Journal of Emergency Medicine. 2002; 20(4):287–290. Hall, J. E. Guyton and Hall Textbook of Medical Physiology, 12th ed. Philadelphia: Elsevier, 2010. Hennes, H., Kim, M., Prehospital pain management: current status and future direction. Clinical Pediatric Emergency Medicine 2006; 7:25–30 Hennes, H., Kim, M. K., Pirrallo, R. G. Prehospital pain management: a comparison of providers’ perceptions and practices. Prehospital Emergency Care. 2005; 9(1):32–39. Ho, K., Spence, J., Murphy, M. F. Review of pain-measurement tools. Annals of Emergency Medicine. 1996; 27(4):427–432. Hockenberry, M. J., Wilson, D. Wong’s Essentials of Pediatric Nursing, 8th ed. St Louis: Mosby, 2009. Holdgate, A., Asha, S., Craig, J., Thompson, J. Comparison of a verbal numeric rating scale

with the visual analogue scale for the measurement of acute pain. Emergency Medicine. 2003; 15:441–446. Hubert, H., Guinhouya, C., Richard-Hibon, A., Wiel, E., Durocher, A., Goldstein, P. Prehospital pain treatment: an economic productivity factor in emergency medicine? Journal of Evaluation in Clinical Practice. 2009; 15:152–157. Jennings, P. A., Cameron, P., Bernard, S., Determinants of clinically important pain severity reduction in the prehospital setting. Emergency Medicine Journal 2010;, doi: 10.1136/emj.2010.107094. [[Epub ahead of print]]. Jennings, P., Cameron, P., Bernard, S. Epidemiology of prehospital pain: an opportunity for improvement. Emergency Medicine Journal. 2011; 28:530–531. Jensen, P., Mark, Karoly, P., Braver, S. The measurement of clinical pain intensity: a comparison of six methods. Pain. 1986; 27:117–126. Lee, J. S. Pain measurement: understanding existing tools and their application in the emergency department. Emergency Medicine. 2001; 13:279–287. Lord, B., Woollard, M. The reliability of vital signs in estimating pain severity among adult patients treated by paramedics. Emergency Medicine Journal. 2011; 28:147–150. Lord, B. A., Parsell, B., Measurement of pain in the prehospital setting using a visual analogue scale. Prehospital & Disaster Medicine. 2003;18(4):353–358 [Erratum appears in Prehospital & Disaster Medicine 2005, 20(1), v.] Luger, T. J., Lederer, W., Gassner, M., Lockinger, A., Ulmer, H., Lorenz, I. H. Acute pain is under-assessed in out-of-hospital emergencies. Academic Emergency Medicine. 2003; 10(6):627–632. MacIntyre, P. A., Scott, D. A., Visser, E., Walker, S. M. Acute Pain Management: Scientific Evidence, 3rd ed. Australian and New Zealand College of Anaesthetists and Faculty of Pain Medicine, 2010. MacIntyre, P. E., Schug, S. A.Acute Pain Management. A Practical Guide. Philadelphia: Elsevier, 2007. Maio, R. F., Garrison, H. G., Spaite, D. W., Desmond, J. S., Gregor, M. A., Stiell, I. G.,

O’Malley, P. J. Emergency Medical Services Outcomes Project (EMSOP) IV: pain measurement in out-of-hospital outcomes research. Annals of Emergency Medicine. 2002; 40(2):172–179. Marco, C. A., Plewa, M. C., Buderer, N., Hymel, G., Cooper, J. Self-reported pain scores in the emergency department: lack of association with vital signs. Academic Emergency Medicine. 2006; 13(9):974–979. McLean, S. A., Domeier, R. M., DeVore, H. K., Hill, E. M., Maio, R. F., Frederiksen, S. M. The feasibility of pain assessment in the prehospital setting. Prehospital Emergency Care. 2003; 8:155–161. McManus, J. G., Jr., Sallee, D. R., Jr. Pain management in the prehospital environment. Emergency Medicine Clinics of North America. 2005; 23(2):415–431. Merskey, H., Bogduk, N.Classification of Chronic Pain. IASP Task Force on Taxonomy. Seattle: IASP Press, 1994. Meyer, R. A., Ringkamp, M., Campbell, J. N., Raja, S. N. Peripheral mechanisms of cutaneous nociception. In McMahon S., Koltzenburg M., eds.: Wall and Melzack’s Textbook of Pain, 5th ed., Philadelphia: Elsevier, 2006. Michael, G. E., Sporer, K. A., Youngblood, G. M. Women are less likely than men to receive prehospital analgesia for isolated extremity injuries. American Journal of Emergency Medicine. 2007; 25:901–906. Mkandawire, N. C., Boot, D. A., Braithwaite, I. J., Patterson, M. Musculoskeletal recovery 5 years after severe injury: long-term problems are common. Injury. 2002; 33(2):111–115. Moore, C. M., Leonardi-Bee, J. The prevalence of pain and disability one year post fracture of the distal radius in a UK population: a cross sectional survey. BMC Musculoskeletal Disorders. 2008; 9:129. National Health and Medical Research Council (NHMRC)NICS National Emergency Care Pain Management Initiative Final Report 2011. Melbourne: NHMRC, 2011. National Institute of Clinical StudiesEmergency Care Acute Pain Management Manual. Canberra: National Health and Medical Research Council, 2011.

Price, D., Bush, F., Long, S., Harkins, S. A comparison of pain measurement characteristics of mechanical visual analogue and simple numerical rating scales. Pain. 1994; 56:217–226. Ricard-Hibon, A., Belpomme, V., Chollet, C., Devaud, M.-L., Adnet, F., Borron, S., Marty, J. Compliance with a morphine protocol and effect on pain relief in out-of-hospital patients. Journal of Emergency Medicine. 2008; 34(3):305–310. Rickard, C., O’Meara, P., McGrail, M., Garner, D., McLean, A., Le Lievre, P. A randomised controlled trial of intranasal fentanyl vs intravenous morphine for analgesia in the prehospital setting. American Journal of Emergency Medicine. 2007; 25:911–917. Rivara, F. P., Mackenzie, E. J., Jurkovich, G. J., Nathens, A. B., Wang, J., Scharfstein, D. O., et al. Prevalence of pain in patients 1 year after major trauma. Archives of Surgery. 2008; 143(3):282–287. [discussion 288.]. Rupp, T., Delaney, K. A. Inadequate analgesia in emergency medicine. Annals of Emergency Medicine. 2004; 43(4):494–503. Shields, B. J., Cohen, D. M., Harbeck-Weber, C., Powers, J. D., Smith, G. A. Pediatric pain measurement using a visual analogue scale: a comparison of two teaching methods. Clinical Pediatrics. 2003; 42(3):227–234. Shipton, E. A., Tait, B. Flagging the pain: preventing the burden of chronic pain by identifying and treating risk factors in acute pain. European Journal of Anaesthesiology. 2005; 22:405–412. Simpson, P., Bendall, J., Middleton, P. Prophylactic metoclopramide for patients receiving intravenous morphine in the emergency setting: a systematic review and meta-analysis of randomized controlled trials. Emergency Medicine Australasia. 2001; 23(4):452–457. Solomon, P. Congruence between health professionals’ and patients’ pain ratings: a review of the literature. Scandinavian Journal of Caring Sciences. 2001; 15(2):174–180. Swor, R., McEachin, C. M., Seguin, D., Grall, K. H. Prehospital pain management in children suffering traumatic injury. Prehospital Emergency Care. 2005; 9(1):40–43. Thomas, S. H., Shewakramani, S., Prehospital trauma analgesia. Journal of Emergency Medicine 2008; 35:47–57

Todd, K. H., Sloan, E. P., Chen, C., Eder, S., Wamstad, K. Survey of pain etiology, management practices and patient satisfaction in two urban emergency departments. Canadian Journal of Emergency Medicine. 2002; 4:252–256. Turturro, M. A. Pain, priorities and prehospital care. Prehospital Emergency Care. 2002; 6(4):486–488. Watkins, N. Paediatric prehospital analgesia in Auckland. Emergency Medicine Australasia. 2006; 18(1):51–56. Weisman, S. J., Bernstein, B., Schechter, N. L. Consequences of inadequate analgesia during painful procedures in children. Archives of Pediatrics & Adolescent Medicine. 1998; 152(2):147–149. Williamson, O. D., Gabbe, B. J., Cameron, P. A., Edwards, E. R., Richardson, M. D. Predictors of moderate or severe pain 6 months after orthopaedic injury: a prospective cohort study. Journal of Orthopaedic Trauma. 2009; 23(2):139–144.

CHAP TER 29

Lower back pain By Janet Curtis

C O N C E P TS U S E D I N TH I S C H A P TE R • The paramedic’s clinical approach: Section 2 • Perfusion: Chapter 55 • The autonomic response: Chapter 56 • The inflammatory response: Chapter 57

O V E RV IE W • Approximately 85% of adults will experience lower back pain at some point in their lives (Hayes, Huckstadt & Daggett, 2006). • Some 90% of back pain cases have a nonspecific cause (Gullick, 2008; Hayes, Huckstadt & Daggett, 2006). • There are a number of causes of back pain including muscle strains, prolapsed discs, degeneration of spinal structures, infection, cancer and some abdominal and renal complaints. • The pain associated with acute lower back injuries can be debilitating and may need significant pharmacotherapy. • Although most back pain is musculoskeletal in nature, there are a number of red flags that help identify a serious underlying pathological cause of back pain. • Nonspecific back pain is a diagnosis of exclusion. • Acute back pain becomes a chronic problem in only 5–10% of patients (Bouton et al., 2008). • About 90% of episodes of acute back pain will improve with minimal intervention in the first month (Hayes, Huckstadt & Daggett, 2006).

• Minor cases of lower back pain may not require transport to hospital, but rather a recommendation to see their GP. For more serious cases, treatment by paramedics includes pain relief, positioning and transport to hospital. • Back pain in children is rare and is more likely to be due to a serious pathological cause.

Introduction Acute lower back pain can be defined as pain between the lower rib cage and the gluteal muscles, with or without pain radiating down one or both legs (Casazza, 2012; Hayes, Huckstadt & Daggett, 2006; Huether & McCance, 2012). About 1% of individuals with acute lower back pain have pain radiating down one or both legs, usually due to sciatic nerve (sciatica) involvement (Huether & McCance, 2012). The timeframes for this pain vary in the literature from less than 6 weeks (Hayes, Huckstadt & Daggett, 2006) up to 12 weeks (Casazza, 2012; Gullick, 2008). Chronic lower back pain is defined as more than 3 months of continuous pain in the lumbar region, in the absence of any serious identifiable cause (Bouton et al., 2008). This is explored in case study 3. Acute back pain becomes a chronic problem in only 5–10% of patients (Bouton et al., 2008). A herniated disc is a rupture of the fibrocartilage surrounding an intervertebral disc, releasing the nucleus pulposus that cushions the vertebrae above and below. The resultant pressure on spinal nerve roots may cause considerable pain and damage the nerves, resulting in restriction of movement (Harris, Nagy & Vardaxis, 2009). A herniated disc most often occurs in the lumbar region. It is also called a herniated intervertebral disc, herniated nucleus pulposus, ruptured intervertebral disc, slipped disc and prolapsed disc (Harris, Nagy & Vardaxis, 2009). The lower end of the spinal cord resembles a horse’s tail where the bundle of lumbar, sacral and coccygeal nerve roots emerge from the spinal cord at the first or second lumbar vertebra and descend through the spinal canal (Harris, Nagy & Vardaxis, 2009). If a disc herniates in this area, it is called cauda equina syndrome.

Pathophysiology Lower back pain is a common health problem, so paramedics will frequently encounter this complaint, usually at the point when the patient is unable to cope with the pain or unable to move because of it. Up to 85% of adults will experience lower back pain at some point in their life (Hayes, Huckstadt & Daggett, 2006; Huether & McCance, 2012), with the episodes of pain occurring between the ages of 20 and 65 years (Casazza, 2012; Gullick, 2008). Women report lower back pain more often after the age of 60, possibly due to the presence of osteoporosis (Huether & McCance, 2012). Back pain in children is relatively rare and is much more likely to be due to a serious pathological cause (Della-Giustina & Kilcline, 2002; Hayes, Huckstadt & Daggett, 2006). Often the cause of back pain cannot be determined, as no abnormal findings are evident on x-rays or other screening tests and the patient has no neurological impairment (i.e. no loss of sensation, no numbness or pins and needles, and no weakness in the affected limbs). This gives rise to a diagnosis of nonspecific back pain (Gullick, 2008). At least 90% of back pain cases have a nonspecific cause (see Box 29.1; Gullick, 2008; Hayes, Huckstadt & Daggett, 2006). B O X 2 9 . 1B a c

k pain statistic s

• Unspecified back pain: 90% of cases • Muscle sprain: most common • Disc involvement: 2–3% of cases • Vertebral fractures: 3–5% of cases • Other causes: 125 BPM • BP 40 km/h • patients who are trapped for >30 min. Over the next decade changes in vehicle safety and protective equipment are likely to change the speeds used to determine the various trigger mechanisms. A collision at 60 km/h involving a vehicle with up-to-date safety equipment will cause different injuries to a collision at the same speed involving an older vehicle without this safety equipment. However, the mechanisms are evidence-based and you should assess the factors in each case before you dismiss them as irrelevant to a particular patient.

Pattern of inj ury The process of conducting a VSS requires the paramedic to access various parts of the patient’s body and this should be used to inspect these areas in order to identify the pattern of injury (POI). Similar to the factors described above under mechanisms of injury, a number of specific injury types have been identified as sensitive predictors of mortality. Once again, the body’s ability to temporarily compensate for these injuries can deceive paramedics and most ambulance services have created a list of patterns of injury that require early transport and treatment. Patients presenting to paramedics with any of the following injuries should be considered to be moving towards decompensation (regardless of their current vital signs), and while they may not yet fit the criteria for actual time critical they should be considered to be emergent time critical and managed accordingly: • penetrating injury to head, neck, chest, abdomen, axilla or groin • single significant blunt injury to head, neck, chest, abdomen, axilla or groin • multiple blunt injuries to head, neck, chest, abdomen, axilla, groin • spinal cord injuries • partial/full-thickness burns >15% (or involving the airway) • fractures to two or more long bones

• fractured pelvis • open fractures or dislocations • serious crush injuries. With a significant pattern of injury, the patient with two stab wounds becomes the priority. A review of his vital signs shows him to be tachycardic (124 BPM) and pale, with a blood pressure of 110/70 mmHg.

The secondary survey While the inspection associated with conducting the VSS may provide some clues to the POI, it is no substitute for a detailed secondary survey where the prime purpose is to detect the presence of any of the high-risk injuries. Conducting a full-body assessment of the medical patient is not normally required and most clinicians will limit the areas inspected to include or exclude a diagnosis (i.e. checking for peripheral oedema in a patient suspected of right ventricular failure). However, a thorough secondary survey is essential for the trauma patient, as obvious and painful injuries such as fractured limbs can be distracting to both the patient and the paramedic and may obscure more dangerous injuries such as puncture wounds that have caused internal bleeding. Regardless of the injuries identified during the VSS, a detailed secondary survey should be conducted on all patients who have experienced a significant MOI (see Fig 31.3). Drugs and alcohol are contributors to trauma and can mask the effects of injuries: inspect patients carefully and systematically once you have full access. In extremely hot or cold conditions, in public places or when the dangers at a scene cannot be controlled for long, exactly when and where a full secondary survey can be performed will vary, but definitive clinical decisions regarding the patient’s condition must not be made until the secondary survey has been completed.

FIGURE 31.3 The use of time-critical guidelines can enable integration of MOI and POI into scene management and triage. At the completion of the structured patient assessment, those patients with abnormal vital signs should be considered actual time critical and transported without

delay. Those with normal vital signs but a POI should be considered the next priority, followed by those with normal vital signs and a positive MOI, then those with normal signs and an insignificant MOI. Like other aspects of the standardised assessment process, developing a checklist to conduct a secondary survey will ensure a comprehensive assessment for the patient but at a low cognitive cost for the paramedic. Most secondary surveys divide the process by body location or system and a sample secondary survey for the trauma patient is described in Table 31.1. In conscious patients use the same divisions and ask them whether they have any pain in a particular region before you examine it physically. TABLE 31.1 Sample trauma secondary survey

CSF = cerebrospinal fluid. Alcohol, drugs and the psychological response to trauma can all mask the pain of injury. The other two patients in this case are examined for stab wounds but none are found.

Saving the saveable There are a number of traumatic conditions that paramedics can accurately diagnose in the field and need to treat without delay, but there are also injuries that can only be effectively treated in a hospital. For these injuries any delay in transport to a trauma centre or hospital is likely to negatively impact on patient outcomes. Understanding the pathology behind these conditions is essential in order for paramedics to differentiate between these clinical decisions confidently and safely. Withholding treatment when an intervention is possible can be extremely difficult to resist, but to do so with confidence reflects an ability to combine a detailed patient assessment with evidence-based practice, strong clinical knowledge and an awareness of how paramedics integrate into the emergency health system. In most of these cases there is strong evidence that patients benefit only from surgical intervention and that delaying transport or attempting to restore their vital signs with interventions such as intravenous fluid that do not definitively correct the problem will only increase mortality. Patients who die soon or immediately after trauma often have overwhelming injuries

that are outside the realm of clinical intervention. Some patients have critical injuries that will cause death unless they are addressed in a timely fashion. Injuries such as acute airway obstruction, acute respiratory issues (pneumothorax) and hypovolaemia are correctable problems that paramedics can address if they are identified during the assessment process. These injuries cause such alterations in vital signs that they are readily identifiable and are generally managed accordingly. Of greatest concern are those patients who initially compensate for their injuries but who ultimately need medical intervention. These time-critical patients require early recognition and rapid transport to appropriate trauma centres. Some will require paramedic treatment while others need to be transported without delay. The term ‘Golden Hour ’ was coined to describe this cohort of patients who are at risk of dying from correctable causes if they are not recognised quickly. The concept of the Golden Hour was not intended to imply an exact time but to give an indication of urgency. Puncture wounds to the axilla or groin have the potential to cause life-threatening internal haemorrhage for which surgical intervention is necessary. Based on the pattern of injury and vital signs the paramedics in this case elect to transport the patient with stab wounds without delay and direct the other two patients to back-up crews.

The challenge to reasoning The MOI and POI charts can act as useful checks to capture patients who would otherwise be missed but the complexity of the charts, combined with the unpredictable nature of trauma scenes, makes it difficult to describe when the charts should be included in the assessment process. One approach is to apply them as best you can during the assessment phase and then use them as a checklist at the conclusion of this phase to determine your next step. Although the mechanisms and patterns of injury described here are widely accepted, their applicability to individual patients needs to be considered. Pregnant women and elderly people have a greater propensity for injury and elderly people take prescription medications that limit their cardiovascular response to blood loss. It is not unreasonable to ‘upgrade’ these patients to the next highest triage category.

Trauma systems Developed in a number of states, trauma systems integrate centres specialising in the resuscitation and management of trauma victims with ambulance services. Trauma systems are based on transporting patients directly to a specialist treatment centre the first time and avoiding the need for subsequent transfers. The development of paramedics who are capable of timely and effective emergency interventions in the field and en route has made the trauma system a practical reality. If patient extrication is delayed, consider bringing elements of the trauma system to the patient in the form of high-level medical and paramedical clinicians. Strategic planning about transport routes, use of helicopters and hospital notification needs to occur early and is part of the multitasking approach to trauma assessment and management that threatens to overwhelm novice clinicians.

Summary Trauma patients represent an opportunity for paramedics to provide life-saving treatment. This opportunity can only be realised if paramedics are able to overcome the challenges posed by the nature of these cases, conduct an accurate patient assessment and integrate the findings into a clinical plan. Patient outcomes almost certainly require teamwork across the entire trauma system, but they start with an individual paramedic’s systematic approach to assessment and management.

Reference Deasy, C., Bray, J., Smith, K., Harriss, L., Morrison, C., Bernard, S., Cameron, P. Traumatic out-of-hospital cardiac arrests in Melbourne, Australia. Resuscitation. 2012; 83:465–470.

CHAP TER 32

Head injuries By Virginia Plummer and Matt Johnson

C O N C E P TS U S E D I N TH I S C H A P TE R • The paramedic’s clinical approach: Section 2 • Perfusion: Chapter 55 • The autonomic response: Chapter 56 • The inflammatory response: Chapter 57

OVERVIEW • The term ‘head injury’ is a broad classification that includes injuries to the face, scalp, skull or brain. Facial and scalp injuries can be painful and distressing but brain injuries have the most potential for mortality and morbidity. • Early recognition and management of traumatic brain injuries (TBIs) can reduce mortality and morbidity. • TBIs are usually the result of direct trauma to the head but can also occur as a result of severe acceleration or deceleration without head strike. TBI is the leading cause of death and disability in young adults (Shum, 2007). • Primary TBI occurs at the time of impact due to direct neuronal damage (Dunn et al., 2010) and describes the destruction of neurons and vascular structures by the mechanical forces of impact or deceleration (Atkinson & Wilberger, 2003). • Secondary TBI evolves as a result of the body’s inability to maintain normal brain perfusion following the primary injury. Inflammation, haemorrhage, oedema and blood pressure all contribute to the development of a secondary injury. Unlike the primary injury, the degree of secondary injury is subject to paramedic management. • TBIs are classified as mild (GCS 13–15), moderate (GCS 9–12) or severe (GCS Hypoglycaemic agents > Sedatives > Anxiolytics or antidepressants > Anticholinergic drugs • Alcohol • Acute illness • Cerebrovascular accident/transient ischaemic attack • Chronic illness • Postural hypotension • Visual disorders • Confusion or cognitive disorders • Gait disturbance due to arthritis • Musculoskeletal disorders

• Balance disorders • Weakness • Environmental hazards: mats, slippery surfaces

• Brown-Séquard syndrome presents with dysfunction differing on either side of the patient. Injury to one side of the cord will affect motor function on the same side of the injury but altered sensory and pain input on the opposite side (Medscape, 2014). This is because the sensory fibres for fine touch running in the lateral spinal thalamic tract cross over at the level of entry to the cord, while those motor fibres running in the corticospinal tract cross over high above the cord itself. • Anterior cord syndrome is most commonly associated with injury to the anterior spinal column and subsequent interruption of the anterior spinal artery supply. It will give signs on both sides of the body as the tracts are affected equally. Motor function is usually more significantly altered with sensation frequently less affected given the lateral tracts used through the cord (Radiopaedia.org, 2014). • Conus medullaris syndrome and cauda equina syndrome are injuries of the very distal end of the spinal cord. Conus medullaris syndrome affects both the lower and the upper motor neurons. This syndrome usually presents quickly and bilaterally but is less severe than cauda equina syndrome. Cauda equina syndrome presents more slowly and unilaterally. These syndromes most notably affect the bladder, bowel and lower limbs (Spector et al., 2008).

Other signs and symptoms Spinal shock The term ‘spinal shock’ does not refer to collapse of the circulatory system as do other forms of shock. Rather it refers to loss of usual neurological activity at and below the level of injury including motor, sensory and autonomic function. This is when autonomic dysreflexia can occur (see the section on long-term care below). Loss of bladder and bowel control accompanies spinal shock. Neurogenic shock Injury to the thoracic spine or above, especially cervical injury, can severely interrupt sympathetic outflow from the spinal cord nerves. Following SCI a brief initial rise in blood pressure from noradrenaline release occurs. Soon afterwards, vagal tone from the intact cranial vagus nerve goes largely unopposed, with the predominant effect being bradycardia. The presence of bradycardia denotes an injury above the level of innervation of the sympathetic chain. Hypotension results from both the slowed heart rate and vasodilation. Vasodilation below the level of the injury is a reflection of interruption to sympathetic supply. The skin is frequently warm and dry, without the usual sympathetic response of redirecting blood from the peripheral circulation. However, it must be noted that this classic presentation may be delayed and may not occur at all with some injuries. Its absence should

not be considered diagnostic (Guly, Bouamra & Lecky, 2008). Priapism An SCI patient with complete transection can present with priapism due to unopposed parasympathetic stimulation. Without sympathetic tone in the vasculature, blood pools in the peripheries, resulting in an accumulation of blood in the penis. Where this is found, it occurs at the time of injury and usually requires no specific treatment as it will resolve over time (Todd, 2011). Hypovolaemic shock Neurogenic shock ensures that a normal body response to circulatory dysfunction cannot be mounted. The SCI patient is also a trauma patient and possibly a severe multi-trauma patient. Hypotension cannot simply be assumed to be due to SCI and paramedics should consider blood loss from other injuries. The absence of clear SCI neurological deficit should suggest that hypotension is likely to be from some other cause. Furthermore, where patients have other injuries consistent with blood loss and hypovolaemia, management for hypotension must be a priority. It may be difficult to differentiate the cause of shock during early assessment, with estimation of central venous pressure (hence preload) an important tool in assessment. Other forms of shock Since the patient may also have other injuries, other causes of shock than hypovolaemia or neurogenic shock should be considered when assessing vital signs and presentation. For example, chest trauma including tension pneumothorax, pulmonary and myocardial contusions and pericardial injury is possible. Temperature Following the development of neurogenic shock, the patient may very quickly become hypothermic. Vasomotor control is no longer under autonomic control below the level of injury. Given the inability to redistribute blood from the exposed periphery and to generate heat through muscle activity, the patient will essentially become dependent on ambient air temperature for body temperature. Although they may present as warm and dry for a time, it is far more likely that an exposed and injured patient will become quite cold. Hypothermia is an ever-present complication in many trauma patients and is particularly problematic in a patient with SCI.

Consider! Check the environment the patient is in and how long they have been there. The patient will be vasodilated and susceptible to heat loss, particularly if they are wet, lying on cold ground or exposed to the elements. Move them to a warm place and cover them up as soon as possible without compromising spinal care.

The patient in this case is very much at risk of hypothermia, as he is wet, immobile and vasodilated. Other injuries It is imperative to remember that any patient with a potential spinal injury may have other injuries. The lack of proper sensation and motor function will make it more difficult to examine for physical injuries. A thorough secondary examination should be undertaken concurrently with the spinal examination and initial spinal care. Paramedics have to rely more on visual clues to assess injury rather than the typical clues of pain and altered movement.

Look for! • Head injury • Chest injury • Abdominal injury • Limb trauma

Initial assessment summary

Problem Motorcycle accident, conscious but unable to move Conscious GCS = 15 state Position Supine Heart rate 60 BPM Blood 90/50 mmHg pressure Skin Pale, cool, dry (skin is wet where the wet clothing is) appearance Speech Normal pattern Respiratory 18 BPM rate Respiratory Even cycles rhythm Chest Good breath sounds bilaterally auscultation Pulse 96% oximetry Temperature 35.2°C Motor/sensory Altered sensation in his arms and loss of sensation and motor function function in his lower limbs Pain 4/10 neck pain History As the patient went over the handlebars he would have potentially hit the ground face first (hyperextension), striking the back of his head (hyperflexion), hitting his head directly on the ground (compression) or even suffering rotational trauma. He was then dragged by his friends, potentially causing further trauma to any injuries sustained. He is also wet, so hypothermia may develop. Physical Neck pain, altered sensation in his arms and loss of sensation and assessment motor function in his legs. Possible closed fracture of his left lower leg. D: There are no dangers to the patient or crew. A: The patient is conscious with no current airway obstruction. B: Respiratory function is currently normal. C: Heart rate and blood pressure are both low. The patient is hypotensive (with no obvious haemorrhage) with a pulse at the lowest end of normal. This is not consistent with hypovolaemia but it is consistent with SCI. He also has motor and sensory deficits. Given the mechanism, his whole spine is at risk and so care of the whole spine is required.

CONFIRM The essential part of the clinical reasoning process is to seek to confirm your initial hypothesis by finding clinical signs that should occur with your provisional diagnosis. You should also seek to challenge your diagnosis by exploring findings that do not fit your hypothesis: don’t just ignore them because they don’t fit. Unlike medical cases where a number of possible causes need to be excluded, the mechanism of injury is usually obvious in trauma cases. However, the most obvious injury is not always the most serious and visually dramatic and painful injuries can distract both the patient and the paramedic from other possibilities.

What else could it be? Stroke Perhaps the patient had a stroke precipitating the fall. Both stroke and spinal injury may present as hemiplegia. It is possible for a patient to appear to have traumatic injuries and yet still have an underlying medical problem that either preceded the trauma or followed it. History is an important discerning tool. This patient’s history does not suggest a medical cause for his presentation.

DIF F ERENT IA L DIA GNOSIS Spinal injury Or • Stroke • Stroke mimics • Head injury • Limb injury • Pre-existing injury • Other cause of poor perfusion

Stroke mimics The altered sensation and movement could be a result of some other medical condition that would be considered and eliminated in a stroke assessment. Hypoglycaemia, migraine or febrile illnesses can be dismissed with a thorough history and assessment. Head injury Head injuries, particularly penetrating, may cause neurological dysfunction of the lower body that may be similar to SCI. It is usually prudent for all patients with significant head injury to be managed as if they have spinal injury as well.

Limb injury The fact that the patient cannot move a limb does not mean that there has been a loss of central motor control. A localised injury may result in a similar presentation to SCI. This would be less likely to be the cause of a classical spinal injury presentation. Pre-existing injury A patient presenting with acute signs of SCI may actually have a pre-existing injury. Such signs should be evident, including a disability sticker on a vehicle or a stored wheelchair. Other causes of poor perfusion Chest injury or other blunt trauma may produce hypotension; and cardiovascular medications may interfere with physiological responses, as may hypothermia. Vital signs may be suggestive of an injury but there should be no rush to discount possible alternatives or concurrent problems. In any event, it is important to provide good spinal care so as to not underestimate the potential for injury.

T REAT Emergency management An injury above the level of C4 may mean that the patient will require ongoing ventilation and associated head trauma may lead to loss of consciousness. Airway management priorities depend on presentation. It is important to establish a baseline of vital signs to assist in determining the extent of physiological compromise caused by the trauma. A thorough secondary physical examination not only provides evidence of spinal injury but also indicates other presenting injuries and so enables prioritisation of management. Spinal injury may occur in isolation or with other injuries and complications. Box 35.2 outlines the principles of management for spinal injury. B O X 3 5 . 2P

rinc iples o f manag ement

Spinal injury • Safety of patient and rescuers • Airway care • Respiratory support • Cervical care • Antiemesis • Spinal immobilisation • Careful handling • Perfusion support

• Management of other injuries

Injury stabilisation The essential prehospital management of a patient with suspected spinal injury is spinal immobilisation and careful handling to avoid worsening the injury. The most mobile part of the spine is obviously the neck but due care must be paid to the entire spine. Spinal immobilisation has the same aim as any other fracture management, namely to restrict movement and so reduce pain and further injury. A fracture may involve vascular, nerve and soft-tissue injury. With spinal injury, the critical aim is to avoid further injury to the spinal cord itself. There are two key options for spinal immobilisation: • manual immobilisation • use of immobilising devices. Despite spinal immobilisation typically being considered as routine prehospital management, it should not be considered lightly. A Cochrane systematic review of available evidence found no randomised controlled trials with regard to spinal immobilisation of injured patients. There is some prospective evidence pertaining to non-injured volunteers in studies (Kwan, Bunn & Roberts, 2001), and there is also some retrospective evidence that immobilisation may have little or no effect and may even increase neurological injury (Hauswald et al., 1998). For most patients the damage will be done at the time of injury and will not be worsened by subsequent handling. Furthermore, there are complications that can accompany spinal immobilisation that must be considered during patient care. The most obvious is that the practice is uncomfortable for patients and so they are unlikely to want it. For example, rigid cervical collars and hard backboards soon become uncomfortable and potentially can cause pressure areas. In addition, the restriction of movement and chest strapping involved can adversely impact on breathing (Bauer & Kowalski, 1988; Lieberman & Webb, 1994; Totten & Sugarman, 1999) and can increase aspiration risk in supine patients. However, thoracic strapping has been shown to significantly reduce lateral motion for any patient managed on a spineboard (Mazelowski & Manix, 1994). As with any area of patient management, the benefit must be seen to outweigh any disadvantage. For this reason careful screening is required for patients for whom spinal immobilisation may be necessary. It should also be noted that many potential complications of spinal immobilisation result from prolonged immobilisation (in excess of 48 hours) and are much less of a concern in the prehospital setting (Davis et al., 1995). The clinical committee of the Council of Ambulance Authorities recommended that spineboards be used as an extrication device only because of the difficulty in immobilising the trunk when the head is relatively fixed. This recommendation, first made in 2000 and reaffirmed since then, is based on observation only, as there have been no high-level studies of the effects of spineboard strapping on shearing forces in the neck. A vacuum mattress has the advantage of providing the same degree of support to all sections of the

spine as well as conforming to the normal curves of the spine. Strapping to a flat relatively slippery board with independent head immobilisation (fixed more rigidly) is still taught in some countries, including Australia and New Zealand, and provides a difficult dilemma for emergency clinicians in the absence of quality evidence. Helmet removal One of the great conundrums of first-aid management is whether to remove the helmet of an injured patient. Much of the available literature refers to sporting helmets; these are often a very different design to motorcycle helmets and the principles of removal and the need for removal are not necessarily translatable. Also, the potential complications for an open-face helmet as opposed to the full-faced variety may differ. In Australia paramedics will most frequently encounter helmets related to motorcycles or motor sport (excluding bicycle helmets). The helmet of a sports player or motorcyclist should be removed as soon as practicable by paramedics (as opposed to on-scene firstaiders). The reasons for this are numerous and include: • an inability to properly assess and manage airway and breathing, including dealing with a soiled airway and performing intubation • an inability to place the head and neck in the neutral position—or worse, the head may be forced into an undesirable position of flexion • an inability to apply a cervical collar or immobilise the spine • a full-face helmet may cause rebreathing and CO2 retention (Segan, Cassidy & Benkowski, 1993; Branfoot, 1994). One method of helmet removal is to manage the patient (ideally supine) with one rescuer kneeling or lying above the patient’s head holding the helmet stationary (see Fig 35.6), while the second removes the patient’s glasses (if worn) and undoes the helmet chin strap. The second rescuer then takes responsibility for head stabilisation by holding the patient’s jaw and under the patient’s neck. The second rescuer may need to take the weight of the patient’s head and must be prepared to resist any movement from the first rescuer who removes the helmet. The first rescuer should gently spread the base of the helmet and lift the front of it past the patient’s nose. The helmet can then be slid off but it may require careful manipulation, pulling the back of the helmet over the top towards the patient’s face to ensure that it can slide off completely. The correct neutral position for the patient can then be established and the first rescuer can return to providing head and neck stabilisation.

FIGURE 35.6 The helmet should be removed as soon as practicable. Source: Jeff Kenneally. The patient in this case is still wearing his helmet. It is a full-face helmet and requires removal using the two-person method as soon as practicable. The neutral position No matter what position the patient is found in, the head should be returned to the neutral position unless the patient complains of pain in so doing, resistance is felt against the movement or the patient describes not being able to move the neck from the current position. If this is the case, one rescuer needs to hold the patient’s head in that current position until the patient can be immobilised by a more secure method than the paramedic holding them. It should be noted that once a rescuer is tasked with cervical stabilisation this task must remain continuous and the person will be unable to assist with any other function. Coordination of patient movement should occur via this person so that spinal care remains considered. Careful consideration should thus be given to the person allocated this role, as they must be senior and assertive enough to perform the role and yet remain expendable from any other task.

P RACT ICE T IP Immobilisation should encompass a whole-of-spine approach: neither the head nor the body should be immobilised in isolation.

The neutral position is relative and unique to each patient. When placed

supine, the adult head will fall back into a partially extended position in as many as 98% of people (Schriger et al., 1991). To maintain the neutral position in an adult padding should be placed beneath the occiput. The amount of padding can vary considerably within a range of no more than +/– 5° flexion/extension of the head (Boswell et al., 2001). Although there is considerable variation between adults, raising the occiput between 2 and 5 cm will provide optimal positioning (De Lorenzo et al., 1995). Emphasis must be placed on personalising the position for each patient, with the intention being to avoid any flexion or extension (see Fig 35.7).

FIGURE 35.7

The neutral position. Source: Jeff Kenneally.

For patients with a head injury and no spinal injury, it is well-established that the optimal position to balance intracranial pressure and cerebral perfusion pressure is a 15–30° head-up posture flexed at the hips (Durward et al., 1983). However, the typical human head weighs 4–5 kg, providing significant downward force on any unstable cervical injury. Patients with a potential spinal injury should be managed in a supine or lateral position until clearance is provided or more substantial stabilisation of the injury occurs. For patients found in an upright position who cannot immediately be placed supine (such as in road trauma), the head should be returned to the position that best approximates the neutral position and maintained there. In children younger than 8 years of age the relatively larger occiput may require either a supine position or some padding beneath the shoulders to raise the thorax and prevent flexion of the head (Boswell et al., 2001; see Fig 35.8). The neutral position has been shown to be poorly managed in paediatric patients, with no single method reliable in all cases (Curran et al., 1995; Boswell et al., 2001).

FIGURE 35.8 The neutral position in children varies with age and development. Source: Roberts (2009). Spinal abnormalities Some conditions exaggerate normal spinal curves or produce curves when there should be none, including scoliosis (lateral curving), kyphosis (exaggerated upper spinal curve) and lordosis (exaggerated lower spine curve). Although a history of previous spinal abnormality may not be clearly known to the paramedic, in many cases they may have a strong suspicion of this during examination, particularly if there are signs of disability (such as a wheelchair). In any event, paramedics should never attempt to force an unusually appearing spine back into a ‘normal’ presentation. Instead, the patient should be supported in that position with the use of padding to fill the curves as they are found. Where kyphosis is found, the neutral position will have to be tailored specifically to suit. Manual inline stabilisation Manual inline stabilisation can be provided with the patient effectively in any position, including seated, supine or lateral. The ideal method, however, is with the rescuer ’s fingers spread across the greatest surface area of the patient’s

head, as this produces the greatest stability (see Fig 35.9). It is also important to ensure that there is no contact with the patient’s neck, to minimise the risk of affecting venous return. By holding the head only, there is no direct support to the lower body allowing for uncoordinated movement between the head and the body, placing the cervical spine at risk. This is particularly so when the patient is being moved, such as during log rolling. Alternatively, the patient’s head can be held between the rescuer ’s forearms with the fingers grasping the (uninjured) clavicles on either side. Where the patient requires advanced airway techniques or ventilation support, the rescuer can use their own knees and thighs to provide some stabilisation to the patient’s head. Whichever method of stabilisation is used, traction should not be applied as it may increase the likelihood of exacerbating any injury (Gerling et al., 2000).

FIGURE 35.9 A Holding the head only. B Holding the head and clavicles. Source: Jeff Kenneally. Airway management Airway management includes addressing current needs as well as considering ongoing needs such as antiemetics, intubation and assisted ventilation. The usual airway adjuncts of oropharyngeal and nasopharyngeal airway devices may be necessary in the first instance, although relative contraindications must be considered, including avoidance of inducing the gag reflex in a patient with head injuries and of inserting any airway device for a patient with facial or skull fracture. Patients may be positioned in the lateral position as a first management option but this must be done with great care to maintain the head in a neutral inline position. Ideally this will include more than one rescuer coordinating, with good head support throughout. Managing patients with spinal injuries supine also provides for maximal tidal volume, as respiratory

inadequacy is a commonly associated complication (Berlly & Shem, 2007). Intubation Where necessary, intubation may be safely performed, provided the parasympathetic response to airway manoeuvres has been blocked with atropine (avoiding a dramatic unopposed parasympathetic-induced bradycardia). The usual positions for achieving the best view during intubation, such as by elevating the occiput, are best avoided with a preference for maintaining the neutral position and using supportive tools of direct laryngeal pressure (and use of a bougie if the patient is chemically paralysed, preventing laryngospasm). A secondary assistant tasked with holding the patient’s head and resisting any movement during the procedure is an ideal support (Nolan & Wilson, 1993). This person, in providing manual inline stabilisation, may be in conflict with the person performing laryngoscopy both by restricting head movement (intentional) and by being in close proximity (unavoidable). The use of manual inline axial stabilisation reduces anteroposterior movement during intubation attempts (see Fig 35.10). Similarly, the use of the Miller™ blade technique has been shown to reduce such movement (Gerling et al., 2000). The use of varying intubation devices aside from a standard laryngoscope technique may improve the view without compromising manual inline axial cervical spine stabilisation.

FIGURE 35.10 Head stabilisation during intubation. Source: Adams (2008). Where a cervical collar is applied, the ability to view the vocal cords may be reduced, placing greater reliance on the force of the technique. Release of the collar may thus be required during intubation, with a reliance on manual axial inline stabilisation. However, such stabilisation may adversely impact on the view and lead to a delay in intubation and ventilation, which is undesirable in a patient with traumatic head injuries (Manoach & Paladino, 2007). Movement during cricothyroidotomy is unknown but is likely to be small and clinically insignificant (Crosby, 2002; Malik et al., 2008). Rapid-sequence intubation remains a safe and effective method of securing an airway in a patient with cervical injuries (Criswell, Parr & Nolan, 1994). Cervical collar The cervical collar is intended to minimise the amount of movement possible for the cervical spine. It does not provide complete immobilisation of the neck and of course provides no care for the rest of the spinal column. The collar is at

best an integral component of a management package. A poorly fitted cervical collar may force the neck to remain in a compromised position of poor alignment, which may affect the injury. Patients who are agitated or regain consciousness may attempt movement against the collar and further risk injury (Morris & McCoy, 2003). The cervical collar has also been implicated in causing complications for patients during management, such as soft-tissue injury from prolonged application. More significantly, it has been suggested that the collar can interfere with jugular venous return and potentially worsen any head injury (Holly et al., 2002; Lida et al., 1999; Davies, Deakin & Wilson, 1996; Raphael & Chotai, 1994). However, application of a cervical collar remains a core component of prehospital spinal care and it is recommended for shortterm use. It should be used in conjunction with multiple other spinal care principles including gentle coordinated movement of the patient and manual immobilisation of the patient’s head. Even if the collar provides little benefit, its placement may highlight the ongoing need for spinal care to both the patient and other medical personnel. For a cervical collar to be effective, it must be properly measured and fitted. Some collars come in a variety of sizes and are best measured for each patient, while others can be adjusted to suit each patient. The collar must be in close contact with the patient’s skin across the chest, upper back, shoulders and jaw line, so clothing should be removed first to allow best fit. Similarly, jewellery should be removed to ensure that the collar does not compress the item and cause discomfort or injury. In a typical rescue situation a cervical collar is fitted to the patient as first found. Later, movement of the patient, particularly readjusting to ensure correct neutral position, may cause the collar to lose best contact with the skin and so a different-sized collar will be needed. The cervical collar can be applied with the patient in any position and only requires the patient to be in the neutral position first. The rescuer delegated to provide manual stabilisation should continue uninterrupted while the collar is fitted. Patient extrication Numerous methods can be used to immobilise the whole spine but the spineboard is common for both extrication and carrying of patients (see Fig 35.11). A vacuum mattress is usually considerably more expensive and bulky to store than a spineboard (see Fig 35.12), but the spineboard has major disadvantages compared to the vacuum mattress in terms of comfort and overall stability of the spine (Luscombe & Williams, 2003). The vacuum splint may also provide superior thoracic spine immobilisation (Johnson, Hauswald & Stockhoff, 1996). The scoop stretcher is another lifting device; its sides can be separated and placed under the patient. Although this reduces the need to lift and roll the patient, it does not necessarily work on all surfaces and is not designed for immobilisation. Notwithstanding this, the scoop stretcher can be a useful tool in spinal care (Krell et al., 2006).

FIGURE 35.11 Spineboard immobilisation. Source: Laerdal (2011).

FIGURE 35.12 Vacuum mattress for spinal immobilisation. Source: RAPP Australia Pty Ltd (2014), www.neann.com.au/neann-vim-vacuumimmobilisation-mattress-6-ft-157. It is particularly important that whenever a patient is managed with spinal immobilisation the head and body are never managed independently or with differing degrees of immobilisation. Immobilising either the head or the body independently of the other allows for the possibility of movement or shearing between the parts. This would expose the neck to great risk and defeat the purpose of immobilisation. For small children, immobilisation can be improvised using an inverted Kendrick Extrication Device™ (see Fig 35.13) or a standard adult vacuum mattress, paying particular attention to variations in the neutral position. Children are more likely to remain unsettled and the decision to immobilise may require parental support. If it proves to be too unsettling for the child, improvisation using a capsule or car seat may be possible. Consider inline manual support with the child’s head between the rescuer ’s forearms and their upper body between the rescuer ’s hands initially. This will enable the rescuer to maintain close contact and provide reassurance to the child. Once rapport has

been established it may be possible to apply a cervical collar and whole-of-body immobilisation.

FIGURE 35.13 Kendrick Extraction Device™: for very small children the device can be inverted and used as a spineboard. Source: FernoWashington Inc. (2011). There are two broad methods of moving any patient onto a bed or spineboard: • Log rolling involves a coordinated roll of the patient from supine to either lateral or back (see Fig 35.14). It may initially involve the patient being turned from the prone position or similar. Prone is clearly more difficult and the return movement to neutral may have to be made simultaneously with rotation into the

lateral position to avoid placing the patient’s face directly downwards. The rescuer providing head support is critical as they are the vital link between the patient’s head and body. Application of a cervical collar may have to be delayed until after completion of the roll.

FIGURE 35.14 The team log roll. Source: Swartz (2009). • Team lifting involves multiple rescuers lifting the patient while keeping them in a constant plane. This is potentially heavier for the rescuers but could offer better head and body stability (Del Rossi, Horodyski & Powers, 2003). There are purpose-built devices for extricating patients with spinal injuries while providing whole-of-spine care, such as the Kendrick Extraction Device™ (see Fig 35.13). With such devices, a thoracic flexible frame is applied to the patient, which includes extension to the head and straps for harnessing the legs. The device can be applied to a patient in situ and has handles/straps to allow rescuers to lift and carry the patient. Not all patients will be found lying on the ground and the Kendrick Extraction Device™ is useful for extricating patients found in the sitting position. Some patients may be moved with a combination of spineboard and coordinated manual handling. Sometimes patients with a spinal injury may be found ambulating at the scene, but this should not preclude proper spinal immobilisation where indicated. The extrication of the patient in this case can be completed with a coordinated lifting method using a scoop stretcher, spineboard or flat lift and providing proper spinal immobilisation. Antiemesis Since typically patients with spinal injuries are managed in the supine position, the risk of nausea and vomiting is of concern. Any movement of the patient to facilitate vomiting will be problematic for spinal care, particularly if spinal immobilisation has been applied. Patients in vacuum mattresses and those with a cervical collar restricting their ability to open their mouth may have an increased risk of aspiration. Intubation should be considered for patients who are in an altered conscious state and unable to protect their own airway. For conscious patients where this is not appropriate, administration of antiemetic

prophylaxis is important to reduce the likelihood of vomiting. Transportation to hospital may also produce motion sickness in supine patients, as there may be an imbalance between the vestibular system perceiving movement and the visual clues the patient can receive. General care Pressure area formation is a lifelong risk for SCI patients so any body parts that contact hard surfaces should be appropriately padded. Limbs that cannot selfsupport should be placed into anatomically normal positions and not allowed to hang dependently as further soft-tissue injury can occur or the limb may be exposed to injury during movement. Patients placed on flat surfaces or firm beds will complain very quickly of pain in the lumbar spine area but a small 1–2 cm layer of padding in the lumbar arch can greatly improve comfort. This is particularly important if the patient is restrained to the flat surface or is unable to move. Patients with abnormal curvatures of the spine should have padding support modified accordingly. The discomfort and complications of spinal immobilisation suggest that it should not be regarded as a therapy for all patients. Screening tools should be used appropriately so that immobilisation is restricted for those patients who are considered at real risk of spinal injury. Fluid resuscitation To compensate for vasodilation following spinal cord trauma, an initial fluid bolus is suitable for early resuscitation. For isolated SCI, up to 10 mL/kg is a suitable initial volume to maintain an adequate mean arterial pressure and tissue perfusion. Fluid resuscitation must not become overzealous, however, as pulmonary oedema from fluid overload is a very real risk. Where a fluid bolus does not correct blood pressure in isolated SCI the patient should be assessed for other injuries. Patients with other injuries consistent with causing hypovolaemia should have fluid resuscitation appropriate to those injuries. If fluid resuscitation has been adequately provided for either other injuries or isolated SCI, vasopressors may be required to restore adequate blood pressure and perfusion. Temperature management Patients with a spinal injury should be managed so as to maintain normal body temperature, in particular to avoid hypothermia. Regular and ongoing temperature assessment using a reliable method of measurement (e.g. tympanic thermometer) should be a standard part of all paramedic assessment. In this case the patient’s wet clothing should be removed, as this will exacerbate heat loss.

P RACT ICE T IP Temperature control can be an issue when large amounts of fluid are administered to SCI patients in the prehospital setting. Depending on the injury, some patients may lose heat due to vasodilation or conduction into cold surfaces (which they cannot feel), or gain heat from a hot environment from which they cannot

move. Spinal patients exposed to hot or cold environments should have their temperature monitored frequently.

EVALUAT E Evaluating the effect of any clinical management intervention can provide clues to the accuracy of the initial diagnosis. Some conditions respond rapidly to treatment so patients should be expected to improve if the diagnosis and treatment were appropriate. A failure to improve in this situation should trigger the clinician to reconsider the diagnosis. However, in the setting of SCI paramedics should accept perfusion parameters outside of what they would usually accept. Manual temperature control may be difficult in these patients, meaning that they will need to be re-evaluated more often. In addition, the patient’s motor sensory perception should be repeatedly re-evaluated to ensure that their condition is not worsening.

Hospital admission De fi ni ti ve spi na l a sse ssm e nt Radiological assessment is usually required for definitive exclusion of bony injury unless the patient can be easily and confidently screened with preliminary assessment (Morris, McCoy & Lavery, 2004). Children may be screened using radiographs but where there is any uncertainty, computed tomography (CT) may be required (Slack & Clancy, 2004). Despite vertebral fractures being evident on most plain radiographs, a number of spinal column injuries are not as easy to detect and magnetic resonance imaging (MRI) remains a highly sensitive means for evaluating any patient in whom there remains concern. MRI is particularly effective in evaluating soft-tissue injuries such as ligament damage (Morris & McCoy, 2004). Patients who remain difficult to examine, particularly unconscious patients, will require judgement to determine when clearance can be provided. Combinations of radiography and CT scans can usually be reliable and effective in providing confident clearance (Morris & McCoy, 2004).

Continued immobilisation Although the spineboard has a defined role in extrication of the trauma patient with a suspected spinal injury, it has no further role in transport, the ED or hospital admission (Vickery, 2001). Essential components of resuscitation should occur without interruption but removal of the patient from the spineboard should occur as soon as practicable (once on the ambulance stretcher; Cooke, 1998; Yeung, Cheung & Graham, 2006; Lubbert, Schram & Leenen, 2005).

Respiratory care Respiratory complications are a major problem when managing acute SCI and account for a significant number of deaths with most deaths occurring within the first few days after injury. The most common complications are respiratory infection and pneumonia along with atelectasis. The need for ventilation, management of respiratory complications and the need for tracheostomy all add to the cost and duration of care for patients with spinal injuries. The more complete the injury, the more likely respiratory complications will occur (Berlly & Shem, 2007). In the earliest instance, respiratory failure as a result of injury to the spine or associated chest trauma can be problematic. The latter is commonly associated with thoracic spine injuries. Similarly, aspiration from loss of airway reflexes is a risk. Chest trauma, the development of adult respiratory distress syndrome (ARDS) and overhydration for neurogenic shock are all possible causes of pulmonary oedema in SCI patients (Berlly & Shem, 2007). In-hospital management requires the effective removal of airway secretions and good hygiene. Careful monitoring of blood gases and other clinical signs of respiratory failure are important. Mechanical ventilation is commonly employed to assist ventilation and avoid atelectasis. Postural drainage positioning and chest percussion can be used to help maintain effective ventilation. Similarly, respiratory therapy techniques can be used in longer-term management.

Although intubation may be an early adjunct in airway maintenance, patients requiring ongoing airway care may require a tracheostomy. This has the advantage of increased comfort for the patient, is easier to care for than an endotracheal tube and enables patient mobility where this is possible. Not all patients move from an endotracheal tube to tracheostomy, however: many patients undergo attempts to wean them off ventilation completely first and so avoid any further need for airway adjunct.

Spinal cord concussion SCI is the most feared outcome in spinal injury, but a small number of injuries that present with initial signs of cord injury recover in a short period of time. Just as the brain may show signs of temporary dysfunction when concussed, so too can the spinal cord. Spinal concussion can be said to have occurred when a traumatic mechanism leads to the onset of SCI deficits and yet full recovery occurs within 48–72 hours (Zwimpfer & Bernstein, 1990; Del Bigio & Johnson, 1989). The mechanism for spinal cord concussion is not well understood; there is speculation that it may be associated with movement of the cord within the column or with pre-existing structural abnormality. Long-term recovery for patients is usually good. Since this diagnosis can be made only after recovery, all patients with spinal injuries are managed with standard spinal care. Where recovery occurs, any spinal column injury found is managed accordingly. The absence of any major structural injury is common.

Temperature As discussed earlier, the body temperature of a patient with SCI is under far greater influence of ambient environmental temperature due to vasodilation. Therefore, body temperature will be closely monitored and managed with temperature-controlled fluids and warming equipment such as Bair Hugger™ therapy.

Bowel and bladder SCI often causes a loss of bladder and bowel control. The loss of function may occur at the time of injury or afterwards and it may not be permanent. The changes will vary not only with the severity of the injury but also with the location. Higher-level injuries may cause an increase in bladder tone, leading to frequency and incontinence. Lower-level injuries may cause loss of bladder tone, leading to an inability to urinate and retention of some urine, which may increase the risk of recurring infection. Loss of bowel control presents similarly. Higher injuries can take away the ability to identify when a bowel motion is required. Bowel movements occur on a reflex basis with the anal sphincter retaining its tone; the patient stimulates this reflex at a time that is suitable. Lower injuries may remove the tone of the anal sphincter and hence cause retention of faeces. Depending on the nature of the symptoms, a combination of manual stimulation techniques, diet management, medications, laxatives and enemas may become a regular part of life for the patient. The first few days post-SCI are frequently accompanied by a paralytic ileus. This usually self-resolves and requires little intervention other than insertion of a nasogastric tube to

facilitate drainage. Secondary to unopposed parasympathetic activity is a prevalence for gastric ulcer disease and this may need to be managed with ongoing medication.

Deep vein thrombosis Limb stasis predisposes SCI patients to deep vein thrombosis—another lifelong complication. Some patients can be assessed using ultrasound for increased risk, and anticoagulant drugs such as heparin and compression stockings are a common strategy for management.

Length of hospital stay Length of hospital stay varies with the severity of the injury and other associated injuries. Typically, SCI patients have a median stay of 16 days in acute care followed by a median of 133 days in a rehabilitation unit. The duration of hospital stay for persisting SCI varies between 77 days and 221 days. The overwhelming majority of patients are discharged home, with only a small percentage moving to a nursing home. In Australia, it is estimated to cost almost $500 million per year to care for these patients (Norton, 2010). Given that the typical age of injury is 25 years, the ongoing cost of care is huge.

Long-term issues and care P re ssure a re a s Constant care of pressure areas is required for life for all SCI patients. Healing pressure ulcers is a major healthcare cost, with the best management strategy clearly avoiding the problem in the first place (Cobb et al., 2014).

Coronary heart disease The incidence of coronary heart disease is both more common and seen earlier in those with SCI. The reasons for this are unclear but may be related to dysfunction of the adrenergic system and changes with lipids and cholesterol, and insulin resistance (Myers, Lee & Kiratli, 2007). Coronary heart disease is a long-term common cause of death in people with SCI.

Respiratory muscle training Many patients with SCI, particularly those with tetraplegia, lose some or all control of the muscles required for effective ventilation. Various training techniques can be undertaken to increase the strength and use of the respiratory muscles, such as forced breathing against the resistance of a blocked airway (Liaw et al., 2000; Van Houtt, Vanlandewijck & Gosselink, 2006). Improvement in inspiratory muscle use can increase vital capacity and reduce atelectasis. Any improvement in expiratory muscle effectiveness can increase cough ability and hence clearing of secretions and reduction of infections (Roth et al., 2010).

Phrenic and diaphragm nerve pacing Intramuscular electrodes can be implanted into the diaphragm of a patient who is dependent on a ventilator. This can enable substantial increases in inspiratory effort and tidal volume as well as periods without ventilator support. Similarly, direct stimulation of the phrenic nerve can produce diaphragm activity with consequent benefits (DiMarco et al., 2002, 2005; Zimmer, Nanti & Goshgarian, 2007).

Autonomic dysreflexia Although SCI is usually permanent in most patients, a return of spinal cord reflexes below the injury site will eventually occur. Autonomic dysreflexia is an abnormal and excessive spinal reflex response and involves alpha-adrenoreceptor hyperresponsiveness producing an excessive pressor response (Teasell et al., 2000). This is a true medical emergency. For SCI above the level of T6 a dangerous hypertensive crisis can result. Intact peripheral nerves return stimuli to the cord from sources including a distended bladder, bowel motion, pain from an injury or illness or even mild discomfort such as sheets tucked in too tightly. These sensory impulses, though blocked at the level of injury, can set up a reflex arc response in

the cord itself leading to a sympathetic response. Peripheral vasoconstriction and hypertension can ensue. The brain will become aware of this hypertension, gaining feedback via baroreceptors linked to the cranial nerves. The intentional response to halt the crisis cannot get past the spinal cord injury and so may prove largely ineffective. The other mechanism of response is to produce a compensatory bradycardia. Typically a patient with autonomic dysreflexia will present with headache, flushing in the upper body and profuse sweating from upper body vasodilation. In stark contrast, the lower body may present as pale and cold. Key to effective paramedic management is recognition and a prompt response. Search for possible stimuli and manage accordingly, including clearing and draining a catheter bag, clearing impacted bowel, loosening clothing or bedding and providing analgesia if pain is thought to be the cause. Analgesia may be required even if pain is not described by the patient. If these options fail, use of a vasodilator, particularly glyceryl trinitrate, in a regimen similar to treatment of cardiac chest pain is appropriate.

Life expectancy for SCI survivors The life expectancy of patients who survive SCI is considerably reduced. Varying with the severity of the injury, the most common causes of death for SCI patients include infection (septicaemia, pneumonia and urinary tract disease leading to renal failure predominantly), heart disease, pulmonary embolism and, tragically, suicide (Soden et al., 2000).

CA SE ST U DY 2 Case 11054, 1530 hrs. Dispatch details: A four-year-old boy has been struck by a motor vehicle in the street. He is conscious and crying and still lying in the road. Initial presentation: When the crew arrive they find a crowd of people around the child. A bystander is waving at oncoming cars to slow down as the police are not yet in attendance. The crew park the ambulance to block traffic from proceeding past the scene.

ASSESS 1538 hrs Primary survey: The patient is conscious, talking and crying. 1539 hrs Chief complaint: The child has an obvious forehead abrasion and appears to have a lot of pain in his left mid-thigh. 1541 hrs Vital signs survey: Perfusion status: HR 120 BPM, strong and regular; BP 90/50 mmHg; skin cool and dry. Respiratory status: RR 28 BPM; good, clear air entry bilaterally; his breathing appears fast although there is no use of accessory muscles. Conscious state: GCS = 15. 1542 hrs Pertinent hx: The child was riding his bicycle; when the vehicle hit him it was travelling at approximately 40 km/h. He was thrown across the car bonnet before landing on the road a few metres from the car. He was wearing his bicycle helmet and did not get up afterwards. He is crying and has suffered no apparent loss of consciousness. 1545 hrs Secondary survey: There are no visible injuries or pain to the chest or abdomen. His left thigh is markedly swollen compared to the right and is

painful mid-thigh. There is a small haematoma on his temple with some minimal bleeding. He is not complaining of pain or tenderness in the back of his neck. He can move all limbs except his left leg.

CONFIRM In many cases paramedics are presented with a collection of signs and symptoms that do not appear to describe a particular condition. A critical step in determining a treatment plan in this situation is to consider what other conditions could explain the patient’s presentation.

What else could it be? Head injury The history of the event suggests that the patient has a mechanism and pattern of injury that includes blunt trauma to his head. He has an abrasion on his forehead, which indicates that his head has struck either the car or the ground. Although he is conscious and crying, a full neurological assessment is required, including any loss of consciousness reported by bystanders. However, the child’s age and distressed state will make it difficult to fully assess his neurological function.

DIF F ERENT IA L DIA GNOSIS Fractured left femur Or • Head injury • Spinal injury • Something else

Spinal injury The patient also has a mechanism and pattern of injury that may suggest a spinal column or cord injury. His age and distressed state will make it difficult to fully assess his injuries or any neurological deficits. The pain in his left thigh is a distracting injury and makes it difficult to thoroughly assess him while he is in significant pain. Narcotic analgesia will undoubtedly relieve the pain to a degree, but it may also have an effect on his conscious state making an accurate assessment even more difficult. Although the leg pain and vital signs suggest that there is no significant spinal cord injury, identifying any bony damage to the spine that may yet cause a cord injury will be difficult. As such, children should not be cleared using

spinal clearance parameters. Any child with a mechanism or pattern of injury that may suggest a spinal injury must be immobilised and managed as such and cleared after medical and/or radiological assessment. Something else The incident was clearly traumatic. The extent of the child’s injuries is not known: apart from the left mid-thigh pain suggestive of a fractured femur he may have other injuries. A thorough vital signs survey is required to provide a baseline set of observations and regular monitoring is required to detect changes or trends early. A thorough secondary survey is also required to identify any other injuries that may not immediately be evident due to the distraction of the painful leg and the child’s distress. Consideration should be given to chest, abdominal and pelvic injuries with this mechanism of injury.

T REAT This patient should be treated as a multi-trauma patient. The abrasion on his head and his painful leg suggest that his injuries encompass more than one body region. He requires manual spinal immobilisation immediately until he can be fully immobilised. Immediately, one paramedic should provide manual inline spinal immobilisation and provide reassurance and build rapport with the child. This will make it easier to apply a cervical collar and immobilise him prior to loading and transporting. The probably fractured femur requires splinting as this will assist with pain management and reduce further injury to the soft tissues, nerves and blood vessels, as well as minimising haemorrhage from the injury that may result in perfusion issues. This child is clearly distressed and in pain and he requires narcotic analgesia as per local guidelines. Ideally, IV access should also be obtained early to manage any pain and perfusion issues that may develop. Finally, transport to a facility offering the highest level of trauma is required. 1545 hrs: The paramedics request other resources as appropriate (e.g. intensive care or aeromedical retrieval, depending on location) and give the patient intranasal fentanyl for pain. 1547 hrs: The paramedics commence inline manual spinal immobilisation of the patient’s left leg, followed by a traction splint. 1553 hrs: They place a cervical collar on the patient, but he tries to remove it and shakes his head around, so they decide to leave him without a collar at this stage as he is more immobile without it. As the pain relief becomes effective the patient may become more compliant, but manual stabilisation is a compromise that often has to be made in the field. 1554 hrs: The paramedics establish IV access and administer IV fluid TKVO (to keep vein open) and IV analgesia titrated to the patient’s weight and response. 1557 hrs: The paramedics complete full spinal immobilisation once the patient has become more settled with further analgesia and then reapply the

cervical collar.

EVALUAT E Evaluating the effect of any clinical management intervention can provide clues to the accuracy of the initial diagnosis. Some conditions respond rapidly to treatment so patients should be expected to improve if the diagnosis and treatment were appropriate. A failure to improve in this situation should trigger the clinician to reconsider the diagnosis. In this case the patient would be expected to remain stable during transport and any deterioration should trigger a reassessment. An undetected internal bleed, positional hypoxia and sedation from too much pain relief are possible complications of treatment.

CA SE ST U DY 3 Case 10983, 0830 hrs. Dispatch details: An 80-year-old woman has been found lying on the floor at home. She is conscious and has a laceration to her head. Initial presentation: The crew are led inside a private house by a carer who found the patient. The patient is lying on her back in the bedroom where she fell.

ASSESS 0841 hrs Chief complaint: The patient is complaining of pain at the back of her head and is unable to get up. 0841 hrs Vital signs survey: Perfusion status: HR 96 BPM, weak and irregular; BP 95/50 mmHg; skin cool and dry; temperature 34.1°C.

Respiratory status: RR 14 BPM; good, clear air entry; L = R; normal work of breathing; no complaint of dyspnoea. Conscious state: GCS = 14; confused to time, place and event. 0842 hrs Secondary survey: The patient is able to move all her limbs. 0843 hrs Pertinent hx: The patient is normally unsteady and has a history of falls. Despite this, she looks after herself well with daily home help support around the home. She is in her pyjamas and cannot say how long ago she had the fall. She has been incontinent of urine. The bedside table has been knocked over, suggesting that she struck this as she fell to the floor. 0845 hrs Secondary survey: There are no visible injuries or pain to the chest or abdomen. Similarly, all limbs appear free from pain or injury. There is dried blood on the back of her head with a small amount observable on the bedside table. She also complains of pain and tenderness in the back of her neck.

CONFIRM In many cases paramedics are presented with a collection of signs and symptoms that do not appear to describe a particular condition. A critical step in determining a treatment plan in this situation is to consider what other conditions could explain the patient’s presentation. This patient has an obvious head injury as evidenced by the laceration on her head. She is reportedly confused so it is important to gauge whether this is ‘normal’ for her or a result of the injury. If there is any doubt, the change in conscious state should be considered to be new and either a result of the fall or contributing to the fall. The patient is more susceptible to sustaining a spinal injury as a result of a low-level fall. Neurological changes that occur with age also predispose this patient to falling, including postural instability, a slowed reaction time, a decline in proprioceptive senses and changes to visual perception such as acuity, depth, peripheral and night vision. Medications used to treat other chronic conditions may predispose patients to haematoma formation, such as anticoagulant medications. This patient is complaining of bony tenderness along her cervical spine. While there are not many symptoms suggesting a spinal injury or spinal cord injury, neither can be ruled out yet.

P RACT ICE T IP The complications of lying on the floor for a prolonged period of time include: • hypothermia • dehydration • crush syndrome.

What else could it be? Cardiac event This patient has a history of falls and this has been attributed to her unsteadiness. Although this may be the cause of her fall on this occasion it is prudent to consider whether an event may have precipitated this fall. One potential cause is a cardiac event such as arrhythmia. An ECG can be carried out, but it may not show any sign of the event leading to the fall. For this reason, a cardiac event cannot be ruled out.

DIF F ERENT IA L DIA GNOSIS Fall Or • Cardiac event • Stroke • Metabolic cause • Infection

Stroke A neurological event precipitating the fall is also a possibility for this patient. While it is not definitive, a neurological assessment is prudent to determine whether this patient has any stroke symptoms. Metabolic cause An assessment of this patient’s history and a blood glucose test will enable hypoor hyperglycaemia to be ruled out. Further metabolic testing will need to be carried out in hospital. Infection While temperature is a simple indicator of infection, in the elderly it is not a reliable indicator. Due to alterations in the autonomic nervous system in the elderly they may not present with a temperature if they have infection. A history of recent illness, including symptoms such as a cough, consolidation in the chest or urinary tract symptoms to name a few, give some clues as to whether infection could be the cause of the fall. Regardless of the cause of the fall, this patient’s current presentation dictates that spinal care must be carried out, in addition to management of any other issues found. She is dressed in her pyjamas, is hypothermic and has been incontinent of urine. This suggests that she fell at some point during the night and that a medical cause might have precipitated the fall. The hypothermia may be contributing to her confusion but other reasons need to be considered. The vital signs survey suggests that she has no respiratory distress and that her perfusion status is within normal parameters, although this will need to be assessed in the context of her usual medications.

T REAT This patient is at risk of spinal injury due to her age and she cannot be cleared using normal spinal clearance parameters. She also has the potential for a closed head injury. Whole-body spinal immobilisation should be applied with careful consideration given to padding areas of bony prominence and curves such as occiput, lumbar region and iliac crests. The ideal tool is a vacuum mattress. Any abnormal spinal curvature or deformity will have to be accommodated when immobilising this patient. Other medical conditions likely to impede spinal immobilisation include chronic respiratory and cardiac disorders that may make supine positioning difficult. Anomalies identified as part of assessment should be managed and include wound care and hypothermia management. 0855 hrs: One of the crew maintains manual inline cervical support while the other applies a cervical collar. They remove her wet clothing, wrap her in warm blankets and attend to her wounds. 0905 hrs: The patient is fully spinally immobilised.

EVALUAT E Evaluating the effect of any clinical management intervention can provide clues to the accuracy of the initial diagnosis. Some conditions respond rapidly to treatment so patients should be expected to improve if the diagnosis and treatment were appropriate. A failure to improve in this situation should trigger the clinician to reconsider the diagnosis. In this case the patient would be expected to remain stable during transport and any deterioration should trigger a reassessment. An undetected internal bleed, positional hypoxia and sedation from too much pain relief are possible complications of treatment.

Future research During the inflammatory phase a significant amount of demyelination can occur, resulting in permanent injury to nervous tissue. One promising area of research is the transplantation of cells, including stem cells, early in the acute phase to enable either new cellular growth or remyelination of remaining cells. This includes ways to improve or enhance the actions of the remaining nerves that have been demyelinated. The research includes an investigation of the optimal time for such activities, as there is some promise of neuronal regrowth, albeit insufficient, that can be enhanced in later post-acute stages. Strategies revolve around directly enabling cellular regrowth and enhancing the environment for it to occur (Rowland et al., 2008). Scar tissue in CNS injury, known as the glial scar, is responsible for inhibiting the regrowth of axonal tissue. Various models for cellular transplant and enhancing the environment for scar inhibition, thus allowing for regrowth, are being explored (Rowland et al., 2008; Silver & Miller, 2004).

Summary Spinal column injury and spinal cord injury are different injuries with potentially different long-term care pathways. SCI often leads to a response from all body systems, resulting in the need to consider all systems throughout the recovery and rehabilitation processes. In the prehospital setting SCI must be a primary consideration for all patients who have experienced even the lowest level of trauma, particularly if they are elderly. Avoidance of any further traumatic or medical injury is the primary goal of prehospital management.

References Adams, J. G.Emergency Medicine. Philadelphia: Saunders, 2008. American Spinal Injury Association. International Standards for Neurological Classifications of Spinal Cord Injury, rev ed. Chicago, Ill: American Spinal Injury Association, 2000. Armstrong, B. P., Simpson, H. K., Deakin, C. D. Prehospital clearance of the cervical spine: does it need to be a pain in the neck? Emergency Medicine Journal. 2007; 24(7):501–503. Bauer, D., Kowalski, R. Effect of spinal immobilisation function in the healthy, non-smoking man. Annals of Emergency Medicine. 1988; 17(9):915–918. Berlly, M., Shem, K. Respiratory management during the first five days after spinal cord injury. Journal of Spinal Cord Medicine. 2007; 30(4):309–318. Boswell, H. B., Dietrich, A., Shiels, W. E., King, D., Ginn-Pease, M., Bowman, M. J., Cotton, W. H. Accuracy of visual determination of neutral position of the immobilized pediatric cervical spine. Pediatric Emergency Care. 2001; 17(1):10–14. Branfoot, T. Motorcyclists, full face helmets and neck injuries: can you take the helmet off safely, and if so, how? Journal of Accident & Emergency Medicine. 1994; 11:117–120. Cirak, B., Ziegfeld, S., Knight, V. M., Chang, D., Avellino, A. M., Paidas, C. N. Spinal injuries in children. Journal of Pediatric Surgery. 2004; 39(4):607–612. Cobb, J. E., Bélanger, L. M.A., Park, S. E., et al. Evaluation of a pilot Pressure Ulcer Prevention Initiative (PUPI) for patients with traumatic spinal cord injury. Journal of Wound Care. 2014; 23:211–226. Cooke, M. W. Use of the spinal board within the accident and emergency department. Journal of Accident & Emergency Medicine. 1998; 15:108–113. Criswell, J. C., Parr, M. J.A., Nolan, J. P. Emergency airway management in patients with cervical spine injuries. Anaesthesia. 1994; 49(10):900–903. Crosby, E. Airway management after upper cervical spine injury: what have we learned? Canadian Journal of Anesthesia. 2002; 49(7):733–744.

Curran, C., Dietrich, A. M., Bowman, M. J., Ginn-Pease, M. E., King, D. R., Kosnick, E. Pediatric cervical spine immobilisation: achieving neutral position. Journal of Trauma Injury Infection & Critical Care. 1995; 39(4):729–732. Davies, G., Deakin, C., Wilson, A. The effect of a rigid collar on intracranial pressure. Injury. 1996; 27(9):647–649. Davis, J. W., Parks, S. N., Detlefs, C. L., Williams, G. G., Williams, J. L., Smith, R. W. Clearing the cervical spine in obtunded patients: the use of dynamic fluoroscopy. Journal of Trauma. 1995; 39:435–438. De Lorenzo, R. A., Olson, J. E., Boska, M., Johnston, R., Hamilton, G. C., Augustine, J., Barton, R. Optimal positioning for cervical immobilization. Annals Emergency Medicine. 1995; 28(3):301–308. Del Bigio, M. R., Johnson, G. E. Clinical presentation of spinal cord concussion. Spine. 1989; 14(1):37–40. Del Rossi, G., Horodyski, M., Powers, M. E. A comparison of spine board transfer techniques and the effect of training on performance. Journal of Athletic Training. 2003; 38(3):204–208. DiMarco, A. F., Onders, R. P., Ignagni, A., Kowalski, K. E., Mortimer, J. T. Phrenic nerve pacing via intramuscular diaphragm electrodes in tetraplegic subjects. Chest. 2005; 127(2):671–678. DiMarco, A. F., Onders, R. P., Kowalski, K. E., Miller, M. E., Ferek, S., Mortimer, J. T. Phrenic nerve pacing in a tetraplegic patient via intramuscular diaphragm electrodes. American Journal of Respiratory and Critical Care Medicine. 2002; 166(12):1604–1606. Durward, Q. J., Amacher, A. L., Del Maestro, R. F., Sibbald, W. J. Cerebral and cardiovascular responses to changes in head elevation in patients with intracranial hypertension. Journal of Neurosurgery. 1983; 59(6):938–944. Gerling, M. C., Davis, D. P., Hamilton, R. S., Morris, G. F., Vilke, G. M., Garfin, S. R., Hayden, S. R. Effects of cervical spine immobilization technique and laryngoscope blade selection on an unstable cervical spine in a cadaver model of intubation. Annals of Emergency Medicine. 2000; 36(4):293–300. Guly, H. R., Bouamra, O., Lecky, F. E. The incidence of neurogenic shock in patients with

isolated spinal cord injury in the emergency department. Resuscitation. 2008; 76(1):57–62. Holly, L. T., Kelly, D. F., Counelis, G. J., Blinman, T., McArthur, D. L., Cryer, H. G. Cervical spine trauma associated with moderate and severe head injury: incidence risk factors and injury characteristics. Journal of Neurosurgery. 2002; 96:S285–S291. Johnson, D. R., Hauswald, M., Stockhoff, C. Comparison of a vacuum splint device to a rigid backboard for spinal immobilization. American Journal of Emergency Medicine. 1996; 14(4):369–372. Krell, J. M., McCoy, M. S., Sparto, P. J., Fisher, G. L., Stoy, W. A., Hostler, D. P. Comparison of the Ferno scoop stretcher with the long backboard for spinal immobilisation. Prehospital Emergency Care. 2006; 10:46–51. Kwan, I., Bunn, F., Roberts, I. G. Spinal immobilization for trauma patients. Cochrane Database of Systematic Reviews. 2, 2001. [art. no. CD002803.]. Liaw, M. Y., Lin, M. C., Cheng, P. T., Wong, M. K.A., Tang, F. T., Resistive inspiratory muscle training: its effectiveness in patients with acute complete cervical cord injury. Archives of Physical Medicine and Rehabilitation 2000; 81:752–756 Lida, H., Tachibina, S., Kithara, T., Horiike, S., Ohwada, T., Fujii, K., et al. Association of head trauma with cervical spine injury, spinal cord injury or both. Journal of Trauma. 1999; 46:450–452. Lubbert, P. H.W., Schram, M. E., Leenen, L. P.H. Is there a reason for spine board immobilization in the emergency department for patients with a potential spinal injury? European Journal of Trauma. 2005; 31(4):375–378. Lustrin, E. S., Karakas, S. P., Ortiz, O., Cinnamon, J., Castillo, M., Vaheesan, K., Brown, J., Diamond, A., Black, K., Singh, S. Pediatric cervical spine: normal anatomy, variants and trauma. Radiographics. 2003; 23:539–580. Malik, M. A., Maharaj, C. H., Harte, B. H., Laffey, J. G. Comparison of Macintosh, Truview EVO2, Glidescope and Airwayscope laryngoscope use in patients with cervical spine immobilization. British Journal of Anaesthesia. 2008; 101(5):723–730. Manoach, S., Paladino, L. Manual inline stabilization for acute airway management of suspected cervical spine injury: historical review and current questions. Annals of

Emergency Medicine. 2007; 50(3):236–245. Martin, B. W., Dykes, E., Lecky, F. E. Patterns and risks in spinal trauma. Archives of Diseases in Children. 2004; 89(9):860–865. Mazelowski, P., Manix, T. H. The effectiveness of strapping techniques in spinal immobilization. Annals of Emergency Medicine. 1994; 23(6):1290–1295. McCance, K., Huether, S. Pathophysiology: The Biologic Basis for Disease in Adults and Children, 7th ed. Philadelphia: Mosby, 2014. Medscape. Brown-Sequard Syndrome. Retrieved 28 October 2014 from http://emedicine.medscape.com/article/321652-overview, 2014. Morris, C. G.T., McCoy, E. Cervical immobilization collars in ICU: friend or foe? Anaesthesia. 2003; 58(11):1051–1053. Morris, C. G.T., McCoy, E. Clearing the cervical spine in unconscious polytrauma victims, balancing risks and effective screening. Anaesthesia. 2004; 59(5):464–482. Morris, C. G., McCoy, E. P., Lavery, G. G. Spinal immobilization for unconscious patients with multiple injuries. British Medical Journal. 2004; 329:495. Muhr, M. D., Seabrook, D. L., Wittwer, L. K. Paramedic use of a spinal injury clearance algorithm reduces spinal immobilization in the out-of-hospital setting. Prehospital Emergency Care. 1999; 3(1):1–6. Myers, J., Lee, M., Kiratli, J. Cardiovascular disease in spinal cord injury: an overview of prevalence, risk, evaluation and management. American Journal of Physical Medicine and Rehabilitation. 2007; 86(2):142–152. Nolan, J. P., Wilson, M. E. Orotracheal intubation in patients with potential cervical spine injuries. Anaesthesia. 1993; 48(7):630–633. Norton, L.Spinal Cord Injury, Australia 2007–08. Canberra: AIHW, 2010. [Injury Research and Statistics Series No. 52. Cat. no. INJCAT 128]. Patton, K. T., Thibodeau, G. A. Anatomy and Physiology, 7th ed. St Louis: Mosby, 2012. Radiopaedia.org. (2014). Retrieved 28 October 2014 from

http://radiopaedia.org/articles/anterior-cord-syndrome. Raphael, J. H., Chotai, M. B. Effects of the cervical collar on cerebrospinal fluid pressure. Anaesthesia. 1994; 49(5):437–439. Reilly, C. W. Pediatric Spine Trauma. JBJS. 2007; 89(1):98–107. Roberts, D. Clinical Procedures in Emergency Medicine, 5th ed. St Louis: Elsevier, 2009. Roth, E. J., Stenson, K. W., Powley, S., Oken, J., Primack, S., Nussbaum, S. B., Berkowitz, M. Expiratory muscle training in spinal cord injury: a randomized controlled trial. Archives of Physical Medicine and Rehabilitation. 2010; 91:857–861. Rowland, J. W., Hawryluk, G. W.J., Kwon, B., Fehlings, M. G. Current status of acute spinal cord injury pathophysiology and emerging therapies: promise on the horizon. Neurosurgical Focus. 2008; 25(5):E2. Schriger, D. L., Larmon, B., LeGassick, T., Blinman, T. Spinal immobilization on a flat backboard: does it result in neutral position of the cervical spine? Annals of Emergency Medicine. 1991; 20(8):878–881. Segan, R. D., Cassidy, C., Benkowski, J. A discussion of the issue of the football helmet removal in suspected cervical spine injuries. Journal of Athletic Training. 1993; 28(4):294. [296, 298, 300, 302, 304–305.]. Silver, J., Miller, J. H. Regeneration beyond the glial scar. Neuroscience. 2004; 5:146–156. Skellet, S., Tibby, S. M., Durward, A. Immobilisation of the cervical spine in children. British Medicine Journal. 2002; 324:591. Slack, S. E., Clancy, M. J. Clearing the cervical spine of paediatric trauma patients. Emergency Medicine Journal. 2004; 21(2):189–193. Soden, R. J., Walsh, J., Middleton, J. W., Craven, M. L., Rutkowski, S. B., Yeo, J. D. Causes of death after spinal cord injury. Spinal Cord. 2000; 38:604–610. Somers, M. Spinal Cord Injury: Functional Rehabilitation, 3rd ed. New Jersey: Pearson, 2010. Spector, L. R., Madigan, L., Rhyne, A., Darden, B., Kim, D. Cauda equina syndrome. Journal

of American Academy of Orthopedic Surgery. 2008; 16(8):471–479. Swartz, M. Textbook of Physical Diagnosis, 6th ed. Philadelphia: Saunders, 2009. Teasell, R. W., Arnold, J. M.O., Krassioukov, A., Delaney, G. A. Cardiovascular consequences of loss of supraspinal control of the sympathetic system after spinal cord injury. Archives of Physical Medicine and Rehabilitation. 2000; 81(4):506–516. Todd, A. J., Moe, L. R., Joon, L. Y.Cervical Spine Surgery Challenges: Diagnosis and Management. Thieme Medical Publishers, 2008. Todd, N. V. Priapism in acute spinal cord injury. Spinal Cord. 2011; 49:1033–1035. Totten, V. Y., Sugarman, D. B. Respiratory effects of spinal immobilization. PreHospital Emergency Care. 1999; 3(4):347–352. Van Houtt, S., Vanlandewijck, Y., Gosselink, R. Respiratory muscle training in persons with spinal cord injury: a systematic review. Respiratory Medicine. 2006; 100(11):1886–1895. Vickery, D. The use of the spinal board after the prehospital phase of trauma management. Emergency Medicine Journal. 2001; 18:51–54. Yeung, J. H.H., Cheung, N. K., Graham, C. A. Reduced time on the spinal board: effects of guidelines and education for emergency department staff. Injury. 2006; 37(1):53–56. Zimmer, M. B., Nantwi, K., Goshgarian, H. G. Effect of spinal cord injury on the respiratory system: basic research and current clinical treatment options. Journal of Spinal Cord Medicine. 2007; 30(4):319–330. Zwimpfer, T. J., Bernstein, M. Spinal cord concussion. Journal of Neurosurgery. 1990; 72(6):894–900.

CHAP TER 36

Burns By Nick Goodwin, Jason Wasiak and Fiona Wood

C O N C E P TS U S E D I N TH I S C H A P TE R • The paramedic’s clinical approach: Section 2 • Perfusion: Chapter 55 • The inflammatory response: Chapter 57

O V E RV IE W • Burn injuries encompass a wide range of mechanisms and severity. • Patients at the greatest risk of a poor outcome after a burn injury are infants and the elderly. • Patients at the highest risk of sustaining a burn injury are young children, the elderly and young males. • Burn injuries present particular challenges in pain management, fluid administration and airway management. • Early and effective intervention can result in significant and life-long improvement in functional and cosmetic outcomes.

Introduction Burn injuries are sustained when tissues are subjected to excessive heat. Chemically reactive agents, strong electrical currents, radiation, radioactive substances and friction can also cause the cellular changes seen in burn injury. In addition, similar cellular damage can occur when tissue is exposed to extremely cold substances such as liquid nitrogen; these are often referred to as ‘cold burns’. The inflammatory response triggered by burn injuries can damage viable tissue that surrounds the burn and, if the burn site is extensive and severe enough, can cause cardiovascular collapse (shock) and/or airway occlusion. Burn injuries occur in all age groups and in many settings, and range from minor wounds requiring little treatment to severe, life-threatening injuries (see Box 36.1). In Australia, approximately 10,000 people are hospitalised every year as a result of burn-or scald-related injury. The elderly, children and young males are more likely to sustain a burn injury requiring hospitalisation (Harrison & Steel 2006; Wasiak et al., 2009). B O X 3 6 . 1E p i d e m i o

lo g y o f burns

High mortality/morbidity risk factors • Age >60 • Large burn surface area >40% • Airway burns/inhalational injury • Hypothermia • Concurrent major secondary trauma • Presence of fungi or multi-resistant organisms in the burn

Leading causes of mortality • Sepsis • Respiratory failure • Shock • Multiple organ failure • Anoxic brain injury • Abdominal compartment syndrome

Outcome measures of greatest significance for patients • Survival • Cosmetic and functional outcomes • Resolution of pain • Recovery from emotional and psychological trauma

Most common mechanisms of burn injury • Flame/flash (adults) • Scalds (children) Source: Adapted from Herndon (2007).

There is no better example of the challenges facing paramedics than when confronted with the patient suffering from burns. These extremely painful, highly emotive injuries often occur in front of family or workmates, in the presence of ongoing dangers and in conjunction with other traumatic injuries. In this setting paramedics not only have to ensure the safety of themselves, the patient and bystanders, but must also determine the extent and nature of the patient’s injuries in order to accurately and rapidly initiate treatment and select an appropriate destination. The ability to prioritise and make correct decisions in this setting relies on a solid knowledge of the pathophysiology of burn injuries and of how burns can rapidly evolve into a life-threatening situation. In addition to the acute challenges, decisions made at the scene can have long-term functional and cosmetic impacts on patients. Despite major advancements in hospital management, prehospital burns care remains poorly researched and its true impact on patient outcomes unclear. Given the critical importance of early intervention in burn injuries, research into effective prehospital care is imperative.

Pathophysiology Burns produce intensely painful injuries that are extremely challenging to manage in the prehospital setting. An understanding of what occurs at the cellular level is essential to managing burns effectively and reducing associated morbidity and mortality.

Anatomy of the skin The skin is the largest organ of the body and acts as a physical barrier to infection and fluid loss. It is also essential for the regulation of body temperature and acts as a sensory interface with the external environment. Any one of these functions may be compromised by a burn injury—and if the injury is significant enough in severity, the effects can rapidly become life-threatening. In order to accurately classify and treat burn injuries, paramedics need an understanding of the anatomy of the skin and how local tissue response to burns can ultimately lead to systemic changes such as cardiovascular collapse (shock). The skin consists of two layers—the epidermis and the dermis—beneath which is a layer of subcutaneous fat (see Fig 36.1). The outermost layer, the epidermis, contains no blood vessels or nerve endings and is comprised largely of layers of slowly maturing epithelial cells that form at the junction between the dermis and the epidermis. As the epithelial cells are ‘pushed’ towards the surface by new cells forming underneath they lose their normal cellular contents, become flattened and are infused with keratin. Eventually these cells reach the surface where they are constantly being shed. The epidermis forms the barrier to fluid loss and infection (Herndon, 2007).

FIGURE 36.1 Classification of burns. Partial-thickness burns include first-and second-degree burns. Full-thickness burns include third-degree burns. Fourth-degree burns involve tissues under the skin, such as muscle or bone. Source: Patton & Thibodeau (2012).

Directly underneath the epidermis, the dermis is a relatively thin layer composed primarily of connective tissue but it is rich in blood vessels and contains nerves, pain and pressure receptors, sebaceous (sweat) glands and hair follicles. Blood flow to the dermis allows for control of thermoregulation and in addition to providing nutrients to the growing cells in the lower epidermis, the dermis also provides the skin with its elasticity and strength (Herndon, 2007). The dermis is divided into two layers: the thin and superficial papillary region (named because of its irregular surface) and the deeper and stronger reticular region where the hair follicles and glands reside. Just as the epidermis varies in thickness according to location, so does the dermis: it is less than half a millimetre on parts of the face but up to 3 mm thick on the back (Scott & Fong, 2004; Herndon, 2007). Below the dermis is a layer of fat sometimes referred to as the hypodermis. Although not considered part of the skin, this subcutaneous tissue is rich in fat cells and white blood cells and anchors the skin to underlying bone or connective tissue. Burns due to heat (thermal burns) are the most common burn injuries but tissue damage can also occur when tissue is exposed to chemicals, electricity, radioactive substances or extremely cold temperatures (the pathophysiology of chemical and electrical burns is discussed in case studies 5 and 6). Human cells become irreversibly damaged when the cell temperature rises above 45°C and the rate of cell death doubles with each degree above 45°C. This is because the proteins in human cells are stable to a point but ‘denature’ rapidly once they exceed a threshold (Pham & Gibran, 2007).

Burn classification Burn injuries are classified by depth and size because both independently guide treatment and predict the likely outcome of the injury.

Depth Classification is based on clinical observation and examination, knowledge of the burning agent and its temperature, history of the burn, the time elapsed since occurrence and the length of exposure or contact time (Fowler, 1998). Historically, burn depth was classified as first, second, third or fourth degree; however, the descriptors superficial, partial-thickness and full-thickness are now more commonly used (see Table 36.1). In emergency or paramedic practice the important distinction is between superficial burns and the deeper categories of burns. This is because deeper burns require more aggressive and specialist treatment.

TABLE 36.1 Depth assessment of burns Classification Superficial

Description Dry and red, blanches with pressure, no blisters. May be painful. Heals with no scarring. Superficial Pale pink with fine blistering, blanches with pressure. Usually extremely partial-thickness painful. Can have colour-match defect. Low risk of hypertrophic burns scarring. Mid-dermal Dark pink with large blisters. Capillary refill sluggish. May be painful. Moderate risk of hypertrophic scarring. Deep partialBlotchy red, may blister, no capillary refill. In child may be dark lobster thickness burns red with mottling. High risk of hypertrophic scarring. Full-thickness White, waxy or charred. No blisters. No capillary refill. Will scar. burn Source: Craft, Gordon & Tiziani (2011). Superficial burns involve only the epidermis. They are red and painful to touch, but because they do not penetrate and damage the dermis they do not form blisters. Sunburn generally fits into this category of superficial injury. In the acute phase superficial burns require only symptomatic treatment in the form of pain relief (Pham & Gibran, 2007). Partial-thickness burns extend beyond the epidermis into the dermis and are classified as either superficial partial-thickness burns (superficial dermal burns; see Fig 36.2) or deep partial-thickness burns (deep dermal burns; see Fig 36.3). In superficial partialthickness burns, the injury extends into the upper (papillary) region of the dermis. If the epidermis remains intact this will result in blisters, but if the epidermis is broken or burnt away the exposed dermis will appear red and moist and is extremely painful to touch. In most cases, the dermis will still blanch with pressure, indicating good preservation of dermal circulation. Superficial partial-thickness burns generally heal within 14–21 days with minimal scarring. By contrast, deep partial-thickness burns extend into the reticular dermis and damage structures such as sweat glands and hair follicles. These injuries tend to be paler than superficial partial-thickness burns, may appear mottled (pink and pale white) and do not blanch (or are slow to refill) with pressure (Pham & Gibran, 2007). Pain on contact is less than for superficial partial-thickness burns. Healing can take weeks to months, with scarring common.

FIGURE 36.2 A superficial partial-thickness burn injury following a scald. Source: Craft, Gordon & Tiziani (2011).

FIGURE 36.3 A deep partial-thickness burn. Note the pale appearance and minimal exudate. Source: University of Utah Health Care Burn Center. Full-thickness burns extend through the epidermis and dermis and into the subcutaneous tissue (see Fig 36.4). The centre of these burns can be charred or pale (depending on the source of heat that has been applied), but they are generally not sensitive to touch and are ‘leathery’ in texture. This ‘leathery’ tissue is referred to as eschar. These burns require surgical repair including excision and grafting (Schwartz & Balakrishan, 2004).

FIGURE 36.4 Full-thickness thermal burn. The wound is dry and insensate. Source: University of Utah Health Care Burn Center. It is important to note that burns rarely present with a single depth of injury (Hettiaratchy & Papini, 2004). Full-thickness burns will almost certainly be surrounded by an area of partial and superficial burns and the pain associated with these ‘lesser ’ areas is likely to be severe, even if the centre of burn is desensitised due to nerve damage. The heat source can also affect the appearance of the damaged tissue, making it difficult to assess wound depth: even experienced clinicians struggle to correctly assess burn depth in more than 70% of cases ( Johnson & Richard, 2003; Jaskille et al., 2010). This ‘bullseye’ pattern where the centre represents the most damaged tissue is typical of partial-and fullthickness burns and is often referred to as Jackson’s thermal wound model (Jackson, 1953; see Fig 36.5). The zone at the centre of the burn (the Zone of Coagulation) is where the damage is greatest and the damage to tissue is irreversible. Immediately surrounding this (laterally and underneath) is the Zone of Stasis, an area where tissue is injured but may survive if managed correctly. This zone has been shown to react positively to initial first aid but can enlarge for several days if not properly managed (Shupp et al., 2010). Finally, in the Zone of Hyperaemia (literally, increased blood) cells are not damaged by the heat but are affected by the inflammatory mediators (Gray & O’Reilly, 2009).

FIGURE 36.5 Jackson’s thermal wound model demonstrates how the inflammatory response to burn injury needs to be managed in order to maximise the patient’s chance of a quick and scar-less recovery.

Surface area Calculating the surface area of any irregular-shaped three-dimensional object is difficult, but far more so when the ‘object’ is partially clothed, moving and in pain. Assessing burn size as a percentage of total body surface area (TBSA) is critical, as this estimate is part of the burns fluid resuscitation calculation (see discussion below under ‘Treat’). There are many methods of assessing burn size but three are commonly used in the emergency setting: • the Lund and Browder chart (see Fig 36.6), which divides the body into sections and allocates a percentage to each section

FIGURE 36.6

Lund and Browder chart. Source: Marx et

al. (2014). • the Rule of Nines (see Fig 36.7), which is similar but uses larger sections

FIGURE 36.7 The Rule of Nines. A Adult, B Child. Source: Smith et al. (2010). • the Palmar method, which uses the size of the patient’s palm to represent 1% of their total body area (Schwartz & Balakrishan, 2004). Regardless of which method is used, it is essential that erythema is not included in the calculation (Connolly, 2011). There is no evidence that one method is more accurate than the others or improves patient outcomes (Hussain & Ferguson, 2009). It is worth noting, however, that small burns are generally overestimated and large burns are underestimated, with burns around the 20% range being the most accurately assessed (Saffle et al., 2009). A number of studies have demonstrated that TBSA estimations are extremely difficult during the acute phase of injury even for treating doctors in referring hospitals. Saffle and colleagues (2009) compared doctor-only estimations from referring hospitals against consultative estimations with the treating burns centres via telemedicine links and

highlighted wide divergences in accuracies between the two groups. A number of factors cloud accuracy, including the presence of extensive erythema masking the size of the burn, inaccuracies inherent in existing assessment methods, the skill of the assessor and changes to the burn injury before the patient arrives at the hospital burns unit or ED.

The inflammatory response to burn injury As described in detail in Chapter 57, the inflammatory response is the body’s normal reaction to injury and is the start of the healing process. There are a range of triggers and substances that drive this response, but the net result of all these mediators is to increase blood flow to the injured area while simultaneously increasing the permeability of the capillaries close to the injured tissue. These reactions facilitate the movement of white blood cells from the capillaries to the extracellular space to help fight infection and remove cellular detritus.

DEF INIT ION Mediator: a substance or structure that controls a specific response in bodily tissue.

Local inflammatory effects While the inflammatory response is essential for healing, an overly aggressive response can direct so much blood to an area, and cause so much oedema, that viable cells surrounding the injury (the Zones of Stasis and Hyperaemia) can become inadequately perfused and start to die. At the local tissue level, the changes to the microvascular blood flow and vessel permeability result in a shift of fluid, electrolytes and protein from the intravascular space into the interstitial space (Latenser, 2009). Most of the oedema forms within minutes to hours of the injury and reaches its maximum by 24 hours post-injury (Demling, 2005; Tricklebank, 2009). If the inflammatory response extends beyond the burn site it can lead to widespread vasodilation and oedema and progress to burns shock (see Fig 36.8).

FIGURE 36.8 After surviving the initial insult, the greatest initial threat to a patient with a major burn is hypovolaemic shock as the inflammatory response spreads

away from the burn site. Source: Brown & Edwards (2012).

Systemic inflammatory effects: burns shock In larger partial-thickness burns the consequences of the inflammatory response can extend far beyond the burn site and cause systemic vasodilation and increased capillary permeability (see Fig 36.9). Although the precise mechanism of this process has not been established, it is suspected that the inflammatory mediators released by local tissue damage (histamine, prostaglandins, thromboxane and nitric oxide) are supported by additional inflammatory mediators such as interleukins 1, 2, 5 and 8 to produce far-reaching, widespread systemic effects (Schwartz & Balakrishan, 2004). The involvement of these mediators seems to occur when the partial area of the burns exceeds 20% of TBSA and some authors describe this situation as the entire body becoming the Zone of Hyperaemia (Connolly, 2011).

FIGURE 36.9

Phases of burns shock.

Compounded with the evaporative fluid loss from the burn site itself, the form of distributive shock can cause hypotension and organ hypoperfusion. This is often referred to as burns shock (Schwartz & Balakrishan, 2004) and once it is fully evolved it is a combination of hypovolaemic, distributive and (possibly) cardiogenic shock. Histamine and other inflammatory mediators potentially have potent effects on almost all of the cardiovascular system. They are potent dilators of both arterioles and veins, which can lead to distributive shock. They increase capillary permeability and potentially lead to a fluid shift sufficient to result in hypovolaemic shock and may even have a direct effect on the heart, causing arrhythmias, decreasing myocardial function and resulting in cardiogenic shock (Brown, 2007). The loss of intravascular volume to the interstitium also occurs in the first 8–12 hours post-injury and the patient can potentially lose the ability to maintain adequate cardiac output and overall tissue perfusion. Tissue hypoperfusion may impair other organ systems as they become involved in the general response to the stress caused by the burn injury (Tricklebank, 2009). The severity of the reaction and the individual contribution of each mechanism are difficult to predict, but in one UK study the resultant hypotension was reported as the main cause of death in 25% of all fatal cases and as present in 54% (Pumphrey, 2000, 2004; Soar et al., 2008). The manifestation of these effects needs to be carefully considered during paramedic assessment. Dilation of the small vessels leading into the capillary beds results in large amounts of blood pooling in the capillaries, particularly those near the skin.

This erythema can make patients flushed and they can radiate large amounts of heat.

T HE MECHA NISM OF CHEMICA L B U RNS Although acids are commonly perceived to be associated with burn injuries, alkaline substances are a more common cause and the exposure can be in the form of a liquid, powder or gas that damages tissues from direct contact or by inhalation or ingestion (Hardwicke et al., 2012). Like thermal burns, the extent of the chemical injury will be dependent on the type of agent, its concentration and volume, and the duration of contact. Most chemical burns damage the skin not by heat but by the chemical reacting with water, proteins or fats in body tissue. Like a thermal burn, this necrotising reaction damages the outer layer of the skin; however, unlike a thermal burn where the heat is partially dissipated by the underlying tissue, the water in the tissues under the skin can actually fuel a chemical burn.

The characteristic oedematous swelling caused by fluid shifts into the interstitial spaces —called angio-oedema—is often first noted in the feet, hands, face (lips and eyelids) and upper airway. Swelling caused by oedema may be seen in the hands by asking the patient to make a fist or may be observed as changes to facial appearance or voice.

Burn progression Burn wounds are three-dimensional and this is an important concept in understanding burn progression. As the skin is exposed to heat the burn spreads both across the skin and beneath it involving more and more layers. The inflammatory response is subject to graduation—that is, small injuries produce a limited release of mediators, while larger deeper burns produce a marked response. This can lead to swelling associated with the burn causing compression of viable tissues in the Zones of Stasis and Hyperaemia bordering the central injury. This oedema can restrict perfusion to otherwise healthy tissue and cause progressive cell necrosis. This extension or progression of the burn has serious implications for surgeons responsible for creating grafts and there is an increasing emphasis on limiting the loss of viable tissue due to inflammation in the first 24 hours after a burn injury (Wood, 2012). Burn wound progression will persist in tissues not immediately destroyed in the burn event unless halted through treatment.

Chemical burns Although only 3–10% of burn injuries are caused by chemicals, they account for approximately 30% of burn fatalities (Hardwicke et al., 2012). Historically, chemical burns were associated with industrial accidents but they are increasingly occurring in domestic settings (Hardwicke et al., 2012). Chemical burns can also occur as a result of chemicals being used as weapons. This is more frequent in domestic rather than terrorist or military settings.

Alkali burns Caustic agents such as sodium hydroxide and potassium hydroxide are common causes of alkali burns. Lime (cement) and ammonia also contain dangerous amounts of alkalis. Alkaline chemicals combine easily with water to dissolve protein and collagen and react with the fats in tissue in a process called saponification. This is the same process that turns animal fats into soap. The compounds formed when alkalis react with skin allow the passage of damaging hydroxyl ions deep into the tissues and limit their contact with water used to flush the wound. Nonetheless, irrigation with large amounts of water remains the primary form of treatment. The eventual damage is proportional to the length of chemical exposure: when contact time exceeds 1 hour, the pH level of tissue damaged by a sodium hydroxide burn cannot be reversed.

Acid burns Unlike alkali burns that are typically moist and produce large amounts of localised oedema, acid burns tend to be ‘dry’. Acids denature the proteins of the skin and create a mass of damaged tissue known as coagulum or eschar, the colour of which will depend on the acid involved—nitric acid burns create a yellow eschar, sulfuric acid eschar is black or brown and hydrochloric acid or phenol eschar ranges from white to greyish-brown. The dehydrating effect of the chemical reaction results in the characteristic dry surface of acid burns. Liberal irrigation with water remains the primary form of treatment and, like alkali burns, prolonged exposure leads to more significant tissue damage.

Elemental metals Elemental metals (sodium, potassium) are harmless until mixed with water, when the resulting exothermic reaction releases not only large amounts of heat but also hydrogen gas and hydroxide ions. The liberated heat can be sufficient to ignite the hydrogen gas and cause additional thermal burns. These are complex and dangerous situations that require the use of specific fire extinguishers (class D) or sand to suppress the flames. Consult with the local fire brigade about handling these chemicals and a specialist burns unit about ongoing patient management.

Systemic effects Chemicals involved in burns can enter the bloodstream and cause systemic effects. In most cases these can be managed symptomatically until the patient arrives at hospital. A frequent cause of systemic symptoms is prolonged exposure to petrol. Patients trapped in motor vehicle accidents will suffer cutaneous chemical burn injuries if they are in contact with petrol for a prolonged period, but may also display neurological, pulmonary, cardiovascular, gastrointestinal and hepatic symptoms.

‘Cold burns’ Cell damage caused by exposure to very cold gases and liquids is relatively uncommon (Camp et al., 2003). The exact mechanism by which ‘cold burns’ damage cells is not certain but the protein denaturation associated with thermal burns does not occur and there is a reduced risk of burn progression. Liquid nitrogen and dry ice are common causes, but the cooling effect of rapidly escaping gases from LP gas leaks and even deodorant bottles can cause these burns. One study found that a personal aerosol bottle sprayed from 1 cm for 20 seconds could reduce a thermometer to –15°C (Camp et al., 2003).

CA SE ST U DY 1 Case 10254, 1330 hrs. Dispatch details: A 35-year-old male has thrown petrol onto a barbecue at his home in an attempt to light it. The petrol vapour has ignited and caused burns to his outstretched hand, arm, upper chest, back and neck. Initial presentation: On arrival the paramedics find the patient standing on the lawn beside a barbecue area at the rear of the house. Family members have removed the remains of his burnt singlet and are cooling his burns with water from a garden hose. The skin on the burned areas is reddened and there are several sections where the skin is hanging off and appears blackened. The patient is shivering and yelling in pain.

ASSESS Safety Before assessment can commence the paramedics must ensure that the scene is safe. This may involve moving the patient to a safe location and ensuring that any smouldering clothing has been extinguished. Burned clothing, jewellery and other encumbrances must be removed quickly if they are not adhered to tissue as they can retain heat, complicate assessment and interfere with later hospital management.

HIST ORY Ask! • Has the fire been extinguished? • Is the patient still at the source of the burn? • What type of fuel was used? (mechanism of injury) • When did the burn occur? • Did the burn occur in an enclosed environment? • How old is the patient? • Has cooling been provided? If so, when did it begin?

Patient history History taking is fundamental to establish the rationale for management decisions in burn injury. A comprehensive and accurate case history also provides valuable information to minimise hazards to paramedics. The fuel source, heat, fumes, body fluids and large amounts of water used to cool burns are all potential dangers. Paramedics should attempt to determine the type of fuel, whether the fire has been extinguished and if the burn occurred in an enclosed space before arriving. This will reduce the potential for unanticipated dangers. Remember, burn injuries cause considerable anxiety and emotional distress for all involved: it’s easy to get drawn into a dangerous situation by distraught relatives or friends. Establishing the time of the burn injury is of particular importance given the potential for burn ‘progression’ and the onset of airway and cardiovascular complications. For people suffering burns in remote areas such as mines, forests and farms there can be long delays before definitive treatment is available. Establishing the time of injury will also determine whether cooling remains a feasible option, particularly in remote settings or where access to medical care or first aid is delayed. Determining the mechanism of injury will aid in the identification of hazards (e.g. in chemical burns), the prioritisation of treatment options (e.g. cardiac management in electrical injury) and the likely pattern of injury and possible complications (e.g. fluid resuscitation for significant thermal burns). The mechanism of injury will also have implications for hospital management. Further information on the patient’s age and medical history will help identify those at an increased risk of a poor outcome. The patient’s age guides both how the case will be managed (e.g. paediatric pain relief guidelines are often different from adult guidelines) and the likely outcome (increasing age is strongly associated with increased morbidity and mortality). By establishing these facts at the outset, a patient injury profile can be created, facilitating the treatment pathway most likely to provide maximum clinical benefit. Vapour combustion from ignited accelerants is a common source of burn injury, particularly in males, and is often associated with social occasions and

excessive alcohol consumption. Such combustion events produce a radiant heat plume, flame source and heated gas component. Ignition is typically very fast and can cause an instinctive inhalation reflex in the patient (Rainey et al., 2007).

A I R WAY Look for! • Burnt facial hair • Burnt nasal hair • Burnt tongue, lips and mucosa • Change in patient’s voice • Stridor

Airway The inflammatory combination of vasodilation and increased capillary permeability can potentially cause the tissues lining the upper airway to swell and obstruct the airway. This can occur if the burns are severe enough to cause a systemic inflammatory response, but will happen much more quickly if the tissues of the airway have been burnt by the ignited petrol vapour. A visual inspection of the patient’s oral and nasal cavities for burnt hairs, redness, swelling or sooty sputum (carbonaceous sputum) will help determine whether an immediate threat is present and provide clues to the extent of airway involvement (more on airway burns in case studies 2 and 4). The patient should be examined for burnt facial hair (eyebrows and lashes). Airway swelling often manifests first at the larynx, as it is the narrowest point of the airway. (Note, in a young child the narrowest point is the cricoid cartilage.) Irritation of the airway and vocal cords from heat, chemical irritants and/or inflammatory response changes can alter speech, so ask the patient’s family if their voice sounds normal: hoarseness and/or stridor is a poor sign. Similarly, ask the patient if their tongue feels swollen, they are having difficulty swallowing or experience pain or discomfort when coughing or talking. In this case the patient’s facial hairs are intact, his voice has not changed and he is breathing normally. There are no signs of early airway involvement.

Breathing Only small quantities of toxic irritants or super-heated gases are required to injure the delicate tissues of the small airways. At the least this is likely to cause bronchospasm and subsequent wheezing, a common finding for paramedics during the assessment of a patient with burns (see Ch 17). Inhalation of smoke, especially from burning furniture and carpets, can also lead to systemic complications such as carbon monoxide poisoning, cyanide poisoning or other toxic contamination of the bloodstream, organs and tissues (Reade et al., 2012).

A history of exposure to noxious gases in an enclosed environment should raise serious concerns. Remain vigilant for signs of respiratory compromise such as wheezing, coughing (Haberal et al., 2010), difficulty speaking or swallowing, copious sputum production or an increased work of breathing. Alterations to conscious state, seizures and severe headache also indicate potential carbon monoxide or cyanide poisoning.

B RE AT HI NG Look for! • Coughing • Wheezes • Respiratory distress Patients with pre-existing respiratory disease such as COPD are at higher risk of symptoms.

In this case the patient has a respiratory rate of 20 BPM, with good tidal volume and no obvious increased work of breathing or signs of respiratory distress.

Circulation The hypovolaemia that eventually results from burns shock takes some time to evolve and is generally preceded by tachycardia. In this case, the patient may be presenting with tachycardia as a response to fear, pain and stress. However, persistent tachycardia (despite treatment) is an ominous sign of cardiovascular compromise and a sensitive indicator of impending hypovolaemia in shock. Hypotension in the burns patient is a perilous indication requiring urgent correction (Haberal et al., 2010). Assessing vital signs in burns patients can be problematic: measuring blood pressure, applying cardiac electrodes or auscultating over burnt, painful tissue may not be feasible. You may need to use alternative sites (e.g. apply a blood pressure cuff to the thigh, palpate for popliteal pulses and place ECG dots in different locations), delay some assessments until after analgesia is administered or avoid them completely. You may have to examine general skin colour and capillary refill to indicate perfusion status. Despite these potential difficulties, all vital signs should be obtained if possible.

Burn area and depth Recall that large areas of erythema may be present immediately or soon after the injury. These superficial reddened and hot areas with brisk capillary refill, although painful, have relatively minor injury that will heal spontaneously. Erythema will gradually subside as the burn cools (or is cooled), the inflammatory response mediates and the skin heals. It may, however, complicate TBSA calculations. Assessment using the Rule of Nines gives an

estimated burned TBSA of 2 hours) from hospital. Infection risk and antibiotic therapy Prophylactic administration of antibiotics is not routine in either the hospital or the prehospital environment. If the burn has been cooled by water from a tank, bore, dam or other untreated source, providing a sample of the cooling water to the receiving hospital can assist in planning early, targeted antibiotic treatment. If dirty water has been used to cool the burn, irrigating with clean water or sterile solutions (e.g. normal saline) at the earliest opportunity may reduce the level of contamination. The effectiveness of this approach is yet to be confirmed in studies. Nonetheless, some cleansing of the wound may be achieved without risking complications. This may also flush loose or adhered material from the wound. Pain relief The patient in this case requires early administration of effective doses of analgesics. Initial management with an inhaled opioid analgesic such as intranasal (IN) fentanyl is ideal, providing rapid and effective pain relief while IV access is obtained. Methoxyflurane may be considered for small, painful burns on limbs, as it is quick-acting and has no cardiovascular side effects. However, even small burns may need subsequent IN or IV opioid analgesics due to the short, variable duration and intensity of analgesia obtained with methoxyflurane (Wasiak et al., 2014). Given these limitations, IN/IV opioids are the preferred option. Inhaled analgesics such as methoxyflurane and nitrous oxide are not suitable when lung function or mechanical ventilation has been compromised. Deep ventilation is likely to cause a significant increase in pain where chest wall injury is present. Furthermore, the patient is unlikely to be able to effectively self-administer in this circumstance. Inhaled analgesics should never be used where the patient presents with respiratory distress and signs of inhalation injury, such as wheezing and coughing, stridor or changes to voice. IV pain relief is likely to be required following initial, alternative measures. Expect to titrate doses according to pain level and consult with senior clinicians before you reach the limits of your local guidelines. Pain from burns can be severe and the doses described in some paramedic guidelines may be insufficient to provide adequate pain relief. Ketamine is used in some prehospital jurisdictions, as well as doctor-staffed retrieval services. There is in-hospital evidence of its efficacy for the management of burn pain and prehospital evidence for its use in acute burn pain is emerging (Reid et al., 2011). Ketamine may be administered intranasally, adding to its usefulness in the management of burns.

Perfusion support The combination of fluid loss directly from the wound site and the effects of a systemic inflammatory response can lead to a significant fall in circulating blood volume, especially in severe burns. Thus, large volumes of fluid are administered in burns resuscitation, proportional to the significant fluid losses. Without IV fluid administration, there is likely to be inadequate perfusion to the kidneys, gastrointestinal tract and other organs, leading to ischaemic injury, renal failure and potentially cardiovascular shock. Fluid loading in the first 8 hours reflects the need to stay ahead of the fall in perfusion and to maintain blood supply to the organs. Any isotonic fluid is considered suitable, although several fluid types have been considered including colloids, albumins and crystalloids. At this time, definitive evidence on the best fluid alternative is lacking. Delayed fluid resuscitation is now linked to poor patient outcomes (Warden, 1992; Kramer et al., 2007; Diver, 2008). As a result, most organisations now employ early fluid resuscitation in the field, typically commencing fluid resuscitation and then adjusting using a standardised formula such as the Parkland formula. However, trigger points for the commencement of fluid therapy vary between jurisdictions and no universal consensus exists. Some prescribe fluids for burns >10% TBSA, others restrict it to burns >15–25% and still others restrict therapy to burns where no airway involvement or major burns to the face, neck or chest are present. There are several formulae for fluid resuscitation in major burns, but the Parkland formula is most commonly employed in Australia and New Zealand. It determines the total fluid load as follows: • 2–4 mL × (TBSA burnt %) × body weight (kg), with • 50% to be given in the first 8 hours after injury, and • 50% to be given in the remaining 16 hours. So an 80-kg patient with a 20% burn would receive a total of up to 6400 mL. This is given to major burn victims regardless of blood pressure at the time of assessment. A minimum of one IV line must be established and, if possible, two large-bore lines should be established to meet fluid targets. Early fluid replacement is the highest priority treatment for patients with severe burn injuries and is associated with improved outcomes, but the best volume and type of fluid remain unclear. Requirements may also vary depending on the type of burn, with fluid administration based on TBSA calculations questionable for patients with severe electrical burns. The treatment tendencies of practitioners have also been called into question in relation to over-resuscitation despite following fluid formulae—a problem now referred to as ‘fluid creep’ (Saffle, 2007). Paramedics should be aware that excessive fluid administration in the burns patient might ‘fuel’ the fluid shift and lead to excessive oedema and other complications. Temperature regulation (warming) Tasks and treatments undertaken during management (e.g. removal of clothes, cooling, fluid administration) may exacerbate heat loss already occurring as a result of the burn. This can significantly lower core body temperature. Hypothermia in major burns is associated with significantly increased morbidity

and mortality (Singer et al., 2010). Shivering may also contribute to pain as wounds are moved or abraded against clothing/dressings. It is therefore fundamentally important for paramedics to ensure that patients are kept as warm and dry as possible while maintaining treatment. This includes covering non-affected areas during cooling procedures and using ambulance heaters during transport, irrespective of the ambient temperature. Warming of the patient should commence immediately from the time the crew arrive and should not be delayed while initiating other procedures. Ambulance IV fluids are often stored at less-than-body temperature and, given the high volumes to be administered, patients can easily become hypothermic. Where fluid warmers are fitted in ambulances, paramedics should consider using only normothermic fluids. Ongoing airway vigilance A patient does not need to have suffered airway burns to develop perilous swelling and airway oedema. This can also result from fluid administration or the development of systemic inflammatory complications. Remain vigilant during transport for any developing airway compromise. Controlling a deteriorating airway through endotracheal intubation is much more likely to be successful if attempted before swelling obstructs the airway.

A I R WAY Look for! • Change in voice • Coughing • Wheezes • Stridor

Transport Unless the patient is under immediate life-threat there is evidence that transport directly to a specialist burns unit improves patient outcomes (ACI, 2011). The Australian and New Zealand Burn Association (2011) has adapted and modified a series of indications for referral to a burns unit from the American Burn Association (ABA). These guidelines should be used together with local protocols to determine the best destination for the patient. Aeromedical evacuation should be considered for all major burns.

EVALUAT E Assessment of the burns patient during transport provides the opportunity to

evaluate the outcomes of your management and to ascertain whether new signs and symptoms are developing. Vital signs and secondary examinations conducted en-route are key to determining whether further interventions are required and should be used to contrast the current clinical presentation with the baseline assessment at the scene. Deterioration or changes in patient condition en route may also alter the choice of destination. Is the patient: • Maintaining an adequate airway? • Demonstrating voice changes? • Coughing or wheezing? • Breathing normally? • Suffering more pain than they need to? Expect larger than normal doses of analgesia. Consult early if needing to exceed guidelines. • Shivering? Keep the patient warm at all times.

Specific concerns during transport of burns patients Once loaded into the ambulance, a patient with burns (more than any other patient) needs close observation and adjustments to their treatment. In particular, consider the following: • Airway support. Remain vigilant for signs of airway occlusion. Listen for any changes to the patient’s voice. • Cooling en route. Ongoing cooling of burns while avoiding patient hypothermia is difficult during transport. Place towels on the floor prior to transport to capture the running water and maintain a safe working environment. • Warming en route. Use of the ambulance’s heater to raise the ambient temperature is highly recommended. Monitor the patient’s body temperature for the onset of hypothermia regularly. (Safety tip: don’t allow yourself to become hyperthermic in this environment, especially during hot seasons: keep yourself cool.) Additional warming may be required at any time.

P RACT ICE T IP Hypothermia is such a significant clinical problem in major burn injuries that surgical procedures such as excision and grafting are undertaken in super-heated theatres (>30°C) with surgical staff wearing ice vests for personal protection.

Pain relief Providing adequate pain relief is absolutely essential. Subject to side effects, it may be necessary to provide continuous analgesic increments right up until hospital admission. Consult your clinical supervisor if you need to exceed your local guideline and ensure that all drug administrations are noted and detailed in the hospital handover.

Perfusion support Perfusion support in burns should be prepared for and/or acted on depending on the patient’s clinical presentation or on the basis of TBSA estimations for fluid resuscitation. Systemic complications in large injuries should always be anticipated and all burn injury patients should have IV access and fluids established at the outset. Ongoing perfusion support will be a clinical choice based on protocol or consultation, particularly where secondary trauma has occurred concurrent to the burn injury. This is often the case in patients with electrical burns. All fluid administration during care should be carefully noted and detailed to staff at the hospital handover. Hospital fluid loading will be a continuation of that which has been commenced in the field.

Burns and secondary trauma Paramedics should always consider other injuries accompanying a burn. The presence of traumatic injuries associated with the burns (e.g. fractures, pneumothorax, penetrating injury) is recognised as a risk factor for significantly increased mortality (ANZBA, 2011). The case history, mechanism of injury and the patient’s signs and symptoms provide early clues to possible secondary trauma, common in explosive burn events and electrical burns. Always carry out a thorough head-to-toe examination (secondary survey) to identify other injuries. ALL burn patients are trauma patients.

Hospital admission (burns unit) The choice of patient destination is a critical consideration for paramedics, particularly where large or deep burns are involved (Gabbe et al., 2011). Specific transfer criteria enable prehospital clinicians to triage patients to the most appropriate facility. In Australia and New Zealand, most services use the ANZBA criteria listed in Box 36.3. B O X 3 6 . 3A N Z B A

c r iter ia f o r tr ansf er to a

spec ialist bur ns unit • Burns >10% TBSA or >5% in a child • Full-thickness burns >5% TBSA • Burns of special areas (i.e. face, hands, feet, perineum and major joints) • Electrical or chemical burns • Burns with associated inhalation injury • Circumferential burns of the limbs or chest • Burns at the extremes of age (i.e. children and the elderly) • Burn injury in patients with pre-existing medical disorders that could complicate management, prolong recovery or affect mortality • Any burn patient with associated trauma

On admission to the burns ward/intensive care unit, the following procedures are standard care: • continuous cardiorespiratory, haemodynamic, temperature and oxygen saturation monitoring • carboxyhaemoglobin estimation • intubation and ventilation; a tracheostomy may be performed if long-term ventilation is required • frequent arterial blood gas analysis during the acute stage of illness • central venous and arterial cannulation • nasogastric tube and nasogastric feeding • IV fluid replacement; close monitoring of fluid volumes is essential, as excessive resuscitation is as problematic as inadequate resuscitation • indwelling urinary catheter with hourly urine output measure • regular monitoring of infection markers • ± prophylactic therapy for gastric ulcers. Prophylactic systemic antibiotic therapy is not recommended. Wound cleansing and debridement are often performed initially in the operating theatre. Oedema, increased blood viscosity and the poor perfusion that occur with burns can cause compartment syndrome. This is particularly problematic in circumferential burns and venous stasis and ischaemia distal to the burn may result. Escharotomy and/or fasciotomy may be required. Rehabilitation begins on admission to maximise functional recovery.

Investigations A patient with burns will require a large number of investigations. Some of these will be used to determine the extent of the injury, the evolution of the inflammatory response or the presence of other injuries. A typical suite of tests would include: • chest x-ray • arterial blood gas (ABG) analysis • electrolytes (to guide IV fluid replacement therapy) • full blood count, C-reactive protein, blood cultures and sensitivities (to monitor infection) • blood glucose level • continuous blood pressure monitoring via a peripheral arterial line • continuous cardiorespiratory, SpO2/CO2 and temperature monitoring (to monitor cardiorespiratory stability and ventilation requirements) • renal function monitoring.

Ongoing management Ai rw a y The primary focus in early hospital management is the airway. The aggressive fluid administration required to maintain perfusion can combine with a systemic inflammatory response to cause severe airway swelling in the 4–12 hours after a burn. In the controlled environment of the ED, endotracheal intubation is often performed well before any airway compromise is apparent in anticipation of severe airway. Intubation is also indicated if wounds require surgical debridement, grafting or excision under a general anaesthetic.

Fluid therapies Fluid resuscitation after severe burn, specifically in the first 24 hours after injury, remains a challenging assignment for all burn care providers, regardless of the level of training. Therapy for this systemic insult is aimed at supporting the patient’s vital signs. There are as many guidelines as there are formulae, each providing a foundation for focused resuscitation boundaries. The general principles of fluid resuscitation in the burns patient include the following: • administration of isotonic crystalloid solutions to replace the large volumes of fluid displaced due to tissue oedema, with half the fluid given in the first 8 hours post-burn injury • minimisation of the use of colloids in the first 24 hours in order to minimise the leakage of delivered proteins into the interstitial space • titration of crystalloid solutions according to the patient’s vital signs, respiratory rate, lung sounds, capillary refill and, in some cases, urine output • consideration of the fluid resuscitation formula based on the type of patient (i.e. adult vs paediatric) and the type of injury (e.g. high-voltage electrical injuries).

Pain control Immediate pain experienced at the burn site is due to the stimulation of local nociceptors and the transmission of the impulse via the nerve fibres A and C to the dorsal horn of the spinal cord. The pain experienced will be dependent on predisposition (e.g. genetics, personality type), context (e.g. expectation, culture, past experiences), cognition (e.g. attention) and any coexisting depression or anxiety. The release of local vasoactive mediators from the inflammatory response will continue to sensitise and stimulate pain fibres. The area of injury will be sensitive to mechanical touch and movement (primary hyperalgesia) and there will be increased sensitivity at adjacent undamaged areas of skin (secondary hyperalgesia). Opioids are the cornerstone of burn pain management and the variety of opioid agents provides a range of potencies, methods of administration and durations of action (Richardson & Mustard, 2009). Oral analgesics may be required for procedural or background pain and can include paracetamol and non-steroidal anti-inflammatory drugs. Both these agents are known to be effective against inflammatory pain and work in a synergistic manner with other opioids, producing an analgesic effect comparable to a higher opioid dose.

During the prehospital and emergency phase of care, the preferred route for most medication is intravenous (IV) because of the potential problems with absorption from the muscle and gastrointestinal tract related to decreased perfusion or delayed gastric emptying. Morphine and fentanyl are the drugs most widely used for pain relief.

Wound care Covering the wound decreases pain, fluid and temperature loss while protecting underlying structures that are important for the promotion of wound re-epithelisation. There is little consensus regarding the most appropriate burn dressings: a recent systematic review showed that there are inconsistent findings with most dressing products (Wasiak et al., 2008). Superficial burns do not require any specific topical agents and can be covered with a moist ointment or moist dressing. Superficial partial-thickness burns involve the loss of epithelium and considerable exudate, so a non-adherent dressing should be applied. The early application of biosynthetic dressings (e.g. hydrocolloid or film dressings) is recommended later down the track until epithelialisation is complete. Partial-and fullthickness burns should be covered with silver-based dressings to minimise burn wound colonisation and contamination and should be referred to a burns unit for more advanced therapies such as debridement, excision and grafting. Early and aggressive surgical debridement of deep dermal and full-thickness burns result in substantial reductions in burn mortality and morbidity, infection rates, hospital length of stay and costs, as well as reduced rates of scarring. Deep burns that extend around the circumference of a limb may cause sufficient local swelling to obstruct blood flow past the burn site. This form of compartment syndrome can threaten the survival of the limb and requires surgical intervention. Monitoring pulses and the appearance of limbs distal to a circumferential burn can assist in early identification of the threat, while Doppler flow probes can provide a more accurate picture. Longitudinal incisions through the burn wound (escharotomy) are the recommended treatment, but the process is painful and likely to cause substantial bleeding. Deeper incisions that penetrate the fascia (fasciotomy) may be required if escharotomy fails to restore distal circulation.

Follow-up The patient’s length of stay in hospital will vary according to their age, comorbidities and complications and the severity of their burns. Compression garments are used to prevent hypertrophic scarring and physiotherapy is initiated as soon as possible to manage and prevent contractures. The prolonged pain of dressing changes and scarring means that mental health issues such as depression and post-traumatic stress disorder (PTSD) are not uncommon.

Burns across the lifespan: elderly patients Around 70% of burn injuries to the elderly occur in the home (Redlick et al., 2002). The dermis and epidermis are thinner in the elderly and subject to atrophy, and the elderly have less subcutaneous fat and reduced sensation and blood supply. This makes them much more susceptible to full-thickness burns (Fish & Davidge, 2008). In fact, the elderly are especially vulnerable to burn injuries due to their aged physiology and pre-existing pathologies. They are also at higher risk of incurring burns due to reduced mobility, hearing, smell, mentation, visual acuity and reaction time, and issues of dependence (Mahar et al., 2008). In addition, they are more susceptible to complications as a result of malnutrition and comorbidities. They are more likely to develop infection, cardiovascular compromise, renal failure and organ dysfunction after a burn injury. Burns >40% TBSA may incur an 80% mortality rate or higher in patients more than 70 years of age (Reid et al., 2011), and in patients more than 60 years of age who also have inhalation injury they may incur a mortality rate as high as 100% (Ryan et al., 1998).

CA SE ST U DY 2 Case 13004, 1938 hrs. Dispatch details: An 18-month-old girl has been burnt with hot tea. Initial presentation: The patient is an 18-month-old child who has pulled a mug of boiling hot tea off a table, spilling it down her chest and abdomen. She is distressed and screaming. There is an obvious red mark where the tea has burned her skin.

ASSESS For paediatric patients the differences in body proportions and physiology critically impact on burn severity and the likelihood and severity of complications. 1950 hrs Primary survey: The patient is conscious and responding with a clear airway and normal breathing.

1951 hrs Vital signs survey: Perfusion status: HR 140 BPM, sinus tachycardia, BP not taken, skin warm and pink, capillary refill 96%, but his heart rate and blood pressure are unlikely to improve significantly unless the paramedics administer adrenaline or another inotrope. A failure to improve should trigger the paramedics to reconsider the diagnosis. Is the patient: • Improving after IV crystalloid fluids? 〉 Continue with the highest level of available care • Deteriorating or unchanged after IV fluids? 〉 Continue with the highest level of available care • Now unconscious? 〉 Start the primary survey • Now pulseless? 〉 Check the monitor. Not VT or VF? Commence CPR!

Ongoing management Corti coste roi ds There is a lack of research to support the use of IV corticosteroids in the acute management stage of sepsis. Previously, corticosteroids were indicated early in the management algorithm, but the Surviving Sepsis Guidelines now support only low-dose hydrocortisone therapy in patients with a poor response to fluid therapy and vasopressor therapy (Tintinalli, 2010). Corticosteroids are therefore no longer recommended for administration in the prehospital phase of care and are almost strictly reserved for patients in the intensive care unit. In extreme cases of prolonged transport time or inter-facility transfer, consultation with the receiving hospital for the administration of hydrocortisone may be appropriate, depending on the clinical context.

Mechanical ventilation and airway management Although ventilatory support and airway management are uncommon in the prehospital setting, they may be required, especially in patients with respiratory sepsis and respiratory failure. Assisted ventilation should be provided when oxygen saturation cannot be maintained >90% on high-flow oxygen or when respiratory failure is imminent (Tintinalli, 2010). Non-invasive ventilation (CPAP or BiPAP) may be considered if expertise and equipment are available, but hypotension secondary to positive end-expiratory pressure should be anticipated. If drug-facilitated endotracheal intubation is required, the need for vasopressors/inotropes post-intubation should be anticipated due to a significant decrease in venous return secondary to positive pressure ventilation. The intricacies of managing the non-invasively or invasively ventilated septic patient are beyond the scope of this text.

Transport The unwell patient with sepsis should be placed in the context of their likely outcome. For example, a very frail and elderly patient with septic shock who is living in a high-level aged care facility is unlikely to have a positive outcome; this is probably a terminal event (Finfer et al., 2004). These patients may have a clear anticipatory directive that provides direction in this difficult circumstance. On the other hand, a middle-aged patient with pneumonia and sepsis will have a much greater chance of survival, and consideration should be given to transporting this patient to an appropriate facility. If a higher level of care is within a reasonable transport distance, this should be considered over a closer but smaller regional hospital, thus negating the need for secondary transfer later on. Similar to major trauma patients, patients with sepsis can benefit from being delivered to the appropriate facility in a timely fashion.

Hospital admission Patients who remain unstable after treatment in ED will be admitted to ICU. Sepsis carries a high mortality rate even if treated, and patients are usually committed to a long stay in ICU. Ongoing care involves improving vital organ perfusion, mechanical ventilation, antibiotic therapy to target the offending organism and management of complications such as ALI, ARDS, MODS and DIC.

Sepsis across the lifespan Sepsis varies in cause, pathophysiology and underlying physiological characteristics across the lifespan. The most at-risk patients are the very young and the very old (Tintinalli, 2010). • 0–14 years. The paediatric population, especially the very young, are at high risk of sepsis, primarily due to immature immune function. Infants and neonates have 10 times the risk of sepsis than older children. Boys are more likely to suffer sepsis up to the age of 10. In children younger than 1, sepsis is the fourth-leading cause of death, and in those aged 1–14 it is the second most common cause (Watson & Carcillo, 2005). • 15–35 years. This age group shows a decrease in the incidence of sepsis, probably due to the immune system being at the height of its function. Although this group can be at risk, especially if significant comorbidities are present, the late teens and early 20s have the lowest incidence, at a rate of about 0.2–0.5% of the population (Angus et al., 2001). • 65+ years. Sepsis in the elderly is a major concern for western countries as their populations age. US data shows that nearly 60% of patients admitted to hospital for sepsis are older than 65 years of age. In addition, these patients carry a much higher mortality rate than other age groups, approaching an average of 40% (Destarac & Ely, 2002).

CA SE ST U DY 2 Case 13023, 1520 hrs. Dispatch details: A 64-year-old male with a history of cellulitis, hypertension and morbid obesity has called an ambulance as he is feeling generally unwell. Initial presentation: The crew arrive and are led inside a private house. The patient is sitting on a chair in the lounge room. He is pale and seems to weigh approximately 150 kg.

ASSESS 1528 hrs Primary survey: The patient is conscious and talking, but drowsy. 1529 hrs Chief complaint: Leg infection for last 3 weeks, tired, dizzy, short of breath and diaphoretic.

1530 hrs Vital signs survey: Perfusion status: HR 150 BPM, sinus tachycardia, BP 60/90 mmHg, skin pale and moist, temperature 40.5°C. Respiratory status: RR 28 BPM, good air entry bilaterally, increased work of breathing, speaking in full sentences, dyspnoeic, SpO2 85% on room air. Conscious state: GCS = 13 (eyes open to voice, confused). 1531 hrs Pertinent hx: The patient has high blood pressure and cholesterol. He has had a skin infection on his lower right leg (cellulitis) for 3 weeks. He saw his GP 2 weeks ago and was prescribed antibiotics, but they ran out 1 week ago and he never went back to his GP. 1535 hrs Secondary survey: Obvious cellulitis that looks red and infected to right lower leg. The most likely diagnosis seems to be sepsis from the cellulitis. The crew call for back-up.

CONFIRM In many cases paramedics are presented with a collection of signs and symptoms that do not appear to describe a particular condition. A critical step in determining a treatment plan in this situation is to consider what other conditions could explain the patient’s presentation.

What else could it be? AMI The patient has numerous risk factors for AMI including obesity, hypertension and hyperlipidaemia. He also has hypotension, sinus tachycardia and shortness of breath with a clear chest, all symptoms that are common in AMI. However, the two signs that point away from AMI are significant fever and an identifiable source of infection. Although it is recognised that almost 25% of patients with AMI will not have ST segment changes, the absence of these in combination with the fever and the cellulitis make AMI an unlikely cause for his inadequate perfusion.

DIF F ERENT IA L DIA GNOSIS Sepsis Or • AMI • Pulmonary embolism (PE) • Anaphylaxis

Pulmonary embolism Obesity and sedentary lifestyle are risk factors for pulmonary embolism (PE). Massive PE may lead to right heart failure and significant hypotension, and also respiratory distress and desaturation in the presence of a clear chest. However, this patient does not complain of chest pain, common in PE, and the cellulitis and fever point towards sepsis. Anaphylaxis Anaphylaxis presents in a similar fashion from a haemodynamic point of view, due to the shared pathophysiology of widespread peripheral vasodilation and increased capillary permeability. However, this patient has no history of allergies, nor has he ingested any known allergen. Although many of the symptoms between anaphylaxis and sepsis are shared, clinical problem solving should point away from anaphylaxis and towards sepsis and probably septic shock. This patient fits the definition of SIRS/sepsis as he has tachycardia and tachypnoea, with an obvious infective source or cause. Inadequate organ perfusion (including the brain) is occurring as a result of widespread release of inflammatory mediators and the immune response causing a systemic increase in capillary permeability, peripheral vasodilation and a likely metabolic acidosis.

T REAT If possible serum lactate should be measured to establish a baseline. This patient needs immediate fluid resuscitation. His vital organs have compromised perfusion, intravascular volume is insufficient. There is likely to be metabolic acidosis and he will probably need more fluid than the paramedics can give him. The organism causing the infection is not known and blood cultures should be taken prior to antibiotic administration. Treatment is aimed at the symptoms and not the cause at this stage. This is not meningococcal septicaemia— essentially, that is the only current indication for prehospital antibiotic therapy. 1540 hrs: The paramedics place the patient in the semi-recumbent position and give high-flow oxygen. They then give the patient 2500 mL of normal saline over 20 minutes. 1550 hrs: The patient’s oxygen saturations improve to 94% on 8 L. Within 10 minutes his symptoms start to improve slightly and he says the dizziness and shortness of breath are better. Perfusion status: HR 140 BPM, sinus tachycardia, BP 90/60 mmHg, skin colour improving slightly. Respiratory status: RR 26 BPM, good air entry bilaterally, increased work of breathing, speaking in short sentences, patient states he is still dyspnoeic. Conscious state: GCS = 14; confused. 1600 hrs: The paramedics place the patient onto the stretcher with the assistance of a second crew. It is important not to walk this patient: preload is

crucial to maintaining cardiac filling in a patient who has lost vascular tone and volume.

EVALUAT E Evaluating the effect of any clinical management intervention can provide clues to the accuracy of the initial diagnosis. Some conditions respond rapidly to treatment so patients should be expected to improve if the diagnosis and treatment were appropriate, whereas other conditions are unlikely to respond in the timeframes normally associated with ambulance transport times. In such cases, a failure to improve should not be considered an indication of a misdiagnosis. In this case the patient is very unwell and he is unlikely to improve during the short time he is in ambulance care. His heart rate and blood pressure are unlikely to improve unless the paramedics administer adrenaline or another inotrope.

CA SE ST U DY 3 Case 11412, 0932 hrs. Dispatch details: A 19-year-old female at a campsite is generally feeling unwell. Initial presentation: The crew arrive and are led inside a large tent. The patient is lying on a camp bed, surrounded by multiple friends of the same age. She seems oblivious to her surroundings. Her friends deny that she has ingested any alcohol or drugs and have been encouraging her to drink large volumes of water.

ASSESS 1007 hrs Primary survey: The patient is drowsy and agitated but rousable to pain. 1010 hrs Chief complaint: The patient refuses to talk and open her eyes. She feels hot. Her friends explain that she has had the flu for the last 3 days and won’t stop complaining about a headache. 1015 hrs Vital signs survey: Perfusion status: HR 120 BPM, sinus tachycardia, BP 90/40 mmHg, skin mottled and dry, temperature 39.2°C. Respiratory status: RR 24 BPM, good air entry bilaterally, increased work of breathing, SpO2 95% on room air. Conscious state: GCS = 12; eyes open to voice, confused, localises to pain. BGL: 6.6 mmol/L. 1020 hrs Pertinent hx: The patient has a history of flu-like symptoms for the last 3 days. She takes no medications and is allergic to penicillin. 1024 hrs Secondary survey: Spotty, purple rash to lower legs and arms. The cardinal sign of meningococcal septicaemia is a non-blanching purpuric rash. The paramedics perform the ‘glass test’, which involves rolling a clear glass over the rash to see whether it disappears when compressed: it does not.

CONFIRM In many cases paramedics are presented with a collection of signs and symptoms that do not appear to describe a particular condition. A critical step in determining a treatment plan in this situation is to consider what other conditions could explain the patient’s presentation. This patient has subtle signs of a serious problem. Although it is difficult to pinpoint a specific cause of her symptoms, she is exhibiting some very concerning signs, including photophobia, headache, borderline hypotension, tachycardia at rest, an odd-looking rash, increased respiratory rate and fever.

What else could it be? Flu-like illness Health professionals occasionally dismiss nonspecific symptoms such as these as simply being a viral illness and the secondary survey (i.e. physical examination of the patient in the medical setting) is often neglected: it has become routine in trauma patients, but should not be left out of any comprehensive assessment. This patient’s symptoms are too significant to dismiss without further investigation and comprehensive assessment combined with thorough history taking suggests that this is more than just the flu.

Drug effects Given the social situation of a large gathering of young adults where the intent is probably to have some fun, it would be easy to assume that drugs and/or alcohol may play a part in the patient’s presentation. However, if history taking is thorough, it should be easy to discount this, as in this case. Her friends have explicitly told the paramedics that although the patient normally drinks alcohol, she has not in this instance. Thus, probing further into the history and clinical presentation is essential.

DIF F ERENT IA L DIA GNOSIS Meningococcal septicaemia Or • Flu-like illness • Drug effects • Dehydration • Diabetic ketoacidosis

Dehydration It is very common for dehydration to manifest in signs and symptoms similar to those of meningeal irritation (i.e. headache, photophobia, irritability and fatigue). Hydration can be assessed by investigating signs such as skin turgor, mucosal membrane moisture and urine output. Septic patients will have signs of dehydration. Also, the friends have explicitly said that she has been consuming large volumes of water, so dehydration can be ruled out for this patient.

P RACT ICE T IP If the only available antibiotic is penicillin and the patient has a stated penicillin allergy, the paramedics will have to decide whether to administer penicillin. Factors to be considered include distance from hospital (for an alternative antibiotic), confidence in the diagnosis (and thus the urgency) and the exact history of any previous allergic reactions if known. If the paramedics decide to administer penicillin, they should first prepare to manage a potential anaphylactic reaction.

Diabetic ketoacidosis Polydipsia, or insatiable thirst, is a hallmark of diabetic ketoacidosis and hyperglycaemia. To rule this out as a diagnosis, a simple blood glucose level will

answer the question. All patients with a GCS of 14 or less should have a blood glucose level taken to rule out hypo-or hyperglycaemia as a cause of the presenting symptoms. This patient’s blood glucose is 6.6 mmol/L so hyperglycaemia can be eliminated as a cause. The most likely diagnosis is meningococcal septicaemia and the patient should be treated for this.

T REAT 1031 hrs: The paramedics place the patient in the semi-recumbent position and give high-flow oxygen. They also establish IV access and administer 1 g of ceftriaxone. Given the patient’s history of an allergic reaction to penicillin the paramedics closely monitor for signs of anaphylaxis, but the slight chance of a reaction to the ceftriaxone is outweighed by the need to treat the meningococcal septicaemia. 1040 hrs: The patient’s oxygen saturations improve to 99% on 8 L. Perfusion status: HR 110 BPM, sinus tachycardia, BP 90/60 mmHg, skin colour improving slightly. Respiratory status: RR 20 BPM, good air entry, L = R, increased work of breathing, speaking in short sentences, patient states no shortness of breath. Conscious state: GCS = 14; confused. 1043 hrs: The paramedics administer 20 mL/kg of normal saline for ongoing fluid resuscitation, recognising that early goal-directed therapy improves outcomes, even after antibiotics have been given.

EVALUAT E Evaluating the effect of any clinical management intervention can provide clues to the accuracy of the initial diagnosis. Some conditions respond rapidly to treatment so patients should be expected to improve if the diagnosis and treatment were appropriate, whereas other conditions are unlikely to respond in the timeframes normally associated with ambulance transport times. In such cases, a failure to improve should not be considered an indication of a misdiagnosis. Responses to the treatment of meningococcal with ceftriaxone can be unpredictable, ranging from no response to a slight improvement but also to a sudden deterioration. In severe cases, the action of ceftriaxone to break down the bacterial walls can trigger an immune response that worsens the shock.

Research Sepsis is one of the most researched and significantly funded areas in medicine. Research is primarily focused on determining how and why the immune response occurs in sepsis and ways to modulate this response. Some studies include the use of novel drugs to support blood pressure and promote organ perfusion. Antibiotic resistance is also a significant concern and researchers are looking into novel antimicrobial agents to combat the evergrowing number of medication-resistant viruses, fungi, parasites and bacteria. Prehospital assessment of serum lactate has been proposed recently as an effective tool in measuring the degree of anaerobic metabolism and acidosis and the effectiveness of early goal-directed therapy. In a Dutch study, researchers found that by measuring the serum lactate level of prehospital septic patients and then managing those patients who showed signs of septic shock based on the lactate level, patients spent less time in ICU and had improved long-term outcomes (van Beest et al., 2009). Devices and consumables used to measure serum lactate are affordable and readily available. As such, this cheap, yet effective assay is likely to become a commonly used assessment tool in prehospital care in the near future.

Summary Sepsis is a progressive disorder that begins with bacterial, viral, parasitic or fungal infection. If the infection is not able to be managed by the body or by first-line medical care, it may progress to sepsis, as identified by widespread inflammatory response (i.e. SIRS). If sepsisinduced SIRS progresses, inflammation abounds, vascular integrity is compromised, myocardial function is suppressed, respiratory function may be compromised and progressive clotting and/or endogenous fibrinolysis may lead to multi-organ failure and death. Sepsis is a life-threatening medical emergency and paramedics are often the first healthcare professionals to assess these patients. Patients meeting SIRS criteria in the presence of a suspected or confirmed infection may be readily diagnosed, but some signs and symptoms may be discreet, so thorough assessment and history taking are vital. It is important to manage these patients aggressively and early, even in the case of diagnostic uncertainty. As such, paramedics must be able to recognise sepsis and institute early treatment to minimise morbidity and mortality.

References Amaral, A., Opal, S., Vincent, J. Coagulation in sepsis. Intensive Care Medicine. 2004; 30(6):1032–1040. Ambulance Victoria Medical Advisory CommitteeAmbulance Victoria Clinical Practice Guidelines. Ambulance Victoria, 2011. American College of Chest Physicians/Society of Critical Care Medicine (ACCP/SCCM) Consensus Conference. Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. Critical Care Medicine. 1992; 20:864–874. Anderson, D., Keith, J., Novak, P., Elliot, M. Mosby’s Medical, Nursing, & Allied Health Dictionary, 6th ed. St Louis: Mosby, 2002. Angus, D., et al. Epidemiology of severe sepsis in the United States: analysis of incidence, outcome, and associated costs of care. Critical Care Medicine. 29(7), 2001. Cohen, J., Powderly, W. G. Infectious Diseases, 3rd ed. Philadelphia: Elsevier, 2010. Cunha, B., Bronze, M. Bacterial sepsis. Retrieved 21 January 2012 from http://emedicine.medscape.com/article/234587-overview, 2012. Dellinger, R., Levy, M., Carlet, J., et al. Surviving Sepsis Campaign: international guidelines for the management of severe sepsis and septic shock. Critical Care Medicine. 2008; 36:296– 327. Destarac, L., Ely, E. Sepsis in older patients: an emerging concern in critical care. Advances in Sepsis. 2(1), 2002. Ebby, O. Community-acquired pneumonia: from common pathogens to emerging resistance. Emergency Medicine Practice. 7(12), 2005. Finfer, S., Bellomo, R., Lipman, J., French, C., Dobb, G., Myburgh, J. Adult-population incidence of severe sepsis in Australian and New Zealand intensive care units. Intensive Care Medicine. 2004; 30(4):589–596. Hart, C. A., Cuevas, L. E., Marzouk, O., et al. Management of bacterial meningitis. Journal of Antimicrobial Chemotherapy. 1993; 32(suppl A):49–59.

Heinz, G. Infection, sepsis and cardiac arrhythmia. Wiener klinische Wochenschrift Gesellschaft der Ärzte in Wien. 1999; 111(21):868–875. Kellum, J., Lan, K., Fink, M., et al. Understanding the inflammatory cytokine response in pneumonia and sepsis. Archives of Internal Medicine. 2007; 167(15):1655–1663. Kumar, A., Roberts, D., Wood, K. E., et al. Duration of hypotension prior to initiation of effective antimicrobial therapy is the critical determinant of survival in human septic shock. Critical Care Medicine. 2006; 34:1589–1596. Latto, C. An overview of sepsis. Dimensions of Critical Care Nursing. 2008; 27(5):195–200. Leibovici, L., Shraga, I., Drucker, M., et al. The benefit of appropriate empirical antibiotic treatment in patients with bloodstream infection. Journal of Internal Medicine. 1998; 244:379– 386. Longo, D., Fauci, A. S., Kasper, D. L., Hauser, S. L. 18th ed. Harrison’s Principles of Internal Medicine; Volumes 1 and 2. McGraw-Hill Professional, New York, 2011. Marieb, E., Hoehn, K. Human Anatomy and Physiology, 7th ed. Redwood City, CA: Pearson Benjamin Cummings, 2007. Marin, C., Papazian, L., Perrin, G., et al. Norepinephrine or dopamine for the treatment of hyperdynamic septic shock? Chest. 1993; 103:1826–1831. Mikkelsen, M., Miltiades, A., Gaieski, D., et al. Serum lactate is associated with mortality in severe sepsis independent of organ failure and shock. Critical Care Medicine. 2009; 37:1–8. Peake, S., Bailey, M., Bellomo, R., Cameron, P., Cross, A., Delaney, A., Finfer, S., Higgins, A., Jones, D., Myburgh, J., Syres, G., Webb, S., Williams, P., the ARISE Investigators for the ANZICS-CTG. Australasian Resuscitation of Sepsis Evaluation (ARISE): a multi-centre prospective, inception cohort study. Resuscitation. 2009; 80:811–818. Rangel-Frausto, M., Pittet, D., Costigan, M., Hwang, T., Davis, C., Wenzel, R. The natural history of the systemic inflammatory response syndrome (SIRS): a prospective study. JAMA. 1995; 273:117–123. Schwartz, B., Al-Tobaiqi, A., Al-Ruwais, A., et al. Comparative efficacy of ceftriaxone and rifampicin in eradicating pharyngeal carriage of group A Neisseria meningitidis. Lancet.

1988; 1(8597):1239–1242. Tintinalli, J.Emergency Medicine: A Comprehensive Study Guide. New York: McGrawHill, 2010. van Beest, P., et al. Measurement of lactate in a prehospital setting is related to outcome. European Journal of Emergency Medicine. 2009; 16(6):318–322. Vincent, J. L., Korkut, H. A., Defining sepsis. Clinics in Chest Medicine. 2008;29(4):585–590, doi: 10.1016/j.ccm.2008.06.001. [vii.]. Watson, S., Carcillo, J. Scope and epidemiology of pediatric sepsis. Pediatric and Critical Care Medicine. 6(3), 2005.

CHAP TER 45

Bleeding from the gastrointestinal or urinary tract By Hugh Grantham

C O N C E P TS U S E D I N TH I S C H A P TE R • The paramedic’s clinical approach: Section 2 • Perfusion: Chapter 55 • The autonomic response: Chapter 56 • The inflammatory response: Chapter 57

OVERVIEW • Bleeding from the gastrointestinal (GI) tract can be gradual or rapid, chronic or acute. • Bleeding from the urinary tract tends to be gradual. • Rapid bleeding may lead to haemodynamic instability and require resuscitation. • Gradual bleeding can be sign of malignancy and requires investigation and observation. • Haematuria and melaena can be extremely distressing and confronting for patients. • Gastrointestinal haemorrhage has a mortality rate of 7–10% (British Society of Gastroenterology, 2007). • It may be difficult to accurately diagnose the site of bleeding solely from external clinical observation.

Introduction Acute gastrointestinal (GI) bleeding can be a medical emergency if the blood loss is significant. Measuring blood loss from the bowel can be difficult (even a small amount can stain toilet water bright red) so pre-hospital assessment and management should focus on identifying patients with life-threatening haemodynamic compromise and rapidly initiating appropriate resuscitation. The reported mortality rate of patients admitted to hospital with acute GI bleeding is 7–10% (British Society of Gastroenterology, 2007), with most deaths occurring in elderly patients with significant comorbidities. Gastrointestinal haemorrhage is bleeding into the GI tract from any site between the oesophagus and the anus. Upper GI haemorrhages originate in the oesophagus, stomach or duodenum, while lower GI bleeding originates from the small bowel or colon. GI haemorrhage may be chronic or acute, with acute haemorrhages ranging from minor to life-threatening catastrophic bleeds. Approximately 75% of emergency department (ED) patients diagnosed with GI bleeding have an upper GI tract origin, 20% have a lower GI tract origin and the remaining 5% have bleeding in both the upper and the lower GI tracts (SIGN, 2008). Acute upper GI tract bleeding generally has a worse prognosis than lower GI tract bleeding, and the prognosis is significantly worse for older, comorbid patients. The mortality rate is doubled for patients presenting with haematemesis (vomiting of brightred blood) and patients initially presenting in shock are nearly four times more likely to die (Rockall et al., 1995). The major causes of upper GI haemorrhage include the following: • Peptic (stomach) ulcer disease is the most common cause of upper GI bleeding, accounting for approximately half of all acute cases (British Society of Gastroenterology, 2007). • Oesophageal ulcers, erosions or malignancies are a common cause of mild upper GI bleeding, but they rarely cause clinically significant acute haemorrhage. • A Mallory-Weiss tear at the gastro-oesophageal junction (usually as a result of severe vomiting or coughing) may cause significant bleeding (Cappell & Friedel, 2008). • A rupture of oesophageal varices (dilated veins) is likely to result in catastrophic haemorrhage. Oesophageal varices are generally associated with portal hypertension and cirrhosis. The mortality rate of patients presenting with variceal haemorrhage is 14% (British Society of Gastroenterology, 2007). • Gastric malignancies may also bleed, but this is generally chronic or minor bleeding (Cappell & Friedel, 2008). • Duodenal ulcers can produce GI haemorrhage in the same way as gastric ulcers. For approximately 20% of patients presenting with upper GI bleeding no cause is identified (Cappell & Friedel, 2008). Acute lower GI tract bleeding occurs most often in the elderly (Farrell & Freidman, 2005). As with upper GI bleeding, the presence of comorbidities or shock increases the mortality rate. Patients taking aspirin or non-steroidal anti-inflammatory drugs (NSAIDs) are at increased risk of severe, acute lower GI haemorrhage (Velayos et al., 2004). The causes of acute lower GI bleeding vary with age, the most common being: • diverticular disease—this is the most frequent cause of rectal bleeding in patients aged over 50 years (23–48% of acute lower GI haemorrhages; Longstreth, 1997). • colorectal neoplasms

• ischaemic colitis • colorectal polyps • inflammatory bowel disease (IBD)/ulcerative colitis such as Crohn’s disease • congenital vascular malformations (angiodysplasia) • damage to the intestinal epithelium from radiation treatment (radiation enteropathy) • ruptured haemorrhoids and anal fissures—these are the most common causes of rectal bleeding in patients younger than 50 (Cameron et al., 2009). Loss of blood into the urinary tract can originate at any site between the kidneys and the urethra but unlike bleeding into the GI tract the volume of blood involved is rarely sufficient to present as an acute emergency. For patients unused to the sight of blood in their urine, however, a toilet bowl stained bright red can be extremely confronting and upsetting.

Pathophysiology Uppe r GI bl e e ds Bleeding from the oesophagus usually results in clinically subacute bleeding and most of the blood is swallowed. In small amounts this blood passes into the lower GI tract and through the bowel with food, resulting in dark stools. But in larger volumes the blood acts as an emetic and can trigger vomiting. Blood that has been mixed with gastric acid becomes clumped and dark and once vomited appears as ‘coffee grounds’. If the bleeding is prolonged and undetected the patient can become anaemic; shortness of breath and lethargy may be the first noticeable symptoms. The most catastrophic upper GI bleed occurs when an oesophageal varix ruptures. Oesophageal varices are dilated superficial veins located in the lower third of the oesophagus. These veins drain into the portal system via the left gastric vein. If they develop an obstruction of portal blood flow (often associated with liver cirrhosis), blood ‘backs up’ in the oesophageal veins. Normally, the pressure in the portal vein is approximately 4 mmHg, allowing adequate return of venous blood to the heart. If damage or scarring in the liver increases this pressure to greater than 10 mmHg, venous return is slowed and oesophageal varices often form (Grow & Chapman, 2001). Rupture of an oesophageal varix may cause a dramatic haemorrhage with a large amount of blood rapidly entering the stomach. The patient will often vomit before the action of gastric acid has had a chance to change the appearance of the blood (haematemesis). Blood that is not vomited progresses through the bowel and exits as dark, sticky altered blood or faeces (melaena). Sometimes the rate of bleeding is so rapid that blood from the upper GI tract (oesophageal varices or ulcers) can appear relatively unchanged at the lower end of the GI tract and bright-red blood may be passed through the rectum (haematochezia). It is estimated that up to 15% of rectal bleeding originates in the upper GI tract (Oakland & Dawson, 2010). The complications of bleeding oesophageal varices include: • massive hypovolaemia and hypovolaemic shock • possible aspiration and aspiration pneumonia associated with a decreased conscious level and vomiting • exacerbation of hepatic encephalopathy. The mortality from bleeding oesophageal varices is 50% and if bleeding is stopped, 50% will bleed again within a week (Grow & Chapman, 2001). Oesophageal varices are the most common cause of death associated with GI bleeding (Klebl et al., 2005). Out-of-hospital management of a ruptured oesophageal varix is limited to management of the associated haemodynamic instability or shock and concurrent management of any airway compromise. Definitive treatment requires urgent surgical or endoscopic intervention. In-hospital emergency treatment pivots on immediate control of bleeding with sclerosis (Palmer, 2007), banding of the oesophageal varices via endoscopy or, for refractory haemorrhage, direct pressure using an inflatable oesophageal balloon (Klebl et al., 2005). Pressor drugs, generally terlipressin, somatostatin and octreotide, are used to induce splanchnic vasoconstriction. Longer-term measures to reduce portal pressure include portocaval shunts and drugs to lower portal vein pressure, beta-blockers or nitrates and, in some cases, liver transplant. Mallory-Weiss tears in the mucosa at the gastro-oesophageal junction may produce

bleeding, usually evident as frank red blood in the vomit. Causes include violent or sustained vomiting, retching, coughing or hiccupping. Mallory-Weiss tears were thought not to cause substantial bleeding, but significant bleeding can occur. Most patients diagnosed with significant bleeding from a Mallory-Weiss tear will have other mucosal abnormalities associated with portal hypertension or liver disease. In one study patients presenting to ED with Mallory-Weiss–associated bleeding had a 20% incidence of shock; a similar case series reported a mortality rate of 10% (Akhtar & Padda, 2011; Yu, White & Iannuccilli, 1982). GI ulcers are found most commonly in the stomach or duodenum. When these ulcers erode, the result is a low-volume chronic blood loss. The patient generally presents with anaemia and dark stools that test positive for occult blood. GI ulcers that damage larger blood vessels may produce significant haematemesis (see Table 45.1). Of the ulcers that erode into larger blood vessels, 30% produce haematemesis or ‘coffee-ground’ vomit (Capell & Friedel, 2008). Elderly patients, patients taking aspirin or NSAIDs and patients with comorbidities are at increased risk of developing gastric ulcers. Infection with Helicobacter pylori is associated with an increased risk of bleeding from gastric ulcers (Hopper & Sanders, 2011), as is taking antiplatelet medications (Henriksen, Palmer & Boon, 2008).

TABLE 45.1 Common causes of haematemesis and melaena

Lower GI bleeds Bleeding from the lower GI tract will resolve spontaneously without treatment in 80–85% of patients (Farrell & Freedman, 2001); however, 10% of patients presenting with gross rectal bleeding (haematochezia) will require active fluid resuscitation and/or immediate surgical intervention (Pfeifer, 2011). The most frequent source of bleeding in patients presenting to hospital with severe haematochezia is diverticulitis (40% of presentations); however, bleeding from a colorectal malignancy should always be considered, especially in patients with a history of weight loss and pain. Colorectal malignancies account for approximately 10% of cases of acute rectal bleeding (Longstreth, 1997).

CLINICA L COMMENT • Chronic low-grade blood loss into the intestinal tract causes anaemia and should always be investigated urgently (within days). • Acute high-volume GI blood loss often leads to haemodynamic instability requiring active resuscitation.

Bleeding directly from the anus can be associated with haemorrhoids, an anal fissure or, rarely, an anal malignancy (Longstreth, 1997). In this situation, a small amount of brightred blood is seen on the toilet paper and sustained significant haemorrhage does not usually occur. However, the patient will be concerned and should have the problem formally investigated. The patient can be reassured that the majority of anal bleeding is benign and easily treated. The possibility of local trauma due to the insertion of a foreign body or anal sex should be considered.

Urinary tract bleeds Bleeding from the urinary tract can present as blood-stained urine (haematuria) or, less frequently, frank blood clots in the urine. The more common causes include urinary tract, prostate or kidney infection; kidney, bladder or prostate cancer; kidney or bladder stones; post-prostate surgery; and trauma. A cause cannot be determined for more than 60% of patients presenting with haematuria (Khadra et al., 2000). Urinary tract bleeding is rarely life-threatening, generally causing chronic bleeding and anaemia. However, in patients with an impaired clotting ability (medication-induced or pathological) haematuria may present as an acute medical emergency. Bleeding into the bladder may lead to the formation of clots that can obstruct urinary outflow through the urethra or through a urinary catheter. The resultant urinary obstruction causes pain and distress, autonomic nervous system stimulation and pressure on the kidneys. Unless the paramedic is trained and equipped to perform catheterisation, the management of this is outside the realm of paramedic practice.

CA SE ST U DY 1 Case 10466, 0735 hrs. Dispatch details: A 70-year-old male with diarrhoea and vomiting. Initial presentation: When the paramedics arrive, they find a pale, diaphoretic male sitting on the toilet and holding a bucket. He is conscious and alert and seems to be breathing normally.

ASSESS Patient history The patient’s wife states that he has been complaining of abdominal pain for the past week and that the vomiting and diarrhoea started abruptly at about 3 am. She adds that both the vomit and diarrhoea are ‘dark and smelly’. The patient has a past history of hyperlipidaemia and hypertension. His medications include aspirin. He also drinks two standard drinks per day and gave up smoking 10 years ago.

Airway The patient is currently managing his own airway. However, if his conscious level decreases, his repeated episodes of vomiting put him at high risk of a compromised airway.

HIST ORY Ask! Ask specifically about: • previous history (many people with gastric ulcer disease re-bleed) • use of NSAIDs, aspirin or steroids • a comprehensive history leading up to the event • progress of symptoms (increasing shortness of breath, dizziness and tachycardia) • alcohol use and previous illnesses—anything suggesting cirrhosis?

Breathing Hypovolaemia causing poor tissue oxygenation and lactic acid production has caused increased stimulation of this patient’s respiratory centre. Both of these factors (hypoxaemia and acidosis) increase his sensitivity to CO2, increasing his respiratory drive. A raised respiratory rate is an indicator of prolonged poor perfusion.

Cardiovascular The patient’s cardiovascular observations confirm that he is currently hypotensive despite a sympathetic response, generating a tachycardia and pale, sweaty skin. His cardiovascular observations are consistent with either an acute, rapid loss of blood volume or a longer episode of gradual bleeding

resulting in a prolonged period of poor perfusion. A raised respiratory rate would indicate that he has been poorly perfused for a longer period of time because he is now showing compensatory signs to metabolic acidosis. It is also a possibility that without appropriate intervention, he will progress to a generalised inflammatory response and irreversible shock due to the prolonged period of poor perfusion and poor tissue oxygenation.

Abdomen Examining the abdomen can be of limited diagnostic use as it is likely that the gastric ulcer will produce some tenderness. The presence of a large amount of blood within the bowel may also produce tenderness and if the ulcer has eroded through the gastric wall, allowing gastric acid into the peritoneal space, peritonitis may have developed.

Vomiting and diarrhoea The patient is holding a bucket that contains about 800 mL of a brown, ‘grainy’ liquid with some fresh blood, which his wife says he has vomited over the last couple of hours. The toilet contains a very dark and odorous liquid. The coffeeground blood in the vomitus with fresh blood streaks in it indicates that although a lot of the blood has been altered by gastric acid, the rate of bleeding is brisk enough that some is being vomited up unchanged. He is also passing melaena, which the patient has described as diarrhoea. It is clear that he has a haemorrhage from the GI tract and that it is significant enough to cause hypovolaemia. He is not passing frank blood per rectum (haematochezia), so the rate of bleeding has not been catastrophic. This positive sign should be interpreted cautiously, as there may be a delay between significant bleeding onset and haematochezia.

P E RF U SI ON ST AT U S Look for! • Raised respiratory rate and depth • Tachycardia • Skin colour (capillary refill time) • Hypotension: late sign • Altered conscious state

Initial assessment summary

Problem Diarrhoea and vomiting Conscious GCS = 15 state Position Sitting Heart rate 110 BPM Blood 90/70 mmHg pressure Skin Pale, cool, diaphoresis appearance Speech Normal pattern Respiratory 22 BPM rate Respiratory Even cycles rhythm Chest Good breath sounds bilaterally auscultation Pulse 95% oximetry Temperature 37.1 °C Motor/sensory Normal function Pain 4/10 upper left quadrant abdominal pain History The patient’s wife states that he has been complaining of abdominal pain for the past week and that the vomiting and diarrhoea started abruptly at about 3 am. D: There is no immediate danger. A: The patient is conscious with no current airway obstruction but this needs frequent reassessment. B: Respiratory function is currently normal but this needs frequent reassessment. The respiratory rate is elevated but ventilation is normal. C: Heart rate is elevated and the blood pressure is poor. The patient is displaying the cardiovascular symptoms of acute hypovolaemia. The history of this incident is consistent with a gastric or duodenal ulcer causing ongoing abdominal pain and eventually eroding a blood vessel, precipitating an acute haemorrhage. This could be exacerbated by use of aspirin. This patient also has tachycardia, hypotension and a raised respiratory rate associated with the metabolic acidosis of poor perfusion. These signs indicate that he has lost a significant amount of blood, potentially up to 1500 mL (see Table 45.2, overleaf ).

TABLE 45.2 Estimated blood loss1 based on patient’s initial presentation

1For a 70-kg man. Source: American College of Surgeons (2012).

CONFIRM The essential part of the clinical reasoning process is to seek to confirm your initial hypothesis by finding clinical signs that should occur with your provisional diagnosis. You should also seek to challenge your diagnosis by exploring findings that do not fit your hypothesis: don’t just ignore them because they don’t fit.

DIF F ERENT IA L DIA GNOSIS Gastric ulcer with significant bleed Or • Mallory-Weiss syndrome • Oesophageal variceal rupture • Bleeding from a duodenal ulcer • Bleed from the lower GI tract

What else could it be? Mallory-Weiss syndrome Not all Mallory-Weiss bleeding is associated with a clear history of vomiting. This is not as unlikely as traditionally thought but does not alter the immediate management. Oesophageal variceal rupture This patient has no history of cirrhosis or liver disease so is not likely to have portal hypertension. The extent of his haemorrhage could be consistent with bleeding from an oesophageal varix. Bleeding from oesophageal varices can be catastrophic, which is one of the reasons they are associated with the highest mortality of any GI haemorrhage (SIGN, 2008). Other reasons behind the high mortality rate include the high rate of re-bleed, the underlying hepatic pathology and the associated problems of encephalopathy and aspiration. This patient may still have bleeding oesophageal varices despite the lack of history and any clinically obvious signs of cirrhosis. In the pre-hospital setting, management of bleeding from oesophageal varices is the same as for bleeding from a gastric ulcer. The immediate concern is fluid resuscitation and protection of his airway, which is at risk if his conscious level falls. Bleeding from a duodenal ulcer Bleeding from a duodenal ulcer could cause significant haemorrhage as the ulcer erodes the gastroduodenal artery but is less likely than a gastric ulcer. Because the duodenal ulcer lies beyond the pylorus, massive reflux of blood into the stomach is not likely in normal circumstances. This degree of hypovolaemia and production of melaena is consistent with a duodenal ulcer that has eroded a blood vessel. Bleeding from the lower GI tract Bleeding from the lower GI tract is generally not associated with coffee-ground vomit or haematemesis and if brisk enough to cause hypovolaemia should present with recognisable blood per rectum. Clinically it seems unlikely that this is bleeding from the lower GI tract.

T REAT Emergency management This patient is showing signs of hypovolaemia and his respiratory response indicates a metabolic acidosis due to sustained poor perfusion. His immediate need is for volume replacement. Venous access should be established immediately and cautious fluid resuscitation commenced. Crystalloid fluids should be administered at a rate sufficient to maintain a palpable peripheral pulse, which will generally correspond to a systolic blood pressure of approximately 80 mmHg. Attempting to reach a ‘normal’ blood pressure with IV fluids risks increasing the rate of haemorrhage.

At the moment the patient presents no challenges in terms of maintaining his airway but as his bleeding is ongoing, it would be wise to be prepared for a decrease in his conscious level necessitating ventilatory and airway support. Should he become unconscious, endotracheal intubation is the best way to prevent aspiration of blood or vomit. As this patient has a pain score of 4/10, appropriate pain relief should also be administered, in line with local protocols. Not least of the patient’s immediate needs is urgent transfer to a place of definitive care for active fluid resuscitation. A clear and timely prior notification will assist in ensuring an efficient reception.

EVALUAT E The paramedics’ pre-hospital goals were to support this patient’s circulating volume to maintain a base level of perfusion and safely transfer him to definitive care. Monitoring trends in his respiratory rate, skin colour, cardiovascular observations and conscious state will give some indication of either further bleeding or response to volume replacement if needed. A sustained improvement following IV fluid administration would indicate either minimal or no further bleeding, while a transient improvement may indicate continued bleeding. No improvement would indicate either catastrophic haemorrhage or some other cause of poor perfusion. Obvious external haemorrhage, either haematemesis or haematochezia, may not reflect current bleeding and is therefore of dubious value in ongoing patient monitoring.

Ongoing management These patients require ongoing fluid resuscitation, potentially including a massive transfusion of fresh frozen plasma, platelets and whole blood (British Society of Gastroenterology, 2007). Gastroscopic assessment will reveal the site of bleeding, allowing further management to be planned. Approximately 80% of upper GI bleeds resolve spontaneously; the other 20% that re-bleed require endoscopic haemostasis or surgery (Fulde, 2006). Drugs to reduce gastric acid production (proton pump inhibitors and H 2receptor antihistamines) are used for non-variceal bleeding.

GI/urinary tract haemorrhage in the field Minor presentations of GI and urinary tract haemorrhage do not require emergency treatment. There is a risk that the paramedic’s reassurance that the situation is not critical may be interpreted as confirmation that any subsequent investigation is unnecessary. Significant painless haematuria is the classical clinical sign of bladder cancer and an early investigation may make the difference between cure and palliation. It should be a reminder of the importance of carefully choosing words when reassuring patients. GI haemorrhage can be a trap for the unwary in that the initial presentation may not appear to be significant blood loss but it may progress to continued and/or accelerated haemorrhage causing significant hypovolaemia. Transport to hospital for evaluation and further investigation is prudent for all patients presenting with GI haemorrhage. Cases of urinary tract haemorrhage still require investigation and unless a guaranteed efficient alternative investigation plan can be devised, a similar approach is wise.

CA SE ST U DY 2 Case 11054, 1142 hrs. Dispatch details: A 62-year-old female with PR (per rectum) bleeding. Initial presentation: The paramedics find the patient sitting in her lounge room in her dressing gown, looking anxious. Her husband and daughter are present and are also concerned.

ASSESS 1205 hrs Primary survey: The patient is conscious and alert. 1206 hrs Chief complaint: The patient is complaining of passing a large amount of blood and blood clots when she used her bowels about an hour ago. 1209 hrs Vital signs survey: Perfusion status: HR 82 BPM, strong and regular; BP 130/85 mmHg; skin pink and dry; temperature 37.0°C; capillary refill 2 seconds. Respiratory status: RR 14 BPM; good, clear air entry bilaterally; SpO2 99% on room air. Conscious state: GCS = 15.

1212 hrs Pertinent hx: The patient explains that when she went to the toilet about an hour ago, she noticed a large amount of blood and blood clots in the toilet bowl. This has not happened before and she has no pain or discomfort in her abdomen. She called for an ambulance as the amount of blood made her quite anxious. She is postmenopausal and hasn’t menstruated for 11 years. She had an appendicectomy as a child. She takes fish oil daily and NSAIDs occasionally for headaches. The patient’s presentation is consistent with lower GI bleeding.

CONFIRM In many cases paramedics are presented with a collection of signs and symptoms that do not appear to describe a particular condition. A critical step in determining a treatment plan in this situation is to consider what other conditions could explain the patient’s presentation.

DIF F ERENT IA L DIA GNOSIS Lower GI bleeding due to: • haemorrhoids • anal fissure • colorectal neoplasm/polyp • diverticular disease • inflammatory bowel disease/ulcerative colitis • congenital vascular malformations (angiodysplasia) Or • Bleeding from the genital tract

What else could it be? Haemorrhoids A haemorrhoid is a dilated vein that may be forced through the anus with straining, causing pain and bleeding. Haemorrhoids are commonly associated with constipation and may also be associated with raised portal venous pressure—the haemorrhoids are formed between the portal and systemic systems in a similar fashion to oesophageal varices. Bleeding associated with haemorrhoids is generally minimal and short-lived and is usually seen as blood on the toilet paper or a few drops in the toilet bowl. Haemorrhoids are the most common cause of rectal bleeding in patients younger than age 50 (Cameron et al., 2009). The volume of blood passed makes this diagnosis seem unlikely. Anal fissure An anal fissure is a split in the mucosa of the anus, usually associated with

constipation or trauma. Anal fissures can bleed a minimal amount after passing stool and present as a smear of blood on the toilet paper. The volume of blood passed makes this diagnosis seem unlikely. Colorectal neoplasm/polyp Bleeding from a polyp or neoplasm in the rectum or colon generally results in the expulsion of blood from the rectum. The blood loss may be significant enough to provide a dramatic appearance, including clots of blood. This could well be the source of bleeding in this case. Diverticular disease Bleeding from diverticulitis is arterial, acute and painless and can be alarming in volume. Diverticula (outpouches of large bowel wall caused by straining against constipation) are the source of bleeding in up to 60% of cases in adults over the age of 50 (Cameron et al., 2009). Patients with diverticulitis often have a history of abdominal pain and changed bowel habits (Yang & Chen, 2005). Inflammatory bowel disease/ulcerative colitis Bleeding from ulcerative colitis generally presents as small amounts of blood mixed with stool. Patients are generally young and have pre-diagnosed and widespread disease. Congenital vascular malformations (angiodysplasia) Angiodysplastic lesions account for up to 12% of cases of rectal bleeding in adults (Cameron et al., 2009). Blood loss is generally chronic; very rarely, a patient may present with an acute haemorrhage. Bleeding from the genital tract In this patient, there is a possibility that the bleeding may originate from the genital tract and in a postmenopausal patient it could be a sign of a neoplasm of either the cervix or the uterus. The presenting history and the patient’s age suggest that the most likely cause of the bleeding is a colorectal polyp or neoplasm.

T REAT The patient is not showing signs of significant hypovolaemia and so at this stage IV fluid infusion is not seen as a priority. However, compensatory mechanisms may sustain vital signs at near-normal levels despite a loss of up to 15% of total blood volume. Also, the patient may progress to more rapid bleeding or a catastrophic re-bleed. She requires careful observation and continual reassessment of her vital signs. If possible, establishing early venous access would be prudent.

EVALUAT E

Evaluating the effect of any clinical management intervention can provide clues to the accuracy of the initial diagnosis. Some conditions respond rapidly to treatment so patients should be expected to improve if the diagnosis and treatment were appropriate, whereas other conditions are unlikely to respond in the timeframes normally associated with ambulance transport times. In such cases, a failure to improve should not be considered an indication of a misdiagnosis. In this case, there should be no change to the patient’s condition during transport.

CA SE ST U DY 3 Case 10983, 2230 hrs. Dispatch details: A 45-year-old male has collapsed. He has been vomiting blood. Initial presentation: The paramedics arrive at a private house and are led to the bathroom by the patient’s wife. The patient is lying on the floor near the toilet.

ASSESS 2243 hrs Chief complaint: There is a large amount of frank blood in the toilet and on the floor and walls around the toilet. The patient has blood on his face and in his mouth. He is lying on his side, breathing quietly. He doesn’t respond to anyone speaking to him and only groans in response to one of the paramedics squeezing his trapezium. 2245 hrs Vital signs survey: Perfusion status: HR 140 BPM, weak; BP 80/50 mmHg; skin pale, diaphoretic, jaundiced; temperature 37.0°C. Respiratory status: RR 18 BPM, clear air entry bilaterally, SpO2 97%. Conscious state: GCS = 7; eye opening to pain, groaning and withdrawing. BGL: 3.9 mmol/L. 2248 hrs Pertinent hx: His wife and one teenage child are present and they

give a history of the patient feeling sick, going to the bathroom and vomiting copiously. Then they heard him collapse. His wife says that he is a chronic alcoholic and has been drinking all evening. He has had alcohol-induced cirrhosis for the past 10 years, as well as type 2 diabetes mellitus, and he is a heavy smoker. 2249 hrs Secondary survey: The paramedics find abdominal ascites and distended abdominal veins. The patient is not responsive and appears to be suffering from profound hypovolaemic shock. Considering his current presentation and medical history, the most likely cause is haemorrhage from ruptured oesophageal varices (see Fig 45.1). The dilated veins around the patient’s umbilicus are a result of portal hypertension causing a backflow of blood from the left portal vein through the paraumbilical veins and into the periumbilical systemic veins in the abdominal wall. These umbilical veins are normally closed in adults, originally functioning to return fetal blood from the placenta in utero (Yang & Chen, 2005).

FIGURE 45.1 Actively bleeding varices. Courtesy of David L. Carr-Locke, MD, Brigham and Women’s Hospital. The patient’s distended abdomen is a late complication of cirrhosis. Cirrhosis causes systemic vasodilation, effectively decreasing arterial blood pressure. Compensatory activation of the renin-angiotensin-aldosterone system and the sympathetic nervous system and the release of antidiuretic hormone lead to renal retention of sodium and water. Fluid leaks through the abnormally permeable splanchnic vasculature into the peritoneal space, resulting in ascites (Kashani et al., 2008). The patient’s decreased conscious level is most likely the result of impaired cerebral perfusion from hypovolaemic shock, but hepatic encephalopathy may also contribute. In hepatic encephalopathy, a cirrhotic liver fails to remove some neurotoxic by-products of digestion, including ammonia and manganese. These neurotoxins cause morphological changes within the brain and have

been shown to cause raised intracranial pressure, coma and death (Donovan, Schafer & Shaw, 1998). The cirrhosis will also impair the functioning of his clotting factors, exacerbating any bleeding.

CONFIRM In many cases paramedics are presented with a collection of signs and symptoms that do not appear to describe a particular condition. A critical step in determining a treatment plan in this situation is to consider what other conditions could explain the patient’s presentation.

DIF F ERENT IA L DIA GNOSIS Ruptured oesophageal varices Or • Rectal bleed • Gastric ulcer • Mallory-Weiss tear

What else could it be? Rectal bleed The paramedics find no evidence of rectal bleeding, indicating that no blood has transited through the gut. The patient has collapsed, indicating that he has lost a significant amount of blood in a short space of time. The blood that he has vomited is bright red and has not been contained within the stomach for long enough to be chemically altered by gastric acid. Gastric ulcer In a patient with cirrhosis and decreased clotting factors bleeding from a gastric ulcer may be more marked than usual. Up to 40% of patients with cirrhosis and GI bleeding have gastric erosions as the source of haemorrhage (Cameron et al., 2009). Mallory-Weiss tear A Mallory-Weiss tear can potentially cause significant haemorrhage, especially in the context of repeated vomiting, as seen in this patient. Although the history and examination indicate oesophageal varices as the most probable source of haemorrhage for this patient, this needs to be confirmed by gastroscopy, as the definitive treatment of these conditions differs significantly. Gastroscopy also offers strategies such as sclerosing and banding to reduce or control haemorrhage. The pre-hospital treatment for this patient is

the same for all potential causes.

T REAT The immediate treatment for this patient is fluid with a target of raising perfusion sufficiently to improve his conscious state and to enable him to protect his own airway. If his conscious state does not improve with treatment, endotracheal intubation will need to be considered as the optimal way to maintain a safe airway. If intubation is not possible due to scope of practice, the patient will have to be managed on his side at all times, as he is at high risk of aspirating blood. If he needs respiratory support and is not intubated, considerable care will have to be taken not to inflate his stomach, potentially precipitating vomiting and aspiration. Two large-bore IV cannulae should be established and IV fluid should be administered until an improvement in the patient’s conscious state is witnessed: this often coincides with a palpable brachial pulse. At this stage it would be prudent to titrate the fluid administration to his conscious state and pulse, as continued bleeding from the oesophageal varices combined with excessive fluid administration may result in overdilution of haemoglobin, platelets and clotting factors. A nasogastric tube to decompress the stomach and drain free blood will not only reduce the volume in the stomach and the risk of aspiration but also indicate whether bleeding is continuing. This may be replaced with an oesophageal balloon tube in hospital as a last resort. Rapid transfer to a hospital resuscitation unit with the capacity to manage massive transfusions is indicated.

EVALUAT E Evaluating the effect of any clinical management intervention can provide clues to the accuracy of the initial diagnosis. Some conditions respond rapidly to treatment so patients should be expected to improve if the diagnosis and treatment were appropriate, whereas other conditions are unlikely to respond in the timeframes normally associated with ambulance transport times. In such cases, a failure to improve should not be considered an indication of a misdiagnosis. In this case, the paramedics cannot directly manage the underlying cause and can provide only symptomatic treatment while expediting rapid transport to definitive care. The patient’s response will depend on the extent of the ongoing bleed and the paramedics’ ability to maintain a patent airway. If the bleed remains uncontrolled, the patient is likely to progress to a pulseless

electrical activity (PEA) arrest. Despite the relatively young age of this patient, his presentation of dramatic collapse and massive bleeding from oesophageal varices does not carry a particularly optimistic prognosis. Given the long-term and chronic nature of alcoholic cirrhosis, his family may be aware of his poor prognosis and may appear less distressed than you might expect. This does not imply that the family, or the patient, should be treated with any less respect or clinical rigour than any other critically ill patient.

Hospital management Hospital management will include replacement of blood volume, platelets and clotting factors using a massive transfusion protocol. Drugs to promote splanchnic vasoconstriction may reduce portal pressure and haemorrhage rate. Banding of the oesophageal varices will often control haemorrhage, as will injecting inflammatory chemicals to promote sclerosis in and around the varix. In refractory bleeding, a modified orogastric tube containing a large balloon or an oesophageal balloon inflated within the oesophagus can function as a tamponade (see Fig 45.2).

FIGURE 45.2 The modified Sengstaken-Blakemore tube. Note the accessory nasogastric tube for suctioning of secretions above the oesophageal balloon and the two clamps, one secured with tape, to prevent inadvertent decompression of the gastric balloon. Source: Rikkers (1981).

Surgical and intravascular procedures to create a shunt from the portal system directly to the systemic system will reduce the pressure on the portal veins and thus the pressure on the oesophageal varices. While these shunts control pressure, allowing blood to effectively bypass the liver may exacerbate hepatic encephalopathy. A liver transplant is also an option, dependent on the patient’s eligibility and the availability of a suitable donor.

Summary Significant GI haemorrhage is a life-threatening emergency and may occur following a less significant initial haemorrhage. Pre-hospital assessment and management of patients with GI tract bleeding should focus on identifying those patients with life-threatening haemodynamic compromise and on initiating appropriate resuscitation. Pre-hospital management should maintain fluid administration to a level that ensures essential organ perfusion, while limiting delays in transferring the patient to definitive care.

References Akhtar, A., Padda, M. Natural history of Mallory-Weiss tear in African American and Hispanic patients. Journal of the National Medical Association. 2011; 103(5):412–415. American College of Surgeons Committee on Trauma. Advanced Trauma Life Support for Doctors (ATLS) Student Course Manual, 9th ed. Chicago, IL: American College of Surgeons, 2012. British Society of Gastroenterology. UK comparative audit of upper gastrointestinal bleeding and the use of blood. Retrieved 27 February 2013 from www.bsg.org.uk/pdf_word_docs, 2007. Cameron P., Jelinek G., Kelly A-M., Murray L., Brown A.F.T., eds. Textbook of Adult Emergency Medicine, 3rd ed., Sydney: Elsevier, 2009. Cappell, M. S., Friedel, D. Initial management of acute upper gastrointestinal bleeding: from initial evaluation up to gastrointestinal endoscopy. Medical Clinics of North America. 2008; 92:491–509. Donovan, J. P., Schafer, D. F., Shaw, B. W. Cerebral oedema and increased intracranial pressure in chronic liver disease. Lancet. 1998; 351(9104):719–721. Farrell, J. J., Friedman, J. S. Gastrointestinal bleeding in the elderly. Gastroenterology Clinics of North America. 2001; 30(2):377–407. Farrell, J. J., Friedman, J. S. The management of lower gastrointestinal bleeding. Alimentary Pharmacology & Therapeutics. 2005; 21(11):1281–1298. Grow, P. J., Chapman, R. W. Modern management of oesophageal varices. Postgraduate Medicine Journal. 2001; 77(904):75–81. Henriksen, P. A., Palmer, K., Boon, N. A. Management of upper gastrointestinal haemorrhage complicating dual antiplatelet therapy. QJM: An International Journal of Medicine. 2008; 101(4):261–267. Hopper, A. D., Sanders, D. S. Upper GI bleeding requires prompt investigation. Practitioner. 2011; 255(1742):15–19.

Kashani, A., Landaverde, C., Medici, V., Rossaro, L. Fluid retention in ascites: pathophysiology and management. QJM: An International Journal of Medicine. 2008; 101:71– 85. Khadra, M. H., Pickard, R. S., Charlton, M., Powell, P. H., Neal, D. E. A prospective analysis of 1930 patients with hematuria to evaluate current diagnostic practice. Journal of Urology. 2000; 163(2):524–527. Klebl, F. H., Bregenzer, N., Schöfer, L., Tamme, W., Langgartner, J., Schölmerich, J. Comparison of inpatient and outpatient upper gastrointestinal haemorrhage. International Journal of Colorectal Disease. 2005; 20(4):368–375. Longstreth, G. F. Epidemiology and outcome of patients hospitalized with acute lower gastrointestinal hemorrhage: a population-based study. American Journal of Gastroenterology. 1997; 92:419–424. Oakland, K., Dawson, J. Gastrointestinal bleeding. General Practitioner. 2010; 11 December:42–43. Palmer, K. Acute upper gastrointestinal haemorrhage. British Medical Bulletin. 2007; 283(1):307–324. Pfeifer, J. Surgical management of lower gastrointestinal bleeding. European Journal of Trauma and Emergency Surgery. 2011; 37(4):365–372. Rikkers, L. F. Portal hypertension. In: Goldsmith H., ed. Practice of Surgery. Philadelphia: Harper & Row, 1981. Rockall, T. A., Logan, R. F., Devlin, H. B., Northfield, T. C. Incidence of and mortality from acute upper gastrointestinal haemorrhage in the United Kingdom. Steering Committee and members of the National Audit of Acute Upper Gastrointestinal Haemorrhage. British Medical Journal. 1995; 311(6999):222–226. Scottish Intercollegiate Guidelines Network (SIGN). Management of acute upper and lower gastrointestinal bleeding a national clinical guideline. Retrieved 22 January 2013 from www.sign.ac.uk, 2008. Velayos, F. S., Williamson, A., Sousa, K. H., Lung, E., Bostrom, A., Weber, E. J. Early predictors of severe lower gastrointestinal bleeding and adverse outcomes: a prospective

study. Clinical Gastroenterology and Hepatology. 2004; 2(6):485–490. Yang, P-M., Chen, D-S. Caput medusae. New England Journal of Medicine. 2005; 353:e19. Yu, P. P., White, D., Iannuccilli, E. A. The Mallory-Weiss syndrome in the pediatric population. Rare condition in children should be considered in the presence of hematemesis. Rhode Island Medical Journal. 1982; 65(2):73–74.

SECTION 15

THE PARAMEDIC APPROACH TO COMPLEX CASES: SPECIFIC CHALLENGES TO PARAMEDIC REASONING AND MANAGEMENT

O U TL I N E INTRODUCTION TO THE PARAMEDIC APPROACH TO COMPLEX CASES: SPECIFIC CHALLENGES TO PARAMEDIC REASONING AND MANAGEMENT CHAPTER 46: The socially isolated patient CHAPTER 47: The dying patient CHAPTER 48: The patient on out-of-hospital dialysis CHAPTER 49: Indigenous Australian patients CHAPTER 50: Māori patients

INTRODUCTION TO THE PARAMEDIC APPROACH TO COMPLEX CASES: SPECIFIC CHALLENGES TO PARAMEDIC REASONING AND MANAGEMENT IN THIS SECTION Chapter 46 The socially isolated patient Chapter 47 The dying patient Chapter 48 The patient on out-of-hospital dialysis Chapter 49 Indigenous Australian patients Chapter 50 Maori patients

At the completion of this section you should be able to • Describe the paramedic assessment of the socially isolated patient. • Discuss the specific paramedic management issues in treating the socially isolated patient. • Discuss concepts of palliative care and the role of the paramedic in supporting palliative care. • Describe the pathophysiology associated with dialysis management. • Discuss the integration of emergency medical treatment with dialysis management. • Discuss the issues that influence paramedic care of Indigenous Australian and M ori patients. While a standardised approach to patient assessment and clinical reasoning underpins every patient encounter, paramedics will regularly need to adapt their tendency to view their work from a purely clinical focus. The opportunity to respond to patients in their own homes adds a unique aspect to paramedic practice and often presents challenges not encountered by clinicians who operate in specialist medical facilities. The chapters in this section focus on patients whose environment, ethnicity or social situation renders their assessment and management even more complex than usual. In many cases it can be quickly determined that there is no need for immediate medical intervention, but that does not mean there is no role for the paramedic. Identifying patients who have become socially isolated and are struggling to manage their health is a unique aspect of paramedic practice, but one that is largely ignored in clinical practice guidelines. Similarly, being called on when the family members of a terminally ill patient are confronted by a sudden deterioration in their loved one’s condition requires a much broader understanding of the paramedic role than determining the underlying pathophysiology of the condition. In this case, the confidence to withhold clinical care requires an especially strong approach to clinical reasoning. In addition, changes in healthcare are impacting paramedic practice. The growing number of people with renal disease combined with the limited availability of organs for transplantation has seen the number of patients undergoing dialysis at home increase significantly. The underlying disease, the process of dialysis and how these impact on acute deterioration in the patient’s health present a challenge to paramedics asked to respond to these patients. Finally, it is well recognised that ethnicity has significant influences on health. It is also clear that there are genetic aspects that influence the frequency and severity of certain diseases. We now have a better understanding of how social and cultural influences alter patients’ views of their illness and how they engage with the healthcare system. Paramedics are often the interface between these patients and the greater healthcare system. We look at the unique aspects of two Indigenous groups (Indigenous

Australians and Ma–ori) and examine how their cultural beliefs need to be incorporated into the clinical reasoning process. This section reinforces that while paramedics maintain a clear clinical focus they must be able to incorporate non-clinical factors into their assessment and management. Managing these patients in their complex environments and situations is an excellent illustration of the value of the reasoning professional paramedic over a procedure-or protocol-driven technician.

CHAP TER 46

The socially isolated patient By Bronwyn Tunnage and Tony Ward

C O N C E P TS U S E D I N TH I S C H A P TE R • The paramedic’s clinical approach: Section 2

OVERVIEW • Social isolation describes the absence of meaningful contact with other people and is a term used to describe a person’s lack of participation in, and integration into, society. • Humans are social beings and the absence of contact with others can lead to feelings of loneliness, low self-esteem and depression. • Social isolation is associated with negative health outcomes and an increased rate of mortality. • Disease and illness can impair mobility, decrease the ability to communicate and/or create a sense of shame. These can all contribute to social isolation. • Specific groups within society are at a greater risk of social isolation. These include elderly people, people with mental health issues, the unemployed and refugees. • Working in the community setting, paramedics will be exposed to socially isolated patients and need to both adapt their treatment to the conditions and use the opportunity to engage patients in the wider healthcare system where appropriate.

Introduction The definition of social isolation has evolved from simply meaning a loss of social attachments and community ties to a broader description that incorporates an individual’s feelings of being socially cut-off, combined with an actual lack of engagement with others —social contacts are few in number and superficial or non-supportive (Nicholson, 2008). It differs from loneliness, which is entirely subjective, and varies between people according to their need for companionship and attachment through relationships. It is also distinct from social exclusion, where an individual’s non-participation is beyond their control. Disease and illness can affect mobility, decrease the ability to communicate and/or create a sense of shame. Similarly, an inability to interact with society can directly affect an individual’s health by excluding them from visiting their doctor or pharmacist. Isolation from friends and family also removes the ability of these groups to monitor the health of the patient. Paramedics need to be aware of the propensity for some patients to be socially isolated and adapt their treatment plans accordingly, as well as taking the opportunity to engage these people in the wider healthcare system where appropriate.

Background Much of the research on social isolation has been undertaken among the older population. This group is exposed to many of the causes of isolation and is at a higher risk of becoming isolated. Addressing issues that impact on the health and wellbeing of elderly adults is becoming more important because the number of elderly people living in Australia and New Zealand is growing rapidly. For example, the number of centenarians living in Australia increased by 300% between 2000 and 2007 from 2000 to 6000 people (the most recent data at the time of writing). In addition, the current age-structure transition, as the Baby-Boomer generation ages, is increasing the proportion of older people within the total population (Jackson, 2007).

The health consequences of social isolation Humans need and desire contact and relationships with others. Social connectedness and integration are associated with a wide range of positive health outcomes including an improvement in life expectancy, comparable with the benefits of smoking cessation (HoltLunstad, Smith & Layton, 2010). People with strong social relationships also report higher levels of health than those with weaker social connections (Cornwell & Waite, 2009; Hawton et al., 2010). In contrast, social isolation has been linked to a range of negative health outcomes such as poor nutrition (Locher et al., 2005), heavy alcohol consumption, greater chance of rehospitalisation (Mistry et al., 2001), depression (Gorst-Unsworth & Goldenberg, 1998), cognitive decline (Bassuk, Glass & Berkman, 1999) and increased susceptibility to dementia (Fratiglioni et al., 2000).

Factors associated with the development of social isolation The identification of social isolation in an individual typically includes some, or all, of the following features: • an extremely low number of social contacts, by any form of communication • a failure to initiate contact with others • contact with others that does not add to wellbeing or is even abusive • a feeling of not belonging • a feeling that present relationships are not fulfilling (Nicholson, 2008). The main precursors of social isolation are a lack of relationships with a partner, family, friends and/or colleagues (de Jong Gierveld & Havens, 2004). For older adults, the combination of losing a life-partner through death, adult children relocating, pursuing a career or raising their own family and not participating in the workforce can all lead to a drastic decrease in the number and quality of social contacts. For recently arrived refugees, the loss of a partner and family members (often in traumatic circumstances), difficulties entering the workforce and joining social organisations in their adopted country, and the absence of their extended family and the wider community from their country of origin can lead to a nexus of isolation. As well as an absence of relationships, physical, psychological, environmental and

economic factors contribute to a lack of social connection (Nicholson, 2008). Poor health, disability and declining mobility can act as physical barriers to sharing in social events and activities. Psychological conditions such as depression or dementia and increasing frailty combined with the fear of falling can lead to withdrawal. Where the individual lives and their distance from social contacts also limits participation; vulnerable groups typically do not have access to private transport and public transport may be infrequent, impractical or dangerous. In addition, housing design, typified by blocks of flats with poor access, can contribute to isolation. Finally, poverty can act as an economic barrier to participation in society.

Implications of social isolation for paramedic practice The proportion of people living alone in Australia increased from 7% of the population in 1986 to 9% in 2001 (the most recent data at the time of writing). This is projected to increase from 1.8 million in 2001 to between 2.8 million and 3.7 million by 2026, representing an increase of between 57% and 105% (ABS, 2006). As social isolation is prevalent in the elderly population, it is anticipated that the increase in older people living alone in the community will lead to a rising number of cases of social isolation. The elderly are more likely to have chronic health conditions and may be frequent users of ambulance services. When paramedics attend older patients they should use it as an opportunity to make a holistic assessment of the person’s wellbeing and to determine whether they are sufficiently supported within the community. Paramedics need to be able to identify people at risk of social isolation and to be aware of the associated negative health outcomes. They should also be familiar with, and know how to access, services that support elderly people living in the community by providing social contact. Unfortunately, systems that paramedics can use to refer at-risk patients for multidisciplinary assessment and intervention are not widely established (Snooks et al., 2006). Telephone befriending services are one means of re-engaging older people in society that has been demonstrated to increase participants’ feelings of wellbeing and self-esteem (Cattan, Kime & Bagnall, 2011). This intervention has an affinity with the wider role of ambulance service providers and some organisations provide this service as part of their community programs.

Social isolation and falls in the older patient Falls are common among the elderly and can have serious consequences, including injury and death. After falling, the patient typically suffers a reduction in quality of life and physical activity and this can trigger a negative cycle of decreasing functionality and increasing social isolation, ultimately leading to dependency, institutionalisation and death (Snooks et al., 2006). Even when the fall does not result in injury, patients may restrict their activities out of a fear of falling again and may withdraw from contact (Davison & Marrinan, 2007; see Fig 46.1).

FIGURE 46.1 Potential negative cycle resulting from falls. Falls in older people are not uncommon as mobility, eyesight and balance are affected by age. Even if a patient does not suffer an acute injury after a fall, fear and loss of confidence as a result of the fall can lead to a restriction of activities and increased social isolation. Visiting patients in their homes, paramedics have a unique opportunity to assess both the patient and the home for the risk of falls. Falls and related injuries frequently require medical attention and the ambulance service is often the first point of contact for patients. They are a significant component of the ambulance service workload, accounting for approximately 10–25% of all call-outs in the over-65 age group (NHS, 2012). They also impact on hospital emergency departments, accounting for 10–15% of all visits. The injuries that most often lead to hospital admission

after a fall are hip fractures, traumatic brain injuries and upper limb injuries. Falls incur high financial costs for the health system: in the UK, falls account for approximately 3% of the total health budget (Snooks et al., 2006). By 2051 it is estimated that the cost of falls to the Australian healthcare system will be $1375 million per annum and that an additional 2500 hospital beds will be required to manage falls alone (Moller, 2003). In Australia in 2008–2009, more than 78,600 people aged over 65 were hospitalised as a result of a fall. The majority were women and the rate of subsequent hospitalisation as a result of the fall was also higher for women than men (Bradley, 2012). Although more women suffer falls than men, the rate of fatal falls is higher among men than women of the same age. The World Health Organization (WHO) reports that mortality from a fall accounts for 40% of all injury deaths (WHO, 2007). Rates of falls increase with age: in New Zealand, falls account for 55% of all hospitalised unintentional injuries among patients aged 65–69 years, 65% for 70–74 year olds, 73% for 75–79 year olds and 85% for those aged 80+ years (ACC, 2006).

Refugees The experience of living as a refugee is different for each individual but typically refugees suffer ongoing physical, psychological and social consequences due to the events they have endured. Many have witnessed or suffered severe brutality, including abuse and torture. Having survived a dangerous journey, they must then live in overcrowded refugee camps, which frequently have limited provision of the necessities of life such as food, sanitation and medical care, and are unsafe due to attacks from both other inhabitants and external agents. Female refugees are particularly vulnerable to violence and exploitation. They are often the head of their family unit and are entirely responsible for the welfare of their dependants. Low levels of literacy and education, a consequence of sexual discrimination in their homeland, contribute to their position of powerlessness. In many cases they have been subjected to frequent and extreme levels of sexual violence (DeSouza, 2012). Refugees arriving under quota or humanitarian programs participate in a coordinated resettlement program. The Australian government provides a 5-day Australian Cultural Orientation Program prior to arrival and the Onshore Orientation Program delivers an individualised case management approach to settling refugees (Department of Immigration and Citizenship, 2011). Further resources are administered at state level. In New Zealand, newly arrived refugees attend a 6-week residential orientation program, which includes general orientation, medical screening and treatment, some English lessons and assistance with accommodation and employment (Ministry of Health, 2012). However, the early stage of resettlement is often a confusing and overwhelming time and information is not always retained. Asylum seekers do not have an organised program of support and are not always aware of their entitlements.

Determinants of social isolation among refugees Refugees have a high risk of becoming profoundly socially isolated. Many refugees have lost partners and close family members to violence or while fleeing from their country. Establishing social contacts and new relationships within their adopted country is difficult due to a lack of fluency in English. Acquiring new friendships outside of their own culture

is difficult if they are not involved in an organised activity such as study or work. Feelings of being different are reinforced by different clothing, speaking with a different accent and racism (DeSouza, 2012). For women especially, the impact of the changed family structure (where they may be the sole adult in the household) and the reduction in family size with a resultant lack of family support can be profound. In addition, neighbours may be less likely to be involved in their lives than in their previous community. Community organisations for refugees are thus an important source of social contact as well as support and information. As well as a lack of relationships, refugees experience physical barriers to social activity as a result of injuries, disability and sickness. The profound grief for family members they left behind and at being exiled from their homeland forms psychological barriers to participation. While humanitarian programs provide assistance to find housing, it is not always close to where refugees from the same country have settled. New arrivals may become isolated from the established refugee community if they need to travel long distances to socialise. This geographical barrier to maintaining contact, compounded by the physical difficulties of travelling on public transport with young children and the financial barrier of transport costs if they have difficulty entering the workforce, increase the likelihood of social isolation. Even when refugees are housed near others from their country of origin, social isolation can occur if deep-seated group differences, such as religious beliefs or clan membership, are retained in the new country (Ministry of Health, 2012).

CA SE ST U DY 1 Case 10489, 1530 hrs. Dispatch details: A personal alarm belonging to a 73-year-old female has been activated and she hasn’t replied to a telephone call from the emergency key holder, a neighbour. The patient lives alone and has a history of falls. Initial presentation: The paramedics arrive and find the patient sitting on her kitchen floor; she is visibly upset. She states that she has fallen and cannot get up.

ASSESS The paramedics’ questions should be clear and concise and they should weigh

all facets of the patient’s past and present medical history against the four risk categories for falls: biological, behavioural, environmental and socioeconomic. The cause of the patient’s fall may range from a complex interaction of medical conditions to simple mechanics. It is important not to underestimate the significance of what may appear to be a simple fall but is actually indicative of a more serious underlying problem. This patient does not appear to have any injuries but she is unable to get up unassisted. She refuses transport to a medical facility. People aged 60–90 years are characteristically stoical by nature and often reject medical attention or fuss. There is a great deal of fear among the elderly that their independence will be lost and apprehension about what the future will bring if they are moved from their home.

Look! • Is the house clean? • Is there any fresh food in the fridge? • Is the garden neglected? • Are there any trip hazards? • Does the patient have a medical alert bracelet/pendant?

The clinical reasoning behind a decision to leave an ‘at-risk’ person at home alone must be weighed against the risk of a subsequent fall and therefore the increased risk of morbidity or mortality. A patient who suffers recurrent falls is at higher risk of suffering a fall-related fracture (Tromp et al., 2001). A closer investigation of the patient’s living conditions—including the state of the bedding, the bathroom facilities and what food and fluids are in the fridge and cupboards—can reveal a more detailed picture of the potentially isolated client.

Initial assessment summary

Problem Fall Conscious GCS = 15 state Position Sitting Heart rate 65 BPM Blood 165/95 mmHg pressure Skin Warm and dry appearance Speech Normal pattern Respiratory 14 BPM rate Respiratory Even cycles rhythm Chest Good breath sounds bilaterally auscultation Pulse 96% oximetry Temperature 36.2°C Motor/sensory Normal sensation function Pain The patient denies any pain. History The patient has fallen in the kitchen. She claims she just needs assistance to get up and doesn’t want to go to hospital. Physical No abnormalities detected. assessment D: There are no dangers to the patient or the crew. A: The patient is fully conscious and protecting her own airway. B: The patient is breathing normally. C: Her perfusion is within normal limits. At the moment, this patient appears simply in need of help to get up from the floor and, provided she receives appropriate follow-up/support, many would consider that she doesn’t need to be transported to a medical facility.

CONFIRM The essential part of the clinical reasoning process is to seek to confirm your initial hypothesis by finding clinical signs that should occur with your provisional diagnosis. You should also seek to challenge your diagnosis by exploring findings that do not fit your hypothesis: don’t just ignore them because they don’t fit.

DIF F ERENT IA L DIA GNOSIS A simple fall with no underlying medical condition and no traumatic injury Or • A fall with an underlying medical cause, resulting in syncope, loss of balance or loss of motor power • A fall that has resulted in an occult traumatic injury (e.g. a fractured pubic ramus)

What else could it be? A fall with an underlying medical cause There are a large number of possible factors that could have caused this patient to fall. • Biological causes should be investigated by reviewing body systems, with particular emphasis on: < the cardiovascular system, including myocardial ischaemia and infarction, cardiac arrhythmias, orthostatic hypotension, syncopal attack, stroke and transient ischaemic attack < the gastrointestinal system, particularly low food and fluid intake, which can cause hypoglycaemia and hypotension, respectively < the musculoskeletal system and its impact on stability and gait < the genitourinary system, as urinary tract infections are commonplace among the elderly and can cause gait imbalance < the central nervous system, including changes in vision. • Behavioural causes for the fall should be explored and include: < Has the patient inadvertently overdosed or underdosed on her prescribed medications? < Is alcohol a factor? • Finally, the environment should be examined for possible contributory factors to a mechanical fall, such as: < loose mats < slippery surfaces < obstacles. This patient is not suffering any arrhythmia and did not complain of symptoms typical of poor perfusion prior to making the call. Her blood sugar, temperature and behaviour are normal and do not suggest any underlying medical cause. A fall that has resulted in an occult traumatic injury The patient denies any pain and has normal movement, strength and sensation of all limbs. A thorough investigation and an open mind are essential to avoid errors in

clinical judgement caused by cognitive biases such as anchoring, confirmation bias, overconfidence bias and premature closure (Croskerry, 2002).

T REAT Initial management Safety Older people living alone are at a particular risk of falls as most falls occur in the home. Being able to quickly and competently assess a patient’s ability to perform their activities of daily living is a complex task. The need for training within paramedicine programs on both physical assessment of the elderly and assessment of their homes is becoming more apparent. Paramedics have the opportunity to refer patients to a social services team: if patients are referred early enough, the potential for a subsequent fall with a worse outcome may be averted. Factors that reduce the chance of referral include a lack of wellestablished local care pathways, paramedics being unaware of these care pathways or referral being outside the paramedic’s scope of practice. Most ambulance services, however, are actively engaging in falls management programs. Pain management If the patient has signs of pain or is complaining of pain, their underlying injuries need to be assessed and managed. It is not unusual for older patients to minimise their complaints to the point where there is a risk that significant injuries may be overlooked. This behaviour may simply be an attempt to avoid causing a fuss but it may also be an attempt to avoid transport for further treatment. Assessing the patient thoroughly after assisting them to stand is important in order to detect hidden injuries. Providing the patient with oral pain relief should be done with caution and only after more serious injuries have been excluded. Non-steroidal anti-inflammatory drugs (NSAIDs) are often contraindicated in the elderly so consultation with the patient’s GP is advisable. Transport The decision to transport an elderly patient from their home environment should be balanced and well-considered. Anxiety and apprehension often place increased stressors on the frail and already vulnerable, and overcrowding in hospital emergency departments and the paramedic’s unwillingness to expose a patient to a long wait in hospital can add to the pressure not to transport the patient. Leaving a patient with no apparent injuries at home would be considered the correct course of action, because keeping people independent is vital for patient wellbeing and reducing healthcare costs. However, research from the UK has shown that 49% of patients who were not transported to hospital after a fall had a second healthcare attendance within 2 weeks and an increased risk of death and hospitalisation compared with their

peers (Snooks et al., 2006). Emerging evidence within pre-hospital research suggests that leaving a patient at home with advanced pre-hospital support through the use of extended care paramedics and appropriate social and medical follow-up may lead to a reduction in secondary admissions (Thompson et al., 2013). Improvements in health integration, in linking relationships between paramedics and GPs and in the assessment skills of extended care paramedics will enable more sound clinical decisions regarding which patients to transport and which to leave at home. The process of safely arranging the support strategies to leave someone at home and documenting this thoroughly takes a lot longer than simply transporting the patient, although in the long run it may be a much better option. Across various ambulance services, the minimum criteria for leaving a patient at home include the following: • A medical cause for the fall has been excluded. • Traumatic injury has been excluded. • A clinical review program has been implemented. • The person has immediate social support (not living alone). • The person has food and is capable of preparing it. • The person is capable of attending to their own daily living needs. • The above has been well documented, along with a series of vital sign observations proving stability. • A call-back plan has been established, including triggers and actions to follow if problems occur.

P RACT ICE T IP Home alarm devices are popular among the elderly, their families, carers and GPs. Knowing that help can easily be summoned increases the older person’s confidence to continue living at home but it also increases ambulance attendance for non-medical–related calls. In addition, these alarms can be seen as a further tool that socially isolates the elderly: family members may believe their loved one is fine and will simply ‘push the button’ if something is wrong.

EVALUAT E Even for patients who are left at the scene, a period of time should be allocated to evaluate the patient again after they have been assisted from the floor. A fall in blood pressure, uneven gait and confusion can all indicate an underlying medical cause that may have been missed in the first assessment. Spending a few minutes evaluating the patient can also reveal risk factors for future falls

such as a loss of balance or vision problems; in many cases the patient may not have noticed the slow deterioration in these abilities.

Ongoing management P a i n re l i e f Polypharmacy is rife within the elderly population and adherence to prescription treatment regimens is variable. Simple oral analgesics such as paracetamol and ibuprofen may well suffice for the majority of falls victims and classic soft-tissues injuries and muscular strains can be well-managed with these relatively simple, cost-effective and lowrisk medications. Stronger medications like codeine may have negative dissociative effects and a more prolonged anaesthetic effect than is required. Inhaled medications like methoxyflurane may have varied results due to compliance and reduced capacity to inhale effectively, but can be very effective for one-off movements such as standing or rolling, alignment of fractured limbs and difficulty with vascular access. Opioid-based products (synthetic and natural) and benzodiazepines have a high potency and are typically rapid-acting in the IV form. Titrating small aliquots of these medications may lead to very effective results in a short period of time.

Social isolation Family and friends are a vital part of the network required by older people to feel socially accepted and part of a community. Social isolation is associated with an increased risk of mortality and a fall exponentially increases the risk of morbidity and mortality (Dickens et al., 2011). Offering social activity and support within a group format and interventions in which older people are active participants appears to be an effective means of reducing social isolation within the elderly.

Falls prevention Falls prevention programs aim to reduce the number of people who have a fall. Outcomes of fall prevention programs in the UK saw emergency call-outs for falls decrease by 75% between 2006 and 2011, leading to increased capacity for emergency services to deal with higher-acuity calls (NHS, 2012). Several falls prevention models exist within Australian and New Zealand governmental agencies promoting strategies on how best to reduce falls. Multifaceted programs including environmental modifications (occupational therapists), physical exercise, review of medications (general practitioner) and review of visual acuity or aids are among some of the methods that have shown to reduce fall numbers. Behavioural changes to adopt a healthy lifestyle, including reducing alcohol intake, smoking cessation, maintaining weight within normal parameters and self-health initiatives such as walking, are fundamental to healthy ageing. Emergency medical service providers have a role to play in health promotion and many already include falls prevention in their community programs.

Hospital admission Following any medical intervention in hospital, the patient will often be assessed in terms of their safety and independence. Questions to be considered include: • Is this patient safe at home? • Did any underlying pathology cause this fall? • Is there an alternative care pathway or support service available to the patient? • Is the patient able to perform activities of daily living? • Is the patient socially integrated with family and/or community, with systems in place to cope with a change in circumstance?

CA SE ST U DY 2 Case 10980, 1453 hrs. Dispatch details: A 28-year-old woman is complaining of feeling unwell with abdominal pain. Initial presentation: The paramedics are met by a volunteer refugee support visitor, who is visiting the patient for the first time and called the ambulance. She explains that the patient is a Somali refugee who arrived within the last 2 months with two of her children.

ASSESS Assessing a patient who is a refugee can be a challenging experience for paramedics for a number of reasons, including language-based communication difficulties and the patient’s possible lack of understanding of the healthcare system, previous experiences of abuse and/or feelings of shame about their health problems. Patients who speak some English may find it difficult to communicate in such a stressful situation or may agree with what is said out of confusion or politeness. Some paramedics may use family members or friends as informal interpreters but this has the potential to create miscommunication. Some cultures have strong beliefs about the appropriateness of contact between males and females and mixed crews should offer a same-sex paramedic where the patient clearly prefers this (Kansu in Burnett & Peel,

2001; see Box 46.1). If the patient has suffered abuse or torture they may be suspicious or fearful of physical examination, or they may react aggressively towards people wearing uniforms who are assumed to be authority figures. Prehospital emergency care is not an appropriate setting to address or explore these issues and doing so may cause the patient anguish or psychological harm. B O X 4 6 . 1S t r a t e g

ies fo r interac ting with

patients who are refug ees • Be flexible and if possible offer the choice of a same-sex paramedic. • Speak slowly and clearly. • Use simple words; do not use slang or jargon. • Be specific and offer the patient clear choices. • Avoid making assumptions and generalisations based on your cultural biases. • Consider family participation, especially as a translator. • Avoid asking closed (yes/no) questions. • Encourage the patient to ask you questions in order to confirm they have understood.

In addition, there are some extra potential issues to consider clinically. The patient may not have received routine childhood immunisations and they may demonstrate disease specific to the region they came from—for example, tuberculosis is still prevalent in Asia and the Indian subcontinent, malaria is a definite concern in Southeast Asia and for patients with an African background sickle-cell anaemia is worth considering. Effective communication is a critical paramedic skill. Establishing rapport with this patient and gaining her trust sufficiently to be able to assess her, to some degree, is vital. If it is not possible to gain her permission to carry out an assessment, or if undertaking the assessment is causing her great distress, the paramedics’ aim should be to rule out the worst-case scenario. They should treat the patient with respect and not probe with questions that are more to satisfy their curiosity than to treat the patient. In this case the patient appears seated upright but has a very flat affect, speaks very quietly and refuses to make eye contact but does not appear discomforted. She moves freely and is holding her youngest child. She is more animated when addressing the child. She is complaining of abdominal pain but the paramedics’ ability to use history and examination to clarify the situation will be impaired in this case. They need to enlist the assistance of interpreters and support strategies to ensure that the patient’s pain is appropriately investigated and managed. It is likely that this cannot be achieved effectively in the out-of-hospital environment.

CONFIRM In many cases paramedics are presented with a collection of signs and symptoms that do not appear to describe a particular condition. A critical step in determining a treatment plan in this situation is to consider what other conditions could explain the patient’s presentation.

DIF F ERENT IA L DIA GNOSIS Undifferentiated abdominal pain Or • An unrelated medical condition described as abdominal pain • An expression of distress described as abdominal pain

What else could it be? An unrelated medical condition Refugees can have multiple, complex or unusual health conditions that are not commonly seen, or are not seen at all, in the general population. For this patient, in addition to the usual differential diagnoses, the paramedics need to consider whether a common presentation is complicated in some way or an unfamiliar condition is present. Abdominal pain in a woman of child-bearing age always requires consideration of ectopic pregnancy or a complication of pregnancy. Female genital mutilation (FGM) is a traditional but harmful body modification prevalent in the Horn of Africa and is estimated to affect 97.9% of women in Somalia (Ministry of Health, 2012). It is defined by the WHO as ‘partial or total removal of the external genitalia or other injury to the female genital organs whether for cultural or other non-therapeutic reasons’. Paramedics should be aware of the complications caused by FGM in obstetric and gynaecological conditions such as spontaneous abortion or imminent childbirth. Abdominal pain can be caused by infectious and parasitic diseases. For example, infection with Helicobacter pylori is high among the general refugee population and is associated with peptic ulcers and persistent abdominal discomfort. Parasitic worms are common in underdeveloped countries, entering the human host through contaminated food or drinking water. Infections of some parasitic worms, such as schistosomiasis, can be asymptomatic for years before causing serious disease, with symptoms including abdominal pain. A sickle-cell crisis is identified by severe pain that can occur in a number of sites including the abdomen. Sickle-cell disease is a genetically inherited blood

disorder found in Africa and parts of the Middle East and causes significant morbidity and mortality. People with sickle-cell disease suffer from a crisis in response to hypoxia, which causes the haemoglobin to clump, changing the shape of the red blood cells. The abnormally-shaped red blood cells block capillaries, causing ischaemia and infarction of the distal tissue. An expression of distress Abdominal pain can be a symptom of psychological disorders such as depression, anxiety or an eating disorder. Refugees are especially prone to feelings of intense guilt, loss and homesickness, which place them at a higher risk of developing psychological disorders. Abdominal pain could also arise from the ongoing physical effects of prolonged malnutrition, physical abuse, sexual abuse or sexually transmitted infection.

T REAT This patient does not appear to be in any form of physiological distress or to have any overt symptoms that suggest a particular disease process. The likely progression of her abdominal pain is difficult to predict, however, and any suspicion that her presentation is primarily a response to social stress cannot override the possibility that she may also have a physical complaint. Her normal vital signs and lack of overt symptoms suggest that the paramedics have some time to make their decision regarding treatment and that immediate transport to hospital may not be the best management path for her. Ultimately, although she needs further medical assessment to exclude any serious pathology, alternatives such as being assessed by a local doctor or having a refugee support service arrange a medical examination may be better than delivering her to a crowded ED with limited resources to support her needs. Assessment and planning may take a lot longer than usual, allowing for time to gain the patient’s confidence, sort out interpreters and provide support for the family.

EVALUAT E Evaluating the effect of any clinical management intervention can provide clues to the accuracy of the initial diagnosis. Some conditions respond rapidly to treatment so patients should be expected to improve if the diagnosis and treatment were appropriate. A failure to improve in this situation should trigger the clinician to reconsider the diagnosis. In this case the recent onset of symptoms, combined with the lack of any physiological signs, suggests that the patient is unlikely to deteriorate during transport. Given the possible social factors involved in this case, an improvement in the patient’s anxiety and discomfort once she has been

transported from the site may provide some clues to the cause of her symptoms but a physical cause should not be completely ruled out.

Summary Socially isolated patients are disconnected from society and lack relationships with a partner, family or friends. Physical, psychological, environmental and economic barriers may act to limit the individual’s ability to engage with others. Social isolation is strongly associated with morbidity and mortality. Paramedics are in the unique position of attending to patients in their own homes. This gives them the ability to make a holistic assessment of the person’s living situation and to refer isolated patients to appropriate services.

References Accident Compensation Corporation (ACC)Preventing Injury from Falls. The National Health Strategy 2005–2015. Te Arai i nga Aitu a Hinga Te Rautaki a Motu 2005–2015. Wellington: ACC, 2006. Australian Bureau of Statistics (ABS)Future Living Arrangements. Canberra: ABS, 2006. Bassuk, S., Glass, T., Berkman, L. Social disengagement and incident cognitive decline in community-dwelling elderly persons. Annals of Internal Medicine. 1999; 131:165–173. Bradley, C.Hospitalisations Due to Falls in Older People, Australia, 2008–09. Canberra: AIHW, 2012. [INJCAT 138]. Burnett, A., Peel, M. Health needs of asylum seekers and refugees. British Medical Journal. 2001; 322:544–547. Cattan, M., Kime, N., Bagnall, A. The use of telephone befriending in low level support for socially isolated older people: an evaluation. Health and Social Care in the Community. 2011; 19:198–206. Cornwell, E. Y., Waite, L. J. Social disconnectedness, perceived isolation, and health among older adults. Journal of Health and Social Behavior. 2009; 50:31–48. Croskerry, P. Achieving quality in clinical decision making: cognitive strategies and detection of bias. Quality in Clinical Decision Making. 2002; 9:1184–1204. Davison, J., Marrinan, S., Falls. Reviews in Clinical Gerontology 2007; 17:93–107, doi: 10.1017/S0959259808002426. de Jong Gierveld, J., Havens, B. Cross-national comparisons of social isolation and loneliness: introduction and overview. Canadian Journal on Aging. 2004; 23(2):119–123. Department of Immigration and CitizenshipHumanitarian Settlement Services: Onshore Orientation Program. Belconnen, ACT: Australian Government, 2011. DeSouza, R.Doing it for Ourselves and Our Children: Refugee Women on Their Own in New Zealand. Auckland: Centre for Asian and Migrant Health, AUT University, 2012.

Dickens, A. P., Richards, S. H., Greaves, C. J., Campbell, J. L., Interventions targeting social isolation in older people: a systematic review. BMC Public Health 2011; 11:647–669, doi: 10.1186/1471–2458–11–647. Fratiglioni, L., Wang, H., Ericsson, K., Maytan, M., Winblad, B. Influence of social network on occurrence of dementia: a community-based longitudinal study. Lancet Neurology. 2000; 355:1315–1319. Gorst-Unsworth, C., Goldenberg, E., Psychological sequelae of torture and organised violence suffered by refugees from Iraq. Trauma related factors compared to social factors in exile. British Journal of Psychiatry 1998; 172:90–94, doi: 10.1192/bjp.172.1.90. Hawton, A., Green, C., Dickens, A. P., Richards, S. H., Taylor, R. S., Edwards, R., Greaves, C. J., Campbell, J. L., The impact of social isolation on the health status and health-related quality of life of older people. Quality of Life Research 2010; 20:57–67 Holt-Lunstad, J., Smith, T. B., Layton, J. B. Social relationships and mortality risk: a metaanalytic review. PLoS Medicine. 2010; 7:1–20. Jackson, N. Population ageing in a nutshell: a phenomenon in four dimensions. People and Place. 2007; 15(2):12–21. Locher, J., Ritchie, C., Roth, D., Baker, P., Bodner, E., Allman, R. Social isolation, support, and capital and nutritional risk in an older sample: ethnic and gender differences. Social Science & Medicine. 2005; 60:747–761. Mistry, R., Rosansky, J., McGuire, J., McDermott, C., Jarvik, L. Social isolation predicts rehospitalization in a group of older American veterans enrolled in the UPBEAT program. International Journal of Geriatric Psychiatry. 2001; 16:950–959. Ministry of HealthRefugee Health Care: A Handbook for Health Professionals. Wellington: Ministry of Health, 2012. Moller, J.Projected Cost of Falls-Related Injury to Older Persons as a Result of Demographic Change in Australia. Canberra: Commonwealth Department of Health and Ageing, 2003. NHS Confederation, Ambulance Service Network and Community Health Services Forum. Falls Prevention. New Approaches to Integrated Falls Prevention Services. Retrieved from

www.nhsconfed.org/Publications/Documents/Falls_prevention_briefing_final_for_website_30 2012. Nicholson, N. R. Social isolation in older adults: an evolutionary concept analysis. Journal of Advanced Nursing. 2008; 65(6):1342–1352. Snooks, H. A., Halter, M., Close, J. C.T., Cheung, W., Moore, F., Roberts, S. E. Emergency care of older people who fall: a missed opportunity. Quality and Safety in Health Care. 2006; 15:390–392. Thompson, C., Williams, K., Morris, D., Lago, L., Kobel, C., Quinsey, K., Eckermann, S., Andersen, P., Masso, M.HWA Expanded Scopes of Practice Program Evaluation: Extending the Role of Paramedics Sub-Project Final Report. NSW: Centre for Health Service Development, Australian Health Services Research Institute, University of Wollongong, 2014. Tromp, A. M., Pluijm, S. M., Smit, J. H., Deeg, D. J., Bouter, L. M., Lips, P. Fall-risk screening test: a prospective study on predictors for falls in community-dwelling elderly. Journal of Clinical Epidemiology. 2001; 54:837–844. World Health Organization (WHO)WHO Global Report on Falls Prevention in Older Age. Geneva: WHO, 2007.

Further resources • Learn more about telephone befriending services at www.stjohn.org.nz/What-wedo/Community-programmes/Caring-Caller. • Find out how one emergency service provider delivers falls prevention messages as part of a community partnership at www.ambulance.vic.gov.au/Community/CommunityPartnerships/Preventing-Falls.html. • Discover specific resources developed to assist non-English speakers to call an ambulance at www.ambulance.nsw.gov.au/Community-Info/Community-Education-Programs/NonEnglish-speakers-Calling-an-Ambulance-program.html. • Understand more about female genital mutilation with information and resources for health professionals at www.fgm.co.nz/contact.

CHAP TER 47

The dying patient By Katrina Recoche and Susan Lee

C O N C E P TS U S E D I N TH I S C H A P TE R • The paramedic’s clinical approach: Section 2 • Perfusion: Chapter 55 • The autonomic response: Chapter 56

O V E RV IE W • Patients who are expected to die of an established disease often engage with ambulance services during episodes of sudden deterioration. • Differentiation of reversible and inevitable deterioration requires decisions about active treatment versus active comfort measures. • The physiological changes associated with dying include a gradual shutdown of organ function that may have no obvious effect for periods but then causes episodes of sudden change. • Immunological compromise, immobility and pain-relieving medications can all lead to an acute change in the patient’s condition. These changes are not caused directly by the underlying terminal condition and are often treatable. • The psychological aspects of care of both the patient and their family are part of the holistic management of the dying patient.

Introduction Like most health professionals, paramedics are regularly faced with patients suffering from conditions for which treatment is futile and that will shortly lead to death. However, paramedic training is focused almost entirely on responses to acute events where the intent is to restore the patient to health. As one of the few resources able to respond to patients in the community setting, paramedics are therefore often faced with the difficult situation of an acute exacerbation of a terminal condition for which their guidelines are inappropriate or clearly ineffective. This chapter provides a structure to underpin the (often difficult) clinical decision making that can occur in these cases. End of life is ‘the part of life where a person is living with, and impaired by, an eventually fatal condition, even if the prognosis is ambiguous or unknown’ (Palliative Care Australia, 2008). In many cases advance care planning will determine what the person’s goals are regarding their end-of-life care. This planning process may result in an advance care plan or directive that sets out the person’s values and preferences for care and may include the appointment of an advocate or proxy decision maker. Death from terminal conditions is rarely linear, however, and most patients will suffer sudden health changes as death approaches. These changes can cause increased and noisy respirations or alterations in conscious state; faced with these sudden changes in a loved one, family members are often distressed and request emergency assistance. For paramedics the decision-making process must consider the advance care plan as well as whether the acute condition is treatable or part of the dying process. The World Health Organization (WHO) defines palliative care as ‘an approach that improves the quality of life of patients and their families facing the problem associated with life-threatening illness, through the prevention and relief of suffering by means of early identification and impeccable assessment and treatment of pain and other problems, physical, psychosocial and spiritual’ (WHO, 2011). It is provided by an interdisciplinary team of specialist professionals who work mainly in the field and takes place in the patient’s home as well as hospitals, aged care facilities and specialist palliative care inpatient settings.

Pathophysiology One of the most challenging aspects of the care of emergency patients is identifying when a person with a fatal illness is in a dying trajectory as opposed to suffering a reversible condition that may be related to the complications of medical intervention or errors in drug administration. This is further complicated because illness trajectories follow different paths. For example, the terminal cancer trajectory tends to have periods of exacerbation and remission with a return to relative health before an ultimately sharp decline at the end of life. Compared to chronic diseases such as COPD, the trajectory of remission and exacerbation rarely sees the person returning to former health: their decline is more linear and can take much longer from the time of diagnosis to death (Downey & Engelberg, 2010). People who are imminently dying have noticeable physiological changes in the way their body functions. These changes may occur over a period of hours or days prior to death and the course is both unpredictable and inevitable. There may be some variations between individuals who have different diagnoses, such as the presence or absence of particular symptoms like nausea and vomiting or bleeding. If a gradual decline is experienced before death, the following physical changes may be observed.

Central nervous system As death approaches the alterations in conscious state usually lead to the person becoming more introspective and socially isolated, sleeping more and spending less time interacting with those around them. In some cases these changes in conscious state progress steadily to coma as the person approaches death. Different levels of consciousness approaching death have been reported (Twycross & Lichter, 1998), with between 6% and 30% of patients being conscious up to 15 minutes before death. Some individuals seem to rally for a short time prior to death, becoming more conscious, but this momentary clarity is unlikely to be sustained. Physiologically, these changes may be a result of accumulating toxins from tissue destruction caused, for example, by a tumour or hypoxia. Up to 88% of individuals suffering a terminal disease will experience some form of delirium in the last weeks of life (Keely, 2010). Most often the delirium is hypoactive, represented by moaning and mumbling, but it can take a hyperactive form with hallucinations, florid speech, paranoia, restlessness and confusion or myoclonic seizures (Keely, 2010). These responses can be particularly distressing for relatives. Peripheral reflexes decrease as circulation to the periphery decreases. This also results in reduced peripheral sensation, so touch perception may be reduced, although pressure sensation may still be present, in addition to pain.

Circulation As cellular function deteriorates approaching death, cardiac rate and rhythm may be altered and arrhythmias such as tachycardia and bradycardia are common. As cardiac output diminishes, pulse pressure decreases, so peripheral pulses are less palpable and heart sounds fainter. With less peripheral circulation, often skin takes on a pale, waxen appearance. In cases where hypoxia contributes to cell death, there may be increasing

peripheral or central cyanosis. As peripheral circulation diminishes, core temperature may increase, while the periphery cools. Sweating in order to cool the body occurs. Cardiac failure, both right-and left-sided, is a feature of end-stage cardiac decline. The drop in cardiac output results in poor perfusion, which in turn generates inflammatory mediators. This may cause fluid to enter the interstitial spaces, leading to peripheral or (more often) pulmonary oedema.

Respiratory system Pneumonia is a common infection in people with cancer, the elderly and those with terminal illnesses. Consolidation caused by infection reduces air entry and contributes to poor gas exchange at the alveoli, resulting in dyspnoea. Copious bronchial exudates may also contribute to increased cough, though the cough reflex diminishes as the dying trajectory extends. Air hunger, as a result of lung failure at the end of life, can cause severe distress and restlessness and rapid grunting respirations. There are two more common significant changes to respirations as a person is dying. The earlier change is called Cheyne-Stokes breathing and refers to an irregular pattern of breathing in both rate and depth, with the presence of periods of apnoea. This sign appears in the comatose patient, indicating interruption of the respiratory drive mechanisms in the brainstem. The normal drive to breathe is driven by CO2 levels, but as death approaches the respiratory centre’s response to varying CO2 levels can become erratic. Although Cheyne-Stokes breathing is seen in patients with brain trauma (Wilson & Giddens, 2009), its presence in a person with terminal illness indicates biochemical changes associated with either hypoxaemia or chemical mediators associated with tissue breakdown. The second change occurs later in the dying trajectory and is often referred to as the death rattle: this respiratory noise may develop as a result of both upper and lower airway changes (Wilson & Giddens, 2009). The coarse crackles associated with this phase can develop as a result of left ventricular failure causing pulmonary oedema or because secretions pool in the upper airways. At this stage the patient is often unable to clear these secretions and the noise becomes louder; it can be particularly distressing for family members and carers. Repositioning of suctioning is often effective in reducing upper airway noises.

Gastrointestinal system Gastrointestinal motility and absorption diminish as circulation to the gut decreases. This results in anorexia and constipation. Often, family members and health professionals may be concerned about lack of eating and attempt to ‘force feed’ the person, which only results in nausea and vomiting. Dysphagia or difficulty swallowing may make taking oral medications difficult and this should be anticipated, as most drugs necessary at the end of life can be administered by the subcutaneous route. Thirst as a result of dehydration is not a common problem at the end of life, despite a reduction in fluid intake. Reduced hydration may assist in reducing other more noxious symptoms such as fluid accumulation in the lungs, vomiting and incontinence. Drying of the tongue and lips is not uncommon but may not be directly related to hydration levels; rather, it may be the result of an

increased respiratory rate, the side effects of medications or oral candidiasis.

Renal system Urine output decreases with a reduction in hydration and circulation. This is unlikely to cause symptoms, but incontinence or retention caused by loss of sensation to the bladder may contribute to agitation. Urinary concentration and stasis may contribute to the development of urinary tract infection, resulting in increasing pain, which can contribute to agitation.

Hepatic system With the failing perfusion status comes a reduction in liver function and therefore a reduction in the body’s ability to clear drugs. It is not uncommon to see a reduced need for opiates in the last stages due to the reduction in drug clearance that occurs. Drug administration should be guided by symptoms and acknowledging that there may be a reduction in drug clearance.

Other changes Catastrophic bleeding occurs in 6–10% of patients with palliative care needs, particularly those with haematological malignancies (McGrath & Leahy, 2008). It may, however, be associated with liver failure, comorbid haematological disorders, chemotherapy, medications, radiotherapy, surgery and the underlying disease progression, such as damage of blood vessels by tumour (Hulme & Wilcox, 2008). Bleeding may be episodic, a lowvolume oozing or catastrophic depending on the underlying cause (McGrath & Leahy, 2008). Bleeding may present as bruising, melaena, haemoptysis, haematuria, haematemesis, epistaxis, or vaginal or rectal bleeding. The site of the bleeding may give some indication of the cause and provide direction for management. Patients at risk of catastrophic bleeding should have advance care plans in place and standing orders for sedation and pain management available if they are being cared for in their own home. Paramedics should contact the patient’s GP and community-based palliative care providers before starting aggressive resuscitation for bleeding. In addition, simple measures such as using dark-coloured towels to disguise the colour and amount of bleeding can reduce the family’s distress (McGrath & Leahy, 2008). The patient’s family and carers often require reassurance that the patient is in an altered conscious state and that any pain is being managed (McGrath & Leahy, 2008). Administration of sedation during a catastrophic bleed is standard palliative care practice but sits outside the normal guidelines used by paramedics: consultation with the patient’s care team is strongly recommended in this situation. Spinal cord compression may be caused by a primary tumour and have an insidious onset or commonly by metastases from lung, breast, prostate or renal primary malignancies. Displacement of the spinal cord is caused by the metastatic lesion affecting function and leading to irreversible paralysis if not treated (Quraishi & Esler, 2011). The signs and symptoms may include back pain, limb weakness or sensory changes and bladder dysfunction, followed by ataxia and paralysis if it progresses (Patchell et al., 2005; Quraishi

& Esler, 2011). The skeleton is the third most common site for metastases after the lungs and liver (Patchell et al., 2005). Bony metastases most commonly occur in the vertebrae (Selvaggi & Abraham, 2006). Spinal cord compression occurs in 5–14% of patients with a cancer diagnosis and is considered a palliative care emergency that requires immediate hospitalisation (Patchell et al., 2005). The paramedic’s role includes calm explanations to allay the patient’s and family’s fear and anxiety and liaison with the treating palliative care team or GP to arrange hospital admission.

CA SE ST U DY 1 Case 14058, 0435 hrs. Dispatch details: An unconscious 67-year-old man with a history of lung cancer is in respiratory distress and an altered conscious state. Initial presentation: The paramedics are taken to the bedroom by the patient’s distressed wife. The patient is lying supine in bed on three pillows. He appears cachexic, pale and diaphoretic, and his breathing is stertorous. Peripheral cyanosis is also noted.

ASSESS Patient history Determining the underlying cause of the patient’s deterioration is important. In particular, understanding whether the patient’s condition is due to some reversible side effect of medical treatment or an end-of-life trajectory is key to determining the paramedic’s next step. Patients with advanced cancer are likely to have recently had medical advice about their condition and treatment options. Asking the patient’s wife about medical discussions in relation to his cancer and treatment is important. A more thorough physical assessment is appropriate. The paramedics should check the patient’s temperature and ask about his recent cancer treatment. Some cancer treatments such as chemotherapy can increase the risk of infection by causing neutropenia. This risk will be at its maximum within a couple of weeks of chemotherapy. Possible sites of infection such as lungs or urine should be checked.

The paramedics should also ask what medications the patient is taking and any recent changes to these medications. Patients with cancer pain can be on significantly large doses of opioid analgesics but this is unlikely to be the cause of this patient’s condition if he has been on a slowly increasing dose over a period of time. However, the introduction of new opioids or large dose changes should be investigated. The patient’s central nervous system response should be checked by repeating the assessment of consciousness (Glasgow Coma Scale) and pupil size and response to light. Asking the patient’s wife about the patient’s condition over the last few days, particularly his sleep–wake cycles and food and fluid intake, may indicate a pattern of deterioration. However, the paramedics should not conclude a dying trajectory until they have determined that changes in medications such as increases in opioids are not contributing to his decreased conscious state. They should check his peripheral circulation and reflexes. Lack of plantar and radial pulses, peripheral cyanosis and coolness, and sluggish plantar reflexes may be a result of reduced cardiovascular function in a dying patient.

P RACT ICE T IP Cancer Institute NSW (2009) identifies febrile neutropenia as a medical emergency: it is indicated by a temperature of at least 38.3°C (or at least 38°C on two occasions) and a neutrophil count of less than 0.5 × 109 cells/L or less than 1.0 × 109 cells/L and predicted to fall to lower than 0.5 × 109 cells/L.

Initial assessment summary

Problem Conscious state Position Heart rate Blood pressure Skin appearance Speech pattern Respiratory rate Respiratory rhythm Chest auscultation Pulse oximetry Temperature History Physical assessment

Altered conscious state GCS = 6; no eye opening, no verbal response, minimal attempt at withdrawal to pain Semi-recumbent in bed 70 BPM, irregular, shallow 100 on palpation Pale, diaphoretic, peripherally cyanosed No speech 15 BPM Shallow, irregular with periods of apnoea Widespread coarse crackles bilaterally Not sensing 36.1 °C Recent decline in health. His wife was woken by his noisy breathing and was unable to rouse him. Patient cachexic

This patient appears to be in the terminal phase of his illness.

Look for! • Grunting respirations and use of accessory muscles to breathe • Malodourous urine • Lower abdominal pain on palpation

Ask about! • Medication history • Medication chart or record • Palliative care record or referral • Mental state over past 24 hours • Patterns of eating and drinking • Last medical discussions

CONFIRM The essential part of the clinical reasoning process is to seek to confirm your initial hypothesis by finding clinical signs that should occur with your provisional diagnosis. You should also seek to challenge your diagnosis by exploring findings that do not fit your hypothesis: don’t just ignore them because they don’t fit. There are a number of possible reasons for this patient’s deterioration. His cancer may be progressing and he may in fact be near death. Alternatively, he may be septic as a result of his cancer treatment suppressing his immunity or he may have experienced an overdose of medications.

What else could it be? Sepsis If overwhelming sepsis is the problem, the patient may have an increased body temperature, but patients who have suppressed immunity may not exhibit the same response to infection as people with normal immunity (refer to Ch 44; Cancer Institute NSW, 2009). Similarly, the lack of tachycardia normally associated with sepsis may be a result of the patient’s terminal state and cannot be used to definitively exclude sepsis. The risk of infection is increased by both the patient’s bed-ridden state and his underlying disease, but infection may not be the cause of his sudden deterioration.

DIF F ERENT IA L DIA GNOSIS Terminal stage of cancer (dying) Or • A reversible condition associated with sepsis • A reversible condition associated with a change in medication

Medication change In opioid overdose, patients often have a decreased level of consciousness, bradycardia and hypoventilation, as does this patient. A brief assessment of his conscious level using the Glasgow Coma Scale to assess psychomotor response and pupil size will assist in differentiating between drug overdose and disease progression. Constricted pupils are often present in patients who have been on narcotics for a long period of time. In this case the patient’s pupils are normal. Understanding the patient’s recent medication history is likely to assist in the exclusion of drug overdose. Speaking to the patient’s GP, district nurse or palliative care provider may clarify his medication usage and medical management plan and goals of care.

T REAT Emergency management The challenge for paramedics faced with this situation is not to necessarily initiate the emergency care that a patient displaying these vital signs would normally require. The primary concern in managing a terminally ill patient in the community is to slow decision making down as much as possible to ensure that the patient’s wishes are respected, family members are supported and the patient is kept comfortable. Using a palliative approach to care is necessary in order to ensure the comfort and safety of the patient and their family. If the patient is imminently dying as a result of his progressive cancer, there is nothing that can be done to prevent his death. However, determining his wishes in the circumstances is important. Some patients may have indicated their wishes in terms of the place of their death and their desire not to experience medical interventions such as trips to hospital or resuscitation by discussing this with family members, documenting a refusal of treatment, appointing a proxy decision maker in an enduring power of attorney or preparing an advance care plan. A careful and sensitive discussion with the patient’s wife may determine the patient’s wishes and guide the treatment plan. Even when families have discussed death and options such as the patient’s desire to remain at home or to refuse medical interventions, family members may not be sure if these decisions apply to the particular situation they find themselves in. Sometimes they need reassurance that their loved one is dying in order to acknowledge that they can put a discussed plan into action. Because dying often happens at night, or because of panic, family members may call an emergency paramedic instead of the community nurse, palliative care provider, GP or other family members, even though they have been instructed not to do so. Gentle assistance to recall the plan of care in these circumstances may be helpful. Sometimes, the use of oxygen via a mask or nasal cannula will improve oxygenation and enable the patient to participate in these discussions, but if the decision is made subsequently to leave the patient at home, the oxygen will have to be removed, which may be hard for the family. Oropharyngeal suction may also be used to reduce the secretions causing stertorous breathing. This is rarely effective as the fluid re-accumulates and may irritate an otherwise peaceful patient, but it may reduce the noise associated with breathing. Patients with stertorous breathing are normally unconscious and dyspnoea is not apparent, but the noise is often distressing for family members. If the following documents have been completed by the patient, they may assist in determining appropriate treatment in the event of imminent death by identifying either the patient’s wishes or a proxy who has an understanding of the patient’s wishes:

• refusal of treatment • enduring medical power of attorney (MPOA) • advance care plan. A community palliative care service plan of care for end of life may include standing orders of helpful medications for symptoms such as pain, nausea, vomiting, agitation and noisy breathing. Phoning the palliative care doctor, GP or nurse involved in the patient’s care may assist the paramedic in clarifying the patient’s condition and plan of care. In some situations, the decision will be made to transport the patient to hospital for end-of-life care, based on clarification of the patient’s wish not to die at home or consideration that the family is unable to provide care at home. Moving a patient who has very poor cardiac output into a sitting position in order to transfer them to a stretcher can reduce venous return sufficiently to completely compromise cardiac output and cause a sudden deterioration. This should be considered when making the decision to move the patient. If an opioid overdose is suspected, extreme care should be taken in attempting to reverse the overdose with a narcotic antagonist (see Box 47.1). A lack of careful titration is likely to cause severe rebound pain in the terminally ill person, either necessitating emergency hospital admission for some days to reestablish pain control or leading to an excruciatingly painful death if death is imminent. Supportive care is preferable with oxygen/ventilation support until the serum concentration of the narcotic has reduced and the patient’s conscious state has improved, although this may take some time. Often CO2 retention is a significant factor in opiate-induced respiratory failure causing a decreased conscious level: this will reverse with a few full breaths using a bag/mask. When all other options have been exhausted or if imminent death as a result of overdose is suspected, an opioid reversal protocol (not more than 100 mcg IV per dose titrated to effect) devised for palliative care may be used. B O X 4 7 . 1E t h i c

al issue: do uble eff ec t

The principle of double effect was identified by St Thomas Aquinas to describe circumstances in which an action may have good and bad effects but still be morally acceptable (Boyle, 2004; Jolly & Cornock, 2003). A good example of this is that the means of managing intractable symptoms may inadvertently shorten a patient’s life. The intent of the treatment is to palliate the symptoms and death is a foreseen but unintended consequence of that treatment (Boyle, 2004). The principle of double effect does not simply allow bad outcomes because they are not intended, however: the requirement of a ‘proportionally grave reason’ for harmful side effects must give appropriate weight and consideration to the moral justification for the action (Boyle, 2004). Some palliative care legislation is enlightened enough to specifically mention and support the situation where management improves quality of life but may shorten it.

Depending on the patient’s wishes it may be appropriate to either aggressively manage sepsis or actively not manage it. If sepsis as a result of neutropenia is suspected and active management is selected, time to first treatment with antibiotics (1 hour is recommended) is a significant factor in survival. The septic shock is managed with oxygen and IV fluids to maintain blood volume during immediate transport to hospital (Cancer Institute NSW, 2009).

Verification of death In some jurisdictions (check relevant state and/or federal legislation), credentialled paramedics are permitted to verify death by undertaking clinical assessment of a body and establishing that death has occurred (see Box 47.2). B O X 4 7 . 2C r i t e r i a

f o r t h e ve r i fi c a t i o n o f

death • No palpable pulse and • No heart sounds heard for 2 minutes and • No breath sounds heard for 2 minutes and • Fixed (non-responsive to light) pupils and • No response to centralised painful stimulus and • No motor response to peripheral painful stimulus Source: Department of Health (2011).

EVALUAT E Continuous reassessment of the patient’s condition and interventions is important. Liaison with palliative care services or the patient’s GP should also occur in conjunction with the patient’s family.

Ongoing management While disease trajectories are unique to the individual they are also driven by pathophysiology, shaped by strategies used by patients, families and health professionals and of course affected by issues such as access to treatment options and services. In the healthcare setting, clinical care pathways have been used to streamline care management and resource allocation. Clinical care pathways are structured multidisciplinary plans of care designed to support the implementation of clinical guidelines, clinical and non-clinical resource management, clinical audits and financial management. They provide detailed guidance for each stage in the management of a patient for a specific condition over a given time period and include progress and outcome details (Marie Curie Cancer Institute Liverpool, 2010). Care pathways usually have four components: (1) a timeline, (2) categories of care and interventions, (3) intermediate and long-term outcome criteria and (4) a record of deviations from the pathway and how they are managed. They can be viewed as algorithms in that they offer a flow chart for step-wise decision making for a particular patient group or condition. The Liverpool Care Pathway was developed in a partnership between the Royal Liverpool Hospital and the city’s Marie Curie Hospice in the late 1990s, with the aim of facilitating the dying phase for those patients being cared for in acute care settings (Marie Curie Cancer Institute Liverpool, 2010). In Australia, the majority of expected deaths of the elderly and those with nonpalliative care conditions occur in hospitals or extended-care facilities (Jackson, Mooney & Campbell, 2009). The Liverpool Care Pathway has been adapted for use with patients in acute and extended-care facilities all over the world so as to best reflect local practices, needs and resource availability (Jackson, Mooney & Campbell, 2009). The end-of-life care pathway is patient-and family-focused, based on evidence and addresses the four key domains of physical, psychological, social and spiritual needs (Jackson, Mooney & Campbell, 2009; Marie Curie Cancer Institute Liverpool, 2010). Whatever title is given to the pathway, it serves to guide generalist staff through basic palliative care principles and practices. A key to successful implementation is helping staff to identify impending death early enough to facilitate a ‘good death’ for the patient and support for their family (Jackson, Mooney & Campbell, 2009; Marie Curie Cancer Institute Liverpool, 2010). Using the pathway, medications, treatments and other interventions are reviewed and their value, in terms of how they support palliative care goals, is evaluated. Unnecessary interventions and medications are discontinued. Recommended standing orders for medications to manage a range of potentially distressing symptoms that may accompany end of life are also included in the pathway. The most common symptoms are pain, agitation, excessive upper respiratory secretions, dyspnoea, and nausea and vomiting. Medications are balanced to provide the most effective level of symptom management possible. For nonspecialist palliative care staff, the types of drugs used, the combinations and the dosage ranges may be unfamiliar and confronting. The recommended medication guidelines have been developed based on evidence-based palliative care practice.

Hospital admission Managing a ‘good death’ in a home setting is the goal of many palliative care plans but, failing this, admission to hospital or (rarely) direct hospice admission is an alternative. The emergency department (ED) is the main portal of entry to hospital and as such has increasingly been accessed by those with end-of-life needs. The problem is that EDs (like paramedics) are priority-driven more towards resuscitation and prolonging life than providing quality end-of-life care (Bailey, Murphy & Porock, 2011). The focus on diagnosis, stabilisation and complying with performance measures such as waiting times and length of stay does not equip EDs with resources and pathways for palliation and explains why end-of-life care in this setting may be less than optimal (Fullerton, Kenner & Tucker, 2012). In the ED there is little space or privacy for patients and families to prepare for impending death or for staff to be able to offer the quality of end-of-life care and family support that palliative care standards outline. A Western Australian study reviewed hospital and ED use by people who were expected to die. The study excluded people who were residents of extended-care facilities. Over a one-year period, of the 1071 people who died, 61.5% died in hospital and 4% had been seen in an ED on the day of their death (Bailey, Murphy & Porock, 2011; Rosenwax et al., 2011). Rosenwax and colleagues (2011) suggest that such pressures on the acute health system may indicate gaps in palliative care service delivery that the acute sector should not be used to plug. Death in an ambulance on the way to hospital is also not ideal. Consider how the patient and family may be supported at home, particularly if the patient is close to death. Liaison with the patient’s GP and community-based palliative care service provider is important for a plan of care to be complete. In some states extended care paramedics have proved very competent in this area of care, working in conjunction with the patient’s GP and palliative care teams. The patient may have been an inpatient in a specialist palliative care unit in the past and be known to the medical and nursing staff. If so, the GP or community palliative care service may be able to assist with admitting the patient directly into the palliative care unit, rather than an ED.

Death and dying across the lifespan In recent years Australia’s death rate has stabilised at 6.0 deaths per 1000 population, down from 6.3 in 2004 and 12.7 in 1971 (ABS, 2011). Advances in medicine, public health strategies and public awareness have seen deaths from ischaemic heart disease decline from 162.9 per 100,000 in 1998 to 96.9 per 100,000 in 2008 and deaths from stroke reduce from 71.6 per 100,000 in 1998 to 48.5 per 100,000 in 2008. However, deaths from dementia and Alzheimer ’s disease are increasing (ABS, 2011). Men continue to die at a younger age compared with women, but the gap is shrinking (ABS, 2011; see Fig 47.1 [most recent data at the time of writing]).

FIGURE 47.1

Comparative male and female death rates, Australia 2009. Deaths per 1000 of the estimated resident population, as of 30 June 2009. Source: ABS (2011).

Causes of death vary across the lifespan (see Table 47.1). Most deaths in children younger than 1 year old are due to injuries and conditions related to the perinatal period or congenital abnormalities. From 1 to 14 years of age malignant neoplasms and external causes such as injury, drowning or transport accident are common. Between 15 and 24 years of age, transport accidents and intentional self-harm increase, as is the case for the 25–34-year-old group, for whom circulatory disease also becomes a feature. Malignant neoplasms and circulatory diseases take over as the main causes of death for those aged over 45, respiratory disease is notable from age 65 and falls become a feature for those aged over 75 (ABS, 2009, 2011). TABLE 47.1

Comparison of cause of death by age, Australia

Source: Adapted from ABS (2009).

CA SE ST U DY 2 Case 10045, 1600 hrs. Dispatch details: A 78-year-old woman with a 5-year history of breast cancer has been found drowsy and disorientated by her daughter. Initial presentation: The paramedics arrive at a private house and follow the daughter to the bathroom where they find the patient sitting against the basin.

ASSESS 1610 hrs Primary survey: The patient is disorientated to place and time. 1611 hrs Chief complaint: Drowsy and disorientated. 1612 hrs Vital signs survey: Perfusion status: HR 100 BPM strong and regular, BP 110/65 mmHg, skin pale and clammy. Respiratory status: RR 22 BPM, good clear air entry bilaterally. Conscious state: GCS = 12. 1615 hrs Pertinent hx: The daughter (the patient’s carer) called her mother this morning at 11 and found that she had been vomiting; this was unrelieved by antiemetic. She arrived home from work at 4 to find her mother drowsy and disorientated. The patient has not had anything to eat or drink for 48 hours and has recently undergone chemotherapy. She is on cycle three and was reviewed by her GP a week ago, when her medications were reviewed. Initially the patient was diagnosed with ductal carcinoma of the breast with axillary lymph node involvement and had a right mastectomy and axillary clearance with radiotherapy. Two months ago she had liver metastases diagnosed following routine follow-up scans. She has had two cycles of chemotherapy with a limited response. She was referred to a palliative care consultant and community palliative care services in the local area. 1618 hrs Secondary survey: Alopecia related to chemotherapy; dry mouth, coated tongue; pupils equal and reacting; right mastectomy scarring well-

healed; tense abdomen; bowel sounds present and normal; diffuse pain on palpation; nil rebound tenderness. The patient has been incontinent of urine and has a fine tremor in her hands. The patient has a history of decline over the last 2 days and presents confused with a raised respiratory rate and signs of dehydration. The problem appears to be dehydration secondary to nausea and vomiting, but it is unclear what caused the nausea and vomiting in the first place. It is possible that this could be due to the drugs used in her chemotherapy.

CONFIRM In many cases paramedics are presented with a collection of signs and symptoms that do not appear to describe a particular condition. A critical step in determining a treatment plan in this situation is to consider what other conditions could explain the patient’s presentation.

What could it be? Side effect of medication Nausea and vomiting are unfortunately a well-known side effect of many chemotherapy drugs and they can be difficult to manage effectively. Once a patient has started to vomit, administering oral antiemetics becomes difficult. The patient may respond to systemic administration of an appropriate antiemetic and consultation with the patient’s care team is encouraged. Cardiovascular stroke A stroke could cause a decrease in the patient’s conscious level. Patients with cancer can have an increase in coagulation factors and are at a higher risk of an embolic stroke. This would usually present with some unilateral signs, which do not appear to be present in this patient.

DIF F ERENT IA L DIA GNOSIS Terminal stage of cancer Or • Side effect of medication • Cardiovascular stroke • Sepsis • Drug overdose of opiates • Bowel obstruction • Cerebral metastases

Sepsis

Infection is a possibility, with a relative lack of response to the infection being due to the immunosuppression associated with chemotherapy. If this cannot be confidently ruled out, empirical treatment as if this is sepsis is usually recommended. Drug overdose of opiates Opiates cause nausea and a decreased conscious state so could be responsible for this patient’s presentation. Look for changes in drug use, noting that the patient may not have been following the prescribed recommendations exactly. Bowel obstruction The patient could have a bowel obstruction. Unfortunately, it is difficult to assess the patient’s abdomen in this situation as diffuse tenderness is not diagnostic of a bowel obstruction. She wouldn’t be expected to have passed much per rectum as she hasn’t been eating, so this won’t help the assessment. At the moment, this diagnosis remains a possibility. Cerebral metastases Cerebral metastases can present with nausea and vomiting and are quite likely in this setting. Lack of focal signs is reassuring, but does not exclude the diagnosis. This diagnosis still remains a possibility. Establishing the cause of the patient’s nausea and vomiting becomes a process of elimination, which may well rely on in-hospital tests and investigations, as well as the patient’s response (or not) to medication.

T REAT The patient’s first need is for volume replacement and control of her nausea and vomiting. IV fluids and an IV antiemetic are an appropriate first measure. Her condition is complex and identifying the cause of the nausea and vomiting will lead to long-term management strategies. As health professionals working within the greater healthcare team this is the time for the paramedics to share the problem with the clinicians who know the patient’s history well. A joint management plan between the paramedics and the treating palliative care team will probably involve an early review and investigations, either in-hospital or as an outpatient.

EVALUAT E Evaluating the effect of any clinical management intervention can provide clues to the accuracy of the initial diagnosis. Some conditions respond rapidly to treatment so patients should be expected to improve if the diagnosis and treatment were appropriate. A failure to improve in this situation should trigger the clinician to reconsider the diagnosis.

In this case, the paramedics will evaluate whether they have relieved the patient’s symptoms and returned her to a functional state. An improvement in her conscious level, a decrease in the nausea and vomiting and a decrease in her respiratory rate would all be indicative of an initial improvement. In conjunction with her treating team they will evaluate whether it is safe and appropriate to treat her at home or whether she needs hospital investigation for stabilisation and assessment.

Summary Management of the dying patient in a palliative care situation is very different from the normal paramedic approach of treat and resuscitate. However, paramedics are in a position to be able to significantly improve quality of life for the remainder of the patient’s life and to support their family at the time of their death. Managing patients in this situation is very much a multidisciplinary team activity and the professional paramedic has an important role to play.

References Australian Bureau of Statistics (ABS). Causes of Death Australia. Retrieved 27 October 2011 from www.abs.gov.au/ausstats/[email protected]/Products/B6940E9BF2695EE1CA25788400127B0A? opendocument, 2009. [Cat. no. 3303.0.].

Australian Bureau of Statistics (ABS). Gender Indicators. Retrieved 27 October 2011 from www.abs.gov.au/ausstats/[email protected]/Lookup/by+Subject/4125.0~Jul+2011~Main+Features~Death 2011. [Cat. no. 4125.0.]. Bailey, C., Murphy, R., Porock, D. Trajectories of end-of-life care in the emergency department. Annals of Emergency Medicine. 2011; 57(4):362–369. Boyle, J. Medical ethics and double effect: the case of terminal sedation. Theoretical Medicine. 2004; 25(1):51–60. Cancer Institute NSW, Immediate Management of Neutropenic Fever. eviQ. Retrieved 31 October 2011 from

www.eviq.org.au/Protocol/tabid/66/categoryid/568/id/123/Immediate+Management+of+Febri 2009 Department of Health, State Government of Victoria. Guidance Note for the Verification of Death. Retrieved from www.health.vic.gov.au/__data/assets/pdf_file/0006/356667/Feb2011-Guidance-Note-for-the-Verification-of-Death.pdf, 2011. Downey, L., Engelberg, R. A. Quality-of-life trajectories at the end of life: assessments over time by patients with and without cancer. Journal of the American Geriatric Society. 58(3), 2010. Fullerton, S. L., Kenner, D. J., Tucker, M. T. Letter to editor. Anywhere to palliative care: a fast-track pathway from the emergency department to palliative care. Medical Journal of Australia. 196(9), 2012. Hulme, B., Wilcox, S., Yorkshire Palliative Medicine Clinical Guidelines Group. Guidelines on the Management of Bleeding for Palliative Care Patients with Cancer. Retrieved October 2014 from www.palliativedrugs.com/download/090331_Final_bleeding_guideline.pdf, 2008.

Jackson, K., Mooney, C., Campbell, D. The development and implementation of the Pathway for Improving the Care of the Dying (PICD) in general medical wards. Internal Medicine Journal. 2009; 39(10):695–699. Jolly, M., Cornock, M. Application of the doctrine of double effect in end stage disease. International Journal of Palliative Nursing. 2003; 9(6):240–244. Keely, P. Delirium at the end of life. American Family Physician. 81(10), 2010. Marie Curie Cancer Institute LiverpoolWhat is the Liverpool Care Pathway for the Dying Patient (LCP)? Information for Healthcare Professionals. Liverpool: Marie Curie Cancer Institute Liverpool, 2010. McGrath, P., Leahy, M. Catastrophic bleeds during end-of-life care in haematology: controversies from Australian research. Supportive Care in Cancer. 2008; 17(5):527–537. Palliative Care Australia. Palliative and End of Life Care Glossary of Terms, 1st ed. Canberra: Palliative Care Australia, 2008. Patchell, R. A., Tibbs, P. A., Regine, W. F., Payne, R., Saris, S., Kryscio, R. J., et al. Direct decompressive surgical resection in the treatment of spinal cord compression caused by metastatic cancer: a randomised control. Lancet. 2005; 366(9486):643–648. Quraishi, N. A., Esler, E., Metastatic spinal cord compression. British Medical Journal 2011; 342:2402, doi: 10.1136/bmj.d2402. Rosenwax, L. K., McNamara, B. A., Murray, K., McCabe, R. J., Aoun, S., Currow, D. Hospital and emergency department use in the last year of life: a baseline for future modifications to end-of-life care. Medical Journal of Australia. 2011; 194(11):570–573. Selvaggi, K., Abraham, J. Metastatic spinal cord compression: hidden danger. Nature Clinical Practice Oncology. 2006; 3(8):458–461. Twycross, R., Lichter, I. The Terminal phase. In Doyle D., Hanks G.W.C., MacDonald N., eds.: Oxford Textbook of Palliative Medicine, 2nd ed., Oxford: Oxford University Press, 1998. Wilson, S. F., Giddens, J. F. Health Assessment for Nursing Practice, 4th ed. St Louis: Mosby, 2009.

World Health Organization (WHO). WHO definition of palliative care. Retrieved 28 October 2011 from www.who.int/cancer/palliative/definition/en, 2011.

CHAP TER 48

The patient on out-of-hospital dialysis By Leanne Boyd

C O N C E P TS U S E D I N TH I S C H A P TE R • The paramedic’s clinical approach: Section 2 • Perfusion: Chapter 55 • The autonomic response: Chapter 56 • The inflammatory response: Chapter 57

OVERVIEW • Nephrons are the functional units of the kidneys, filtering blood to control blood volume and electrolyte balance and allow the excretion of wastes. • Each kidney contains up to 1 million nephrons. • A person can lose up to 90% of their renal function before becoming symptomatic (Kidney Health Australia, 2011). • End-stage kidney disease (ESKD) predisposes patients to a number of serious conditions and complicates emergency assessment and management. • In 2008, 17,578 Australians received renal replacement therapy (RRT): 7516 had a functioning transplant and 10,062 received dialysis (Cass et al., 2006). • In 2010, dialysis and kidney transplant services cost the Australian government almost $1 billion (Kidney Health Australia, 2010). • The cumulative cost, in today’s dollars, of treating all current and new cases of ESKD to 2020 is estimated to be approximately $12 billion. Increasing the use of home-based dialysis (home haemodialysis and peritoneal dialysis) over this period would lead to an estimated saving of approximately $378-$430 million (Kidney Health Australia, 2010). • Dialysis has dramatically improved the mortality rates of patients with ESKD. However, the therapy does not completely replicate the function of healthy kidneys and the mortality and

morbidity rates of these patients remain unacceptably high. • Paramedic responses to patients on dialysis are likely to increase significantly in the future.

Introduction End-stage kidney disease (ESKD) is the most severe form of chronic kidney disease; it is also known as stage 5 chronic kidney disease (CKD) or kidney failure (AIHW, 2013). In ESKD irreversible damage to the kidneys results in a loss of control of blood volume and waste excretion and a subsequent rise in blood nitrogen levels (AIHW, 2013). The severity of the renal impairment can also affect the kidneys’ other functions, such as promoting the growth of red blood cells (RBCs) and maintaining bone density. Although ESKD is not an acute condition, it compromises the body’s homeostatic ability to such a degree that it complicates emergency management of the host of conditions that are associated with it. Treatment of ESKD with dialysis further complicates the emergency management of these patients. Kidney replacement therapy (KRT) in the form of dialysis or a kidney transplant is required for survival when kidney function is no longer sufficient to sustain life (AIHW, 2013).

Pathophysiology Although the kidneys make up less than 1% of body weight, they receive 20% of cardiac output (Boron, 2012). In the setting of trauma this ‘mismatch’ makes paramedics and other emergency clinicians wary of the potential for rapid blood loss if the kidneys are injured. But the kidneys’ anatomical location provides them with excellent protection: superiorly they sit just below the diaphragm, with the left kidney posterior to the spleen and the right posterior to the liver (Tortora & Grabowski, 2014; see Fig 48.1). Protected by these organs the kidneys are also tightly packed into the retroperitoneal space by two layers of dense fat (Tortora & Grabowski, 2014). From behind they are shielded by the muscles of the back and also receive partial protection from the 11th and 12th ribs (Tortora & Grabowski, 2014). In reality, the kidneys are far more likely to be damaged from internal disease processes than external trauma and it is in their everyday function where the magnitude of their role becomes obvious.

FIGURE 48.1 The location of the kidneys. Source: Adapted from Talley & O’Connor (2013).

The reason for the apparent mismatch between the kidneys’ physical size and the blood supply they receive becomes obvious when the role of the kidneys is examined more closely. The functional unit of the kidneys is the nephron: approximately 1 million nephrons are distributed around the outer portion (the cortex) of each kidney. Nephrons consist of a ‘nest’ of extremely porous capillaries (the glomerulus) surrounded by a capsule known as Bowman’s capsule (Tortora & Grabowski, 2014). Red and white blood cells flowing into the glomerulus are too large to escape into Bowman’s capsule but large amounts of plasma and dissolved electrolytes escape the blood and are collected by the capsule (Tortora & Grabowski, 2014). This pressure-driven filtration is important not only in controlling blood volume, but also for maintaining pH and the excretion of wastes (Tortora & Grabowski, 2014). Once collected in Bowman’s capsule the filtrate flows into a series of convoluted tubules where essential electrolytes and nutrients are reabsorbed while wastes are kept within the increasingly concentrated urine. The kidneys also secrete a number of substances back into the bloodstream that act as vasoconstrictors (renin-angiotensin), as well as secreting erythropoietin (EPO), a hormone that stimulates the production of RBCs and calcitriol, the active form of vitamin D (Elliot, Aitken & Chaboyer, 2012). The processes of reabsorption and secretion are essential for homeostasis but they are dependent on the nephrons creating sufficient filtrate. In a healthy kidney the glomerular filtration rate (GFR) equates to approximately 180 L per day, an amount that clearly cannot be lost as urine: nearly all of this fluid must be absorbed by the tubules that extend from the glomerulus. In the process of reabsorbing this fluid the kidneys are able to closely control the amount of acid in the blood as well as controlling blood volume (Tortora & Grabowski, 2014). With up to 2 million nephrons performing this role, the kidneys can maintain relatively normal blood volume and chemistry in the face of severe disease, and renal dysfunction may not be obvious until approximately 90% of the nephrons are damaged (Kidney Health Australia, 2011).

Stag es o f CRF • Stage 1: Some damage but GFR is often normal: greater than 90 mL/min. • Stage 2: Small fall in GFR to 60-89 mL/min. • Stage 3: GFR falls to 30-59 mL/min. Fluid retention may become apparent. • Stage 4: GFR 15-29 mL/ min. • Stage 5: Kidney failure occurs and GFR is less than 15 mL/min. (National Kidney Foundation of America, 2014)

ESKD is the last and most severe of the five stages of chronic renal failure (CRF): see Box 48.1. Stages 1 to 4 show few or no symptoms despite increasingly severe loss of functional nephrons. Stage 5 is classified as ESKD and represents a range of blood abnormalities and symptoms that are not compatible with life without treatment. The vast majority of cases of CRF and subsequent ESKD are a result of complications with diabetes, smoking, cardiovascular disease, hypertension and obesity (AIHW, 2009). Because ESKD is asymptomatic until it is well advanced it is difficult to determine its true prevalence, but it is estimated to affect one in every seven Australians over the age of 25. Among the Indigenous population the rate can be up to 11 times higher (AIHW, 2009).

B O X 4 8 . 1C h r o

nic renal failure

Prolonged hypoxia and hypotension following trauma and cardiac arrest are known causes of kidney injury and it is in this context that paramedics and emergency care clinicians should most often be considering their impact on the development of renal disease. This is reflected in emergency care guidelines, with adequate ventilation and perfusion being the priorities. In the setting of trauma most cases of kidney damage due to poor perfusion are short term and the dysfunction is classified as acute renal failure (ARF). However, the presence of ARF in critically ill patients is strongly associated with mortality and reflects the importance of the kidneys in maintaining homeostasis. In cases of significant ARF the kidneys may not fully recover and patients will be described as suffering from chronic renal failure (CRF; or chronic kidney disease, CKD). CRF is used to describe reduced kidney function, regardless of the disease or condition causing the disease, that persists for more than 3 months (National Kidney Foundation of America, 2014).

ESKD results from a number ofdifferent pathologies that cause irreversible damage to renal tissue (refer to Table 48.1) but, regardless of the cause, the kidneys are unable to maintain their normal homeostatic functions. Once patients reach ESKD they require renal replacement therapy (RRT) in the form of either dialysis or transplant. Dialysis (see below) can substitute for many of the functions of the human kidney (Anderson et al., 2008).

TABLE 48.1 Causes of end-stage kidney disease Causes of ESKD Glomerulonephritis Diabetes mellitus Polycystic kidney disease Gout Hypertension Renal artery stenosis Reflux nephropathy Systemic lupus erythematosus and other multisystem diseases Stones and other obstructions Drug-related nephropathy Congenital abnormalities

Mechanism of damage Inflammation of the kidneys (usually autoimmune) Damage to small blood vessels of the kidneys Renal tissue destroyed by cysts Excess uric acid in the blood Damage to renal vessels causing nephrosclerosis Reduction in renal perfusion Back pressure of urine causing damage Damage to connective tissue Trauma and infection Direct and indirect damage to renal tissue Mechanism varies

The underlying abnormalities caused by ESKD are uraemia (the presence of urea in the blood) and azotaemia (excessive nitrogen in the blood). Because this change in blood chemistry affects the very nature of homeostasis, the signs and symptoms of ESKD present across a number of systems and the effects can cascade significantly from the initial cause. As such, ESKD cannot be defined by a particular group of symptoms or specific levels of blood components. Instead, ESKD should be considered as a syndrome and it is often diagnosed on its clinical presentation. Although the specifics vary between individuals, these presentations can be described systematically, as follows.

Cardiovascular Rates of cardiovascular disease (CVD) are between four and eight times higher among sufferers of ESKD (AIHW, 2009) and CVD is the main cause of morbidity and mortality in patients with ESKD (Yao et al., 2004). Although ESKD and CVD share a number of risk factors (diabetes, hypertension, hyperlipidaemia, smoking), the grossly exaggerated prevalence of CVD suggests a relationship between the disease pathologies. Links between the low levels of chronic inflammation typical of ESKD and the production of oxidative substances have been proposed as the causes (Yao et al., 2004). Fluid retention also increases blood volume, places increased workload on the heart and vasculature and is present in most patients with ESKD before they commence dialysis. This can be further complicated by the release of vasoconstrictive substances from the kidneys attempting to increase their filtration. Prolonged uraemia can also cause cardiomyo-pathy but more often leads to pericarditis.

This non-infective form of pericarditis can progress to cardiac tamponade if it is not diagnosed and managed effectively.

Respiratory The combination of fluid overload and decreased myocardial function can lead to pulmonary oedema. Emergency management is consistent with non-ESKD patients and is generally effective. Anaemia can also reduce oxygen-carrying capacity sufficiently to present as shortness of breath.

Blood Decreases in the secretion of EPO and reduced RBC life due to uraemia can ultimately cause anaemia in ESKD patients. This cohort of patients is also susceptible to bleeding disorders. Caused by interruptions to several areas of the clotting cascade, this often manifests itself as gastrointestinal bleeding and increased risk of subarachnoid and subdural haematomas. Even before considering the increased bleeding times associated with using heparin to assist in dialysis, this increased bleeding risk needs to be considered in ESKD patients who have suffered falls or minor trauma.

Skin and bone Dry and itchy skin is common in ESKD, as are changes (lightened or darkened) in skin colour and nails. More significant, however, are the superficially contradictory weakening of bones and calcification of joints and soft tissues. The lack of vitamin D associated with ESKD causes a higher turnover of bone tissue, which ultimately weakens the bones and can present as bone pain and muscle weakness. The high levels of circulating calcium and phosphate can cause calcium deposits to form in synovial joints and present as gout-like pain. Calcification can also occur in the heart and vessel walls.

Neurological Persistently high levels of uraemia can affect the conscious state. Slurred speech, drowsiness, confusion and memory loss are all typical signs of uraemic encephalopathy. Severe cases can present as seizure and coma, but clinicians need to exclude trauma and vascular causes before declaring the symptoms to be solely related to uraemia. Peripheral neuropathy and autonomic dysfunction are also common. The neuropathy can present as either pain or anaesthesia, while the autonomic dysfunction most often manifests as postural hypotension, decreased bowel activity and reduced sweating response.

Dialysis Many of the functions of the human kidney (such as maintaining acid—base and electrolyte balance and excreting nitrogenous waste) can be replaced when necessary with a range of artificial processes or interventions, collectively referred to as RRT. These interventions include renal transplantation and dialysis. Dialysis refers to the process of separating colloids and crystalline substances in solution by the difference in their rate of diffusion through a semipermeable membrane (Anderson et al., 2008). After diagnosis, patients (in consultation with their family and health professional team) have to choose between haemodialysis and peritoneal dialysis. The two forms of dialysis use a similar principle but an entirely different method: 1. Haemodialysis involves removing the blood from the body and passing it over a semipermeable membrane (dialyser) to achieve diffusion and ultrafiltration (Thomas, 2014). 2. Peritoneal dialysis uses the peritoneal lining as the semipermeable membrane. Dialysate is pumped into the abdominal cavity and urea, toxins and solutes move across the membrane (peritoneum) via diffusion from the bloodstream into the dialysate, or vice versa, depending on the concentration gradient (Thomas, 2014). Fluid removal is achieved by utilising an osmotic pressure mechanism in which varying dextrose concentrations in the dialysate provide an osmotic gradient for water flow from the patient’s blood to the peritoneum (see Fig 48.2; Abdeen & Mehta, 2002).

FIGURE 48.2 Diffusion across a semipermeable membrane. The higher osmolality of the dialysis solution draws water and wastes from the blood across the semipermeable membrane. Source: Renal Department, Royal North Shore Hospital, Sydney, Australia. There are a number of advantages and disadvantages to each method (see Table 48.2, overleaf ) but they both require the creation of an access point for blood or fluid to be

dialysed. TABLE 48.2 Advantages and disadvantages of haemodialysis and peritoneal dialysis

Haemodialysis If haemodialysis is chosen, a permanent access device will need to be established (see Fig 48.3, overleaf ). The two most common types of long-term access are:

FIGURE 48.3

Access for haemodialysis. Source: kbik/wikipedia.

1. Arteriovenous fistula (AVF). An artery and a vein are anastomosed, most commonly the radial artery and the cephalic vein in the patient’s non-dominant arm. This type of access requires good-quality peripheral vessels. 2. Arteriovenous graft (AVG). If the peripheral vessels are unsuitable for an arteriovenous fistula, a graft will be used. Grafts are usually not the first choice as they are less compliant than fistulas, which can result in higher pressures. Once access has been established, haemodialysis can commence. Patients choose where to dialyse in consultation with their family and health professionals. There are three main choices: 1. centre-based haemodialysis 2. limited care ‘satellite’ haemodialysis 3. home-based haemodialysis. The conventional approach to dialysis, which is used by the first two facility-based options, is 3 days per week for approximately 4 hours each time (Agar, 2011). Home-based dialysis provides more options for individual lifestyles and patients can implement the regimen that best suits them. There has been an increasing trend towards home-based nocturnal haemodialysis (Agar, 2011). This leaves the waking hours undisturbed, allows greater freedom with regards to fluid restrictions and allows for longer, gentler haemodialysis. The Australian and New Zealand Dialysis and Transplant Registry (ANZDATA) has captured data that suggests significant survival advantages for increased hours of dialysis, with 18 hours or more per week being optimal (Agar, 2010). This is more aligned with home-based dialysis than conventional facility-based dialysis regimens. The potential complications that must be considered are outlined in Table 48.3.

TABLE 48.3 Potential complications with haemodialysis Potential Cause complication Hypotension Loss of fluid volume Cramps Ultrafiltration rate set too high Disequilibrium Too-efficient removal of syndrome solutes Haemolysis Damage to red blood cells Air embolism Air in circuit

Initial management Autoinfuse, monitor Reposition limbs, use heat pads, gentle massage

Discontinue haemodialysis and transport to hospital Discontinue haemodialysis, do not return blood, transport to hospital Discontinue dialysis, do not return blood, lay patient on left side, resuscitate as necessary, transport to hospital Dialyser Allergic response to Discontinue haemodialysis, do not return blood, reactions foreign materials within maintain airway, consider anaphylaxis clinical the circuit practice guideline Clotting of Inadequate Discontinue haemodialysis, do not return blood, blood lines and anticoagulation transport to hospital, investigate cause dialyser The haemodialysis circuit commences with blood leaving via a needle inserted into the arterial access device. The patient’s own blood pressure assists in moving approximately 200 mL of blood through the extracorporeal circuit at any one time. A blood pump within the machine also assists by moving the blood through the circuit at a constant rate. A heparin infusion is usually used (pre-filter) to prevent the blood from clotting within the circuit. There are many different brands and types of dialysers, some more basic than others, but most dialysers have the features highlighted in Figure 48.4. The dialyser does the work by filtering the extra fluid and waste from the blood into the dialysate, using countercurrent flow (see Fig 48.5, overleaf ).

FIGURE 48.4 Schematic of a typical haemodialysis circuit. Source: Shodor/wikipedia.

FIGURE 48.5 Countercurrent flow. Countercurrent flow refers to the flow of blood through the

artificial kidney in one direction and the flow of dialysate through the artificial kidney in the opposite direction. This enhances efficiency as the blood is always in contact with fresh dialysate. Source: Shodor/wikipedia.

Peritoneal dialysis If peritoneal dialysis is chosen, access via a peritoneal catheter will need to be established: this is done as a minor surgical procedure (see Fig 48.6, overleaf ). Once peritoneal access has been established, patients, in consultation with their family and health professionals, need to choose which method best suits their needs. There are two choices:

FIGURE 48.6 Location of a CAPD catheter. A Location of the surgical incision. B Location of the catheter in the pelvis. C Dacron cuff at the level of the posterior rectus sheath. D Exit site shown with final placement. Source: Townsend et al. (2008).

P RACT ICE T IP Many cases of ESKD are progressive. As kidney disease progresses, peritoneal dialysis may become inadequate and haemodialysis will eventually be needed.

• continuous ambulatory peritoneal dialysis (CAPD) • automated peritoneal dialysis (APD) CAPD uses the peritoneum to filter the blood on a continual basis. Individuallydetermined amounts of dialysate are introduced into the peritoneal cavity on average four times per day (see Fig 48.7).

FIGURE 48.7 CAPD uses the peritoneum to filter the blood on a continual basis. Source: Renal Department, Royal North Shore Hospital, Sydney, Australia. In contrast, in APD the dialysate is cycled a number of times by a machine, at night, while the patient sleeps (see Fig 48.8). The machine leaves the last cycle to dwell in the peritoneal cavity for the day and the catheter can then be capped off until needed the next night.

FIGURE 48.8 In APD, the dialysate is cycled a number of times by a machine, at night, while the patient sleeps. Source: AAP/Michael Conroy. Peritoneal dialysis is minimally invasive and is commonly used for children. The most common complication is peritonitis; other complications that need to be considered are outlined in Table 48.4. This option may not be available if the disease process is far advanced or the patient has had recurrent peritonitis or other complications.

TABLE 48.4 Potential complications with peritoneal dialysis Potential Cause complication Ineffective Disease progression solute removal Raised Pressure from high volumes of fluid in the intraabdominal peritoneal cavity; can result in genital oedema pressure and dialysate leakage from the catheter exit site Protein Protein lost through the peritoneum deficiency Hyperlipidaemia Glucose absorbed from the dialysate Kinks in the Poor positioning of catheter or tubing tubing Constipation Causes problems with outflow Blood-stained effluent Peritonitis

Initial management Medical consultation Treat symptomatically and transport Dietary advice

Monitor Check and reposition tubing Exercise, high-fibre diet, adequate fluid intake and laxatives Rare, occurring most commonly in menstruating Usually self-resolving females; may be due to endometriosis Introduction of pathogens into the peritoneal Discontinue peritoneal cavity dialysis, pain relief, transport to hospital

CA SE ST U DY 1 Case 10912, 1945 hrs. Dispatch details: A 63-year-old male is complaining of chest pain that started shortly after he commenced haemodialysis at home. Initial presentation: The paramedics find the patient sitting upright in an armchair connected to a haemodialysis machine, with his concerned wife beside him. The patient is alert and his skin is pink and dry.

ASSESS As discussed in Chapter 24 the primary aim of assessing chest pain is to determine the likelihood of the pain being due to cardiac ischaemia, as this is the most serious possible cause. ESKD places patients at a far higher risk of cardiac ischaemia but also of other non-cardiac causes.

Patient history The patient’s pain commenced a few minutes after his wife connected him to haemodialysis. It is typical of his normal angina pain (heaviness across the central chest extending to his jaw) that he gets once or twice a week when he ‘over-exerts’ himself. His wife gave him a single GTN (glyceryl trinitrate) spray but it didn’t relieve the pain is it normally would. They waited 5 minutes and tried the GTN spray again. This time the pain reduced from 7 out of 10 to a score of 5. The patient has now had the chest pain for 20 minutes.

HIST ORY Ask! • How long after you started dialysing did the pain begin? • What was your starting weight? Is that typical? • What is your ‘dry’ weight?

The patient has a history of angina and is able to compare the current pain to his normal angina. Angina as described by this patient (more intense, more persistent) may be caused by a disrupted coronary plaque and as such fits the signs of acute coronary syndrome (ACS) and cannot be discounted as ‘simply angina’. This also needs to be considered in the context of the higher risk of plaque formation in ESKD patients. Given that a disrupted coronary plaque does not necessarily lead to ECG changes it cannot be clinically excluded in the field and the standard practice is to treat ‘unstable angina’ as part of ACS. However, there are complicating factors associated with this case of angina. The patient has just started dialysis so his fluid load (blood volume) should be high. Patients refer to this pre-dialysis state as their ‘wet’ weight and most are extremely vigilant about measuring how much weight gain has occurred since they finished their last dialysis (their ‘dry’ weight). The high fluid load typical of commencing dialysis reflects a large blood volume and subsequently a large preand afterload being placed on the heart. This high demand state could explain his chest pain. Similarly, patients approaching the end of their dialysis have a much-reduced blood volume and the lack of blood can lead to an increase in

sympathetic tone (see Ch 55), resulting in a raised heart rate and vasoconstriction. Indeed, a patient’s ‘dry’ weight is often set by the point at which hypotension prevents any more fluid removal. So, in addition to the description of the pain the paramedics need to gather information on the patient’s state of dialysis.

Cardiovascular Blood pressure, skin and pulse assessments will assist in determining whether the patient is suffering from a high demand (fast heart rate and/or high blood pressure) or low supply (hypotension) state. Hypotension can also result from uraemic pericarditis causing fluid to accumulate in the pericardial space and creating a cardiac tamponade, so it can occur in pre-dialysed patients.

ECG and physical exam Electrolyte imbalances common to ESKD can cause a number of arrhythmias (see Ch 25) that can lead to increased heart rate and subsequently increased myocardial demand. Uraemic pericarditis is also common and is characterised by loud friction rubs, but not the widespread ST elevation of typical pericarditis (unless infective). A brief relief from the pain when the patient sits forwards is typical but not definitive of most types of pericarditis. Decreased renal function can reduce the amount of EPO secreted and result in anaemia. Assessing anaemia in the field is difficult, but pale mucous membranes (inside lower eyelid, gums) can be suggestive.

P HYS I C A L E X A M Look for! • Arrhythmias • ST changes • Pale mucous membranes

Listen for! • Pericardial friction rub

Problem Chest pain Conscious state GCS = 15 Position Sitting upright Heart rate 94 BPM Blood pressure 170/100 mmHg Skin appearance Pink, warm, dry Speech pattern Normal Respiratory rate 18 BPM Respiratory rhythm Normal Chest auscultation Clear breath sounds bilaterally Pulse oximetry 98% on room air Temperature 37.1 °C Pain 5/10 History ESKD, angina, hypertension ECG Normal with no ST segment or T wave changes D: There are no dangers. A: The patient is conscious with no airway obstruction. B: Respiratory function is currently normal. C: Heart rate is normal. The blood pressure is high but typical for ‘wet’ weight. The patient is currently well perfused. He is displaying chest pain typical of his normal angina but unlike normal the pain is not relieved by GTN. Given that he is complaining of central chest pain consistent with myocardial ischaemia and that it is not responsive to normal treatment, the diagnosis has to be considered as ACS until proven otherwise.

CONFIRM The essential part of the clinical reasoning process is to seek to confirm your initial hypothesis by finding clinical signs that should occur with your provisional diagnosis. You should also seek to challenge your diagnosis by exploring findings that do not fit your hypothesis: don’t just ignore them because they don’t fit.

DIF F ERENT IA L DIA GNOSIS ACS Or • Anaemia • Pericarditis • Fluid overload

What else could it be? Anaemia The kidneys produce about 80% of the body’s EPO and anaemia is common among sufferers of ESKD. The process of haemodialysis also damages a significant number of RBCs and in combination these two effects can lead to a lack of oxygen carrying capacity and subsequent development of ischaemic chest pain. Although the routine administration of high-flow oxygen is now being revised in patients presenting with ACS (Burls et al., 2011), it must be remembered that ESKD patients present with several additional complications. Anaemia is common and pulse oximetry is not necessarily an accurate guide in any anaemic patient. High SpO2 readings reflect only that the patient’s RBCs are saturated; the reading does not measure how many RBCs may be present (or missing). This is compounded by the fact that this patient has only just commenced this round of dialysis: approximately 200 mL of his circulating volume has been diverted through the dialyser and replaced with normal saline. The replacement fluid has no oxygen carrying capacity and, combined with anaemia caused by decreased EPO secretion, can create a mismatch in myocardial oxygen supply and demand. Pale mucous membranes (inside lower eyelid, gums) can be suggestive of anaemia. Pericarditis Pericarditis is more common and carries a higher mortality among patients with ESKD compared with the general population. Two forms predominate: uraemic pericarditis and dialysis-related pericarditis. The causes of each are multifactorial but both are related to the degree of uraemia. Neither commonly involves the infective processes of non-uraemic pericarditis so the myocardium does not become inflamed and produce the ECG changes normally associated with the condition (ST elevation in all leads). The ECG may, however, display signs of the electrolyte imbalances caused by severe uraemia. The pain is typically well localised and very short-term relief can be gained by the patient changing position (side to side or leaning forwards). A loud friction rub is usually present but the general malaise symptoms of infective pericarditis (fever, fatigue) can easily be confused with the symptoms of inadequate or missed dialysis, which is when dialysis-related pericarditis is most likely to occur. The most serious consequence of inflammation of the pericardial sac in these patients is pericardial tamponade due to fluid (blood due to poor clotting or serous fluid) building up in the pericardium and compressing the heart. This leads to decreased cardiac output and subsequent hypotension. Although the patient’s dialysis schedule is consistent with pericarditis (high fluid and high uraemia), his normal heart rate and more-than-adequate blood pressure do not suggest tamponade. Fluid overload This patient is due for dialysis so he is most likely close to or above his ‘wet’ weight. In this setting the addition of 200 mL of non-oxygen—carrying saline from the machine may be enough to tip the myocardial supply-and-demand balance into the ‘negative’ and result in ischaemia. Although fluid overload is often considered to be the primary cause of pulmonary oedema in patients

with ESKD, it is more likely to be due to myocardial dysfunction secondary to ischaemic heart disease. The point to remember is that fluid overload can occur without causing pulmonary oedema. While it may be logical to suggest that fluid overload could be the cause of this patient’s unrelieved angina, it must be remembered that CVD is the cause of more than 50% of deaths in patients with ESKD (Collins, 2003). Based on the description of the pain it is extremely difficult to argue the patient does not fit the diagnostic criteria for ACS and, given the risks associated with this condition, it would be perilous to treat him otherwise. That only leaves the question of how to integrate his haemodialysis into the prescribed management plan for ACS.

T REAT Emergency management ACS management The principles of emergency ACS management are described in detail in Chapter 24 but essentially aim to redress the imbalance between myocardial oxygen supply and demand and can be summarised as follows: 1. Reduce myocardial workload by reducing patient activity. 2. Administer GTN to reduce pre-and afterload to reduce myocardial workload. 3. Administer oxygen to increase myocardial supply if there are signs of systemic hypoxia. 4. Administer aspirin (and other anticoagulants) to minimise clot formation. A number of studies have found that ESKD patients are less likely to receive aspirin than other patients presenting with ACS (Berger, Duval & Krunholz, 2003), despite the higher risk of CVD in these patients. 5. Give pain relief to reduce sympathetic drive (decreased myocardial workload). Intravenous (IV) access should be sited on the opposite limb from the fistula. The use of intranasal or inhaled pain relievers should be considered if GTN does not provide pain relief and IV access cannot easily be obtained. Drugs with high levels of renal toxicity (e.g. methoxyflurane) should be avoided. 6. Transport to hospital for further investigation including cardiac enzyme analysis. Given that this patient has a substantial blood pressure and no contraindications for any of the above management this should not be a difficult case, but it is complicated by his current haemodialysis.

S I T U A T I O N A L A WA R E N E S S Be careful with fluid administration: patients with ESKD often have diet and fluid restrictions. For example, a patient on satellite haemodialysis who dialyses three times a week is restricted to 500 mL

of water per day plus the total volume of daily urinary output (many patients with ESKD are anuric). Patients on home-based dialysis have more freedom due to the frequency of their dialysis regimen.

Dialysis Does this patient need to be removed from haemodialysis immediately? While it may be tempting to conclude that his pain is a result of fluid overload and that allowing him to remain on dialysis will eventually resolve the fluid balance, this is an unsubstantiated decision and places him at risk of all the complications of ACS (see Ch 24). Although dialysis can remove up to 500 mL every half hour, it would be difficult to defend the decision to leave this patient on dialysis if the pain was still present after, say, 30 minutes of dialysis, or he developed a dangerous arrhythmia from an evolving myocardial infarction. While it is important to include the patient and family in the decision to cease dialysis for transport and to appreciate their likely reluctance to do so, it is the clinician’s responsibility to provide the patient with the best medical advice and decision making. In this case that decision involves initiating management of ACS while calmly and carefully removing the patient from dialysis. If, as in this case, the patient is not actually time critical, blood circulating through the dialyser should be returned to the patient to help correct any anaemia. The process should not extend on-scene time. In most cases, the patient or their carer will be a good source of advice about this procedure or will actually complete the procedure, but paramedics need to have a basic understanding of haemodialysis machines and how to manage them in an emergency. To return the blood to the patient: 1. Decrease the blood pump rate to 100—150 mL/per min (clarify the normal return rate with the patient or their carer if possible). 2. Open the flow clamp on the normal saline. 3. Clamp off the arterial blood line close to the patient using two plastic arterial clamps (one below and one above the Luer lock). 4. Commence the disconnection procedure after approximately 2—3 minutes or when the return is a light-rose colour (whichever comes first). Take care not to return too much fluid to the patient. To disconnect the patient from the haemodialysis machine: 1. Turn off the pump. 2. Clamp both the fistula needles and dialysis lines (four clamps are needed: they should be available beside the machine). 3. Disconnect the lines from the needles. 4. Remove the needles, ensuring you apply firm pressure (but not occlusive) at both sites until haemostasis is achieved: this may take up to 30 minutes. Many patients become systemically heparinised from the heparin in the circuit and this prolongs bleeding. Given the timeframe required this process may need to be adjusted if the patient is time critical (see case study 2). 5. Ensure the blood lines are disposed of safely.

EVALUAT E Evaluating the effect of any clinical management intervention can provide clues to the accuracy of the initial diagnosis. Some conditions respond rapidly to treatment so patients should be expected to improve if the diagnosis and treatment were appropriate. A failure to improve in this situation should trigger the clinician to reconsider the diagnosis. Cardiac ischaemia induced by the sudden volume loss from commencing dialysis is not uncommon and, provided the management described above is performed, returning the patient’s blood to his cardiovascular system should resolve the imbalance between myocardial oxygen supply and myocardial oxygen demand if this is the cause. Many of the factors that contribute to CRF, however, also contribute to the development of coronary artery disease and there is an increased likelihood of dialysis patients experiencing a disrupted atherosclerotic plaque causing ACS. Continuous cardiac monitoring of these patients is recommended, as the evolution of ST segment changes can indicate the development of a myocardial infarction.

Ongoing management Refer to Chapter 24 for the ongoing management of the patient with ACS. Patients are likely to be admitted to hospital for investigation. They will receive their dialysis as an inpatient once their pain has been evaluated and managed.

Follow-up If a patient has ongoing unstable angina, their suitability for home-based dialysis will need to be evaluated. Satellite haemodialysis would ensure that they are monitored by a health professional at all times.

Long-term role Paramedics are likely to encounter more patients on home-based dialysis in the future. It would be of benefit if paramedics were to liaise with other health professionals in their area and identify who is on home-based haemodialysis. Formalised emergency plans, similar to asthma plans, would assist in identifying the role of paramedics in the out-ofhospital setting.

ESKD across the lifespan ESKD can affect people of all ages. Figures 48.9 and 48.10 show the number of patients on dialysis in Australia and New Zealand, respectively. Overall, glomerulonephritis remains the most common cause of ESKD in children and adolescents, while diabetic nephropathy is a leading cause for adults (ANZDATA Registry, 2010). In Australia, the mean age for commencement of RRT is 60.7 years, with an age range of 3.5 months to 95 years; and in New Zealand, the mean age at commencement is 57.6 years, with an age range of 3.5 years to 88 years (ANZDATA Registry, 2010). The disease is more common in the Indigenous population and particularly affects younger age groups. For every diagnosed case of ESKD it is estimated that another case goes unrecognised (AIHW, 2011).

FIGURE 48.9 Number of patients on dialysis in Australia, 2012. Source: ANZDATA (2012).

FIGURE 48.10 Number of patients on dialysis in New Zealand, 2012. Source: ANZDATA (2012).

CA SE ST U DY 2 Case 19432, 1220 hrs. Dispatch details: A 60-year-old female has collapsed at home during haemodialysis. Initial presentation: The paramedics find the patient semi-reclined in a chair, connected to a haemodialysis unit.

ASSESS 1240 hrs Primary survey: The patient is in an altered conscious state. 1242 hrs Vital signs survey: Perfusion status: HR 118 BPM; sinus tachycardia; BP 80/50 mmHg; skin cool, pale and clammy. Respiratory status: RR 24 BPM, shallow respirations, no adventitious sounds,

normal pattern, air entry bilaterally. Conscious state: GCS = 12 (E3, V4, M5). 1244 hrs Pertinent hx: The patient’s husband tells the paramedics that she complained of sudden chest pain and then collapsed. She has a history of hypertension, angina and ESKD. 1247 hrs Secondary survey: No abnormalities are noted on physical examination but her ECG reveals significant ST elevation in V2, V3 and V4.

CONFIRM In many cases paramedics are presented with a collection of signs and symptoms that could relate to a number of conditions. A critical step in determining a treatment plan in this situation is to consider what other conditions could explain the patient’s presentation. The most time-critical with regards to treatment is an arrhythmia such as ventricular tachycardia or ventricular fibrillation or myocardial infarction. The ECG is suggestive of an anterior myocardial infarction and the decision is made to treat accordingly. This makes transport to definitive care a priority. The increased urgency of this case raises a number of management issues: 1. Should the patient’s blood be returned to her? 2. Should the IV cannulas used for haemodialysis be removed?

T REAT This patient is acutely ill and requires the complex management of poor perfusion with ACS as outlined in Chapter 24. This follows the basic principle of increasing myocardial oxygen supply while reducing myocardial oxygen demand. In this context returning the patient’s blood from haemodialysis should be considered important and if performed concurrently with basic management this should not delay transport to hospital. It is important to recruit someone familiar with the equipment and the decision is made to ask the patient’s husband to assist in this process. The use of heparin during the process of haemodialysis usually requires digital pressure to be placed over the fistula for up to 30 minutes before clotting (haemostasis) will occur and the crew may not have the time or resources to do this. An alternative is to perform the normal disconnection process while establishing basic care of the patient and preparing transport. Once ready to transfer the patient the haemodialysis line can be clamped and cut and the needles left in situ. This has the obvious complication of severe haemorrhage if the clamps are accidentally loosened so they need to be monitored very closely. Of greater concern, however, is the integrity of the AVG or AVF. These

structures are delicate but essential to the patient’s health and ability to dialyse. If urgency requires the crew to choose this alternative the needles and attached tubing must be carefully and securely bandaged to protect the site. Once disconnected, the paramedics should keep the patient’s bandaged arm in view at all times and frequently check for haemorrhage. This alternative is not ideal as it places the AVG or AVF at risk of clotting, haemorrhage and needle trauma, but it may be a better than a prolonged scene time while waiting for haemostasis. Patients and their carers are rightly very protective of a functioning fistula or graft and will be anxious about any activity at the site of this vascular access. Paramedics should always attempt to gain IV access on the opposite arm to the graft—using the graft itself to gain IV access should be considered an avenue of absolute last resort. In many cases intraosseous access would be preferable. Transport to a hospital with interventional cardiac facilities (thrombolysis, percutaneous coronary intervention) would be strongly recommended for this patient (see Ch 24 for details of further treatment and evaluation).

EVALUAT E As with any patient suffering from ACS this patient has the potential to deteriorate suddenly from cardiac arrhythmias and decreased left ventricular function. As a result, frequent reassessment, cardiac monitoring and preparing to manage any arrhythmias according to local guidelines should all be implemented. Effective analgesia will make the patient more comfortable. There is a slight possibility that the clot will partially resolve spontaneously and the symptoms and ECG abnormalities will reduce.

CA SE ST U DY 3 Case 12694, 1420 hrs. Dispatch details: A 37-year-old female complaining of abdominal pain. Initial presentation: The paramedics are met at the house and find the patient sitting upright in an armchair with her knees drawn up to her chest.

ASSESS 1440 hrs Primary survey: The patient is alert and responsive. 1442 hrs Vital signs survey: Perfusion status: HR 124 BPM, sinus tachycardia, BP 100/60 mmHg, skin warm and dry, temperature 39.4°C. Respiratory status: RR 18 BPM, normal respirations, no adventitious sounds, normal pattern, air entry bilaterally. Conscious state: GCS = 15. 1444 hrs Pertinent hx: The patient complains of moderate (8/10) abdominal pain that she describes as sharp, constant and located around her umbilicus. The pain woke her at 7 this morning and she has attempted to self-manage it with oral analgesia. She has a history of glomerulonephritis, which resulted in CRF and the need for peritoneal dialysis. 1447 hrs Secondary survey: The paramedics note a plugged peritoneal catheter in situ, exiting below and to the left of the patient’s umbilicus. The site appears reddened with no exudate. The patient explains that she is on machine-automated peritoneal dialysis (APD) each night.

ASSESS Ask! • Have you noticed any changes in your bowel and bladder function recently? • Have you vomited? • Is the distillate different from normal? (Amount, colour) • What is your normal dialysis cycle?

Check! • Peritoneal dialysis effluent • Access port • Abdomen

The patient on peritoneal dialysis has a far higher risk of abdominal complications due to the need for an access port and the introduction of fluid into the cavity. However, while these factors increase the risks for the patient, they provide paramedics with a form of internal assessment that is not possible in other patients. Fluid removed at the completion of the dialysis cycle should be clear but in this case it is cloudy. Diagnosis of peritonitis is usually made in the presence of abdominal pain and tenderness with pyrexia and cloudy

effluent (Thomas, 2014). The peritoneal catheter exit site should be examined for signs of infection such as redness, heat, pain and purulent exudate. Always maintain aseptic technique when handling or disconnecting the catheter.

CONFIRM In many cases paramedics are presented with a collection of signs and symptoms that do not appear to describe a particular condition. A critical step in determining a treatment plan in this situation is to consider what other conditions could explain the patient’s presentation. In this case, abdominal pain in the presence of peritoneal dialysis necessitates urgent investigation and treatment, with the most likely diagnosis being a peritoneal infection.

T REAT Management and risk assessment of abdominal pain are outlined in detail in Chapter 43 and this patient should be treated according to those recommendations. The only exception is to avoid nephrotoxic drugs and largevolume IV fluid administration. The timeline of the development of the surgical emergency known as the acute abdomen is described in Chapter 15 and the process of peritoneal dialysis should be considered as a risk factor both in the potential to develop this condition and for it to progress extremely quickly. As such, early recognition and treatment are essential. In addition to minimising the risk of developing an acute abdomen, effective management can protect the port site and allow the patient to continue with dialysis. Ongoing patient education regarding aseptic technique when managing dialysis equipment and the peritoneal catheter may be needed. Peritoneal dialysis will not be continued if peritonitis is severe or a frequent problem. Alternative access will need to be established to allow for haemodialysis in the interim and/or in the longer term if the complications of peritoneal dialysis are not well controlled. This is particularly important if the patient is on the renal transplant list, as optimal health is required to maintain eligibility.

EVALUAT E Evaluating the effect of any clinical management intervention can provide clues to the accuracy of the initial diagnosis. Some conditions respond rapidly to treatment so patients should be expected to improve if the diagnosis and

treatment were appropriate. A failure to improve in this situation should trigger the clinician to reconsider the diagnosis. In this case the patient appears to be in the early stages of the infective process and is likely to remain stable during transport. Titrating pain relief to ensure that she is comfortable will provide vital signs that are less likely to be affected by anxiety and pain and are more reflective of the patient’s underlying physiological state.

Future research Epidemiological studies investigating the number and type of cases involving haemodialysis seen by paramedics are needed to assist in developing guidelines and training. The findings would assist in developing formalised clinical practice guidelines for this cohort. For patients, research is currently underway aimed at improving the efficiency of the dialysis process by developing semipermeable membranes that more accurately mimic the functions of the kidneys. This may include biohybrid fabrics impregnated with stem cells (Humes, Fissell & Tiranathanagul, 2006). This technology may ultimately extend to implantable artificial kidneys (Tasnim et al., 2010).

Summary Patients on home-based dialysis add an interesting dimension to clinical problem solving and case management. Paramedics need to have a broad understanding of the principles of dialysis, the individuality of patients’ dialysis programs and the complexity of ESKD. Exposure to cases involving home-based dialysis will increase significantly as the number of patients with ESKD is predicted to increase significantly in the next few years.

References Abdeen, O., Mehta, R. Dialysis modalities in the intensive care unit. Critical Care Clinics. 2002; 18:223–247. Agar, J. Nocturnal Haemodialysis Program. Barwon Health. Retrieved 20 August 2011 from www.nocturnaldialysis.org, 2011. Agar, J. Home dialysis in Australia: is the wheel turning full circle? Medical Journal of Australia. 2010; 192(7):403–406. Anderson, D., et al. Mosby’s Medical, Nursing, & Allied Health Dictionary, 8th ed. St Louis: Mosby, 2008. Australia and New Zealand Dialysis and Transplant Registry (ANZDATA)ANZDATA Registry 2013 Report. Adelaide: ANZDATA, 2013. Australian Institute of Health and Welfare (AIHW)An Overview of Chronic Kidney Disease in Australia. Cat. no. PHE 111. Canberra: AIHW, 2009. Australian Institute of Health and Welfare (AIHW). End Stage Kidney Disease. Retrieved 22 November 2013 from www.aihw.gov.au/ckd/end-stage-kidney-disease/#q01, 2013. Berger, A., Duval, S., Krunholz, H. Aspirin, beta-blocker, and angiotensin-converting enzyme inhibitor therapy in patients with end-stage renal disease and an acute myocardial infarction. Journal of the American College of Cardiology. 2003; 42:201–208. Boron, W. Medical Physiology: A Cellular and Molecular Approach, 2nd ed. Philadelphia: Elsevier, 2012. Burls, A., Cabello, J., Emparanza, J., Bayliss, S., Quinn, T. Oxygen therapy for acute myocardial infarction: a systematic review and meta-analysis. Emergency Medicine Journal. 2011; 28(11):917–923. Cass, A., Chadban, S., Gallagher, M., Howard, K., Jones, A., McDonald, S., Snelling, P., & White, W. for Kidney Health Australia. (2006). The Economic Impact of End-Stage Kidney Disease in Australia: Projections to 2020. Sydney. Australia. Collins, A. Cardiovascular mortality in end-stage renal disease. American Journal of Medical

Sciences. 2003; 325(4):163–167. Elliot, D., Aitken, L., Chaboyer, W. ACCCN’s Critical Care Nursing, 2nd ed. Sydney: Elsevier, 2012. Humes, H., Fissell, W., Tiranathanagul, K. The future of hemodialysis membranes. Kidney International. 2006; 69:1115–1119. Kidney Health Australia. Fast Facts on CKD in Australia. Retrieved 15 September 2011 from www.kidney.org.au/KidneyDisease/FastFactsonCKDinAustralia/tabid/589/Default.aspx, 2011. National Kidney Foundation of America. Stages of Kidney Disease. Retrieved 17 October 2014 from www.kidney.org, 2014. Talley, N., O’Connor, S. Clinical Examination, 7th ed. Sydney: Elsevier, 2013. Tasnim, F., et al. Achievements and challenges in bioartificial kidney development. Fibrogenesis Tissue Repair. 2010; 3(1):14. Thomas, N. Renal Nursing, 4th ed. London: Baillière Tindall, 2014. Tortora, G., Grabowski, S. Principles of Anatomy and Physiology, 14th ed. New York: John Wiley & Sons, 2014. Townsend, C. M., Beauchamp, R. D., Evers, B. N., Mattox, K. L. Sabiston Textbook of Surgery, 19th ed. St Louis: Saunders, 2012. Yao, Q., et al. Traditional and non-traditional risk factors as contributors to atherosclerotic cardiovascular disease in end-stage renal disease. Scandinavian Journal of Urology and Nephrology. 2004; 38(5):405–416.

CHAP TER 49

Indigenous Australian patients By Abigail Trewin, Sandra Schmidt and Shaun Ewen

C O N C E P TS U S E D I N TH I S C H A P TE R • The paramedic’s clinical approach: Section 2

O V E RV IE W • Australia’s Indigenous peoples are culturally diverse with many languages and cultural practices. • Interacting with patients from different cultural backgrounds requires a review of your own cultural expectations. • Indigenous Australians experience a high prevalence of comorbidity issues with subsequent adverse health outcomes. • Kinship is the basis of Indigenous society, describing how relationships between members of that group will interact. • The cultural beliefs of contemporary Indigenous Australians can be located on a continuum, spanning those who have had a traditional upbringing to those who may know they are Indigenous but have lost connections with their heritage and cultural traditions. • Compared with other Australians, Indigenous Australians experience significant inequities in life expectancy, health status, health outcomes (morbidity and mortality) and access to a range of health services. • The ability of paramedics to conduct a detailed health assessment and make sound clinical decisions when dealing with Indigenous patients may require an understanding of their culture and beliefs and how these shape their engagement with health providers.

Introduction Both health professionals and the patients they attend are shaped by their experiences and cultural beliefs. These beliefs also shape how each group views disease and how they express disease to others (see Ch 6). Most clinicians embrace the biomedical (or scientific) view of disease and often fail to accept that their patients do not always share this view. This can limit the clinician’s ability to gain an accurate history, but also fails to engage the patient in the choice of treatment and ensure their adherence to therapy. This discrepancy between the clinician’s view of disease and treatment and the patient’s view can be exacerbated when the two are from significantly different cultures. Culturally appropriate care extends the biomedical model to respect the patient’s worldview, cultural values, beliefs and practices. Each person’s concept of health, wellbeing and illness is developed within their sociocultural context. Identifying a person’s concept of health, wellbeing or illness ensures that healthcare is both relevant to understanding why they have sought medical help and effective in addressing their health concerns (Wilson, 2008). Many Indigenous patients suffer a higher rate of socioeconomic disadvantage and chronic disease (AusMAT, 2011), with a higher number on treatment for pre-existing conditions such as renal disease, diabetes, cardiac conditions (including rheumatic heart disease) and hypertension. Indigenous Australians (Aboriginal and Torres Strait Islander peoples) comprise 2.5% of the country’s total population. Almost 27% of people in the Northern Territory are estimated to be of Indigenous origin, while in the other states and territories Indigenous Australians make up 0.7–4% of the total population (ABS, 2012a). This chapter considers cultural aspects of traditional Indigenous Australian life. It is necessary that these matters are discussed in very broad and general terms and while the term ‘Indigenous Australians’ is used the authors acknowledge that it covers many different groups with different traditions, values and ways of life.

Kinship Kinship can be defined as the relationship between members of the same family, or a feeling of being close or similar to other people or things (Bourke & Edwards, 2004). It is significant to every part of Indigenous Australian society and understanding the role that kinship plays will assist clinicians in managing Indigenous patients in a culturally safe way. Kinship dictates social organisation, but this will differ between regions and groups. Kinship describes whom an Indigenous person can speak to, how they are addressed and whom they are allowed to confide in. Kinship also describes ‘avoidance’ relationships, prohibiting individuals from approaching or speaking to another member of the group. Within the kinship system everyone knows exactly how to behave towards everyone else. The basic principle is that people born of the same sex belong to the same sibling line and are viewed as essentially the same (Bourke & Edwards, 2004). So in a community two brothers are considered equal: their children are referred to as brothers and sisters, not cousins, and they will view their father ’s brother not as their uncle but as another father. The same is true of sisters who have children: the children will refer to each sister as their mother, not their aunt. Their mother ’s brother, who is of the same sibling line but the other sex, is referred to as Uncle, and their father ’s sister is Auntie. It is therefore not uncommon to have many mothers and many fathers and many brothers and many sisters (Bourke & Edwards, 2004). In addition, many regions classify their community through ‘skin names’. This is the name given at birth that describes the section/subsection that a person belongs to. The name relates to the child’s parents’ ‘skin name’ and divides the community further into relevant relationships. When Indigenous Australians refer to someone to whom they are related they usually use the appropriate relationship term for that person, such as auntie; if they are unrelated, they are referred to as so and so’s son or mother. Personal names are used with discretion as they are seen as essentially part of that person. When Indigenous Australians accept an outsider into their group, they name that person in relation to themselves in order for that person to fit into their society. This is because they need to know the kinship relationship of that person to themselves, and that person must have a defined social position. The value of the kinship system is that it structures people’s relationships, obligations and behaviour towards each other, and this in turn affects matters such as who will look after children if a parent dies, who can marry whom, who is responsible for another person’s debts or misdeeds, and who will care for the sick and old. Indigenous people raised in cities and towns may or may not follow kinship systems but they will still usually have close family networks in the area and socialise with other Indigenous people. Many maintain their links with family in remote or regional areas.

Culture Australia is a culturally diverse country: 43% of the population were either born overseas or have a parent who was born overseas (DFAT, 2013). Migrants have enriched many aspects of Australian life, creating new influences while blending into a country of established traditions. The country’s original inhabitants, Indigenous Australians, are the custodians of one of the world’s oldest continuing cultural traditions. Knowing how to behave to avoid offending patients and to demonstrate cultural sensitivity when managing patients is not simply learned through reading or attending a cultural awareness course. It involves continual learning through interaction, participation, reflection and engagement. A person’s behaviour is influenced by a complex mix of human response to a crisis, personality differences and most importantly the culture the person brings to the situation (AusMAT, 2011). Many dimensions influence culture, such as gender equality in a society or the value of individualism, and these can lead to stereotyping of a particular race or group. While culture influences how people may behave, each person remains an individual. Stereotyping often leads to friction when behaviour doesn’t match our expectations, but it is very difficult for people not to stereotype. Paramedics can adjust how they interact with patients by being aware of their own stereotypes and cultural biases, treating people as individuals and describing behaviour rather than judging it. Given that paramedic encounters with younger patients (of all ethnicities) are strongly associated with drugs and alcohol (and sometimes traumatic injuries), dealing with cultural differences adds another dimension to conducting safe and accurate patient assessments.

Specific aspects of Indigenous culture Indigenous representation in the cities It is extremely simplistic to assume that Indigenous Australians who live in major cities or towns are not engaged with many of their traditional ceremonies, customs and beliefs. Culture is not static and, as a way of describing how people express themselves and structure their lives and relationships, it stretches across locations. Many Indigenous Australians maintain a strong connection to the land and describe themselves as coming from places that may not be as familiar to many as other Australian place names. Despite local variations many Indigenous Australians share a similar history in terms of relationships with governments and healthcare systems. As a group they also share an experience of colonisation, albeit at different times and in different ways across the country. Being removed from their land, removing children from families and other discriminatory practices by governments and government agencies stretch across this community to some degree and impact on how they interact with healthcare workers.

P RACT ICE T IP You are encouraged to find out who the local Indigenous people are for the area in which you are working or studying (e.g. the Larakia, the Wurundjeri or

the Jagera). Do they have particular customs? What you learn is likely to be far more precise than the generic cultural principles explained in this chapter.

Payback ‘Payback’ is a term used in customary law, which is part of the kinship system. Kinship relationships determine the processes used to resolve disputes (Northern Territory Law Reform Committee, 2003). Payback is enacted when a wrongdoing has been committed. Public wrongs include breaches of sacred law, incest, sacrilege and murder by magic, while private wrongs include homicide, wounding and adultery. The essential difference lies in the manner in which the dispute is resolved. Elders are actively involved in public wrongs, whereas for private wrongs the person who has been harmed (and their relevant kin) generally determines the appropriate response (Williams, 1987). Therefore, under traditional law, families of the offender and the person who was harmed negotiate the outcome and kin relationships determine who inflicts the punishment (Trees, 2004). Families are involved in deciding the punishment because Indigenous Australian law demands satisfaction between families when a wrong has been committed (Law Reform Committee Western Australia, 2004). Paramedics may sometimes be asked for a bandage for a perceived injury where none is detected. The wearing of a bandage often delays payback. Underlying the emphasis on revenge is a general aim to restore balance and order. If punishment is inflicted properly, the matter is usually at an end; however, if the punishment goes too far as a result of an overemphasis on revenge, further conflict may result (Cousins, 2004). Unfortunately, payback is not always exacted in a traditional way, resulting in life-threatening injuries. Indigenous legal systems including payback revolve around group rights and group control, whereas the Australian legal system has developed out of a more individualistic tradition, with greater emphasis on personal rights and freedoms.

Gender issues Gender issues are important, with ‘women’s business’ and ‘men’s business’ being defined and held separate. This can prevent a practitioner from examining a person of the opposite sex (see Fig 49.1). It may be more appropriate to talk to or instruct family members or friends present to talk on behalf of the patient or to undertake basic treatment only (AusMAT, 2011).

FIGURE 49.1 ‘Women’s business’ and ‘men’s business’ are defined and held separate. Clinicians may find resistance from community members when they attempt to examine an Indigenous person of the opposite sex. Source: AAP/Clive Hyde, Northern Territory Government.

Sorry business Bereavement, known as sorry business, is a very important part of Indigenous Australian culture. When a person dies, sorrow is often expressed through wailing. Funerals can involve entire communities and the expression of grief may occasionally include self-injury. The relatives may cut off their hair or wear white pigment on their faces. The community will refrain from using the name of the deceased, but can refer to them by the name Kwementyaye; people with the same name as the deceased should also be called Kwementyaye. Photographs or videos of the deceased have to be destroyed (Sheldon, 2001).

Shame Encroaching on any area that involves taboos or causes a person to feel judged may result in shame. When shame occurs it can impede treatment: a patient may get angry about being judged or feel very uncomfortable. This may result in ongoing silence and/or refusal of treatment/transport.

Communication Introductory protocols are important: be prepared to spend more time than usual sharing personal information about yourself and the purpose of your visit. Remember that the

patient may not have called for medical assistance: someone with greater authority within the community may have made the decision that the patient required an ambulance. While the patient may comply with this authority, they may be confused if they do not see their level of injury/illness as significant. Reluctance to engage may relate to not understanding why the community has decided that treatment is necessary. The patient’s story needs to be told, but who tells it is related to kinship. The patient may not engage in the story telling but expect an appropriate member of community to tell the story on their behalf. The use of silence should not be misunderstood. In many Indigenous communities it may be considered impolite to answer questions immediately and these pause intervals are a normal conversation style. Silence may also mean that the person does not want to express an opinion at that point in time or that they are listening and reflecting about what has been said (AusMAT, 2011). Rapid-fire direct questioning can cause confusion and does not allow the patient time to follow the question process, resulting in questions being ignored or not fully answered. Where possible explain why you have to ask so many questions, wait for the pause interval after each question and don’t try to fill it. Prolonged eye contact during conversations can make Indigenous people feel uncomfortable. Take your cues from the person: some will be very used to interacting with non-Indigenous people and have no issue with this, while others will refuse to look at you but are still listening—don’t confuse this with dismissal.

Distribution A high proportion of Indigenous Australians are considered socially and economically disadvantaged—and the socially and economically disadvantaged, no matter what their ethnicity, make up a large proportion of those needing emergency healthcare. This can be a challenge for young paramedics, who often have little experience with this section of the community. Many students may feel that they are unlikely to meet Indigenous patients in the major cities but in fact most Indigenous Australians live in major cities or towns: about one-third live in major cities, with only a quarter living in remote or very remote areas (ABS, 2008; see Fig 49.2). However, no matter where Indigenous Australians live, their health status is remarkably similar and it is well-known this is lower than for nonIndigenous Australians. The challenge is to ensure that clinicians are aware of the antecedents that may impact their clinical decision making and care for Indigenous Australians so that the mistakes of the past are not repeated and the gap between Indigenous and non-Indigenous health is closed (see Fig 49.3).

FIGURE 49.2 Indigenous population clusters. City-based paramedics need to be aware of the cultural and communication issues that can arise when dealing with the Indigenous community. Source: AIHW (2011).

FIGURE 49.3 One of the factors in closing the gap between Indigenous and non-Indigenous health outcomes is providing a health service that recognises and responds to cultural factors. Encouraging early engagement with health services is a critical step in eliminating reduced life expectancy among the Indigenous population. Source: AAP/Dan Peled.

Epidemiological profile Morbi di ty Rates of disease are much higher in the Indigenous population. Indigenous Australians also have a much higher rate of comorbidities, which, in turn, causes a greater burden of disease. Some diseases found in the Indigenous population are virtually unseen in the nonIndigenous population. These include trachoma and rheumatic heart disease (AIHW, 2009). Paramedics working in areas with a large Indigenous population should try to develop their own knowledge of these conditions, as they are not often covered sufficiently in modern university courses.

Mortality According to AIHW (2012), the five leading causes of mortality for both Indigenous and non-Indigenous Australians are: • coronary heart disease • cerebrovascular disease • dementia and Alzheimer ’s disease • lung cancer • COPD. For all but respiratory diseases, the mortality rate is far higher in the Indigenous population and almost always extends across a wider age range. According to the Australian Bureau of Statistics (2012b) the four main causes of death among the Indigenous population in 2011 were: • cardiovascular disease (including coronary heart disease and cerebrovascular disease) • cancer • injuries (including self-inflicted injuries and transport accidents; see Box 49.1) B O X 4 9 . 1V i o

lenc e rates amo ng Indig eno us

Austr a lia ns Assault is among the five leading causes of death for Indigenous Australians, both males and females. Over the period 2001–2005 (the most recent data at the time of writing), the Indigenous male age-specific death rates for 10-year age groups from 25 to 54 were between 11 and 17 times the corresponding agespecific rates for non-Indigenous males, while for females the rates ranged between 9 and 23 times the equivalent age-specific rates for non-Indigenous females (AIHW, 2009).

• endocrine, metabolic and nutritional diseases.

Medical information and treatment Historically, health education and health-related information have not been delivered with reference to cultural views. As a result, information about organ functions, disease processes and so on is often delivered in a biomedical western way, which is frequently not well understood or accepted. In addition, many people still consult traditional healers (AusMAT, 2011) before seeking western medicine. Seeking contemporary treatment may be delayed for a variety of other reasons including kinship responsibilities, finances, access to medical care and a lack of recognition of the urgency related to the illness. The resulting frustration for paramedics is often a deteriorating patient with a prolonged medical illness who has received minimal to no treatment prior to the ambulance being called.

Transport to hospital Indigenous people with little experience of the healthcare system may assume that a trip to hospital means they won’t return home alive as this may have happened to relatives in the past. They may be frighted of the ‘unknown’ and consequently reluctant to leave. Providing clear, simple explanations why transport is necessary and what the hospital will do for the patient is important to provide reassurance and reasoning for the patient and their family. Alternatively, their reluctance to go to hospital may be related to the practicalities of being able to return home after they are discharged. If the patient has no money and no way of getting home, they may refuse to go to hospital. Convincing a patient to attend may be dependent on the paramedic being able to assist in the negotiation of guaranteed return travel through relatives or government travel schemes, such as taxi vouchers. Be aware also that social issues may dictate why a patient is reluctant to be transported. If the patient’s association with their community is likely to be adversely affected by their absence, they may simply refuse to go and it will be very difficult to convince them otherwise. Be sensitive to signals that alert you to this situation; for example, a patient refusing to be transported but giving no explanation and kin members refusing to accompany the patient. When transporting an Indigenous patient to hospital take a relative too, where possible. A patient’s reluctance to go to hospital can often be overcome when a suitable relative agrees to accompany them. In fact, kinship may require that a member of the family travel with the patient to provide emotional and social support.

COM M U NI CAT I ON Consider! • How is communication carried out? • Who is allowed to be present during the discussion? • What should or should not be discussed in public? • Who can communicate on behalf of the patient? • Does ‘yes’ really mean yes? • Have you summarised back to the patient what they have said, rather than

asking whether they understand?

CA SE ST U DY 1 Case 14588, 2200 hrs. Dispatch details: A 47-year-old male described as ‘sick’ by the caller for the past week is keeping the residents of his house awake with his coughing. Initial presentation: The paramedics are waved down as they approach the address by a female who states that she is the patient’s wife. She leads them to the patient, who is lying on the floor on a mattress covered in blankets. There is a tin cup next to the bed with what looks like green sputum in it. His wife tries to pull the blankets off her husband, but he grumpily argues with her and pulls them back over his head. The paramedics approach him and seek permission to examine him. He doesn’t answer them, choosing to turn over and face the opposite direction. He appears short of breath. His wife chastises him. She explains that he has been sick for a week coughing ‘that green stuff ’ and demands that the paramedics take him to hospital as she is too tired to continue watching him. The paramedics again ask the patient if they can examine him, explaining that they are here to help and that his wife is worried about him. He reluctantly pulls the blankets from his head and rolls onto his back. He looks flushed and unwell.

ASSESS Patient history The patient is refusing to discuss his illness; only his wife can confirm his condition and the accuracy of her information is unknown. It is very easy for the paramedics to miss the importance of his wife relaying the information and instead demand that the patient talk to them directly. While this may be necessary in some situations, observing appropriate protocols when working with Indigenous people is critical to establishing positive and respectful

relationships. Is the husband refusing to engage with the paramedics because he doesn’t want to speak, because he wants a significant family member to disclose his story or because he doesn’t want assistance? The clues lie in the fact that he has allowed the paramedics to examine him. He hasn’t refused assessment and hasn’t provided contradictory information over the story his wife has relayed in his presence. Further confirmation can be sought by evaluating how other members of the house are behaving towards the patient and his wife. Are they supportive of her story or are they supporting the husband and stating he is okay? Support towards her will generally indicate that she has the right to relay his story. The patient participating in the examination also confirms that he is interested in the assistance offered. The community supporting the patient may indicate that the caller (his wife in this instance) may be involved in other social issues that may have prompted a request for removal of the patient, which may or may not be appropriate. Once the patient’s story has been relayed by his significant kin, there may be an opportunity to separate the wife from her husband, leaving the patient on his own to answer questions. Without significant kin present it is more likely that he will engage in questioning. Respect for her can still be shown by seeking information from her while she is away from him.

Initial assessment summary

D: There are no dangers. A: The patient is conscious with no current airway obstruction. B: Respiratory function indicates a chest infection. The respiratory rate is elevated and the volume is slightly reduced. The SpO2 is at the lower range of normal. C: Heart rate is elevated and blood pressure is on the lower limit, but the patient is not pale or clammy. The patient is displaying respiratory distress consistent with pneumonia in the right lung.

CONFIRM The essential part of the clinical reasoning process is to seek to confirm your initial hypothesis by finding clinical signs that should occur with your provisional diagnosis. You should also seek to challenge your diagnosis by exploring findings that do not fit your hypothesis: don’t just ignore them because they don’t fit.

What else could it be? Asthma The patient’s work of breathing is normal and there are no wheezes, so this diagnosis is not supported. Acute pulmonary oedema While crackles are present they are coarse, localised and resolve or move with a cough. The patient is also supine, which is atypical for acute pulmonary

oedema, as sitting upright reduces the dyspnoea. This diagnosis is not supported.

DIF F ERENT IA L DIA GNOSIS Pneumonia Or • Asthma • Acute pulmonary oedema • Pulmonary embolism • Pleural effusion • Pneumothorax • Sepsis

Pulmonary embolism The patient does not appear to have significant risk factors but this condition is difficult to exclude in the pre-hospital setting. The lower blood pressure is a concern as it could indicate a significant obstruction to pulmonary blood flow. Pleural effusion This diagnosis is difficult to exclude in the pre-hospital setting and is probably present to some degree if pneumonia is present. Pneumothorax Equal breath sounds and a lack of localised resonance help to exclude this diagnosis. The presence of bronchial sounds in the lower right lobe suggests consolidation of lung tissue (the ‘solid’ nature of the lung tissue is transmitting sounds more than air) and assists in excluding this diagnosis. Sepsis While the patient almost certainly has a lung infection, this does not preclude the infection from becoming systemic. Only a blood culture will confirm this finding, but given his vital signs, if he is not currently septic he is likely to progress to this state if left untreated. The patient is indeed unwell and should be transported to hospital. In order to achieve this outcome some significant cultural considerations need to be evaluated.

T REAT Emergency management Management of respiratory distress and sepsis is covered in Section 8 and Chapter 44, respectively, and so the issue here is the impact of the patient’s

Indigenous background in engaging with treatment. While the patient has the right to autonomy and to withhold consent, this can be defended only if he has been given and is capable of understanding the consequences of his decision (see Ch 10). In this case the impediments to the patient agreeing to transport may go beyond those normally encountered by paramedics and they need to be addressed when considering the patient’s wish to remain at the scene. For instance, if the patient was left untreated and succumbed to his illness, his significant kin could be punished by the community for not obtaining help for him. The paramedics should consider the following questions: • Are his significant kin refusing to accompany him? • Does the patient have the finances to return home? • Is he likely to be disadvantaged by leaving his community or home? • Is he afraid of what might happen when he goes to hospital? They should then address each of these questions and again provide an opportunity for the patient to accompany them. If the wife refuses to accompany her husband to hospital and there are no community members present to apply pressure to her to do so, the paramedics should ask for another person to accompany the patient. However, the person assigned to this role may not be the right person to advise in decision making or have the right to tell the patient’s story. As a result, they can provide support and company for the patient but won’t be able to answer questions regarding treatment. If it is not possible to get another community member to accompany the patient, the paramedics should explain the seriousness of the situation to the patient’s wife and encourage her to play her role in accessing help for the patient. In traditional Indigenous culture, if a significant kin member refuses to assist a person they are obligated to help and that person dies, there will be serious ramifications. If return from hospital is an issue, the paramedics may be able to advise what services are available in the area to provide return transportation. This is particularly relevant where it is unlikely that the patient will be admitted to hospital. Alternatively, understanding what government schemes have been arranged may assist in persuading him to go to hospital. However, any arrangements must be communicated to the receiving hospital: one negative experience will not be forgotten and promises will mean little when the next paramedic makes one. Belongings and finances are often shared within the kinship system. As a result, one member of the community may provide support for others and the patient may display a reluctance to leave their home or community if this support is likely to be interrupted. Allowing time for the patient to make alternative arrangements may be critical before they will agree to be transported. The patient may not be familiar with the processes of care in the hospital setting and may be afraid of going to hospital. He may also be concerned about his rights being respected and whether his family will be allowed to be with him. Any such issues should be identified and addressed to put the patient’s mind at ease.

EVALUAT E The response to the management of respiratory distress and sepsis is covered in Section 8 and Chapter 44, respectively.

CA SE ST U DY 2 Case 14659, 2300 hrs. Dispatch details: A 3-year-old has had diarrhoea and vomiting for the past 12 hours. Initial presentation: The paramedics are met on the roadside by a middleaged woman holding the young child. The woman introduces herself as the auntie of the child.

ASSESS 2310 hrs Primary survey: The child is alert but is whining and irritable. She is small for her age, with chronic rhinitis. She is wearing shorts and her chest is bare. 2311 hrs Chief complaint: The child has ‘loose motions’ that are green in colour and offensive-smelling, with around 6–8 loose stools today. She has also been vomiting. 2312 hrs Pertinent hx: The child’s auntie says the child has been unwell since this morning. She started vomiting about 3 hours ago. She thinks the child may have passed urine once today but cannot be sure. 2315 hrs Vital signs survey: Perfusion status: HR 135 BPM; sunken eyes, dry lips, poor skin turgor, skin rash on lower legs that looks like scabies; temperature 39.1°C.

Respiratory status: RR 28 BPM, work of breathing normal, SpO2 98%. Conscious state: GCS = 15. The child sobs when the crew approach her, becoming very distressed at their touch. She is constantly rubbing and pulling at her left ear and trying to wriggle out of her auntie’s arms. The crew decide not to upset the child further by completing a comprehensive examination and resort to observation and a SpO2 monitor. 2318 hrs Secondary survey: The child, although small, appears well nourished and cared for. On further questioning of her auntie it is established that the child’s mother is in the house but sent the child with her auntie. The auntie states that she will travel with the child in the ambulance as the mother doesn’t want to go. She also says that the child is normally well, but other children in the house have had a similar stomach upset over the last week.

CONFIRM The essential part of the clinical reasoning process is to seek to confirm your initial hypothesis by finding clinical signs that should occur with your provisional diagnosis. You should also seek to challenge your diagnosis by exploring findings that do not fit your hypothesis: don’t just ignore them because they don’t fit.

What else could it be? Acute appendicitis Appendicitis is classically associated with paraumbilical pain localising to the right iliac fossa, anorexia, nausea and vomiting. Constipation is more likely to be a feature of acute appendicitis, but diarrhoea is seen when the patient’s appendix is located behind the ileum or protrudes into the pelvic cavity. A key defining feature of gastroenteritis as compared to appendicitis is the pain pattern. This patient’s pain is colicky and generalised across the abdomen. Intestinal obstruction Clinical features of intestinal obstruction include nausea and vomiting and colicky abdominal pain. Abdominal distension and constipation are key signs, with diarrhoea a common presentation but not usually the primary complaint. Inflammatory bowel disease Gastroenteritis and inflammatory bowel disease (Crohn’s disease and ulcerative colitis) share some common clinical features, but with no previous history inflammatory bowel disease is unlikely.

DIF F ERENT IA L DIA GNOSIS Gastroenteritis Or

• • Acute appendicitis • • Intestinal obstruction • • Inflammatory bowel disease

T REAT This situation is clinically quite simple (almost certainly infectious gastroenteritis) but complex socially: the child’s mother doesn’t want to accompany the child or relate her history, sending the child’s auntie to speak to the paramedics instead. It is clear to the paramedics that the little girl is unwell, likely to be dehydrated and requires treatment to stop further deterioration. The types of issues the paramedics need to consider include: • Should they spend time convincing the child’s mother to attend hospital with her child? • Does the child’s auntie have guardianship if the child’s mother is present in the house? • Can they transport the child without her mother? • Does this limit what they can do for the child during transport? • Why wouldn’t the mother want to accompany her child to hospital?

EVALUAT E Evaluating the effect of any clinical management intervention can provide clues to the accuracy of the initial diagnosis. Some conditions respond rapidly to treatment so patients should be expected to improve if the diagnosis and treatment were appropriate, whereas other conditions are unlikely to respond in the timeframes normally associated with ambulance transport times. In such cases, a failure to improve should not be considered an indication of a misdiagnosis. In this case, pain relief should be effective, although the reduction in nausea and vomiting from antiemetic administration can be variable. IV fluids should maintain or slightly improve the patient’s perfusion status but the effect is likely to be minimal.

CA SE ST U DY 3 Case 14590, 1630 hrs. Dispatch details: Police request an ambulance at an alleged assault. Initial presentation: The paramedics arrive and find a 49-year-old male arguing in the middle of a group of people. The police are in attendance and quickly resolve the situation and remove the patient from the group. The man, an Indigenous Australian male, was arguing with his wife when the quarrel became violent. An onlooker witnessed the violence and rang for the police when she saw blood.

ASSESS Members of the group surround the police officers, insisting that the man deserved to be stabbed as he had been seen with a woman other than his wife. The patient is agitated, loudly declaring his innocence. He appears unaware of any injury and won’t stay still long enough for a proper assessment. 1643 hrs Chief complaint: The paramedics notice a small tear in the upper leg of the patient’s jeans and the crutch area and right leg of his jeans are soaked with blood down as far as the knee. The police escort the patient to the rear of the ambulance and sit him down on the back steps. The paramedics then attempt an assessment. 1645 hrs Vital signs survey: Perfusion status: HR 120 BPM, BP 90/60 mmHg, skin cool and dry. Respiratory status: RR 32 BPM, SpO2 94%. Conscious state: GCS = 15. 1650 hrs Secondary survey: There is no obvious wound but a large amount of congealed blood around his upper right leg. On exposure a stab wound is located in the anterior right upper thigh, which pulsates bright-red blood when disturbed. Female members of the group start to wail loudly when they see his blood. No-one will confirm who the perpetrator is and his wife is insisting that she travel with him to hospital. The clinical situation is relatively clear: a penetrating wound to the groin, combined with abnormal vital signs, requires immediate transport to hospital. Expediting transport and ruling out any other injures will be difficult at this

highly emotional scene.

CONFIRM Determining the underlying cause of the patient’s presentation is not difficult. Several witnesses saw him stabbed with a knife, the blood loss is obvious and the treatment is straightforward—immediate transport to definitive care. Assessing his vital signs confirms that he is most likely hypovolaemic and may have an internal bleed that cannot be controlled without surgery. He must be transported to hospital without delay, but there are significant cultural considerations that need to be addressed to enable this. The key to effective engagement in this case involves being culturally sensitive, describing behaviour without judging it and keeping calm. Impatience or assertive behaviour may further agitate the scene. Marital problems aired publicly are likely to produce feelings of shame. Ideally, the treating paramedic should be the same gender as the patient when these issues are discussed, but even then permission needs to be sought from the patient before proceeding. It may be more appropriate for another member of the community to speak about these problems rather than the patient. It is important the patient does not feel judged as this will exacerbate the feeling of shame and make further management more difficult. The paramedics should preface any questions likely to induce these feelings with ‘I’m not trying to shame you, but I need to know …’ This is likely to facilitate more truthful conversations as the paramedics are describing why they should be included in the person’s embarrassment. Acknowledgement of the shame builds rapport and allows the patient to understand that he is not being judged. Wailing, mainly by females, demonstrates their sorrow at what has occurred. It is a mark of respect for the person and may occur even when the injury or illness is not life-threatening. As such, trying to explain the exact nature of an injury to them (if it is minor) may not resolve the reaction. In addition, understanding the meaning behind this reaction should enable paramedics to realise that attempting to console those who are wailing may not be necessary. This patient is agitated and difficult to engage. The paramedics need to establish whether this is due to hypoxia, a sense of shame, the noise and stimulation at the scene or the fact that he is proclaiming his innocence but has received payback regardless. Confirmation can be sought by assessing how other members of the group are behaving towards the patient and his wife. Are they supportive of him or are they angry towards him? Support towards him will normally indicate that he has received payback and is forgiven and his agitation should diminish. Anger towards him could mean he has not taken the payback as he should and this could invoke shame and contribute to his agitated state. The recruitment of an Indigenous male Elder may assist in getting the patient stationary long enough to take his vital signs. This person should be

considered as an appropriate travel companion to keep the patient calm and approachable. Amid the heightened emotions, the patient’s wife asks to go with him to hospital but it is still not clear whether she is the alleged perpetrator. Consulting the patient is appropriate: if he agrees, the paramedics should ensure that his wife understands her role in the ambulance and will assist them and follow their directions. Due to the nature of the scene, giving the wife clear boundaries on what will and won’t be acceptable behaviour, with consequences if she chooses not to follow the instructions, may be necessary to ensure the safety of both the patient and the crew.

T REAT Safety Depending on the circumstances, the patient may be at continued risk from the alleged perpetrator and other family members—as may be the paramedics. Consideration must be given to paramedic safety where violence is present. However, the aggression in this case is predominantly focused inwards and not towards the professionals trying to assist (see Fig 49.4).

FIGURE 49.4 Violence rates among Indigenous Australians are regarded as high, but assaults occur more frequently in lower socioeconomic communities regardless of their cultural background. Source: Corbis/Marianna Massey. The notion of privacy in Indigenous culture is different from traditional Anglo-Saxon Australia. Straightforward, loud conversations or arguments between individuals in a public forum are still considered private. Other community members who are not invited or of relevant kin should not join in, even though the argument can be heard publicly.

EVALUAT E Evaluating the effect of any clinical management intervention can provide clues to the accuracy of the initial diagnosis. Some conditions respond rapidly to treatment so patients should be expected to improve if the diagnosis and treatment were appropriate, whereas other conditions are unlikely to respond in the timeframes normally associated with ambulance transport times. In such cases, a failure to improve should not be considered an indication of a misdiagnosis. In this case, haemorrhage control, IV fluid and pain relief should be effective in maintaining the patient’s vital signs. Small reductions in his heart rate should be the first sign of a positive response to treatment. Improvements in blood

pressure should occur once his heart rate starts to decrease.

Summary Indigenous Australians live with significant health inequities that are compounded by not having access to the necessary determinants of care that optimise health outcomes and to quality health services. It is not unusual for some Indigenous Australians never to have seen a primary healthcare professional and paramedics may be the first health professionals to respond to their acute health conditions or exacerbations of existing chronic conditions. While life-threatening situations demand prioritisation, it is important to consider key cultural factors and appropriate ways to engage with these patients. Paramedics are in a unique position to facilitate patients’ access to health services to have their health needs assessed and treated. To effectively engage and interact with Indigenous Australians, paramedics need to be aware of the stereotypes and prejudices they may hold that can adversely impact on their interactions with patients and their communities. This doesn’t simply mean treating all patients the same: paramedics need to be aware that Indigenous Australians may have encountered negative healthcare providers and discriminatory behaviours; they also need to be genuine, respectful and non-judgemental, and aware of key cultural needs that should be respected.

References AusMAT AusMAT Training, Version 3. NCCTRC, 2011. Retrieved 2 October 2012 from www.nationaltraumacentre.nt.gov.au Australian Bureau of Statistics (ABS). Census of Population and Housing: Counts of Aboriginal and Torres Strait Islander Australians. Retrieved 6 November 2014 from www.abs.gov.au/ausstats/[email protected]/Lookup/2075.0main+features32011, 2012. [Cat. no. 2075.0.]. Australian Bureau of Statistics (ABS). Causes of Death Australia, 2011. Retrieved 6 November 2014 from www.abs.gov.au/ausstats/[email protected]/Lookup/489D9A69EDA30684CA257B2E000D7703? opendocument, 2012. [Cat. no. 3303.0.]. Australian Institute of Health and Welfare (AIHW)National Mortality Database: Recorded Crime: Victims. Canberra: AIHW, 2009. [Cat. no. 4510.0]. Australian Institute of Health and Welfare (AIHW). The Health and Welfare of Australia’s Aboriginal and Torres Strait Islander People, An Overview. Retrieved 6 November 2014 from www.aihw.gov.au/WorkArea/DownloadAsset.aspx?id=10737418955, 2011. Australian Institute of Health and Welfare (AIHW)Australia’s Health, 2012. Canberra: AIHW, 2012. [Cat. no. AUS 156]. Bourke, C., Edwards, B., Family and kinship. Aboriginal Australia. 2nd ed. University of Queensland Press, St Lucia, Qld, 2004. Cousins, M. Aboriginal justice: a Haudenosaunee approach. Justice as Healing: a newsletter on Aboriginal concepts of justice (Native Law Centre). 1, 2004. Department of Foreign Affairs and Trade (DFAT). People: Culture. Retrieved 1 October 2012 from www.dfat.gov.au/facts/people_culture.html, 2013. Law Reform Committee Western AustraliaThematic Summaries of Consultations: Midland, 16 December 2002. Perth: Law Reform Commission of Western Australia, 2004. Northern Territory Law Reform Committee. (2003). Aboriginal Communities and Aboriginal Law in the Northern Territory. Background Paper No. 1 (21).

Sheldon, M. Psychiatric assessment in remote Aboriginal communities. Australasian Psychiatry. 2001; 35(4):435–442. Trees, K. (2004). Contemporary Issues Facing Customary Law and the General Legal System. Roebourne: A Case Study. LRCWA Project 94. Background Paper no. 6 (20). Williams, N.Two Laws: Managing Disputes in a Contemporary Aboriginal Community. Canberra: Australian Institute Studies Press, 1987. Wilson, D. The significance of a culturally appropriate health service for indigenous M women. Contemporary Nurse. 2008; 28:173–188.

ori

CHAP TER 50

M ori patients By Denise Wilson and Bronwyn Tunnage

C O N C E P TS U S E D I N TH I S C H A P TE R • The paramedic’s clinical approach: Section 2

O V E RV IE W • M ori are the Indigenous people of Aotearoa (New Zealand) and they comprise 15% of the population. • Contemporary M ori are not a homogenous group of people, but are diverse in terms of iwi (tribes) and experiences. • The cultural beliefs of contemporary M

ori can be located on a continuum that spans those

who have had a traditional upbringing to those who may know they are M connections with their heritage and cultural traditions.

ori but have lost

• Compared to other New Zealanders, M ori experience significant inequities in life expectancy, health status, health outcomes (morbidity and mortality) and access to a range of health services. • The ability of paramedics to conduct a detailed health assessment and make sound clinical decisions may require an understanding of M engagement with health providers. • Traditional M

ori culture and beliefs and how it shapes their

ori cultural worldviews are holistic and eco-spiritual in nature. This is evident in

the collective (or group) orientation of M

ori in contrast to the individual orientation of the

dominant culture.

Introduction Economic and social deprivations adversely affect health, and Indigenous groups generally have poorer outcomes and poorer survival chances (Whitehead, 1991). In New Zealand, the poor respiratory health experienced by many M ori can be linked to houses that lack insulation and are cold and damp (Howden-Chapman et al., 2005). Research also indicates that the extent and quality of care may differ between non-Indigenous New Zealanders and M ori. For example, they are more likely to experience an adverse event while in hospital (Davis et al., 2006), to postpone buying a prescription medication (Jatrana, Crampton & Norris, 2011), to notice differences in the quality of care they receive (Wilson, 2008) and to experience discrimination and racism within health services (Harris et al., 2006; Wilson, 2008). Despite their overrepresentation in avoidable mortality and morbidity statistics, M ori are less likely to access primary healthcare services. This may be because they do not have the opportunity due to remoteness, or because they do not consider the service to be appropriate to their needs. As a result, when the opportunity to engage with M ori patients does arise in the primary healthcare setting, the ability to engage effectively with their cultural beliefs as well as their illness may have a disproportionately positive and long-term effect. Engaging with culturally distinct groups requires health professionals to undertake a process of reflection on their personal cultural background, professional values and beliefs, and the power they hold in their position. They then need to examine how these might impact on their professional practice when working with others from another culture, like patients and their wh nau (extended family). Box 50.1 provides a glossary of M ori terms.

Specific aspects of healthcare for M ori Qua l i ty of he a l thca re Research with general practitioners (GPs) confirms concerns about the quality of care that M ori may receive when they do access primary healthcare services (Crengle, 2007). GPs report that M ori are likely to have visits of shorter duration, have urgent presentations, are slightly less likely to have tests and investigations and are slightly more likely to have a prescription. Importantly, GPs report that their rapport with their M ori patients is lower than what they have with their other patients.

Institutional racism Institutional racism is evident when those living with high levels of deprivation, as many M ori do, are consequently unable to exercise choice and to access health services in the same way as people with less deprivation (see Fig 50.1). We should be mindful that the high rates of morbidity that M ori experience are caused by a complex set of factors, including not having the necessary resources (such as transport or money) to access healthcare services. Although publicly-funded health systems are set up to give everyone equal access, as Morgan and Simmons (2009) point out, those living with high levels of social deprivation are still not getting the healthcare they need.

FIGURE 50.1 Eighty-three-year-old Rapaki Ma–ori elder Rima Subritzky has helped raise 37 children from her wha– nau and continues to care for her son Charlie, who has disabilities. It is important that healthcare systems promote a cultural understanding of Ma–ori communities to ensure that the specific needs of their people are met. Source: Fletcher EQR (2013).

B O X 5 0 . 1G l o

ssar y

Aroha Hapū

Love A subtribe forming a basic political unit within M

Hui Kia ora Kuia Kupu Manaakitanga Marae

Gathering Greeting, hello Older woman M ori words Caring for others Open courtyard in front of wharenui where formal gatherings are held Life force Common, opposite to tapu Council or committee Men Period of mourning Sacred, restricted, prohibited Hello, thank you Refers to women as bearers of children; the house of humankind

Mauri Noa Rūnanga Tane Tangihanga Tapu Tēn koe Te whare tangata Te reo M ori Tikanga Tuku wairua

M

ori society

ori language

Correct procedures, protocols A verbal ritual said over those who are dying to ease the passage of the spirit into the afterlife Spirit, soul of a person hine Woman/women

Wairua Wahine/w Wh nau Whakam Whakapapa Wharekai Wharenui Whare tupuna

Extended family Shame, embarrassment Genealogy Eating house Meeting house Ancestral meeting house

Epidemiological profile I scha e m i c he a rt di se a se Ischaemic heart disease (IHD) is the second largest cause of death in New Zealand (after all cancers combined) and accounts for one in every five deaths (Ministry of Health, 2010). IHD death rates vary between ethnic groups within the population but are significantly higher among M ori compared with non-M ori. For M ori women, the age-standardised death rate from IHD is more than twice that of non-M ori women, and for M ori men it is 1.85 times higher than for non-M ori men (Ministry of Health, 2010). These figures do not take into account that M ori are a youthful population in comparison with the non-M ori population (only 4% of M ori live beyond the age of 65 years compared with 12% of non-M greater than these figures suggest.

ori) and the actual difference in mortality rates is

Smoking The health risks of smoking are well known, including the link between smoking and heart disease. M ori are more than twice as likely to smoke as other adults living in New Zealand (Ministry of Health, 2010). The health consequences of smoking extend beyond IHD to many other diseases.

Diabetes The age-standardised rates of the diabetes-related complications of renal disease and lower limb amputation are nearly nine and five times higher, respectively, for M ori than nonM ori (Ministry of Health, 2010). M ori are also seven times more likely to die of complications related to diabetes than non-M ori (Harwood & Tipene-Leach, 2007). The ethnic inequalities related to diabetes are complex and involve the interaction of various risk factors such as genetics, environment, social determinants of health (e.g. education, qualifications, income, employment, housing, access to transport) and interpersonal and institutional racism (Harwood & Tipene-Leach, 2007; Reid & Robson, 2007). The ethnic inequalities related to diabetes (and other morbidities often experienced by M ori) are associated with reduced access to, and quality of, healthcare (Harwood & Tipene-Leach, 2007). In other words, absence or delay in the diagnosis and treatment of diabetes has detrimental effects on the health and lives of M ori and their wh nau (Curtis, Harwood & Riddell, 2007).

Rheumatic heart disease New Zealand has one of the highest prevalence rates of rheumatic heart disease globally,

with most cases occurring among M ori and Pacific peoples. Acute rheumatic fever in childhood is associated with geographical region, ethnicity, social determinants of health such as poverty and overcrowding, high rates of streptococcal upper respiratory infections, and a lack of access and use of health services (Wilson, 2010). Acute rheumatic fever in childhood invariably leads to chronic rheumatic heart disease for M ori. The management of chronic rheumatic heart disease is compromised by factors such as geographical location, mobility, access to specialist care, lack of early diagnosis, comorbidities and cultural barriers (White et al., 2010). Paramedics need to be aware that M ori presenting with IHD might have underlying chronic rheumatic heart disease.

Driveway accidents On average, driveway accidents result in the death of 4 New Zealand children every year and the hospitalisation of a further 76 children, some of whom sustain permanent disability (Child and Youth Mortality Review Committee, 2011). In Australia, the number of deaths is about 11 per year. These accidents frequently involve a driver who is either related or known to the child. In many cases the driver assumed the child to be in a safe place, but instead the child wandered into the path of the vehicle (Child and Youth Mortality Review Committee, 2011). Socioeconomic deprivation is associated with higher injury rates among children across all ethnicities and in the case of low-speed driveway accidents this is associated with factors such as type of housing, fencing of play areas, amount and type of child supervision and adoption of safety behaviours (Child and Youth Mortality Review Committee, 2011). Accidents are a leading cause of death for M ori children aged between 1 and 4 years, with transport-related accidents accounting for 36% more deaths for M ori children compared with non-M ori children (Robson & Purdie, 2007). One study identified that of all the deaths caused by low-speed cars reversing, 48% were M ori children (Child and Youth Mortality Review Committee, 2011), despite M ori comprising only 15% of the New Zealand population. M ori children are also more likely to be killed in pedestrian accidents at home than non-M ori children: between 2002 and 2008 the rate was close to 15 per 100,000 among M ori children compared with 3 per 100,000 for non-M ori children (Child and Youth Mortality Review Committee, 2011). In the same period, the rate among the Pacific Islander population was 20.5 per 100,000. This inequity in transportrelated mortality rates continues throughout the lifespan, with the age-standardised mortality rate among M ori from motor vehicle accidents 18.4 per 100,000—more than twice that of the non-M ori population.

Family violence Prevalence studies of women presenting to New Zealand adult and child emergency departments (EDs) found that 34% of M ori women screened positive for partner violence in the previous 12 months and 57% for lifetime exposure to partner violence,

compared with figures of 21% and 44%, respectively, for other women (Martin & Pritchard, 2010). A prevalence study of women attending a M ori health provider found that 27% of M ori women screened positive for partner violence in the previous 12 months and 80% for lifetime exposure to partner violence (Koziol-McLain et al., 2007). Studies have also found that between 60% (Koziol-McLain et al., 2004) and 96% (KoziolMcLain et al., 2007) of M ori women screening positive for partner violence had children living in the same household. Despite M ori comprising only 15% of the population, seven times more young M ori women and four times more M ori children are hospitalised from an assault compared with non-M ori (see Fig 50.2). This disproportionate representation of intimate partner violence (IPV) unfortunately extends into cases where the violence is so severe it causes death (see Table 50.1). TABLE 50.1 Deaths due to family violence, New Zealand

IFV = intrafamilial violence. Source: Family Violence Death Review Committee (2014).

FIGURE 50.2 Young M ori women are seven times more likely to be hospitalised from an assault compared with women from a European background; the risk for M ori children is four times that of other children. Source: iStockphoto/Che McPherson.

M ori have an eco-spiritual, holistic worldview grounded in whakapapa (genealogy) and a collective orientation. Traditional M ori values are based on concepts such as tikanga (correct procedures), aroha (love), manaakitang ° (caring for others), wairua (spirituality), wh nau (extended family) and the notion of collective responsibility and accountability. Values such as these ensure the safety of all concerned and respect the complementary roles that men and women carry out within the context of their wh nau and hapū (a subtribe forming a basic political unit within M ori society).

The ‘warrior’ gene Some commentators have attempted to explain or justify family violence among M ori as being caused by a so-called ‘warrior’ gene. This concept has been perpetuated by some aspects of the media, and the family dysfunction displayed in the movie Once Were Warriors is commonly referenced as being indicative of broader M ori society. While there is no denying that violence rates are

significantly higher among M ori populations, the causes are more likely to be socioeconomic (Marie, Fergusson & Boden, 2008). It has been established that rates of IPV tend to be higher among individuals exposed to economic adversity (Feldman & Ridley, 1995; Bassuk, Dawson & Huntington, 2006) and M ori are at greater risk of socioeconomic disadvantage (Statistics New Zealand, 2010). From this perspective M ori are no more likely to be involved in IPV than non-M ori of a similar socioeconomic background: the disproportionate representation is simply reflective of the increased likelihood that M ori are overrepresented in lower socioeconomic groups (Marie, Fergusson & Boden, 2008). So widespread is wh nau violence that it has been described as ‘imposter’ tikanga (Kruger et al., 2004), meaning that violence has become so normalised and accepted that it is seen as a cultural way for M ori to function. However, culturally M ori have a much broader and more encompassing concept of family, as demonstrated by The Status of Children Act 1970, which recognised that in M ori society children are equally precious to all members of their wider family, regardless of their birth parents’ marital status (see Fig 50.3). Wh nau violence is not historically part of traditional M ori society (Kruger et al., 2004) and is a relatively recent development. In traditional M ori communities, women and children are held in high esteem and importance. This is exemplified in the concept of te whare tangata (women as bearers of children—the house of humankind), whereby women were responsible for maintaining the whakapapa of a wh nau/hapū because they were the bearers of future generations. Similarly, children had an important status because they were seen as the future.

FIGURE 50.3 In M ori society, children are equally precious to all members of their wider family, regardless of their birth parents’ marital status. Here, Tupuhi holds his grandson Rapson during a visit by members of Ng ti P oa to their ancestral land at Maungawhau (Mt Eden) in Auckland. Source: APN/Kenny Rodger.

Wh nau were traditionally a source of collective support, with accountability and obligations within the public domain. Any transgressions against women and children were dealt with swiftly and publicly. The processes of colonisation, patriarchy, capitalism, Christianity, education, legislation and urbanisation, however, have eroded important traditional mechanisms to keep women and children safe. The restructuring of M ori society has created a dislocation of wh nau from their traditional collective support systems, and the perpetrators of family violence are no longer held accountable to the community (Pihama, Jenkins & Middleton, 2003). The contemporary experiences of wh nau violence for M ori are similar to the experiences of other indigenous peoples with histories of colonisation (Berry, Harrison & Ryan, 2009; Brownridge, 2008; Hukill, 2006). To understand the contemporary context of wh nau violence requires an understanding of the past and the impact colonisation has had on many M ori. Settlers, Crown representatives and missionaries documented observations that provide historical evidence that reinforces the revered place M ori women and children held in M ori wh nau and hapū. An example of these observations was recorded by Samuel Marsden, a member of the Anglican clergy who introduced Christianity to New Zealand. He wrote:

I saw no quarrelling while I was there. They were kind to their women and children. I never observed either a mark of violence upon them, nor did I see a child struck. Samuel Marsden inElder (1932).

Delayed access to healthcare Health conditions and diseases can be prevented or treated at the community level through population-based health strategies and at the individual level through timely access to primary healthcare. It is well-established that M ori are less likely to access primary healthcare and more likely to be admitted to hospital or to die from health conditions and injuries that could have been prevented or managed in the community (Ministry of Health, 2010). Paramedics are familiar with encountering patients who are seriously ill because they delayed seeking medical help due to the costs or difficulties in seeing a doctor. In addition to factors associated with socioeconomic deprivation, many M ori who live in rural or semi-rural areas face the added challenges of accessing distant health services. Delayed access to healthcare results in late diagnoses and deferments in receiving potentially life-saving treatments. Thus, the paramedic’s role in gathering a patient’s history and undertaking observations and procedures, such as a 12-lead ECG, is crucial for identification of any problems and transferral to appropriate treatment.

Death among M ori populations M ori, like other people, react in diverse ways to the news that someone they love has died. Some may express profound sadness, others may express anger. Some M ori women express their grief very emotionally by unreservedly crying or wailing loudly, while M ori men tend to grieve quietly —’crying silently’ (Salmond, 1976). Many, but not all, M ori hold traditional beliefs about death and dying and believe that following death a person’s wairua (spirit) leaves the tūp paku (body) and lingers over it for several days prior to embarking on a journey to another dimension of life. A tuku wairua is performed (a° verbal° ritual said over those who are dying to ease the passage of the spirit into the afterlife), although it should be noted that different iwi have different beliefs about the nature of the journey that the wairua takes. The last breath of life signifies both the death of the mauri (life force), which then disappears, and the transition of the person to being a tūp paku. At this time the tūp paku is extremely tapu (sacred) and the person’s wairua is released (Moko Mead, 2003). It is a commonly held belief by many M ori that the tūp paku should not be left alone, meaning close wh nau will want to stay with the body. The wh nau may want to gather and have a kaumatua or church minister to say a karakia (as a form of last rites) over the tūp paku, especially as the injuries that have led to the death are believed to weaken the wairuai (Moko Mead, 2003). It is vitally important to the wh nau that the correct processes and protocols are carried out, such as saying the appropriate karakia and the wh nau staying with the tūp paku. This enables the tuku wairua of their loved to be released and ‘go in peace to the next world’ (Barlow, 1994). It is believed that the tuku wairua watches the events and what people are doing: if things are not carried out correctly, they will not be at peace and will cause difficulties for the wh nau. For this reason, it is important that the correct spiritual and cultural protocols are followed for the peace of mind of the wh nau and for the tuku wairua to begin its journey peacefully (Moko Mead, 2003). However, it is important not to assume that all M ori have traditional beliefs about death: ask and be guided by the wh

nau what their needs are.

CAS E S TUDY 1 Case 30635, 1123 hrs. Dispatch details: A 46-year-old woman has collapsed. She is attending a hui (gathering) on a marae (open courtyard where formal gatherings are held) in a rural location, 45 minutes from the nearest tertiary hospital. Initial presentation: The paramedics arrive and are led to the patient, who is

sitting down in the wharekai (eating house) where she has been helping to prepare lunch. She is pale and sweaty and complaining of feeling dizzy.

ASSESS Patient history As the patient is on a marae it is important for the paramedics to be respectful of and observe tikanga. A sound approach is to follow whoever greets them and observe any protocols such as removing their shoes prior to entering the whare tupuna (ancestral meeting house) or wharenui (meeting house). If time is critical, you can ask to enter the building without removing your footwear. In most circumstances paramedics will not be required to remove their footwear to enter the wharekai. If in doubt, ask. If the situation demands urgent action and involves breaching tikanga, quickly explain what you are doing and why. Research has shown that having a support person to assist M ori women to interpret and answer questions can reduce their stress (Wilson, 2008). If this is the case, allow time for the support person to interpret the questions and answers if language or hearing difficulties are involved.

C OMMEN T When M ori come together, they usually engage in a process called whakawhanaungatanga. This involves introducing where you are from geographically, what you do and what your name is.

This patient states that she was rushing to attend the hui and hasn’t eaten beforehand. Once she arrived she was talking to friends when they said she briefly appeared confused before turning pale and stating she was dizzy. The friends helped her to sit on the ground and she says that made her feel better. Her friends noted that she was sweaty to touch after she nearly fainted. She denies any shortness of breath, chest pain or palpitations prior to this. She was not incontinent or unconscious at any time. She denies central chest pain but reports that she can feel a ‘lump’ in her throat. On further questioning you discover that she has no known medical history. She is overweight, but not obese.

Physical examination Areas on a marae and in the homes of M

ori living by traditional cultural values and

tikanga are governed by the cultural concepts of tapu (sacred, restricted, prohibited) and noa (common, opposite to tapu). It is good practice to seek guidance about where to undertake observations and examinations and where to place equipment. For example, the wharekai is a place of noa. In relation to people, body parts like the head, genitalia and heart are tapu at different times and in various situations. Noa is a state of safety without the impositions, protection and restrictions evident in tapu states (Durie, 1998). For example, while it is always good practice to avoid stepping over any patient, to M ori this would be particularly offensive. Tapu is particularly important when someone dies, as the tūp paku is very tapu. In these situations it is important to seek guidance from wh nau about what is acceptable practice when someone dies. Practically, trying to negotiate tikanga and making sure conditions of tapu and noa are observed is difficult when you are attending a call-out. Getting to know local iwi and/or the rūnanga (council or committee) in the area can assist clinicians who are unsure of appropriate behaviour. Guidelines for attending emergencies can then be established with the support of the community.

Initial assessment summary Problem Conscious state Position Heart rate Blood pressure Skin appearance Speech pattern Respiratory rate Respiratory rhythm Respiratory effort Chest auscultation Pulse oximetry Temperature BGL 12-lead ECG Motor/sensory function History

The patient is complaining of atypical chest pain Alert and orientated; GCS = 15 Sitting upright in a chair 115 BPM, regular 120/90 mmHg Pale, cool, clammy Speaking freely 24 BPM Regular even cycles No use of accessory muscles Clear breath sounds, good bilateral air entry apices to bases 97% on room air 36.9°C 14.5 mmol/L Sinus tachycardia, no ST abnormalities, intervals normal Normal None known

D: There is no danger to the patient or the crew. A: The patient is conscious with no airway compromise. Auscultation of the area around the ‘lump’ sensation reveals no stridor or abnormal sounds. B: Respiratory function is currently normal. C: Heart rate is increased and while her blood pressure is within normal limits the patient appears poorly perfused. Following a near-fainting episode the patient is displaying poor perfusion and

complaining of throat discomfort. She has not eaten prior to this episode.

CONFIRM The differential diagnoses following a near-fainting episode followed by chest pain are outlined in Chapter 24. While these differential diagnoses need to be considered, the patient’s M ori heritage should be also taken into account. The types of issues the paramedics need to consider include: 1. differences in terms of health and risk factors for M ori patients 2. the fact that 46 years old is comparatively more aged for the M ori population than for the Caucasian population 3. cultural differences in terms of the patient’s willingness to access or enter into the healthcare system.

TREAT Emergency management Management of acute coronary syndrome is discussed in Chapter 24. This patient’s increased risk of cardiac disease makes it likely that she is suffering an ischaemic event and needs to be treated according.

EVALUATE This patient’s M ori background should have no impact on her response to treatment, but taking her cultural values into account may reduce her anxiety and have a positive effect on her ischaemia.

CAS E S TUDY 2

Case 10234, 0725 hrs. Dispatch details: A 16-month-old toddler has been struck at low speed by a car reversing out of the driveway. She is unresponsive. Initial presentation: When the paramedics arrive they find the toddler lying motionless in the driveway surrounded by her parents and two other young children. There are several adults nearby who may be extended family or neighbours.

ASSESS 0739 hrs Primary survey: The patient has an obvious severe head injury and no apparent respirations and the paramedics are unable to locate a carotid pulse.

CONFIRM The patient’s failure to progress through the primary survey indicates that a differential diagnosis is not required.

TREAT 0739 hrs: The paramedics commence CPR immediately. They attach the defibrillator and the first rhythm check reveals that the patient is in asystole. They also observe fixed dilated pupils. They continue CPR but after 20 minutes assess that there are no signs of life and terminate the resuscitation attempt. When there has been a death at an accident scene, paramedics may arrive before the police and it can be helpful to notify the police that a M ori wh nau is involved, so that they can activate their cultural policies and involve their iwi liaison personnel (if available) to ensure that the spiritual and cultural needs of the tūp paku and wh nau are addressed in the appropriate manner.

CAS E S TUDY 3 Case 11923, 1546 hrs. Dispatch details: A 26-year-old woman has been assaulted. The call has come from police, who are in attendance. Initial presentation: The paramedics arrive and find the woman outside her house talking to a police officer; there are two young children with her. She is standing but her left eye is bruised and slightly swollen. She refuses to be examined but talks to the paramedics.

ASSESS 1601 hrs Assessment: The patient reports that she tripped on the front doorstep and fell, knocking her head. She denies having any other injuries. Old bruising is visible on her forearms and one of her front teeth is missing but this does not appear to be a recent injury.

CONFIRM The patient refuses close assessment but presents as orientated and alert. The paramedics explain the potential consequences of her injuries, and the patient appears to have sufficient capacity to refuse assessment and treatment (see Ch 10). Although this is never a comfortable position for an ambulance crew, patients have the right to autonomy provided they are supplied with sufficient information and their decision is not subject to coercion.

TREAT In many cases paramedics (and other clinicians) view patients solely through a lens of clinical need—that is, do they require immediate medical intervention? In this case the

patient does not appear to need immediate medical intervention and the crew do not have the right to enforce further assessment, but having been called out it does provide the paramedics with the opportunity to initiate treatments other than medical ones. The patient’s pre-existing injuries, combined with the complexities of cultural and personal factors (the perpetrator and the victim share custody of their child), suggests family violence. Providing her with the opportunity to be removed from the premises under the guise of medical treatment can offer her the chance to engage in support services. Away from the scene she may have the opportunity to reflect on her position and options and seek advice. In most jurisdictions the pathway in which paramedics are forced to operate (transport to an ED) is not particularly suited to this engagement, but it may be better than nothing. Providing the opportunity to the patient privately (away from police and family) can often allow them to engage in this pathway.

EVALUATE The mild extent of injuries suggest that the patient’s physiological condition is unlikely to change.

Summary M ori, like other Indigenous peoples, live with significant health inequities that are compounded by the fact that they have a higher level of socioeconomic disadvantage and less access to quality health services, as well as cultural practices that mean they attempt to access healthcare less readily. When managing M ori patients, it is important to consider key cultural factors and appropriate ways to engage them in addition to the usual clinical considerations. Paramedics need to be aware of the stereotypes and prejudices they may hold and the cultural practices that can impact on the management of M ori patients and their wh nau. Paramedics must remember that they are often the first point of contact for these patients on entering the healthcare system and they need to ensure that the shift into this system is met with as little resistance as possible.

References Barlow, C.Tikanga Whakaaro: Key Concepts in M Press, 1994.

ori Culture. Auckland: Oxford University

Bassuk, E., Dawson, R., Huntington, N. Intimate partner violence in extremely poor women: longitudinal patterns and risk markers. Journal of Family Violence. 2006; 21:387–399. Berry, J. G., Harrison, J. E., Ryan, P., Hospital admissions of Indigenous and non-Indigenous Australians due to interpersonal violence, July 1999 to June 2004. Australian and New Zealand Journal of Public Health. 2009;33(3):215–222, doi: 10.1111/j.1753–6405.2009.00378.x. Brownridge, D., Understanding the elevated risk of partner violence against Aboriginal women: a comparison of two nationally representative surveys of Canada. Journal of Family Violence. 2008;23(5):353–367, doi: 10.1007/s10896–008–9160–0. Child and Youth Mortality Review Committee/Te Rōpū Arotake Auau Mate o te Hunga Tamariki Taiohi Low Speed Run Over Mortality. Child and Youth Mortality Review Committee, Wellington, 2011. Retrieved from www.hqsc.govt.nz/assets/CYMRC/Publications/low-speed-report.pdf Crengle, S. Primary care and M

ori: findings from the national primary medical care survey. In:

Robson B., Harris R., eds. Hauora: M

ori Health Standards IV: A Study of the Years 2000–2005.

Wellington: Te Rōpū Rangahau, 2007. Curtis, E., Harwood, M., Riddell, T. Cardiovascular disease. In: Robson B., Harris R., eds. Hauora: M ori Health Standards IV: A Study of the Years 2000–2005. Wellington: Te Rōpū Rangahau, 2007. Davis, P., Lay-Yee, R., Dyall, L., Briant, R., Sporle, A., Brunt, D., Scott, A., Quality of hospital care for M ori patients in New Zealand: retrospective cross-sectional assessment. The Lancet. 2006;367(9526):1920–1925, doi: 10.1016/s0140–6736(06)68847–8. Durie, M. Whaiora: Maori Health Development, 2nd ed. Auckland: Oxford University Press, 1998. Elder J.R., ed. The Letters and Journals of Samuel Marsden. Dunedin: Coulls, Somerville, Wilkie/A. H. Reed for the Otago University Council, 1932. Family Violence Death Review CommitteeFourth Report: January 2013 to December 2013.

Wellington: Family Violence Death Review Committee, 2014. Feldman, C. M., Ridley, C. A. The etiology and treatment of domestic violence between adult partners. Clinical Psychology: Science & Practice. 1995; 2:317–348. Fletcher EQR. ‘I cried – it was so beautiful!’ Rapaki homeowner overwhelmed by repair. Retrieved 6 November 2014 from http://eqr.co.nz/news/i-cried-it-was-so-beautiful-rapaki-homeowneroverwhelmed-by-repair, 2013. Harris, R., Tobias, M., Jeffreys, M., Waldegrave, K., Karlsen, S., Nazroo, J. Racism and health: the relationship between experience of racial discrimination and health in New Zealand. Social Science & Medicine. 2006; 63(6):1428–1441. Harwood, M., Tipene-Leach. Diabetes. In: Robson B., Harris R., eds. Hauora: M

ori Health Standards IV: A Study of the Years 2000–2005. Wellington: Te Rōpū Rangahau, 2007. Howden-Chapman, P., Crane, J., Matheson, A., Viggers, H., Cunningham, M., Blakely, T., et al, Retrofitting houses with insulation to reduce health inequalities: aims and methods of a clustered, randomised community-based trial. Social Science & Medicine. 2005;61(12):2600–2610, doi: 10.1016/j.socscimed.2005.04.049. Hukill, S. L. Violence in Native America: a historical perspective. Journal of Transcultural Nursing. 2006; 17(3):246–250. Jatrana, S., Crampton, P., Norris, P., Ethnic differences in access to prescription medication because of cost in New Zealand. Journal of Epidemiology and Community Health 2011; 65:454–460, doi: 10.1136/jech.2009.099101. Koziol-McLain, J., Gardiner, J., Batty, P., Rameka, M., Fyfe, E., Giddings, L. Prevalence of intimate partner violence among women presenting to an urban adult and paediatric emergency care department. The New Zealand Medical Journal. 2004; 117:1206. Koziol-McLain, J., Rameka, M., Giddings, L., Fyfe, E., Gardiner, J., Partner violence prevalence among women attending a M ori health provider clinic. Australian and New Zealand Journal of Public Health. 2007;31(2):143–148, doi: 10.1111/j.1753–6405.2007.00032.x. Kruger, T., Pitman, M., Grennell, D., McDonald, T., Mariu, D., Pomare, A. Transforming Wh

nau

Violence: A Conceptual Framework. An Updated Version of the Report from the Former Second M

ori Taskforce on Wh

nau Violence, 2nd ed. Wellington: Te Puni Kokiri, 2004.

Marie, D., Fergusson, D., Boden, J.Ethnic Identity and Intimate Partner Violence in a New Zealand Birth Cohort. Wellington: Ministry of Social Development, 2008. Martin, J., Pritchard, R.Learning from Tragedy: Homicide Within Families in New Zealand, 2002– 2006. Wellington: Ministry of Social Development, 2010. Ministry of Health. Tatau Kahukura: Maori Health Chart Book 2010, 2nd ed. Wellington: Ministry of Health, 2010. Moko Mead, H.Tikanga M

ori: Living by M

ori Values. Wellington: Huia, 2003.

Morgan, G., Simmons, G.Health Cheque: The Truth We Should All Know About New Zealand’s Public Health System. Auckland: PIP, 2009. Pihama, L., Jenkins, K., Middleton, A. Te Rito Action Area 13 Literature Review: Family Violence Prevention for M ori. Retrieved from www.nzfvc.org.nz/PublicationDetails.aspx? publication=13532, 2003. Reid, P., Robson, B. Understanding health inequities. In: Robson B., Harris R., eds. Hauora: M Health Standards IV: A Study of the Years 2000–2005. Wellington: Te Rōpū Rangahau, 2007. Robson, B., Purdie, G. Mortality. In: Robson B., Harris R., eds. Hauora: M IV: A Study of the Years 2000–2005. Wellington: Te Rōpū Rangahau, 2007.

ori

ori Health Standards

Salmond, A. Hui: A Study of M ori Ceremonial Gathering (2nd ed.). Retrieved from http://books.google.co.nz/books?id=TIEOAAAAQAAJ&printsec=frontcover#v=onepage&q&f=false, 1976.

Statistics New Zealand. National Ethnic Population Projections: 2006 (base)–2026 update. Retrieved from www.stats.govt.nz/browsefor_stats/population/estimates_and_projections/NationalEthnicPopulationP 26/Commentary.aspx, 2010. White, H., Walsh, W., Brown, A., Riddell, T., Tonkin, A., Jeremy, R., et al, Rheumatic heart disease in Indigenous populations. Heart, Lung and Circulation. 2010;19(5):273–281, doi: 10.1016/j.hlc.2010.02.019.

Whitehead, M., The concepts and principles of equity and health. Health Promotion International. 1991;6(3):217–228, doi: 10.1093/heapro/6.3.217. Wilson, D. The significance of a culturally appropriate health service for indigenous M Contemporary Nurse. 2008; 28:173–188.

ori women.

Wilson, N., Rheumatic heart disease in Indigenous populations: New Zealand experience. Heart, Lung and Circulation. 2010;19(5):282–288, doi: 10.1016/j.hlc.2010.02.021.

SECTION 16

THE PARAMEDIC APPROACH TO THE PATIENT DISPLAYING ABNORMAL BEHAVIOUR O U TL I N E INTRODUCTION TO THE PARAMEDIC APPROACH TO THE PATIENT DISPLAYING ABNORMAL BEHAVIOUR CHAPTER 51: The patient displaying abnormal behaviour CHAPTER 52: De-escalation in the pre-hospital environment

INTRODUCTION TO THE PARAMEDIC APPROACH TO THE PATIENT DISPLAYING ABNORMAL BEHAVIOUR IN THIS SECTION Chapter 51 The patient displaying abnormal behaviour Chapter 52 De-escalation in the pre-hospital environment

At the completion of this section you should be able to • Describe a standardised clinical approach to assessing the patient displaying abnormal behaviour. • Identify the common causes of abnormal behaviour and typical presentations of common mental illnesses encountered by paramedics. • Identify the common physical illnesses that can generate abnormal behaviour. • Understand the principles of verbal de-escalation that are useful when confronted by aggressive or agitated patients. Abnormal behaviour is not necessarily the result of mental illness: it can be caused by a number of physical diseases or by the effects of both prescribed and illicit drugs. When such behaviour is observed in the community, the public have few options other than to request attendance by paramedics and/or the police. Although it is not widely acknowledged, an increasing proportion of paramedic cases involve mental illness. In the past, mental illness has been underrepresented in paramedic education, which has tended to focus on physical illnesses. Chapters in this section outline a structured approach to assessing and managing the patient displaying abnormal behaviour. Chapter 51 discusses how physical causes of abnormal behaviour must be eliminated prior to the diagnosis of common mental illnesses. Direct treatment of most acute mental illnesses is well beyond the scope of paramedic practice, but transporting these patients to centres where they can be treated requires gaining their consent and cooperation. In rare circumstances, patients can be agitated and even suspicious of paramedics. The law carefully restricts the use of both chemical and physical restraints to transport patients with a mental illness, but regardless of legal issues, these forms of restraint put both the paramedic and the patient at risk of injury. Chapter 52 describes principles and processes to de-escalate acute behavioural episodes and to gain the cooperation of patients being transported for assessment and treatment. This de-escalation process is effective for episodes of aggression regardless of the cause.

CHAP TER 51

The patient displaying abnormal behaviour By Jade Sheen and Matt Johnson

C O N C E P TS U S E D I N TH I S C H A P TE R • The paramedic’s clinical approach: Section 2

O V E RV IE W • Patients displaying abnormal behaviour are increasingly common and they present paramedics with unique clinical and management challenges. • Abnormal behaviour can be based in a physiological cause or it can be a result of mental illness. • Patients presenting with abnormal behaviour require a specialised approach to assessment, including the Mental State Examination. • These patients often have physical injuries as a result of their inability to adequately protect themselves from harm. • Patients who are demonstrating that they are likely to come to harm can be involuntarily transported to hospital under legal provisions.

Introduction According to the World Health Organization (WHO, 2013), mental health is a state of emotional and social wellbeing in which a person can fulfil their abilities, cope with the normal stressors of life, work productively and make a contribution to their community. Changes in mental health functioning may occur in the course of an individual’s life. These changes fall across a spectrum of severity, from common mental health disorders, which cause distress but are short-lived, to more severe mental illnesses. Mental illnesses are thought to last longer than mental health disorders, impair functioning in at least one area of the individual’s life and have a more significant impact on the person’s ability to cope (Mindframe Mental Media Initiative, 2012). It is widely recognised that defining the precise nature of a mental illness (see Box 51.1) is often difficult to apply, requires a special level of knowledge to diagnose and struggles to separate psychopathology from normal variances in human behaviour such as sadness after a loss and shyness (Stein et al., 2010). B O X 5 1 . 1C h a r a c

ter istic s o f a

m e n ta l/ p syc h ia tr ic d iso r d e r Features A mental/psychiatric disorder is a behavioural or psychological syndrome or pattern that occurs in an individual: • the consequences of which must be clinically significant distress (e.g. a painful symptom) or disability (i.e. impairment in one or more important areas of functioning)—that is, they must not be merely an expectable response to common stressors and losses (e.g. the loss of a loved one) or a culturally sanctioned response to a particular event (e.g. trance states in religious rituals) • that reflects an underlying psychobiological dysfunction • that is not solely a result of social deviance or conflicts with society.

Other considerations It must have diagnostic validity using one or more sets of diagnostic validators (e.g. prognostic significance, psychobiological disruption, response to treatment). It must also have clinical utility (e.g. contribute to better conceptualisation of diagnoses, or to better assessment and treatment). Source: Stein et al. (2010).

While studies vary with regards to the most common presentations of mental illness in the pre-hospital setting, five key areas or diagnoses are commonly identified: psychosis/schizophrenia, suicidal ideation, mood/anxiety disorders, behavioural disorders, and drug and alcohol issues. In aged psychiatry, dementia and delirium are also very

common. Mental health treatment may occur in either a hospital or a community setting (AIHW, 2010). While community settings are viewed as less restrictive and therefore preferable, the majority of patients who access emergency services for their mental illness qualify for the more intensive inpatient treatment (Larkin et al., 2006). This is reflected in Figure 51.1. With community treatment the preferred method in many cases, there is often a need to transport patients whose mental illness has unexpectedly exacerbated to either an emergency department (ED) or a psychiatric inpatient unit. Admission to the ED allows for further medical assessment to rule out organic causes as well as a specialist psychiatric assessment to determine the most appropriate treatment option for the patient at that time. Possible outcomes include medical admission to treat an organic cause, admission to a psychiatric inpatient unit or discharge back home with follow-up by community mental health services. In other instances, paramedics will be called to cases where the cause of the abnormal behaviour has already been identified and a mental illness has been diagnosed. In such cases paramedics may transport the patient directly to an inpatient mental health facility as opposed to an ED. The relevance of this pathway may vary according to specific local guidelines and laws.

FIGURE 51.1

The mental health system in Australia.

It should be noted that within the mental health sector the term ‘mental health consumer ’ is used in preference to ‘patient’. For the sake of consistency within this text, however, the collective term ‘patient’ is used. This chapter provides an assessment framework to allow for differential diagnoses in the

face of abnormal behaviour. Once organic causes have been ruled out, a diagnosis of mental illness becomes more likely. Although paramedics are occasionally dispatched to a patient with an exacerbation of a known mental health issue, more often these patients are captured by the much broader dispatch codes ‘abnormal behaviour ’ or ‘altered conscious state’. The challenge for paramedics is to exclude the non-mental health causes of these presentations before determining to treat the patient as suffering from alterations of mental health. Abnormal behaviour can be due to a primary mental health problem, a non-mental health issue (e.g. hypoglycaemia) or an interaction of both. Even when paramedics are dispatched to a patient with a known mental health issue, they must consider that physical illness may be the cause of the exacerbation.

Pathophysiology The patient who presents with abnormal behaviour poses a number of specific challenges. Some mental illnesses are accompanied by abnormal behaviour that is directly observable, while in other cases the behavioural manifestation of the illness will be too discrete or contextually specific to identify. In addition, a number of physical injuries and conditions can cause abnormal behaviour in the absence of mental illness. Faced with a patient who may not be able to provide an accurate history, the challenge for paramedics is to safely identify the symptoms of concern, differentiate between the various causes of abnormal behaviour and engage in the correct pathway of treatment. Mood disorders are very common, with more than 1 million Australians reporting a past depressive episode. Major depressive disorder (MDD) is characterised by disturbances in mood and behaviour. Typical symptoms of a depressive episode include lowered mood, changes in appetite (significant increase or decrease) and sleep (insomnia or hypersomnia), loss of interest or pleasure in usual activities, lowered motivation and energy, social withdrawal and difficulty concentrating. Suicidal thoughts may also be present. To meet the diagnostic criteria for MDD, symptoms must occur over a 2-week period and impact on the person’s ability to perform everyday tasks. Understanding and identifying MDD is extremely important, as it can be a debilitating disorder that has strong links to suicide. Some of the most common disorders that require an ambulance response are psychosis, borderline personality disorder, mania, delirium and dementia.

Psychosis Psychosis is an umbrella term used to describe a group of conditions that are characterised by disturbances in thoughts, perceptions and behaviour. Psychosis involves a loss of contact with reality. The majority of patients with psychosis experience their first episode in adolescence or early adulthood. The lifetime risk of developing a psychotic disorder is difficult to calculate as it relies on individuals presenting to centres where the diagnosis can be made and, as with many mental illnesses, sufferers may actively avoid such services. While classed as a low-prevalence group, accounting for around 3% of cases presenting to Australian specialised mental health services (Department of Health, 2010a), the severity and impact of psychotic disorders means that sufferers are likely to come into contact with the hospital sector when they are acutely unwell (Frost, Carr & Halpin, 2002). Psychosis may be caused by illness such as schizophrenia, organic causes such as drug intoxication or metabolic causes such as diabetes (Queensland Ambulance Service, 2008). When someone is experiencing a psychotic episode for the first time, a definitive diagnosis may be difficult to identify, as some diagnoses require a longitudinal perspective. Common symptoms of a psychotic disorder include hallucinations, delusions and formal thought disorder. A hallucination is defined as a sensory experience that occurs in the absence of any external stimuli (Davidson, Neale & Kring, 2004). Hallucinations may occur in one or more of the five sensory modalities (i.e. they may be visual, auditory, tactile, gustatory or olfactory in nature). Delusions are firmly held beliefs despite evidence to the contrary. Formal thought disorder refers to problems in the organisation of ideas and in speaking so that a listener can understand. Other symptoms that may occur during a psychotic episode include flat or blunted affect, social withdrawal, changes in sleeping

and eating patterns, and an absence of hygiene or personal grooming (Davidson, Neale & Kring, 2004). Checking for compliance to medications is important in patients with psychosis, as between 20% and 80% of patients with schizophrenia fail to self-administer their prescribed medications appropriately (Battaglia, 2001). This non-compliance contributes to a significant number of hospital admissions (Awad, 2004), with symptom relapse being more severe compared with patients who maintain their medications as directed (Saba et al., 2007). Changes in routine and stresses such as job changes can precipitate noncompliance or trigger symptoms.

Guidelines for the out-of-hospital management of psychosis For patients with abnormal behaviour it is impossible to completely separate assessment from management: from the moment paramedics commence communicating with these patients they will be simultaneously assessing, managing and even treating. In almost every case, however, paramedic management will be limited to verbal de-escalation. The guidelines in Table 51.3 later in the chapter provide recommendations to adopt during the assessment. TABLE 51.3 Common mental illnesses encountered by paramedics

— ce ntra l ne rvous syste m (e .g. he a d tra uma , infe ction) — me ta bolic ca use s (e .g. kidne y fa ilure , low blood suga r) — ca rdia c a nd re spira tory syste m (e .g. myoca rdia l infa rction, re spira tory fa ilure ) — syste mic illne ss (e .g. tumour, postope ra tive sta te ; Compton & Kotwicki, 2007). -->

In order to synthesise the available material common medications encountered by paramedics have been identified. *Approved by the US Food and Drug Administration for the treatment of PTSD.

Borderline personality disorder Borderline personality disorder (BPD) refers to a pervasive instability in mood, relationships, behaviour and self-image. Individuals with this disorder fear abandonment and often experience chronic feelings of isolation and emptiness. Impulsiveness is commonly seen in this condition and may contribute to destructive behaviours such as self-harm and addictions (Polk & Mitchell, 2009). As a personality disorder, BPD is not formally diagnosed until the patient is 18 years of age, when personality is considered to be a more stable and developed entity. These traits and symptoms may, however, occur in younger individuals. All patients with a diagnosed mental illness can have a relationship with health services in which they frequently access care on a crisis basis with little ongoing support. This is especially the case for patients with BPD and for this reason most patients will have an established multidisciplinary plan that outlines the expected response for all of the clinicians involved in their care. There is also a perception that the abnormal behaviours associated with bipolar disorder can be interpreted as patients using the ambulance response to seek attention and that their presentation is not equivalent to those suffering a physical illness (see Box 51.2). B O X 5 1 . 2M e n t a l

illness and am bulanc e

m isuse The question of misuse of ambulance services by patients with mental illness has been raised (Roberts & Henderson, 2009). Local and international literature, however, suggests that ambulances are not being misused by these patients (Fry & Brunero, 2004; Larkin et al., 2006). An Australian study by Fry and Brunero (2004) reported that 42% of patients with a mental illness who presented to ED were brought in by ambulance, while 39% were transported by police. They also noted that this group had higher triage codes on average than other attending patients, suggesting a higher urgency for patients with mental illness. An

international study by Larkin and colleagues (2006) supports these findings, with mental health patients deemed as higher urgency and more likely to result in admission than the general patient population, suggesting that ambulance services were not misused by this group. The transport of patients with a mental illness is indeed an appropriate use of ambulance resources and ambulance paramedics are well-placed to support the needs of patients, their families and the community during a mental health crisis.

The guidelines in Table 51.3 provide recommendations for out-of-hospital management of BPD.

Mania Bipolar disorder is the name used to describe a set of ‘mood swing’ conditions, the most severe of which is bipolar I (Black Dog Institute, 2010). Individuals with bipolar I experience long periods of high mood or mania, followed in most cases by periods of depression. First onset of the disorder typically occurs in middle to late adulthood and like many mental illnesses it is more likely to occur at times of heightened stress. Key symptoms of a manic episode include high energy levels, irritability, grandiosity, racing thoughts, decreased sleep and increased engagement in pleasurable or risky activities (e.g. indiscriminate spending or sexual activity). The guidelines in Table 51.3 provide recommendations for out-of-hospital management of mania.

P RACT ICE T IP Ask! • What is the reason for the call-out today? How long has X been an issue for you? What changes or symptoms have you noticed? Can you identify anything that may have triggered this change? • What have you tried so far to manage X? • Has anything been useful in the treatment of X? • Are you on any medications? • What support do you have?

Delirium The term delirium refers to a change in cognition and consciousness that develops over a short period of time. Possible symptoms include an altered conscious state, decreased attention, a reversed sleep–wake cycle, disorientation, rambling or nonsense speech, agitation and seeing things that do not exist (hallucinations). Delirium often has a clear

cause which, if treated, can result in a reversal of symptoms.

Dementia The term dementia describes the symptoms of a large group of illnesses that cause a progressive decline in a person’s cognition, memory and general functioning (CSHISC, 2009). There are many different forms of dementia, each with its own cause. Alzheimer ’s disease is by far the most common cause of dementia, accounting for 50–70% of all cases (CSHISC, 2009). Dementia can occur at any age but is more common after the age of 65.

Explanatory models Mental illness may impact an individual’s biological, psychological, social and occupational functioning (see Box 51.3) and so understanding the aetiology of the illness or identifying one clear causative factor becomes more difficult. Described below are two of the most renowned models of health and illness, namely the biomedical model and the biopsychosocial model. Most clinicians adhere strongly to the biomedical model of illness and treatment, but to diagnose and manage the behavioural and social aspects of mental illness requires an understanding of the biopsychosocial model. B O X 5 1 . 3B i o

lo g ic a l, p syc h o lo g ic a l a n d so c ia l

fac to rs that may impac t o n mental health Biological Genetics, nutritional status, general state of health or, in more specific cases, structural abnormalities in the brain or variable levels of neurotransmitters such as dopamine, serotonin, noradrenaline, GABA.

Psychological Early experiences (childhood), personality, intelligence, attitudes and values, self-image and self-esteem, temperament, coping skills, stress and others.

Social Family relationships, social supports, social skills, cultural background, as well as other environmental factors such as employment and others. Note: Some of the items identified can be considered within multiple categories.

The biomedical model The dominant model of disease in medicine is the biomedical model. It assumes that diseases are fully accounted for by alterations in normal tissue function (caused by injury, infection, malignancy) that result in deviations of measureable biological variables (Engel, 1977; Wade & Halligan, 2004). The model encourages the successful identification of a disease based on symptoms and objective laboratory or field tests, and directs what is often a clear course of treatment (Wade & Halligan, 2004). As it can be used to link most symptoms to diseases, the biomedical model has distinct advantages in the pre-hospital field, where timely intervention is crucial. However, the model leaves no room for an account of the social, psychological and/or behavioural dimensions of an illness (Engel, 1977; Wade & Halligan, 2004). This weakness becomes very apparent when considering individuals with mental illness.

Using the biomedical model, the patient’s health is assumed to be restored once the biochemical treatment has been completed and the ‘abnormality’ addressed. But even in the case of physical illness or disease this is not always true, and the process of suffering an illness can affect the patient long after the symptoms have passed (Engel, 1977; Wade & Halligan, 2004). For example, depression is three times more likely after a patient suffers an acute myocardial infarction (AMI), despite there being no specific physical link that directly ties the damage of myocardial cells to decreased release of serotonin in the brain (Lichtman et al., 2008). Similarly, depressive symptoms after an AMI are predictors of increased mortality and worse health status, despite there being no direct physiological link between brain and cardiac function (Mallik et al., 2006). The biomedical model also fails to account for the importance of the patient– practitioner relationship in terms of successful recovery. Within this model a biochemical defect should indicate the presence of disease, however as Engel (1977) succinctly observed, an abnormality may be present yet the patient may not be ill. Thus biochemical defects account for just one of a myriad of factors that intersect to determine the presence or absence of a disease. Engel proposed consideration of the biopsychosocial model to address these criticisms.

The biopsychosocial model To provide a basis for understanding the determinants of disease and arriving at rational treatments and patterns of health care, a medical model must also take into account the patient, the social context in which he lives, and the complementary system devised by society to deal with the disruptive effects of illness, that is, the physician role and the health care system. This requires a biopsychosocial model. Engel (1977) The biopsychosocial model suggests that illness is the result of a complex interplay of psychological, social and biological factors, each of which should be factored into our assessment and treatment of the patient (Engel, 1977). While the biomedical model seeks to remove the biological factors from the other factors, this approach asserts that no single factor can be considered as an isolated element. Rather, the biological, social and psychological aspects of an individual’s life work together so that deficiency in one area will reflect in each of the other areas. This relationship is represented in Figure 51.2.

FIGURE 51.2 The integrated relationship between the biological, psychological and social domains identified by Engel. The advantage of the biopsychosocial model is that it can account for a greater range of individual variation, ensuring that important factors in the individual’s health status are not missed. It also lends itself to multidisciplinary treatment models, with a combination of social, physical and psychological treatments recognised. Unfortunately the model is not as prescriptive in terms of its assessment and treatment. Additionally, it has been argued that a further separation of biology and psychology can be arbitrary, if not misleading (Tavakoli, 2009). Regardless of the theoretical debate attached, a basic understanding of the biopsychosocial model is important for paramedics, as it directs mental health assessment and treatment models and provides a framework for communication between mental health disciplines. Paramedics are in a unique position to observe patients in their home environment, to identify community supports in place for the patient and to facilitate engagement and communication between the patient and hospital staff. An exclusive

focus on the patient’s physiological status is likely to result in the loss of vital information, which might prolong the patient’s episode of care.

Law and mental health Identifying the legal requirements for pre-hospital treatment of mental health patients can be a challenging task. While mental health legislation exists in all states and territories within Australia and in New Zealand, the jurisdictions differ in terms of the criteria for involuntary treatment, recognised practitioners and requirements. For this reason it is important to understand the agreed universal principles of mental health treatment.

Universal requirements The fundamental aim of mental health legislation is to protect, promote and improve the lives and mental wellbeing of citizens. WHO (2005, p. 1) Key rights outlined by the WHO include quality in treatment delivery, nondiscrimination, the rights to privacy and individual autonomy, freedom from inhumane and degrading treatment, the principle of the least-restrictive environment, and the rights to information and participation in the treatment process (WHO, 2005). The World Medical Association (2006) states that compulsory treatment should be used only when medically necessary and for the shortest possible duration.

Australia and New Zealand Mental health legislation differs across jurisdictions, but each is informed by the universal requirements described above. In Australia, there has been a move towards uniformity with the creation of the National Mental Health Reform Strategy (Department of Health, 2011).

Voluntary versus involuntary A number of patients agree to admission for treatment of their mental illness and they are termed ‘voluntary’ or ‘informal’ patients (Forrester & Griffiths, 2001). The vast majority of ambulance work, however, involves the treatment and transport of ‘involuntary’ patients. Such patients require admission for treatment of their mental illness to ensure their own safety or the safety of others but for whatever reason cannot or will not consent. Although specific guidelines for involuntary treatment differ, some common criteria include: • the person appears to have a mental illness and • immediate treatment is required and • the person presents a risk of harm to self or others and • the person requires admission to a mental health facility for treatment (Forrester & Griffiths, 2001). The decision to enact an involuntary treatment order is clearly a serious one, as it involves the revocation of a person’s right to consent. For this reason a number of checks

are included within mental health legislation to ensure a fair and just process. These include a request for admission from a friend, carer or authorised person; review from a psychiatrist following admission; limitations to detention periods; an appeals process; and, in most jurisdictions, a formal review board to monitor cases and ensure compliance with relevant legislation.

Exclusions According to the United Nations (2002), there are a number of exclusions to involuntary treatment. Grounds for which someone cannot be held include: • political, economic or social status • membership of a cultural, racial or religious group • family or professional conflict • non-conformity with moral, social, cultural or political values or religious beliefs prevailing in the person’s community • any other reason not directly related to mental health status.

Confidentiality Maintaining patient confidentiality is of paramount importance. However, the legal system recognises that there are times when the directive to keep a patient’s information confidential comes into direct conflict with the directive to maintain their safety. As an illustration, consider the case of an 88-year-old female who has attempted suicide following the death of her husband by taking a substantial overdose. Her daughter finds her in time and calls for an ambulance. During the assessment phase the patient confides that she intends to carry out her suicide plan once she is discharged home. She forbids the health professional from disclosing the information to her daughter or anyone else, fearing that her daughter will be distressed and that doctors may attempt to intervene in her plan. Although this information might ordinarily be considered confidential, the risk the patient poses to herself is clear and immediate and therefore outweighs her rights to confidentiality. In this case, the health professional is likely to be permitted to disclose her plan to her doctors to ensure that she remains safe. Thus, rights to confidentiality may be mitigated by risk. For more specific information regarding confidentiality and consent in the case of mental illness and risk-specific behaviour, refer to the mental health legislation and/or health records legislation in your relevant jurisdiction.

CA SE ST U DY 1 Case 14934, 0954 hrs. Dispatch details: A 19-year-old female short of breath and in an altered conscious state in a stairway at her university.

Initial presentation: The paramedics arrive to find a frail, young-looking woman who is visibly distressed and hyperventilating.

ASSESS Armed with an understanding of the biomedical and biopsychosocial models of health and illness, paramedics have a structure to assess the patient presenting with abnormal behaviour (see Fig 51.3). The aim of assessment is to establish whether there is a physical cause for the abnormal behaviour or whether the abnormal behaviour is generating physical symptoms. This is necessary because hypoxia, hypotension, head injury, hypoglycaemia (and other metabolic disturbances), sepsis, intoxication, poisoning and cerebrovascular accident (CVA) can all present with abnormal behaviour but require very different treatments. Possible organic causes must be reviewed first, with all efforts made to rule them out. Only after this process has been completed will a mental illness be considered more likely. For this patient the paramedics must differentiate between physical concerns that may lead to her symptom profile (infection, disease, injury), but also determine whether mental illness is a significant component of her presentation.

FIGURE 51.3

Assessment and treatment plan flow chart.

Should the paramedics’ preliminary observations suggest the presence of agitation or aggression that could threaten their safety, adjustments will need to be made to the assessment and treatment process (see Ch 52). In this case, the observed behaviour is not threatening to the paramedics, so the initial assessment plan is to establish a set of baseline vital signs and to identify any physical abnormalities that may exist. Paramedics who start their assessment in this way not only gain information to help them decide accurately on a diagnosis, but also meet the expectations of the patient and can quickly gain their cooperation. This can be extremely useful when it comes time to ask more delicate details of the patient’s social and mental history. It may also serve to distract the patient, resulting in a decline of her sympathetic nervous response. Having a relaxed body language and position is more likely to create good patient rapport and therefore elicit useful answers. It is possible to maintain a relaxed posture while still keeping an eye on the safety of the situation. Patients

with disturbed behaviour are rarely a threat to paramedic safety if they are handled with respect and sympathy.

Vital signs Provided it is safe to do so, always start by obtaining the patient’s vital signs. Obtaining a full set of respiratory and perfusion observations allows the paramedic to closely observe the patient’s behaviour and start to include these factors in the assessment. Questions at this stage can focus on excluding physical causes such as a recent fall, illness or history of metabolic disorders such as thyroid disease or diabetes.

Mental State Examination The Mental State Examination (MSE, or Mental State Assessment) is a systematic assessment of a patient’s mental health or state of mind at any given point in time (Victorian Government Department of Health, 2008). This formalised process of observation and questioning ensures that clinicians do not miss symptoms of concern (see Table 51.1). While the MSE provides vital diagnostic and handover information it is important to note that it should never be the sole basis for a diagnosis. Different versions of the MSE exist, but most include the categories identified in Table 51.2. TABLE 51.1 Mental State Examination

Appearance

Behaviour

Presentation Interpretation This patient is of slim build Her appearance suggests that and is dressed in neat casual being overweight is not a factor in clothing. Her hair is slightly her breathing difficulties. As her dishevelled and she appears dress and hygiene are well to be very pale. She also attended to, the dishevelled appears distressed. Her health nature of her appearance and hygiene are well provides a contrast of note. attended to. Distress may occur in many instances when an ambulance is called, providing little input for differential diagnosis. The patient’s body appears to Note heaving breaths despite be heaving as if she is clear breath sounds. As she does struggling for breath and she not have a temperature, the is visibly trembling. Her trembling may provide a clue breathing rate slows during suggestive of anxiety or assessment and her trembling adrenaline release. This is diminishes. Her eye contact is consistent with restricted eye initially very restricted but contact on first meeting, which this also improves as rapport may or may not be present in

Speech

develops. No tics or unusual motor movements are observed. She is cooperative throughout. The patient’s voice is barely audible at times during the assessment. Her quantity of speech is limited when she feels short of breath, but later improves.

patients with asthma, but is very common in those with anxiety.

The improvement in speech and breathing rate is important, as no formal physiological treatment has yet been offered, suggesting that the physiological difficulty has resolved itself. The soft tone may be due to lack of breath but is also common in patients with anxiety. Mood She reports that she feels This report is likely to be ’stressed out’ and ’worried’. consistent for most patients who call an ambulance and thus offers few diagnostic clues. It would be worthwhile noting whether her response appears exaggerated compared with other patients. Affect She appears to be visibly This patient’s distress makes some distressed and anxious during psychiatric conditions, such as the assessment. Her mood mania, less likely, but increases the and affect are congruent. likelihood of anxiety or depression. Thought form When able to respond, her Clarity in thought form makes answers are logical, with no head injury, intoxication and more disruptions of connectedness specific psychiatric conditions noted. such as psychosis less likely. It is, however, consistent with anxiety. Thought She identifies a number of This information is vital for content stressors, including her final treatment as it speaks to her risk law exams, uncertainty of harm. She also identifies a regarding future career number of psychosocial stressors choices and whether she that are current, appear actually wants to pursue law, overwhelming and are likely to be and a relationship breakdown. enhanced when she is on She denies any suicidal campus. These stressors could ideation or deliberate selfhave precipitated an anxietyharm. While she is concerned related event. about the possibility of a heart attack, her ideas are not fixed and are not of a delusional quality. Nil obsessions or compulsions noted. Perception Nil perceptual disturbance The absence of perceptual reported. No mannerisms disturbance makes some forms of consistent with perceptual trauma, intoxication and more disturbance. specific psychiatric conditions

Concentration She is easily distracted by onlookers during the assessment. While she is oriented to time, person and place, she has limited insight into the cause of her presentation, believing that she is having a heart attack.

such as psychosis less likely. It is, however, consistent with anxiety. This aspect of the assessment provides vital clues for this patient’s treatment. As she appears distracted by onlookers (and distressed as per affect), all efforts should be made to remove the crowd or the patient. Her belief that she is having a serious medical event may also heighten her distress and thus should be addressed via education; for example ’Our assessment indicates that you are not having a heart attack but may be experiencing x, y, z…’

TABLE 51.2 Mental State Examination categories and features

It is important to note that the MSE is a standard assessment tool useful for patients with varying presentations, not just those presenting with a mental illness. Moreover, while the MSE focuses exclusively on the patient’s mental state, any information regarding the patient’s living environment (e.g. cleanliness, order, indication of ability to attend to daily living skills), sleeping patterns and appetite should be passed on at handover. While paramedics do not engage in formal mental health diagnoses, they must be able to perform a basic differential diagnostic process in order to identify the most appropriate treatment for the patient. You should therefore be able to identify whether the likely cause is a mental illness and, if so, what group of disorders is most likely (e.g. psychotic disorder vs anxiety disorder). The term ‘diagnosis’ is thus used with an understanding that it is in no way final or definitive.

Ask! • What is bothering you the most today? • What is your previous medical history? • [To bystanders] Exactly what behaviour did you observe?

Look for! • Signs of an organic cause for abnormal behaviour • An elevated temperature • Abnormalities in pulse, blood pressure and respiratory rate • Blood glucose level • Sympathetic response giving pale, clammy skin and dilated pupils • Signs of drug use

Risk assessment Risk assessment can take several forms. It is important to assess the risk the patient poses to the paramedic (harm to others) and to themselves (deliberate or accidental self-harm) and so paramedics need to be capable of performing basic risk assessment to ensure their own safety and that of their patients. It may be argued that paramedics are not mental health professionals and as such should not have to perform risk assessments. Although a formal risk assessment will be completed when the patient is transported to hospital, paramedics should be familiar with the process and able to perform a rudimentary risk assessment to account for cases where the patient refuses transport. In such instances the patient may well meet the criteria for involuntary admission on the grounds of their risk. If a risk assessment is not completed, this option will not be available and the patient may well carry out their plans. Transport and access to some form of definitive care is the best option to ensure patient safety and fulfil the paramedic’s duty of care. Types of risk Harm to others In the pre-hospital environment it is essential for paramedics to check for dangers prior to entering any scene. Being able to assess the potential for harm from a third party is also essential. Accidental self-harm Accidental self-harm refers to unintended harm that may come to a patient as a result of their mental state. Individuals with thought disturbance, perceptual disturbance(s) and/or active delusions may be considered to be at greater risk of accidental self-harm. Accidental self-harm can be assessed as a part of a formal MSE, most notably in the areas of judgement and insight. Deliberate self-harm Deliberate self-harm encompasses a spectrum of behaviour from minor selfinflicted injury to more serious suicide attempts. If adequate rapport has been established between patient and paramedic, acts of deliberate self-harm or

intent will generally be disclosed in step 1 in the model below. In some instances, however, previous self-harm or intent may not be as overt. In these instances the paramedic may need to ask the patient directly. The four-stage model The different forms of risk can be assessed using the following four-stage model (see Fig 51.4). To illustrate application of the model, a patient with suicidal intent is considered here (see also case study 2 in this chapter).

FIGURE 51.4 The four stages of risk assessment. • Step 1: Plan. When considering this aspect of the risk assessment you are interested in whether the patient has plans to complete suicide. This is best identified by asking the question directly. If the patient does identify a desire to commit harm, you need to ask further information about their plan, as a more defined plan may be suggestive of a higher degree of risk of actually going through with the intention. • Step 2: Means. Once the patient’s plan has been identified, you need to establish whether the patient has access to the means required to carry out their plan. For example, a patient may have a clearly defined plan to shoot themselves but may not own a gun or have any access to any firearms, whereas a patient who has access to the means is likely to be at increased risk. This element of the assessment may also be important to ensure your own safety. • Step 3: Timeframe. Establishing the intended timing of the attempt is also important. A clear and in many cases shorter timeframe may increase the risk or indicate how long you have to manage the situation. Some patients make plans to self-harm or commit suicide on the anniversary of a significant event (e.g. the death of a partner). It is important to identify these patients and ensure the details are clearly documented and communicated at handover, because although the patient’s immediate risk may be lower, their future risk may be increased and they may need additional support at that time. • Step 4: History. The patient’s history may reflect other risk factors that are important in determining your immediate treatment plan. Other factors may be important in determining a patient’s risk of harm or suicide. Research suggests that the risk factors in Box 51.4 should be considered. B O X 5 1 . 4R i s k

f ac to r s f o r suic ide

History A history of past suicide attempts or having a loved one who has completed suicide may increase risk (Hirschfeld & Davidson, 1998).

Age The ABS indicates that 30–34 year olds are statistically more likely to complete suicide (ABS, 2002). While the rate of suicide completion among adolescents aged 15–19 years is not as high as for other groups, suicide is the second highest cause of death in this age group after motor vehicle accidents (ABS, 2002).

Gender Males are more likely to complete suicide, while females have a higher recorded rate of suicide attempts (Hirschfeld & Davidson, 1998). This difference is not necessarily due to the intent of the patient, but rather the means selected.

Depression Depression has been linked to suicide. Paramedics should take note of patients who have been severely depressed and recently experienced an improvement in their mood. In some individuals this mood shift can be attributed to feelings of relief as they have made a decision to end their life, thus in their mind addressing their concerns. Severely depressed individuals may lack the energy and planning required to action suicidal feelings, but an improvement in their symptoms provides room for them to consider the idea further (Cheng et al., 2000; Hirschfeld & Davidson, 1998).

Alcohol/drug use Substance use lowers inhibitions and may therefore increase risk (Cheng at al., 2000; Hirschfeld & Davidson, 1998).

Social support Social support may be viewed as a protective feature in the person’s history, whereas a lack thereof may increase risk (Australian Government, 2012).

Chronic illness Patients with a chronic illness are more likely to commit suicide (Hirschfeld & Davidson, 1998).

Legal status Assessing the patient’s legal status is important at this juncture, as it may

determine specific treatment options. The paramedic should determine whether the patient is being treated involuntarily for a mental illness or, if they are not, whether they require and are eligible for this form of treatment. This patient does not appear to be a risk to herself or others, she has no clear history of mental illness and does not appear to require inpatient treatment for a mental illness. As such, the paramedics need to (and should be able to) treat her as a voluntary patient.

Initial assessment summary Problem Chest pain and short of breath Conscious GCS = 15 (despite reports of an altered conscious state) state Position Sitting Heart rate 112 BPM Blood 110/80 mmHg pressure Skin Pink, warm, dry appearance Speech Speaks in short sentences pattern Respiratory 28 BPM rate Respiratory Even cycles rhythm Chest Clear air entry auscultation Pulse 99% on room air oximetry Temperature 37.1°C Pain 4/10 History She was climbing the stairs when she began to feel dizzy and faint. Her hands began to shake and she became increasingly nauseated. She felt that her heart was going to burst from her chest and was worried something was ’seriously wrong’ with her. She tried to finish climbing the stairs to remove herself from public view but she almost collapsed trying and so remained on the stairwell. She says that this is the first time she has had these symptoms. She cannot identify any medical issues that might have contributed to her presentation. She has a past history of asthma. If we consider this case with regard to both the biomedical and the biopsychosocial models, even in the absence of a significant underlying cause such as supraventricular tachycardia, the biomedical model can explain some of this patient’s symptoms (e.g. tetany in the hands and palpitations), but it cannot explain why her emotional state ultimately produced these physical symptoms. In this case study social stressors (recent exams and limited social

support) brought on biological changes (increased heart rate, increased respiration rate). Her psychological interpretation of the events (thoughts that she was seriously ill and that her symptoms were harmful) increased her anxiety, resulting in a progression of her physiological symptoms. This case illustrates the manner in which social, biological and psychological factors can interact, resulting in mental health concerns.

CONFIRM The essential part of the clinical reasoning process is to seek to confirm your initial hypothesis by finding clinical signs that should occur with your provisional diagnosis. You should also seek to challenge your diagnosis by exploring findings that do not fit your hypothesis: don’t just ignore them because they don’t fit.

What else could it be? Organic Assessment of the patient’s perfusion status, including an ECG, should rule out hypotension as a cause of an altered conscious state. Accurate assessment of the ECG will exclude paroxysmal supraventricular tachycardia (see Ch 25) as an underlying cause of her elevated heart rate. Chest auscultation that determines equal and good air entry to the lungs will exclude a ventilatory cause of hypoxia such as asthma and this should correlate with a normal SpO2 reading. In this context the signs of hypocarbia (tetany) are consistent with the elevated respiratory rate. A neurological exam should rule out CVA and seizure.

DIF F ERENT IA L DIA GNOSIS Mental illness Or • Organic (e.g. cerebral hypoxia, hypotension, head injury, CVA, infection [especially encephalitis, meningitis], arrhythmias leading to hypotension) • Metabolic (e.g. hypoglycaemia, hyperglycaemia, electrolyte imbalances, renal failure, liver failure) • Intoxicants (e.g. alcohol, stimulants, hallucinogenics) • Other cause (e.g. reactive anger/aggression, exposure to a traumatic scene)

Metabolic A blood glucose reading (BGL) greater than 3.5–4 mmol and an enquiry as to a

history of diabetes or other metabolic disorders should exclude this group of physical causes. Although infection can cause abnormal behaviour, the infection needs to be severe and it is not likely to occur with normal vital signs and without a significant fever. A normal tympanic temperature will exclude an infectious cause severe enough to lead to altered behaviour in a young person. Similarly, disorders causing electrolyte imbalances sufficient to cause abnormal behaviour may also create abnormal vital signs. In this case the pulse is elevated but the blood pressure, temperature and BGL are within normal limits. The ECG reveals no arrhythmia. Intoxicants By now the patient has seen the paramedics perform a number of tests that have produced objective (and normal) results and should be gaining a degree of trust in their assessment. This is an opportune time to enquire if they could be suffering from alcohol or drug effects. But rather than ask these confronting (and accusational) questions directly, explore the more normal aspects of the patient’s dietary intake first. ‘Have you had breakfast today?’ is an innocent question that opens the line of enquiry. ‘Have you taken any medication today?’ followed by ‘Are there any medications you have missed taking today?’ can add to the information base. At this point enquiries about alcohol can seem routine and far less judgemental. The patient denies any drug or alcohol use. Other cause After all of these factors have been ruled out, the paramedic can begin to enquire about events immediately prior to the onset of symptoms. Remember, effective patient care uses the patient to assist. Ask the patient whether they can identify anything that may have triggered this change. If sufficient rapport has been built with the patient by this time and a thorough physical assessment has reassured the patient that the illness is not physical, you may be surprised by the honesty of their answer. The patient cannot offer a trigger for the current episode. Given the above has excluded physical causes of this patient’s presentation, it leaves a working diagnosis of mental illness.

T REAT Despite the frequency and severity of cases of mental illness, these conditions do not fit easily into the minds or practice of many paramedics. This may be because mental illness rarely requires the administration of medication by paramedics. Like most other conditions, however, there is a well-structured treatment plan that will suit most situations (see Fig 51.5).

FIGURE 51.5 For paramedics, managing mental illness is challenging because it does not fit the normal clinical approach. Instead, these cases can be sequenced as communicate, advocate and transport.

Emergency management Communicate Establishing good rapport is essential from the outset of treatment. Rapport is facilitated by the warmth of your approach, attempts to understand the patient’s position and maintaining respect for the patient. This is particularly important for patients displaying abnormal behaviour who may have been laughed at, stared at or dismissed in the past. These experiences often make the patient more sensitive to perceived criticism, making appropriate communication a vital part of treatment. Prehospital care is filled with significant pressures, the most obvious being quick and efficient treatment and transport of patients. As a paramedic you must balance these pressures with the need to engage patients properly, because a loss of engagement may result in treatment refusal or an escalation, which will be far more time-consuming. Patients will recognise and react to a rushed or disorganised assessment. In this patient’s case, the treating paramedic should keep their voice low, their tone reassuring and their manner calm. It may be helpful to coach the patient through some deep-breathing exercises, which will serve the dual purpose of distraction and symptom management. Advocate In some instances the paramedic may be required to advocate for a patient, ensuring that they receive the best possible treatment in the least-restrictive manner. Individuals presenting with abnormal behaviour often attract an audience and you may be required to clear the scene to ensure that the patient’s privacy and dignity are maintained. You may also need to advocate to other professionals, such as the police, to ensure that the patient’s needs are

adequately met. In this case the paramedics may need to clear the scene to minimise distress caused by bystanders. Transport Transportation not only enables access to mental health care but also can be considered a point of care provision itself (Department of Health, 2011). While the transport protocols between police, mental health services and ambulance services may vary across jurisdictions, ambulance services are generally considered to hold primary responsibility for the transport of people with a mental illness if they are too ill to be transported by clinical staff alone (Department of Health, 2011), have a medical illness or other physical condition or require sedation or restraint. If they are agitated or have engaged in criminal activity, the police may be the most appropriate form of transport (Department of Health, 2010b; Health Department of Western Australia, 2012; Queensland Ambulance Service, 2012). Patients may favour an ambulance over a police vehicle as it could be viewed as less stigmatising and in many cases more appropriate, as paramedics have more training in mental health care compared with their police counterparts. As this patient has agreed to transport, is not an involuntary patient and is not aggressive, the primary transport choice is an ambulance. Sedation The question of sedation to facilitate transport of patients with mental illness is often raised. In the vast majority of cases sedation is not necessary. With effective communication most patients will cooperate and agree to transport, although the length of time required to gain their consent may vary. In some cases, however, paramedics will be faced with agitated patients (who may or may not have a mental illness), who require a different approach. The sedation guidelines used in Australia and New Zealand were devised with this group in mind. Primary considerations for these patients include the availability and appropriateness of less-restrictive options such as verbal de-escalation: the mental health Acts in some states and territories specifically prohibit the use of sedation of patients with an involuntary status, while others explicitly support it. Guidelines for safe sedation are described in local jurisdictional guidelines.

EVALUAT E The aim of the evaluation phase is to ensure that the selected intervention is appropriate. This may be assessed by considering the following: • Is the intervention working? The treatment outcomes in the case of mental illness are as varied as the illnesses themselves. In some cases you will see a decrease in concerning symptoms, while in others there may be no apparent change in symptom severity. At the very least, you can assist the patient by building strong rapport and a collaborative relationship. • Is the patient safe? Ensuring your safety and the patient’s is of paramount importance. Safety should be considered from the outset, but you should also re-

evaluate the scene and the patient’s status throughout the intervention period. • Has the patient consented to transport? With appropriate communication and support most patients consent to transport. If the patient refuses transport but requires an urgent psychiatric assessment, you may need to reconsider your choice and communicate in a firmer manner. Highlight the need for transport and your concerns for the patient and consider offering limited options; for example, ‘I am quite worried about the possibility of your harming yourself and, as such, I cannot leave you at home. I have a duty of care to ensure that you are transported to hospital but you do have a choice regarding your transport. You can travel in the ambulance or I can call the (police/CAT team, etc) and ask them to transport you. Which would you prefer?’ If the patient continues to deteriorate, you may need to reconsider your initial diagnosis or communication strategies. Have you effectively eliminated physical causes? Can you approach the patient in a different manner or can your partner approach the patient? In this patient’s case, the paramedics would expect to see a change in her sympathetic activation (e.g. decrease in heart rate, improved respiratory rate) as a result of their intervention.

Specific treatment guidelines Table 51.3 provides an overview of common mental illnesses encountered in paramedic practice and their associated symptoms, medications and specific management strategies.

Investigations Hospital staff will again screen for and eliminate organic causes. Once this screening has been completed and a psychiatric cause is considered more likely, a psychiatric consultant will be called and a determination made regarding the next course of treatment.

Hospital admission Modern psychiatric inpatient treatment is considered to be short-term and intensive intervention to minimise risk and manage symptoms. Care is provided 24 hours a day by a multidisciplinary team of professionals including psychiatrists, psychologists, mental health nurses, social workers and occupational therapists. Treatment is tailored to the needs of the individual, but is likely to include a medication review, short-term psychological treatment and family support. Inpatient wards also run comprehensive activity programs such as cooking, problem-solving groups and art therapy. Occasionally, treatment will be delayed in favour of observation if the patient’s diagnosis or symptom profile is unclear. Admission to a short-stay ward may be required for some intensive treatments, such as electroconvulsive therapy.

Long-term treatment and impacts Patients are generally discharged to a community mental health service for follow-up. A case manager will be allocated and a longer-term treatment plan devised. The case manager links the patient’s mental health supports together, ensuring continuity of care, to monitor the patient’s mental state on an ongoing basis and to evaluate their progress over time (Victorian Government Department of Health, 2008). The course of a mental illness varies according to the individual, their diagnosis and the supports available. While some patients require only one hospital admission, others will have regular involvement with mental health and emergency services. With support and appropriate intervention, recovery from a mental illness is possible.

Mental illness across the lifespan In any single year, one in five Australian adults will experience a mental illness: the prevalence of mental illness decreases with age, with the highest rates noted among 18– 24-year-olds (ABS, 2007). The prevalence of mental illness in Australia is comparable with rates from other Westernised countries including the US (3:10; Kessler et al., 1994), Western Europe (1:10; European Study of Epidemiology of Mental Disorders Committee, 2004) and the UK (1:4; National Centre for Social Research, 2012). The minor discrepancies between these data sets have generally been attributed to differences in measurement and reporting as opposed to true differences in prevalence rates (European Study of Epidemiology of Mental Disorders Committee, 2004). Irrespective, all indications suggest that mental illness is a significant burden of disease, with a wide range of associated disabilities and functional impairments (AIHW, 2010; European Study of Epidemiology of Mental Disorders Committee, 2004; Mauksch et al., 2000). For this reason, mental health has been identified as a National Health Priority Area in Australia. Accurate statistics regarding the number of mental health presentations attended by Australian and New Zealand paramedics are difficult to obtain due to misleading categorisation of jobs at dispatch, uncertainty regarding the individual’s diagnosis at the point of assessment (Roberts & Henderson, 2009) and difficulties linking pre-hospital data with hospital patient care records. Current recording methods also tend to focus on the patient’s primary presentation, meaning that secondary issues or diagnoses are overlooked in the data (Roberts & Henderson, 2009). In a study of South Australian data samples, Roberts and Henderson (2009) reported that mental health presentations represented around 2–3% of their total case sample. It may be argued that these figures are only likely to increase in the coming years, due to the mainstreaming of mental health services and a steadily increasing demand for services, which has not been met by increases in funding (Lowthian et al., 2011). As such, paramedics should be well-educated in the areas of mental health and risk assessments and have a working knowledge of the primary diagnoses likely to present to emergency services.

CA SE ST U DY 2 Case 09755, 1423 hrs. Dispatch details: A 29-year-old male complaining of back pain. Initial presentation: The paramedics arrive at a farm that is relatively isolated. A dishevelled male walks slowly to the door to allow them to enter.

ASSESS 1434 hrs Primary survey: The patient is conscious and talking. 1435 hrs Chief complaint: He has lower back pain. 1437 hrs Vital signs survey: Perfusion status: HR 68 BPM, BP 120/70 mmHg, skin pink and dry. Respiratory status: RR 16 BPM, good clear air entry bilaterally. Conscious state: GCS = 15. 1441 hrs Pertinent hx: The patient says he has had lower back pain for the past 3 months but it has become so bad that it is almost impossible to sleep. As a result he is constantly lethargic, a concern given the physically taxing nature of farm work. He is giving limited eye contact and his voice is flat and detached. He is drawn, tired and has obviously lost weight, based on his loose clothing.

P RACT ICE T IP Psychomotor retardation or a slowing of cognitive processing may occur in individuals during a major depressive episode. In such individuals it is important to limit external stimuli during assessment, which may be taxing on concentration. It is also important to make questions clear and concise, and allow time for the individual to respond. Be patient.

The paramedics are aware that flooding 8 months ago had a significant impact on local farmers, resulting in a loss of stock and, for many, significant financial strain. When asked if he has people to assist him with heavy lifting on the farm, the patient says that he had to let most of his farm hands go, though one remains. This placed a significant burden on him and the stress led to conflict with his wife and a subsequent separation almost 4 months ago. 1444 hrs Secondary survey: There is no specific tenderness to his lower back and his range of movement does not appear particularly limited. Although this patient presents with a clear physical complaint (back pain), strict adherence to this complaint during the assessment period without consideration of his flat affect, monotone speech and limited eye contact may limit the history taking solely to his pain and possible mechanisms of injury. Without prompting he may not disclose his stressors or his risk.

CONFIRM

In many cases paramedics are presented with a collection of signs and symptoms that do not appear to describe a particular condition. A critical step in determining a treatment plan in this situation is to consider what other conditions could explain the patient’s presentation.

What else could it be? Chronic musculoskeletal back pain The lack of any tender areas in the patient’s back and the relatively normal range of movement would seem to exclude chronic musculoskeletal back pain and a range of inflammatory arthritis and myositis conditions.

DIF F ERENT IA L DIA GNOSIS Clinical depression Or • Chronic musculoskeletal back pain • Occult malignancy • Hyperglycaemia (diabetes) • Hypothyroidism • Intracranial tumour • Undisclosed problem with alcohol/drugs of addiction

Occult malignancy Weight loss could be a sign of occult malignancy or diabetes. Lack of any symptoms associated with malignancy makes this less likely but this is still a diagnosis that has to be considered in the background during his hospital investigation. Hyperglycaemia (diabetes) The weight loss could be caused by prolonged hyperglycaemia but little else fits this clinical picture. The normal blood sugar and lack of any history of urinary frequency and excessive thirst effectively exclude diabetes. Hypothyroidism The early symptoms of hypothyroidism include fatigue, joint pain and depression but the disease is generally associated with weight gain, not loss. The patient does not report any increased sensitivity to cold or change to his hair and nails. This does not fit the clinical picture but it should be investigated at hospital. Intracranial tumour Intracranial tumour can present with a mood disorder although it would be unusual to have no other focal signs or symptoms evident. This diagnosis cannot be excluded at this stage. Undisclosed problem with alcohol/drugs of addiction An undisclosed problem with alcohol or drugs of addiction could present with

a depressed mood and weight loss, although it is likely that history or evidence of the problem would have occurred in the evaluation thus far. When asked direct (but not threatening) questions regarding his alcohol/drug use, the patient denies any issues. It should be noted that admission to an addiction doesn’t actually preclude depression and mood disorders as a diagnosis in the field and should not change the management of this patient. In the absence of any physical factors and applying the patient’s history and presentation to the MSE, clinical depression appears as a strong factor in his decision to request help for his back pain. Further assessment by health specialists will be needed to exclude other possibilities.

T REAT With a provisional diagnosis of depression in the setting of isolation and ongoing stress it is essential that this patient is engaged with the wider health system and the paramedics being there is the ideal opportunity to do this. Recognising the need for transport, inexperienced paramedics might use the ‘need to investigate’ his back pain as a way to encourage the patient to agree to transport to hospital. However, during his hospital assessment it will quickly become obvious that the paramedics have lied and this may make him less likely to seek treatment in the future. Open, honest and empathetic exploration of his condition will not only align the patient and crew’s expectations of what should occur, but will also provide more information for the paramedics to make an informed decision regarding treatment options. At this point a risk assessment should be conducted, and this can be done using the four-stage model presented earlier in the chapter. 1447 hrs: The paramedics complete a risk assessment for the patient as follows: Plan: The patient indicates that he has contemplated suicide. The paramedics ask for further information regarding his plan. He details the plan, noting that he has gone so far as to write a goodbye note to his family. Means: The patient admits that he has access to firearms, his chosen method, indicating a high degree of risk. Timeframe: He indicates that he will wait until after his daughter ’s birthday next week, as he does not want her to be sad on her birthday. History: He denies any past suicide attempts, but advises that his paternal grandfather committed suicide when he was 45.

P RACT ICE T IP Small quantities of IV midazolam repeated to effect are safer than large quantities delivered intramuscularly.

Based on the risk assessment, this patient is a very high risk of suicide. He is actively depressed, with a number of current social stressors; he also has a clearly defined plan, access to the means and a timeframe; as well as a family link to suicide. He clearly needs urgent assessment and management within the hospital system. From a pre-hospital perspective, the main care the crew can provide at this juncture is transport in a safe and supportive manner (see Box 51.5). As his risk of self-harm is quite high, it is essential that he understands that this information will be handed over at hospital so that he can receive the most appropriate support possible. B O X 5 1 . 5G e n e r a l

a d vic e in c a se s o f

suic ide r isk • Secure the environment and remove any unwanted distractions or stressors (this may include loved ones). Remove any accessible means of harm. • Do not leave the person alone. • Listen to the person’s story and try to identify the factors that led to an increase in risk at that specific point in time. • Many suicidal patients feel ambivalent about their desire to die or feel that they have no other option. Acknowledge the patient’s feelings and identify protective factors (i.e. reasons they have not acted on their plans or reasons to live). Do not try to talk the patient out of their feelings as they will feel ignored and possibly more helpless. • Be empathetic. While some clinicians may view suicide as pointless or selfish, expressing these views is unprofessional and unlikely to be helpful to the patient. • Encourage access to definitive treatment. If the patient is reluctant, explore legal options such as an involuntary status. The specifics of this option will vary depending on the local jurisdiction. • If all attempts fail and the person acts on their plans, seek immediate support and debriefing. Suicide can be very distressing and it is important that you take care of yourself.

As he contacted the ambulance service, provided he is handled sensitively and with empathy, it is likely that he will agree to be transported voluntarily. The main skill is to facilitate this transport in the most dignified and leastrestrictive way while continuing to assess him. If the paramedics have established a good rapport with him they will be well-placed to deliver a clear handover, including the patient in the process to ensure that he agrees with all the points. If the patient is reluctant to be transported voluntarily, the paramedics will need to start the processes to enact the legal powers to force transport. They

may need to consider administering a chemical restraint using small doses of IV midazolam until he is calm and accepting. If they need to apply physical restraint to obtain the IV line they must take extreme care not to compress his chest or diaphragm in the process. Mental illness should not preclude pain relief and managing this patient’s pain with carefully titrated doses is strongly encouraged.

EVALUAT E Effective pre-hospital management of mental illness rarely requires the administration of medications and as such there is unlikely to be any significant change in the patient’s presentation during transport. Maintaining the patient’s dignity is likely to lead to an uneventful journey to hospital.

CA SE ST U DY 3 Case 09157, 1207 hrs. Dispatch details: A 25-year-old male with uncontrolled haemorrhage to his left arm. The caller states that the patient inflicted the wound intentionally. Initial presentation: When the paramedics arrive they find the patient pacing around the room. His wound has been bandaged by his mother and is no longer bleeding. The patient presents as dishevelled, irritable and suspicious, and asks the paramedics to show their credentials before submitting to a physical examination.

ASSESS 1215 hrs Primary survey: The patient is conscious and talking. 1216 hrs Chief complaint: He reports that he lacerated his arm while

searching for a tracking device that ‘they’ had implanted under his skin. 1218 hrs Vital signs survey: The patient eventually sits at the request of the paramedics, although his legs move restlessly throughout the examination. Perfusion status: HR 90 BPM; unable to obtain BP due to the patient’s agitation; skin pale and dry. Respiratory status: RR 24 BPM, good respiratory effort, no apparent respiratory disturbance evident on visual inspection while questioning the patient. Conscious state: GCS = 14, confused to time. 1220 hrs Pertinent hx: The patient denies a history of mental illness, although his mother reports that he was diagnosed with schizophrenia 5 years ago. She says that he has been well for the past 4 years, but became irritable and withdrawn after losing his job 5 weeks ago. She has noticed a decline in his sleep and appetite since then. 1223 hrs Further mental health questioning: While the patient is able to respond to most questions, the paramedics note long delays in his response times. He has limited eye contact and is unable to identify who ‘they’ are exactly, except to say that they watch him and always seem to know where he is. He also articulates concerns that his mother is trying to poison him and that his friends are talking about him. 1228 hrs Secondary survey: There is good sensation, movement and circulation to his left hand. Unless there is an indication of arterial bleeding, visualising any wound before transport is usually recommended as it may require a specific hospital for treatment, but in this case the crew leave the bandage in place to reduce stimulus to the patient. This case is challenging in that the patient is presenting with both psychosis and a physical injury that requires treatment. His behaviour is likely to make the paramedics wary and may affect their ability to communicate effectively. His discussion provides insight into his thought processes, revealing a paranoid delusion and a lack of insight into his previous medical history and his current state. The clinical picture is consistent with psychosis, although the precipitating cause could be primary schizophrenia alone, an exacerbation due to drug use or possibly a combination of both.

CONFIRM In many cases paramedics are presented with a collection of signs and symptoms that do not appear to describe a particular condition. A critical step in determining a treatment plan in this situation is to consider what other conditions could explain the patient’s presentation.

DIF F ERENT IA L DIA GNOSIS Psychosis

Or • Acute drug reaction • Encephalitis • Focal epilepsy • Hyponatraemia or other electrolyte imbalance • Thyrotoxicosis • Hypoglycaemia

What else could it be? Acute drug reaction A psychotic reaction to drugs, particularly stimulant drugs such as amphetamines, is not unusual and should be managed in a similar way to a primary psychotic state related to schizophrenia. Anecdotally, drug-induced psychosis may be associated with more dramatic delusions resulting in more intense and violent responses from the patient. A psychotic reaction to prescribed medications (including steroids) will occasionally occur: this can be either a direct effect of the drug or an interaction with an underlying psychotic condition. Unfortunately, excluding drug use without the use of toxicology relies on the history, which in this case may be unreliable. Encephalitis An acute psychotic state can be the first presentation of encephalitis and no other signs of infection may be obvious in the early stages. Although this is very unusual it is not impossible and should be considered, particularly if there is no previous history or obvious precipitating cause of the psychosis. This cannot be effectively excluded in the pre-hospital setting and even without an arm wound this factor would necessitate transport to hospital to determine. Focal epilepsy Focal epilepsy can give rise to acute episodes of abnormal behaviour, but this is not usually psychotic and should have a definite onset and offset associated with the epileptic activity. This is not consistent with this patient’s presentation. Hyponatraemia or other electrolyte imbalance An electrolyte imbalance can precipitate disturbed behaviour that may be psychotic in nature. Hyponatraemia associated with excessive drinking of water or adrenal gland failure can present with delusional psychotic behaviour before progressing to cause seizures. An absence of suggestive history is helpful but a normal set of blood tests is really necessary to exclude this hypothesis. It is worth considering in previously undiagnosed patients who are at risk of hyponatraemia (i.e. those attending dance parties or raves where the combination of excessive activity and drug use increase the risk). The patient’s history does not include these activities. Thyrotoxicosis Endocrine abnormalities such as thyrotoxicosis can produce a hyperactive state

with some paranoid component, especially if the patient has an underlying mental illness. The absence of excessive tachycardia, tremors and signs of a hypermetabolic state would make this diagnosis unlikely but formal thyroid function tests would exclude it completely. Hypoglycaemia The presence of a normal blood sugar excludes hypoglycaemia as a possible cause of the abnormal behaviour.

T REAT This patient needs assessment and treatment in hospital where the full range of possible alternative diagnoses can be excluded and he can be offered antipsychotic medication and stabilisation in a controlled environment. He is considered a high risk of accidental self-harm (as noted by his laceration) and could be a risk of harm to others should his paranoid delusions escalate given his current state of agitation. The patient is compliant so he may voluntarily agree to transport, in which case the treatment will be aimed at making the experience as stress-free as possible for him while gaining further insight into his current state of mind and possible precipitating causes. Unusually, his paranoia may preclude the paramedics from treating his wound with pain relief. Always offer patients with physical injuries the option of receiving pain relief, but do not try to force the administration of medications.

P RACT ICE T IP If using physical restraint: • place no pressure on the patient’s chest or abdomen; the patient should be face up to allow good observation of ventilation • ensure that it is possible to rapidly roll the patient onto their side if they vomit.

EVALUAT E Should he not be compliant, legal options will have to be pursued. This patient appears to be suffering from a mental illness, is considered a high risk of accidental self-harm due to his delusions (e.g. laceration to his arm) and thus cannot remain at home, and requires assessment and management in hospital.

This would fulfil the legislative requirements for involuntary treatment and transport in most states. To achieve safe transport, chemical restraint may be considered and is the preferred option over physical restraint, the aim being to use the least-restrictive form of restraint that is compatible with both the patient’s and the crew’s safety. Effective pre-hospital management of mental illness rarely requires the administration of medications or restraints and as such there is unlikely to be any significant change in the patient’s presentation during transport. If physical or chemical restraint is used either temporarily or during transfer, several risks should be considered: (1) the risk of positional asphyxia, in which the victim is unable to breathe properly because of restrictions to chest movement caused by the restraint; and (2) the risk that a sedated patient becomes unconscious and vomits and the physical restraint prevents the paramedics from turning the patient quickly onto their side to clear the airway. While securing the patient’s wrists to each side of the stretcher may act as a better restraint, it can prove fatal if the patient cannot be rolled quickly should they vomit.

CA SE ST U DY 4 Case 10020, 0831 hrs. Dispatch details: A 25-year-old female in a gaming lounge with abnormal behaviour. Initial presentation: Casino staff direct the paramedics to the patient in the gaming lounge where she has been for the past 40 hours and refuses to leave. They called the ambulance when they noticed that she was behaving unusually and had difficulty talking to her. The paramedics notice that she is extremely slim and dressed in bright, vibrant clothing.

ASSESS In response to the paramedics’ greeting the patient reports that she is a

university student studying for her final exams. She goes on to discuss the last movies she has seen. When one of the paramedics firmly redirects her towards her behaviour she reports that in the last 4 weeks she has stopped eating as she has not been hungry. Her sleeping patterns have also altered dramatically: she has had a maximum of 2 hours sleep per night in the last few days. She says that she has been far too busy to sleep as she has significant study commitments and a professional tennis career to prepare for. Without appearing to draw breath, she acknowledges that she has never had formal tennis lessons or played regularly, but remains certain that she will be wildly successful. She is very flirtatious with bystanders and the treating paramedic. 0847 hrs Vital signs survey: Perfusion status: HR 98 BPM, weak and irregular, BP 140/100 mmHg, skin flushed and dry. Respiratory status: RR 18 BPM, good clear air entry, L = R, normal work of breathing, no complaint of dyspnoea. Conscious state: GCS = 15. The treating paramedic notes that the patient is grandiose and disorganised and that when she begins to speak she is very difficult to interrupt. She speaks in a loud voice and her speech is pressured. She admits to using amphetamines in the past 48 hours but denies any sustained or long-term use. Her symptoms are typical of a bipolar I manic episode.

CONFIRM In many cases paramedics are presented with a collection of signs and symptoms that do not appear to describe a particular condition. A critical step in determining a treatment plan in this situation is to consider what other conditions could explain the patient’s presentation.

What else could it be? Amphetamine or stimulant use Hypomania describes a state of euphoria and disinhibition that is often associated with excessive confidence and hypersexuality. It can be distinguished from mania by an absence of psychotic symptoms but the two should be considered as part of a continuum as opposed to separate conditions. The most likely alternative diagnosis for hypomania is amphetamine or other stimulant use. Differentiation will depend on whether there is a history of drug use, a history of bipolar cycles and a previous diagnosis. Without drug screening it can be very difficult to differentiate between pure bipolar hypomania and drug-induced hypomanic behaviour—or, as in this case, a combination of both. The diagnosis is difficult to determine in the field but it could be relevant to immediate management.

DIF F ERENT IA L DIA GNOSIS

Bipolar Or • Amphetamine or stimulant use • Other organic brain syndrome

Other organic brain syndrome There are relatively few organic brain syndromes that mimic this degree of hypomanic behaviour. Possibly hyperstimulation associated with excessive amounts of circulating adrenaline or other catecholamines might present like this. Her pulse and blood pressure are not excessively elevated, though, which does not support a systemic adrenaline-like syndrome. Serotonin syndrome is a potentially life-threatening condition caused by the interaction of serotonin reuptake inhibitors with other drugs that results in the release of too much serotonin. It can produce a hyperactive state but it does not normally have the disordered ideas that are typical of a bipolar hypomanic phase. In addition, serotonin syndrome is always associated with physiological changes such as increases to temperature, heart rate and blood pressure. This does not fit the clinical picture in this case.

T REAT This patient’s use of amphetamines will have exaggerated her hypomanic/manic state and allowed her to remain conscious for long periods of time without sleep. If someone who knows her well can be found they may be aware of a formal diagnosis of bipolar disorder or at least be aware of what medications she has been taking or is supposed to take. They may also be able to provide information regarding possible depressive episodes that are typical of bipolar II and may occur in bipolar I. The patient has no insight into her behaviour and so will be challenging to interact with and convince that she needs help. A slow, steady approach will allow her more opportunity to process information. This interaction should be handled by one member of the crew, who should concentrate on slowing down in response to her hypomanic speech patterns. The paramedics should consider discussing her physical symptoms (i.e. her lack of sleep, drug use, limited food intake) with her to see whether she will engage in treatment for these issues. Wherever possible, she should be encouraged to access treatment voluntarily. The treating paramedic undertakes a risk assessment, which indicates that she will be at risk of accidental self-harm and possible harm to others if left untreated. Given this assessment, legal pathways must be considered. This patient meets the criteria for involuntary treatment for most jurisdictions so the paramedics should be clear that they have a duty of care and cannot leave her in the casino. They can instead give her a choice about which form of transport

she would prefer, ambulance or police. Involving the police has advantages in terms of extra assistance and an authority presence but it can sometimes inflame the situation. The benefits and risks of police involvement need to be weighed up before escalating to this level. This picture is further complicated by the patient’s amphetamine use, which can mimic many of the symptoms of mania. When making a differential diagnosis, clinicians at the receiving hospital will probably construct a careful timeline to identify the presence of symptoms in relation to her substance use. They may also wish to monitor her for an extended period to determine whether her symptoms remain after the amphetamines have been metabolised and excreted from her system. A number of ambulance services support the administration of benzodiazepines such as midazolam to manage amphetamine overdose. This guideline was mostly developed for the small cohort of patients who present with painful bruxism, twitching, scratching and hypertension, but it can also be used as a last resort in aggressive patients. There are very strict guidelines regarding the use of sedatives to facilitate the transport of involuntary patients who are mentally ill. It is perceivable that the paramedics could misinterpret this patient’s history and find themselves administering a sedative against their local Mental Health Act. Consultation to support this decision would be recommended.

EVALUAT E Effective pre-hospital management of mental illness rarely requires the administration of medications and as such there is unlikely to be any significant change in the patient’s presentation during transport. Maintaining the patient’s dignity and not engaging or challenging her delusions is likely to lead to an uneventful journey to hospital.

Summary Patients presenting with abnormal behaviour require a different approach from those presenting with physiological abnormalities. Much more care must be taken in all forms of communication with these patients and a slower, less intimidating approach is often required. These patients are extremely vulnerable and need to be protected from harm. In addition to the abnormal behaviour, any physiological issues must be addressed in an effort to either reverse the abnormal presentation or manage any trauma that has occurred as a result of the presentation.

References Australian Bureau of Statistics (ABS). Year Book Australia, 2001. Retrieved 30 January 2012 from www.abs.gov.au/ausstats/abs, 2002. Australian Bureau of Statistics (ABS)National Survey of Mental Health and Wellbeing: Summary of Results. Canberra: ABS, 2007. [Cat. no. 4326.0]. Australian Government. National Suicide Prevention Strategy. Retrieved 30 January 2012 from www.health.gov.au/internet/mentalhealth/publishing.nsf/content/national-suicideprevention-strategy-1, 2012. Australian Institute of Health and Welfare (AIHW). Mental Health. Retrieved 4 February 2012 from www.aihw.gov.au/publications/index.cfm/title/11415, 2010. Awad, G. A. Antipsychotic medications: compliance and attitudes toward treatment. Current Opinion in Psychiatry. 2004; 17(2):75–80. Battaglia, J. Compliance with treatment in schizophrenia. American Psychiatric Association: 53rd Institute on Psychiatric Services. Retrieved 17 January 2012 from www.medscape.com/viewarticle/418612, 2001. Black Dog Institute. Bipolar disorder explained. Retrieved 14 January 2012 from www.blackdoginstitute.org.au/public/bipolardisorder/bipolardisorderexplained/index.cfm, 2010. Campbell, C., Farrell, G. Personality disorders. In Elder R., Evans K., Nizette D., eds.: Psychiatric and Mental Health Nursing, 2nd ed, Sydney: Elsevier, 2009. Cheng, A. T.A., Chen, T. H.H., Chen, C., Jenkins, R. Psychosocial and psychiatric risk factors for suicide: case-control psychological autopsy study. BJP. 2000; 177:360–365. Community Services and Health Industry Skills Council (CSHISC)Dementia Training for Ambulance Workers: Learner ’s Guide. Strawberry Hills: Department of Health and Ageing, 2009. Community Services and Health Industry Skills Council (CSHISC). Key Principles: Skills for Ambulance Workers in Responding to People with Dementia. Retrieved 24 November 2011 from www.psychology.org.au/publications/tip_sheets/dementia/#s5, 2011.

Compton, M. T., Kotwicki, R. J. Responding to Individuals with Mental Illnesses. Jones & Bartlett, Sudbury, MA, 2007. Davidson, G. C., Neale, J. M., Kring, A. M. Abnormal Psychology, 9th ed. Boston: John Wiley & Sons, 2004. Department of HealthPeople Living With Psychotic Illness. Canberra: Department of Health, 2010. Department of HealthAmbulance Transport of People with a Mental Illness Protocol 2010. Melbourne: Mental Health, Drugs and Regions Division, 2010. Department of Health. Safe Transport of People with a Mental Illness: Chief Psychiatrists Guideline. Retrieved 31 January 2012 from www.health.vic.gov.au/mentalhealth/cpg/safetransport.pdf, 2011. Engel, G. L. The need for a new medical model: a challenge for biomedicine. Science. 1977; 196(4286):129–136. European Study of the Epidemiology of Mental Disorders Committee. Prevalence of mental disorders in Europe: results from the European Study of the Epidemiology of Mental Disorders (ESEMeD) project. Acta Psychiatrica Scandinavica. 2004; 109(420):21–27. Forrester, K., Griffiths, D.Essentials of Law for Health Professionals. Harcourt: Australia, 2001. Frost, B., Carr, V., Halpin, S.Employment and Psychosis: Low Prevalence Disorder Component of the National Study of Mental Health and Wellbeing, Bulletin 3. Canberra: Department of Health and Aging, 2002. Fry, M., Brunero, S. The characteristics and outcomes of mental health patients presenting to an emergency department over a twelve-month period. Australian Emergency Nursing Journal. 2004; 7(2):21–25. Health Department of Western Australia. Protocol between the Western Australia Police Service and the Mental Health Division of the Health Department of Western Australia.

Retrieved 4 February 2012 from www.chiefpsychiatrist.health.wa.gov.au/docs/guides/Protocol_Between_WA_Police_Mental_ 2012.

Hirschfeld, R. M.A., Davidson, L., Risk factors for suicideFrances, A.J., Hales, R.E., eds. Review of Psychiatry, Volume 7. Washington DC: American Psychiatric Association, 1998. Kessler, R. C., McGonagle, K. A., Zhao, S., Nelson, C. B., Hughes, M., Eshleman, S., Wittchen, H. U., Kendler, K. S. Lifetime and 12-month prevalence of DSM-III-R psychiatric disorders in the United States. Archives of General Psychiatry. 1994; 51:8–19. Larkin, G. L., Claassen, C. A., Pelletier, A. J., Camargo, C. A. National study of ambulance transports to United States emergency departments: importance of mental health problems. Prehospital and Disaster Medicine. 2006; 21(2):82–90. Lichtman, J., Bigger, J. T., Blumenthal, J. A., Frasure-Smith, N., Kaufmann, P. G., Lesperance, F., Mark, D. B., Sheps, D. S., Taylor, C. B., Froelicher, E. S. Depression and coronary heart disease. Circulation. 2008; 118:1768–1775. Lowthian, J. A., Jolley, D. J., Curtis, A. J., Currell, A., Cameron, P. A., Stoelwinder, J. U., McNeil, J. J. The challenges of population ageing: accelerating demand for emergency ambulance services by older patients, 1995–2015. Medical Journal of Australia. 2011; 194:574– 578. Mallik, S., Spertus, J. A., Reid, K. J., Krumholz, H. M., Rumsfeld, J. S., Weintraub, W. S., Agarwal, P., Santra, M., Bidyasar, S., Lichtman, J. H., Wenger, N. K., Vaccarino, V. Depressive symptoms after acute myocardial infarction. Archives Internal Medicine. 2006; 166:876–883. Mauksch, L. B., Tucker, S. M., Katon, W. J., Russo, J. Mental illness, functional impairment, and patient preferences for collaborative care in an uninsured, primary care population. The Journal of Family Practice. 2000; 50:41–47. Mindframe National Media Initiative. Mental illness and suicide in the media: a mindframe for police. Retrieved 30 January 2012 from www.mindframemedia.info/site/index.cfm?display=105553, 2012. Muir-Cochrane, E., Barkway, P., Nizette, D.Mosby’s Pocketbook of Mental Health. Sydney: Elsevier, 2010.

National Centre for Social Research. Mental health. Retrieved 4 February 2012 from www.ic.nhs.uk/webfiles/publications/mental%20health/other%20mental%20health%20publi

2012. Polk, D. A., Mitchell, J. T.Prehospital Behavioural Emergencies and Crisis Response. Sudbury, MA: Jones & Bartlett, 2009. Queensland Ambulance ServiceMental Health Intervention Project: Mental State Assessment. Brisbane: Queensland Government, 2008. Queensland Ambulance Service. Transport of Patients with a Mental Illness in Queensland. Retrieved 4 February 2012 from www.ambulance.qld.gov.au/about/pdf/qems_mental_health_transport.pdf, 2012. Roberts, L., Henderson, J. Paramedic perceptions of their role, education, training and working relationships when attending cases of mental illness. Journal of Emergency and Primary Health Care. 7(3), 2009. Saba, G., Mekaoui, L., Leboyer, M., Schuhoff, F. Patient’s health literacy in psychotic disorders. Journal of Neuropsychiatric Diseases and Treatment. 2007; 3(4):511–517. Stein, D. J., Phillips, K. A., Bolton, B., Fulford, K. W.M., Sadler, J. Z., Kendler, K. S. What is a mental/psychiatric disorder? From DSM-IV to DSM-V. Psychological Medicine. 2010; 40(11):1759–1765. Tavakoli, H. R. A closer evaluation of current methods in psychiatric assessments: a challenge for the biopsychosocial model. Psychiatry. 2009; 6(2):25–30. United Nations. Principles for the protection of persons with mental illness and the

improvement of mental health care. Retrieved 4 February 2012 from www.who.int/mental_health/policy/en/UN_Resolution_on_protection_of_persons_with_me 2002. Victorian Government Department of Health. A guide to mental health terminology. Retrieved 30 January 2012 from www.health.vic.gov.au/mentalhealth/termnlgy.htm, 2008. Wade, D. T., Halligan, P. W. Do biomedical models of illness make for good healthcare systems? British Medical Journal. 2004; 329:1398–1401. World Health Organization (WHO)The ICD-10 Classification of Mental Health and Behavioural Disorders: Clinical Descriptions and Diagnostic Guidelines. Geneva: WHO,

1992. World Health Organization (WHO)WHO Resource Book on Mental Health, Human Rights and Legislation. Geneva: WHO, 2005. World Health Organization (WHO). Mental health: strengthening our response. Fact sheet N220. Retrieved 12 January 2013 from www.who.int/mediacentre/factsheets/fs220/en, 2013. World Medical Association. WMA statement on ethical issues concerning patients with mental illness. Retrieved 4 February 2012 from www.wma.net/en/30publications/10policies/e11, 2006.

Resources www.blackdoginstitute.org.au www.beyondblue.org.au anzmh.asn.au www.sane.org

CHAP TER 52

De-escalation in the pre-hospital environment By Jade Sheen and Matt Johnson

O V E RV IE W • Managing patients with mental illness in the community setting is stressful and emotive for both patients and those who care for them. • Managing these patients with physical or chemical restraints increases the chances of harm to both the patient and the paramedic. • The ability to de-escalate patients with mental illness is not usually included in the paramedic skill set, despite the increasing frequency with which paramedics are encountering these patients.

Introduction The unpredictable nature of pre-hospital work may be exciting for prospective paramedics, but the uncontrolled environment that characterises the paramedic workplace is also associated with an element of risk. Although the vast majority of patients and their families are grateful when paramedics arrive, local and international literature suggests that paramedics are at a higher risk of exposure to aggressive incidents precipitated by patients, carers and even bystanders than other health professionals. Studies have found up to 82% of paramedics have been the subject of verbal abuse or harassment (Boyle, 2007). The ability to verbally de-escalate agitated patients and bystanders is the most effective tool paramedics have in dealing with these cases. It is important to note that aggression is presented as a behavioural dysfunction but this is not to suggest that people with mental health issues are by necessity aggressive: in fact, the literature suggests they are more likely to be the victims of violent crimes rather than the perpetrators. During paramedic training, education regarding how to deal with aggressive situations is inconsistent, with a reliance on either escape or chemical restraint strategies. Unfortunately, as Chapter 51 identifies, paramedics are often the only resource that can respond to patients with mental illness who are showing signs of agitation. The crew cannot simply leave and need to manage the patient effectively. While chemical restraint may appear an effective solution, the delicate process of intramuscular (IM) or intravenous (IV) drug administration and then waiting for the drug to reach an effective dose actually requires patient cooperation, which is unlikely. In reality, paramedics may need the assistance of others, including law enforcement, to physically restrain the patient while administering IM/IV sedation, exposing all involved, including the patient, to additional risk.

Theories of aggression Aggression may be defined as any behaviour that is carried out by one individual towards another with the proximate (immediate) goal to cause harm (Krahé, 2013). There are many theories regarding the aetiology of aggression, but we focus here only on the types of aggression that may present in the pre-hospital setting, as this may have direct implications for treatment plans and outcomes. Two specific types of aggression, hostile and instrumental, have been isolated within the literature and require further discussion: • Hostile aggression is seen as impulsive, unplanned, driven by anger and occurring as a reaction to some perceived provocation. Thus, this form of aggression is likely to be highly influenced by the context in which it occurs, providing valuable information for paramedics regarding management. Aggressive cues, provocation, pain and discomfort, drugs and alcohol, incentives and frustration have all been identified as situational factors that may decrease tolerance and increase the likelihood of an aggressive incident occurring. This highlights the importance of scene management when faced with a potentially aggressive incident. • Instrumental aggression is seen as premeditated and occurs as a means of achieving some goal other than harming the victim. In this way it is thought to be proactive as opposed to reactive. Individuals expressing this form of anger have often learnt to achieve their goals through aggression and/or intimidation and are likely to have a history of this behaviour (which may be available at dispatch). Bushman and Anderson (2001) have critiqued the hostile/instrumental dichotomy for a number for reasons, most notably that it fails to account for aggressive acts with multiple motives. They assert that we cannot arbitrarily define an individual’s motivation as being either hostile or instrumental. Sometimes a person may experience mixed motives so that their aggression is driven by anger and a reaction to a specific stressor, yet it occurs much later, after careful planning. Despite this objection, the hostile/instrumental model does hold some utility when thinking about aggression management and specific de-escalation techniques as it allows for two distinct but related approaches: one for the ‘hot’ hostile episodes and one for the ‘cold’ instrumental episodes. In cases where paramedics believe that the individual is clearly exhibiting one form of aggression over another, specific strategies may be of use. If mixed motives are likely, general forms of de-escalation may suffice.

Management of aggression Research suggests that healthcare staff use the method of aggression management that they are most familiar with (e.g. sedation and restraint), despite the potential for other less-invasive methods to be used (e.g. de-escalation). Reasons for this include a lack of training in less-invasive methods of intervention, a lack of resources and time constraints for busy clinicians, concerns for the practitioner ’s own welfare and the security of bystanders. However, these explanations do not warrant the use of an invasive procedure that actually increases the risk of harm when alternatives are available. Paramedics should be familiar with de-escalation, the preferred model of intervention designed to uphold the rights and dignity of the patient using the principle of least-restrictive care.

Principles of de-escalation Cowin and colleagues (2003) describe de-escalation as ‘(the) gradual resolution of a potentially violent and/or aggressive situation through the use of verbal and physical expressions of empathy, alliance and non-confrontational limit setting that is based on respect’. De-escalation requires negotiation and communication, not command and control. The fundamental principles of de-escalation as outlined by Distasio (1994) are as follows: 1. Maintaining the autonomy and dignity of the patient. 2. Using self-knowledge to achieve goals. 3. Being self-aware. Self-awareness includes an understanding of your physical presence and your individual needs and responses (e.g. your body language may have an impact on the success or failure of an intervention). Often your body language may be closed or hostile in these situations without you even realising it. Individual issues can include comments or situations that may trigger your own anger. 4. Intervening early. By intervening early in the anger cycle you will increase the chances of success and hopefully allow for a ‘cognitive’ intervention. If the person is already highly aroused (e.g. a release of adrenalin often accompanies physiological arousal) they need time to wind down: ‘cognitive’ or talking-based interventions will be less successful during this period. 5. Providing options and choice. By providing limited options and choices where possible, you allow the individual to retain some degree of autonomy and dignity and enable them to comply with requests without losing face. 6. Avoiding physical confrontations. Sedation, restraint and seclusion are not always preferable if de-escalation fails. Providing the person with physical space and avoiding early attempts to restrain them physically may ultimately allow paramedics to use the least-restrictive means of treatment. There are times when a successful de-escalation will involve giving the individual space to ventilate and manage their own frustrations before paramedics step in.

De-escalation in practice The highly emotive nature of dealing with verbal aggression (and threats of physical aggression) makes these situations difficult to manage. Having a defined process can assist paramedics in managing—as opposed to reacting to—these events (see Fig 52.1).

FIGURE 52.1 The steps of de-escalation. Effective verbal de-escalation protects both paramedics and patients from harm.

Step 1: Look Before approaching an agitated individual observe their behaviour carefully. This assessment may provide vital clues regarding the stage they are currently in according to the cycle of aggression—for example, if the individual is pacing and gesturing broadly, their major motor movements suggest that they have experienced a significant escalation and are to be approached with caution. Also assess the environment, scanning for weapons or any item that may be used as a weapon as well as other individuals who may pose a threat to the paramedics. In addition, assess any escape options should a quick exit be required. Should the risk of harm be assessed as high, paramedics are encouraged to leave the scene and contact the police for support. If the risk is assessed as low, move on to step 2.

Step 2: Listen Listening to the patient’s verbalisations when they are angry may provide vital clues with regards to the cause of their anger and possibly their motivation (i.e. is the episode ‘hot’ or ‘cold’?). Attempting to gain an understanding of the individual’s motivation is important, as it may indicate the use of a specific de-escalation tactic. Another essential component of this step is to try to gain an understanding of the individual’s objectives. This will provide

essential information when de-escalating the situation and enables the paramedic to identify whether there is a discrepancy between the patient’s objectives and the treatment plan. Discrepancies often occur when treatment is made involuntary for legal reasons.

Step 3: Act Based on the visual and verbal assessment of the patient, a plan of action should be formulated. Aggression management alternatives are assessed in detail below. The plan of action should be revised at regular intervals to identify whether progress is being made. If the paramedic sees no change in the patient’s engagement or demeanour after a reasonable period of time (this will depend on the urgency of treatment required), the plan will need to be reassessed.

Aggression management strategies When formulating a plan of action it is essential to commence with the least-restrictive means of management and to progress to more-invasive responses only if necessary (see Fig 52.2).

FIGURE 52.2 Successful de-escalation follows a distinct path. First, the patient is engaged verbally to establish a non-authoritarian collaborative relationship. This requires the paramedic to avoid the ‘dominant-submissive’ relationship that occurs in most health emergencies. Next, the paramedic establishes a collaborative relationship with the patient but limits the options available to the patient. Finally, allowing the patient to regain some sense of control means they can ‘agree’ on the outcome. For instrumental aggression, set clear, firm boundaries on behaviour and offer

alternatives. Devote less time to listening when the person is acting inappropriately or being manipulative. For hostile aggression, allow time and space for the person to cool down.

Verbal • Allow time for the person to respond if they are confused or disoriented. If the patient is experiencing a degree of thought disturbance they may be easily overwhelmed by external stimuli and need time to consider information. Giving them time and space is respectful and also allows them the opportunity to respond, minimising frustration. Personal space is a concept that can become disordered, particularly in the presence of stimulants, and crews should consider allowing a personal space much larger than they would normally provide. • Allocate one key person to communicate with the patient. Multi-agency responses, an unfamiliar and unpredictable environment and the involvement of bystanders and/or carers may substantially increase the stimuli in the environment. Attempt to minimise frustration and stimulation overload by electing one key person to communicate with the patient. • Employ active listening skills: Listen to the individual and summarise what they are saying where appropriate. • Ask the person’s carer/family for advice and strategies: A common criticism of healthcare workers is that they fail to take the advice of a patient’s caregivers and/or family. These people may hold valuable information regarding the patient’s history, triggers to aggression if it has occurred in the past and useful management strategies. • Use calm and respectful language. • Use open-ended questions if the patient’s mental state allows them to respond. This type of questioning requires active cognitive processing for patients to formulate a response, which may inadvertently decrease their arousal level and therefore the potential for violence. • Avoid challenges and promises that can’t be kept. In the pre-hospital setting this may include promises that the patient will not have to stay in hospital when they may actually require admission. Making such promises creates a lack of trust in paramedics and may result in aggression in hospital if staff advise that the patient actually requires admission. • Be firm but compassionate. It is possible to be firm with the patient regarding their need for transport but to still empathise with any concerns they may have. • Use a calm, lowered tone of voice. Most of us unconsciously raise our tone of voice and volume when presented with an individual who is yelling or being verbally abusive. Unfortunately, responding in this manner may result in the patient raising their tone even higher to compete. It is preferable to use a lowered tone when faced with yelling as the individual is more likely to respond in kind by lowering their own voice. Don’t be afraid to employ silence: no-one likes silence and a reticent patient is far more likely to communicate if there are gaps of silence for them to fill.

Psychological • Give limited choices. While you may not be able to give the individual a choice regarding hospital attendance, giving limited choices regarding other matters allows the patient to maintain some sense of autonomy and control. Feeling powerless is viewed as a significant

trigger for anger. • Encourage the patient to gain control over their behaviour. For example, it may help to identify that the patient appears agitated and is pacing and speaking rapidly and clenching their fists. Drawing awareness to these signs of anger and encouraging the patient to regain control may be most helpful for individuals who do not have a history of aggression or see it as unhelpful. • Try to identify and understand the reasons for the patient’s anger. Understanding the triggers allows you to remove or problem solve them, which may de-escalate the episode. • Use distraction and redirection where appropriate. • Suggest more appropriate behaviour. Some individuals may rely on aggressive responses as they lack an awareness or history of using alternative means of communication. The increase in arousal associated with aggression may also make it difficult for some to identify a more appropriate response at this point in time. Suggesting a more appropriate course of action may assist in these circumstances. • Allow the person an ‘out’ so they can back down without losing face. This technique is particularly important for adolescents who may be less willing to back down from a perceived threat. By avoiding ultimatums and instead offering choices, you can avoid perceiving the lack of options as a challenge to their autonomy. • Be prepared to portray a frail persona and you will not appear to be a threat. For example, ‘Could you please sit down and stop pacing: you’re making me feel very uncomfortable’ makes you the subject of the conversation and takes the pressure off the patient.

Physical • Be aware of your physical presence. Make the patient aware of when you are moving and where you are going and don’t walk behind them, as it may be perceived as threatening. Allow an arm’s length or more space between you where possible and if you need to touch the patient in order to perform any examinations, warn them and look for acknowledgement before continuing. If possible and safe to do so, sit down: it lowers the tension and reduces your power differential. • Remove your sunglasses and ensure that you are not standing with your back to a bright light. This enables the patient to respond appropriately to your face and eye movements. • Remove dangerous objects from your person. Minimise jewellery, ties or scarves around your neck and tuck long hair into the back of your shirt if possible. • Be aware of dangerous objects or projectiles in the environment. • Be aware of the exits. Position yourself near an exit but not in between the patient and the exit as you will become an obstacle to their escape. Stand at 45° to the patient to deflect their blows if the worst-case scenario occurs. • Encourage the patient to sit by sitting yourself but do not force them to do so. Standing over the patient may increase their feeling of vulnerability and therefore lead to increased aggression. Sitting sideways on the chair allows you to look relaxed yet be capable of rapid escape.

References Anderson, C. A., Bushman, B. J. Human aggression. Annual Review of Psychology. 2002; 53:27–51. Boyle, M., Koritsas, S., Coles, J., Stanley, J. A pilot study of workplace violence towards paramedics. Journal of Emergency Medicine. 2007; 24:760–763. Bushman, B. J., Anderson, C. A. Is it time to pull the plug on the hostile versus instrumental aggression dichotomy? Psychological Review. 2001; 108(1):273–279. Cowin, L., Davies, R., Estall, G., Berlin, T., Fitzgerald, M., Hoot, S. De-escalating aggression and violence in the mental health setting. International Journal of Mental Health Nursing. 2003; 12:64–73. Distasio, C. A. Violence in health care: institutional strategies to cope with the phenomenon. The Health Care Supervisor. 1994; 12(4):1–27. Krahé, B. The Social Psychology of Aggression, 2nd ed. New York: Psychology Press, 2013.

SECTION 17

THE PARAMEDIC APPROACH TO OBSTETRIC AND NEONATAL EMERGENCIES O U TL I N E INTRODUCTION TO THE PARAMEDIC APPROACH TO OBSTETRIC AND NEONATAL EMERGENCIES CHAPTER 53: Imminent birth CHAPTER 54: Neonatal resuscitation

INTRODUCTION TO THE PARAMEDIC APPROACH TO OBSTETRIC AND NEONATAL EMERGENCIES IN THIS SECTION Chapter 53 Imminent birth Chapter 54 Neonatal resuscitation

AT THE COMPLETION OF THIS SECTION YOU SHOULD BE ABLE TO • Describe the physiological changes associated with pregnancy. • Describe the physiology of labour. • Describe the stages of labour and assessment of the woman in labour. • Explain the management of a breach presentation and a breech delivery. • Describe the causes, significance and management of shoulder dystocia. • Describe the pre-hospital management of prolapsed cord. • Explain the causes and management of postpartum haemorrhage. • Explain the physiological changes occurring in the infant at the time of birth. • Describe the initial assessment of the newborn infant. • Describe and explain the rationale underlying neonatal resuscitation procedures. • Describe the specific clinical issues and management concerns associated with the care of a premature infant. • Discuss how to maintain an optimum environment for care of the newborn within a pre-hospital setting. Birth is a normal event and only rarely should it be considered as a medical emergency: for the most part mother and infant do well without the clinician having to face complex clinical decisions. Relatively few babies are born before the mother arrives at hospital, although paramedics may occasionally be required to assist in a normal delivery and very rarely they may be required to attend a complex birth or to assist in the resuscitation of a neonate who has been delivered without adequate ventilation or perfusion. Birth and neonatal resuscitation are examples of situations that are relatively rare in paramedic experience and require a clear systematic approach. If the delivery is normal and resuscitation of the infant is unnecessary (as in the vast majority of cases), there are essentially no elements of clinical reasoning to apply and an algorithmic approach to management is both safe and sufficient. The paramedic role is to provide clinical and caring support. Even when complications arise with either the mother or the infant, emergency management tends to follow predictable pathways involving well-specified algorithms and the need for clinical reasoning and problem solving beyond that associated with resuscitation principles is limited. However, this is also a time when the emotional aspect of the scene places further pressure on the paramedic facing an unfamiliar task. As such, a prescriptive and directive approach to managing birth and neonatal resuscitation makes sense. Unlike previous chapters, which explore the ‘what else could it be?’ approach to assessment and decision making, the chapters in this section focus on clear and detailed procedural instructions. The information is intended to give paramedics a systematic approach that minimises clinical challenges and maximises the transfer of clinical responsibility for definitive care. One of the most useful pieces of advice in this setting is to

share the problem with those who work with obstetrics and neonatal resuscitation. Paramedics are part of a larger multidisciplinary team and as team players are not expected to manage all situations alone when expertise and advice is available.

CHAP TER 53

Imminent birth By Gayle McLelland

C O N C E P TS U S E D I N TH I S C H A P TE R • The paramedic’s clinical approach: Section 2 • Perfusion: Chapter 55 • The autonomic response: Chapter 56

O V E RV IE W • There is a little research regarding paramedic encounters with labour and birth and most of the published literature is old (McLelland et al., 2011). • In Australia in 2009, 0.6% of all births were unplanned births before arrival (BBAs) at hospital, for which paramedics could potentially have been the initial primary health provider (Li et al., 2011). • While the number of BBAs remains low, since 1991 it has almost doubled in some areas (McLelland, McKenna & Archer, 2012). • Most of the births encountered by paramedics are normal vertex presentations and require minimal intervention (Moscovitz et al., 2000; Verdile et al., 1995). • Although rare, paramedics may encounter potentially life-threatening obstetric emergencies including breech birth, shoulder dystocia and cord prolapse (Verdile et al., 1995). • The most frequent maternal complication at an unplanned birth is postpartum haemorrhage (Bhoopalam & Watkinson, 1991; Di Benedetto et al., 1996; Haloob & Thein, 1992; Loughney et al., 2006; Verdile et al., 1995). • Admissions to special care units are 2 (Beeram et al., 1995) to 6.25 (Rodie, Thomson & Norman, 2002) times greater for BBAs than for in-hospital births.

Introduction Parturition, or labour, is the process that enables expulsion of the fetus, placenta and membranes through the birth canal. Normal labour is the spontaneous onset of contractions that occurs between 37 and 42 weeks’ gestation and is completed within 18 hours with the presentation of the baby by the vertex. Labour, and the eventual birth of a baby, is a harmonious balance between correct anatomy, precise physiology and the mechanics of the baby travelling through the pelvis. Often referred to as the ‘5Ps’— passage, passenger, powers, psychology and problems (White, Duncan & Baumle, 2011)—a successful birth requires the right combination of all of these factors.

Physiology Although labour is physiologically a continuous process, for educational and clinical purposes it is divided into three stages (Pairman et al., 2010; Stables & Rankin, 2010). The first stage involves the onset of painful contractions causing dilation of the cervix; the second stage starts after the cervix has fully opened and lasts until the birth of the baby; and the third stage involves delivery of the placenta (Pairman et al., 2010; Stables & Rankin, 2010; see Tables 53.1 and 53.2). The factors that initiate labour are not fully understood but it is widely accepted that it commences due to a combination of fetal, placental and maternal factors (Coad & Dunstall, 2011; Fraser & Cooper, 2003; Stables & Rankin, 2010). TABLE 53.1 The three stages of labour

Source: Coad & Dunstall (2011); Fraser & Cooper (2003); Pairman et al. (2010); and Stables & Rankin (2010).

TABLE 53.2 Length of stage of labour

Source: National Institute for Health and Care Excellence (2007).

The female pelvis or passageway The human pelvis consists of four bones. The posterior wall comprises the sacrum and the coccyx bone; and the lateral and anterior walls consist of three fused bones: the ilium, the ischium and the pubis. These bones join to form a border around an empty space, which in females allows the passage of the baby through the pelvis (Pairman et al., 2010; Stables & Rankin, 2010). This passage can be divided into three zones: the pelvic brim, the pelvic cavity and the pelvic outlet. The pelvic brim separates the upper flare of the iliac fossa, or false pelvis, from the lower basin-shaped true pelvis. The pelvic cavity is the area of the pelvis between the pelvic brim and the outlet. It is bordered anteriorly by the symphysis pubis and pubic bones; laterally by the interior of ilium and the body of the ischium; and posteriorly by the sacrum. The obstetric pelvic outlet is the lower portion of the pelvis and is bordered by the lower edges of the symphysis pubis anteriorly, the sacrum posteriorly and the ischial tuberosities laterally. The female pelvis is generally wider and shallower than the male pelvis and is categorised into one of four different shapes—gynaecoid, android, platypelloid and anthropoid, as illustrated in Figure 53.1 (Stables & Rankin, 2010). While the gynaecoid pelvis is thought to be ideal for childbirth, a woman may have any one of the four shapes or a combination of two or more shapes (Coad & Dunstall, 2011). The dimensions of each type of pelvis vary greatly, but the gynaecoid pelvis is the widest (see Table 53.3).

TABLE 53.3 Pelvic measurements of gynaecoid pelvis

Source: Stables & Rankin (2010).

FIGURE 53.1

The four types of female pelvis. Source: Pairman et al. (2014).

The fetal head or passenger Equally important in the passage of the baby through the pelvis is the size, shape and position of the baby’s head. Due to the large brain, the fetal head is comparatively large for the human pelvis but with the skull flexed on the neck the smallest diameter presents to the pelvis (Stables & Rankin, 2010). The passage is optimised further by the pliable nature of the baby’s skull. While the facial and base of skull regions are almost completely ossified by birth, the cranium bones are not completely joined. The five large bones (two frontal, two parietal and one occipital) and two smaller bones (two temporal) that form the cranium (or vault) are connected with membranous sutures with fontanels where two or more bones meet (Stables & Rankin, 2010). The sutures and fontanels facilitate small movements between the bones, which enable them to overlap: the change in the shape of the skull assists with the baby’s journey through the pelvis (Coad & Dunstall, 2011).

Labour First stage The release of prostaglandins and the hormone oestradiol allows the cervix to soften and stretch, or dilate. The support and protection it has provided during pregnancy is now altered and it becomes a gateway to, and eventually a part of, the birth canal. As the cervix changes, there are also changes in the muscle of the uterus, the myometrium. The tone of the myometrium changes to allow the coordinated contractions from the top, or fundus, increasing uterine pressure (Coad & Dunstall, 2011; Stables & Rankin, 2010). Once labour is initiated, a positive feedback loop known as Ferguson’s reflex commences and will not finish until the birth of the baby (see Fig 53.2). Ferguson’s reflex describes the increase in the production of oxytocins caused by the pressure of the presenting part of the baby on the cervix. This increase in oxytocins stimulates the myometrium to contract more strongly, longer and with more frequency, which in turn causes thinning and dilation of the cervix (see Fig 53.3).

FIGURE 53.2 ACTH = adrenocorticotrophic hormone; CRH = corticotrophin-releasing hormone; DHEA-S = dehydroepiandrosterone sulfate; PGs = prostaglandins. Positive feedback loop during labour. Source: McLean & Smith (2001).

FIGURE 53.3 Friedman’s curve, a typical graph depicting the progress of labour where cervical dilation is plotted against time. The curve is divided into latent and active phases, with the active phase further divided into acceleration, maximum slope and deceleration. Source: Pairman et al. (2010). The upper and lower segments of the uterus work together during contractions. With each contraction the myometrium constricts, causing the upper segment of the uterus to descend as the baby moves through the birth canal, further strengthening Ferguson’s reflex. During the first stage contractions occur somewhat irregularly up to 20 minutes apart, becoming more frequent until they are 3 minutes apart. The duration of contractions is typically brief at the start (10–15 seconds) but will increase up to 1 minute by the end of this stage (Coad & Dunstall, 2011; Stables & Rankin, 2010). As the labour progresses the lower segment of the uterus stretches and the cervix continues to thin or efface until there is full dilation. During the stretching of the lower segment, a membrane (the chorion) separating the baby from the mother detaches from the surface of the uterus and traps a small sack of amniotic fluid between the baby’s head and the cervix. This is called the forewaters. The hindwaters is the remainder of the fluid behind the baby. As the cervix dilates, the pressure in the forewaters increases until they burst into the birth canal. While the membranes can rupture at any time during or even before labour, the physiological moment is when the cervix is fully dilated and entering the second stage. Towards the end of the first stage, as the cervix dilates quickly, the woman

may have a bloody mucosal vaginal loss or a ‘show’. During pregnancy the cervix forms a mucus plug called the operculum, which assists in protecting the uterus from ascending infection (Stables & Rankin, 2010). Expulsion of the operculum at the end of pregnancy is known as a ‘show’ and often signifies changes to the cervix. The mucus plug or ‘show’ often continues to be expelled during labour as the cervix is dilating. Unfortunately, a ‘show’ is not a reliable indicator of time to birth, as a woman can have a ‘show’ at any stage during or prior to labour. Although the woman’s body is preparing for labour in the final weeks of pregnancy and she may experience some discomfort, the actual definition of labour is the onset of painful regular contractions until full dilation of the cervix. The process of effacement is illustrated in Figure 53.4 and the cervix usually effaces and dilates faster in women who have previously had a baby.

FIGURE 53.4 Cervical dilation for primagravida and multigravida. Source: Pairman et al. (2014). The first stage of labour can be divided into three phases: latent (early), active and transitional. The latent phase is the period from the commencement of cervical effacement (thinning) and dilation until it is 3 cm dilated. The contractions commence irregularly at 15–20 minutes apart and may last up to 30 seconds but they become more coordinated and closer together. Once the cervix is more than 3 cm dilated, the active phase starts and continues until the cervix is 8–9 cm dilated. Dilation is much more rapid in the active phase, with the cervix dilating at an average of 1.5 cm per hour (Stables & Rankin, 2010). In addition, the contractions become more regular: three occurring in 10 minutes and lasting up to 60 seconds. When the cervix is 8–9 cm dilated, the woman enters the transitional phase. During this period the rate of dilation often slows and there may be a brief lull in uterine activity (Fraser & Cooper, 2003). During transition the woman often experiences restlessness and may become distressed, demanding pain relief.

Second stage The second stage of labour is much shorter than the first; it begins at full dilation of the cervix and lasts until the birth of the baby. It can last up to 2 hours in a primigravida and 1 hour in a multigravida but can be as short as 5 minutes (Stables & Rankin, 2010). Since the length of this stage varies between women the best practice is to allow each woman to follow her own urges. The woman may have short 5–6-second pushes during one contraction or she may have the desire to bear down for longer (Coad & Dunstall, 2011; Stables & Rankin, 2010). Forcing her to push without the desire or stopping her from pushing when she needs to may cause hypoxia to the baby or exhaustion in the mother (Coad & Dunstall, 2011; Stables & Rankin, 2010). At the commencement of the second stage the contractions become less intense as the mother experiences a quiet period or lull as the baby’s head descends into the vagina. This can last between 10 and 30 minutes. During this important period there is no need to force the mother to push until she has the desire to do so herself (Stables & Rankin, 2010). As the baby descends further and the head becomes visible, the second stage progresses to an active period when the woman has an increasing urge to push or possibly defecate (Stables & Rankin, 2010). With each contraction the woman will bear down and the baby moves forwards and rotates in accordance with the pelvic floor. When the contractions subside it is possible that the baby may retreat back up the vagina until the next contraction (Coad & Dunstall, 2011). As the baby descends further, the perineum starts to stretch to allow passage of the baby’s head (refer to the mechanism of labour below). When the widest part of the baby’s head stretches the vulva to its maximum, the head often remains stationary or is said to be crowning. At this point the severity of the pain can cause the woman instinctively to stop pushing as she takes a quick breath or pants. This natural reflex prevents rapid delivery of the head, which could cause trauma to the perineum (Coad & Dunstall, 2011). The baby is born facing the maternal anus but will rotate as its head realigns with the rest of the body in the pelvis (restitution). After restitution the baby continues to turn a

complete 90° until its head is perpendicular with the maternal midline as the anterior shoulder rotates in the pelvis. Rotation of the anterior shoulder continues as it follows the curve of the pelvis until it exits the vaginal introitus and the posterior shoulder immediately follows. With the birth of the comparatively large head and shoulders, the baby’s body is instantly born with a gush of the amniotic fluid of the hindwaters (Coad & Dunstall, 2011). For more detail on the passage of the fetus during this phase, see the mechanism of labour below.

P RACT ICE T IP For the paramedic who may occasionally be involved with obstetrics, the key point in the physiology of normal delivery is that it all occurs automatically without any need for intervention.

Mechanism of labour The journey of the baby into and through the pelvis is often referred to as the mechanism of labour. The successful completion of the mechanism of labour relies on two independent factors: the shape and the size of the presenting part of the fetus (Pairman et al., 2010; Stables & Rankin, 2010). Regardless of the orientation of the fetus in the uterus prior to delivery, there are three common principles to the mechanism: (1) the fetus will descend; (2) the leading part of the fetus will meet resistance against the pelvis floor and then rotate forwards; and (3) the last emerging part of the fetus will rotate around the pubic bone. Normal labour requires that the baby is in a longitudinal lie and that the attitude is one of good flexion so that the occiput is the presenting part, as detailed in Figure 53.5.

FIGURE 53.5

Mechanism of labour. Source: Pairman et al. (2014).

The stages of delivery are outlined below and in Figure 53.6.

FIGURE 53.6

The stages of delivery.

Descent Often the descent of the fetal head into the inlet of the pelvis occurs in the final weeks of pregnancy, especially for a primigravida. It is possible that the head will not descend until after the commencement of labour for a multigravida. As labour progresses the fetal head descends into the pelvis in transverse diameter but ease of entering the pelvis is largely reliant on the attitude or flexion of the fetal head (Pairman et al., 2010; Stables & Rankin, 2010). Flexion The force of the contractions on the fetal spine forces flexion of the fetal head as it enters the pelvis. This facilitates the presentation of the least possible diameter of the fetal head (Pairman et al., 2010; Stables & Rankin, 2010). Internal rotation Due to the force of the contractions and the shape of the pelvis, including the ischial spines, once the fetal head has completely entered it rotates so that it lines up with the anteroposterior diameter of the pelvic outlet. The occiput has now moved forwards and is lying under the symphysis pubis. The position of the neck is slightly changed so that the head is no longer aligned with the shoulders (Pairman et al., 2010; Stables & Rankin, 2010). Extension of the head As the head moves under the pelvic arch it swivels on the pubic bone and pushes through the vagina, causing it to extend upwards. The forehead, face and chin then pass across the perineum (Pairman et al., 2010; Stables & Rankin, 2010), as illustrated in Figure 53.7.

FIGURE 53.7 The head rotating and descending in the second stage. Source: Marshall & Raynor (2014).

Restitution

With the birth of the head, the shoulders enter the pelvis. The head appears to turn slightly externally as it realigns itself with the shoulders. External rotation (shoulders) As the shoulders continue to enter the pelvis, they align themselves with the anteroposterior diameter. The anterior shoulder hits the pelvic floor and moves under the symphysis pubis. This causes the head to continue to rotate so that the baby faces either the woman’s left thigh or her right thigh. After the birth of the anterior shoulder, the posterior follows as it passes the perineum.

Third stage The birth of the baby marks the commencement of the third stage. The contractions change and the rate slows (Pairman et al., 2010; Stables & Rankin, 2010). This stage can last between 5 and 60 minutes and is a vulnerable time for the mother as she has an increased risk of haemorrhage during this period (Coad & Dunstall, 2011). After the birth of the baby the uterus contracts down upon itself; this reduction in size reduces the surface area of the placental site. The veins become more congested and rupture, causing the firm placenta to buckle and detach from the more flexible myometrium. The continuing contraction of the uterus causes the oblique muscle fibres to constrict around the blood vessels supplying the placenta, preventing drainage of blood back into the maternal system (see Fig 53.8). The increasingly congested placenta usually detaches from a central point and its escalating weight forces the separation of the edges followed by the membranes (Coad & Dunstall, 2011; Pairman et al., 2010; Stables & Rankin, 2010). Thus with the continuous contraction of the uterus and the weight of the placenta, the membranes are stripped from the uterine wall. Signs that the placenta is about to deliver are a small gush of blood (separation) and the appearance of the cord lengthening (descent).

FIGURE 53.8 The third stage of labour commences after delivery, A. The uterus contracts and the placenta separates, B, and eventually passes down the birth canal, C. Source: Marshall & Raynor (2014). With the separation of the placenta, there is an increased risk of bleeding as blood continues to flow to the placental site. Three mechanisms assist with the control of blood loss at this stage: (1) the ‘living ligatures’ or muscle fibres constrict around the blood vessels that previously connected the uterus to the placenta; (2) vigorous contraction of the upper segment of the uterus effectively applies pressure to the placental site; and (3) temporary changes in the clotting factors allow a fibrin mesh to form over the damaged veins and then quickly form over the placental site (Stables & Rankin, 2010). Management of the third stage can be either physiological (allowing the process to occur naturally) or active (administering medications and therapy). It has generally been thought that active management helps prevent postpartum haemorrhage (Fraser & Cooper, 2003; Stables & Rankin, 2010) but recent research has questioned this belief (Pairman et al., 2010). At present, physiological management is recommended only for lowrisk births but this presents a challenge in the prehospital setting as—purely by definition— prehospital births are considered high risk in that they always occur in an unplanned setting, without the expected continuity of care, and often are precipitated births. However, most births that occur in the prehospital setting are in fact normal vertex presentations and require little or no intervention (Moscovitz et al., 2000; Verdile et al., 1995). As such, paramedics should be confident that physiological management should be adequate in most cases. In fact, in practical terms there are no in-field options for management of the third stage except allowing the placenta to separate and deliver naturally. The gush of blood that accompanies this may seem dramatic but if palpation reveals a firm uterus (a little bigger than a cricket ball), paramedics can be reassured that there should be no further bleeding from the placental bed.

Maternal physiological adaptation during labour Cardiov ascular system

A progressive rise in cardiac output with each contraction adds 300–500 mL of blood to the circulating volume and increases the woman’s heart rate (Coad & Dunstall, 2011; Pairman et al., 2010; Stables & Rankin, 2010). There are also increases in diastolic and systolic blood pressure: increasing 5 seconds before a contraction and returning to baseline after the contraction. In the first stage, there may be a rise of 35 mmHg systolic and 25 mmHg diastolic; and in the second stage the diastolic can rise up to 55 mmHg and the systolic can rise higher than in the first stage (Coad & Dunstall, 2011; Pairman et al., 2010; Stables & Rankin, 2010). With the delivery of third-stage dramatic haematological changes occur and parameters return to pre-labour levels (Coad & Dunstall, 2011; Pairman et al., 2010; Stables & Rankin, 2010). Supine hypotension remains a risk during labour, with the pregnant uterus pressing on the inferior vena cava and causing a reduction in cardiac return (Coad & Dunstall, 2011; Pairman et al., 2010; Stables & Rankin, 2010; see Fig 53.9). As a guiding principle, paramedics should avoid allowing a pregnant woman to lie supine. In transit this means using either the left lateral position or a wedge under the right hip to tilt the pregnant uterus away from the vena cava. Unfortunately, most ambulances have a stretcher mounted on the right side of the vehicle so the paramedics have to turn the patient away from them, making observations that much harder. Loading the woman feet first is a possible solution but it removes the paramedic’s ability to sit at her head and manage her airway or to secure her using the appropriate safety restraints.

FIGURE 53.9 Supine hypotension. The weight of the gravid uterus can compress the inferior vena cava when the patient is supine, A. This can be

managed by tilting the patient at least 30° to the left, B, or manually displacing the uterus to the left, C. Source: Pairman et al. (2014).

Haematological system To keep blood loss during delivery to a minimum, changes occur in the haematological system, including a state of increased coagulation (this precedes and follows delivery by several weeks) and physiological anaemia as a result of the increase in blood volume (increased plasma volume) but not in the amount of red bloods cells. During labour, however, haemoconcentration can occur as a result of dehydration from exertion. Stress and muscular activity can also precipitate an increase in the formation of red blood cells (erythropoiesis). During labour and immediately postpartum, there is an increase in neutrophils and the white cell count may increase up to 25–30 × 109/L (Coad & Dunstall, 2011; Pairman et al., 2010; Stables & Rankin, 2010).

Respiratory system In active labour, hyperventilation from pain or anxiety can lead to a temporary respiratory alkalosis with the typical signs of hyperventilation (peripheral paraesthesia). A respiratory acidosis can occur if contractions are too close together (unlikely in spontaneous-onset labour) or if the woman holds her breath too long when pushing during the second stage (Coad & Dunstall, 2011; Stables & Rankin, 2010). Both conditions are generally selfresolving and do not require any intervention. However, both may indicate inadequate pain relief.

Renal system Increased aldosterone secretion stimulates an increase in sodium loss (and potassium retention). There is a chance of dehydration so fluid intake should be maintained, particularly in prolonged labour or in labour occurring in hot conditions (Coad & Dunstall, 2011; Stables & Rankin, 2010).

CA SE ST U DY 1 Case 10923, 1036 hrs. Dispatch details: A 37-year-old woman, 39 weeks’ gestation; membranes have ruptured; in labour. Initial presentation: On arrival at the scene the paramedics find the patient leaning over the couch in her lounge room. She is able to answer questions in

between contractions. Her neighbour is in attendance as they are unable to contact the patient’s husband, who has gone to a country town for work. He is out on site, so is unreachable at the moment. The woman’s 3-year-old daughter is also present.

ASSESS Patient history On questioning the patient tells the crew that her membranes ruptured an hour ago and the amniotic fluid was clear. She is having contractions every 6–8 minutes but at this stage can breathe through them. She does not report an urge to push. This is her fifth pregnancy: three of her children are at school and one is with her. In order to prepare a treatment plan the crew need to know: • the history of this labour • the history of this pregnancy • the history of previous pregnancies and births • a general medical history. This labour • When did the contractions start? How often are they coming? It is possible in this situation that a woman may be so distressed that she may state she is feeling contractions long after they finish, so the paramedics should try to feel the contractions if they can (see Fig 53.10).

FIGURE 53.10 Feeling for a contraction. Source: Pairman et al. (2014). • Have the membranes ruptured? The membranes can rupture at any point before or during labour, even when the head is crowning. If the membranes are still intact when the head delivers, they need to be ruptured manually by tearing them. The membranes must not be ruptured manually if they cannot be visualised. Once the membranes have ruptured, the amniotic fluid should be clear to slightly pink in colour. Any other colour is significant: green to brown could indicate a distressed baby and any shade of red could indicate bleeding. • Is there any other vaginal discharge? Mucus mixed with a small amount of blood, or a ‘show’, indicates normal detachment of the membranes as the cervix is dilated. If the mucus becomes more heavily blood-stained, it may indicate that the cervix is nearing full dilation. Any amount of frank bleeding should be considered abnormal. • When did the mother feel the baby move last? Paramedics have no ability to monitor the baby’s wellbeing or health and asking about movements provides only an indication about the baby’s health. Babies do not continually move in utero and often have ‘sleep periods’ where they are very quiet, so a lack of movement does not necessarily indicate a problem. If the mother has had a trouble-free pregnancy and is at term, and the labour is spontaneous and trouble-free, there is no reason to think there is a problem.

• Are there any signs of the second stage or imminent delivery? For example, uncontrollable urge to push, anal pouting, perineal bulging or presenting part on view. • When did the mother last void? It is important to ask when the woman last urinated to assess fluid status, as dehydration can slow the progress of labour and a full bladder can become an obstruction during the second stage of labour (Pairman et al., 2010). This pregnancy • What is the mother’s gravida and parity? Generally, if a woman is a nullipara, the labour will take longer than if she is a multigravida (Pairman et al., 2010). However, there are exceptions to any rule so paramedics should always assess the woman’s physical and clinical signs. • What is the gestation in weeks? Rather than asking the baby’s due date, it is better to ask the gestation in weeks. Determining the gestation of the baby allows the paramedics to assess the risk associated with a premature infant (see Ch 54). • Have there been any obstetric complications during the pregnancy? Complications such as pre-eclampsia, gestational diabetes or antepartum haemorrhage can assist in gauging the risk of associated intrapartum or postpartum complications (Coad & Dunstall, 2011; Fraser & Cooper, 2003; Pairman et al., 2010; Stables & Rankin, 2010). Previous pregnancies and births • Has the mother had any previous pregnancies and births? Were there any complications? Women who have pregnancy and birth complications may be at greater risk of similar complications with subsequent pregnancies. Paramedics should assess the potential risk for this birth by obtaining a thorough history of previous births and pregnancies, such as shoulder dystocia, breech presentation and postpartum haemorrhage. Past or present medical history • Does the woman have any chronic medical conditions? For example, asthma, cardiac conditions. • Is there any acute exacerbation of chronic medical conditions? • Has the patient had any recent acute medical conditions? For example, upper respiratory tract infection, urinary tract infection. • Does the patient have any allergies?

Initial assessment summary

Problem Labour Conscious GCS = 15 state Position Standing Heart rate 92 BPM Blood 125/70 mmHg pressure Skin Pink, warm, dry appearance Speech Normal between contractions pattern Respiratory 18 BPM, becomes more erratic during contractions rate Respiratory Even cycles rhythm Chest Good breath sounds bilaterally auscultation Pulse 99% oximetry Temperature 37.4°C Pain Little to no pain between contractions; 8/10 during contractions History Gravida 5, para 4. Her membranes ruptured an hour ago and the amniotic fluid is clear. She is having contractions every 6-8 minutes but at this stage is able to breathe through them. She does not report an urge to push. Her last labour was over in less than 4 hours. Physical No signs of the second stage of labour. assessment D: There are no immediate dangers. A: The airway is not compromised. B: Breathing is normal. C: The patient is well perfused and there is no obvious haemorrhage. The patient is a multigravida presenting in the first stage of labour of a near full-term uncomplicated pregnancy. Previous vaginal deliveries were uneventful and she has no complicating medical conditions. There does not appear to be any sign of fetal distress.

CONFIRM The challenge facing the crew is this situation is to decide whether there is time to transport the patient to hospital for the birth or whether the birth is imminent and they should prepare to deliver the baby prior to transport. Such are the uncertainties with the progression of labour that this judgement has to

be made on a case-by-case basis considering the resources available, the distance to hospital and the patient’s presentation. Although it is possible to deliver a baby in the ambulance it is not well-suited to the procedure and should be avoided if possible.

DIF F ERENT IA L DIA GNOSIS First stage of labour Or • Second stage of labour and imminent delivery likely

The following criteria should be assessed prior to making a decision about transport: • contractions • vaginal discharge • signs of imminent delivery • wellbeing of the baby • signs of the second stage of labour and an imminent delivery.

Contractions Definitive diagnosis of labour can be made only by performing a vaginal examination to assess cervical effacement and dilation. This skill is not commonly within the scope of practice for paramedics, so they need to rely on clinical assessment of contractions (see Box 53.1). The onset of early labour is often signified by the commencement of irregular contractions occurring 15–20 minutely that may last up to 30 seconds. During this period paramedics may discuss options with the patient and her family regarding staying home longer or travelling independently to hospital versus being transported in an ambulance. They can explain that labour is not fully established and she has time to organise herself further. B O X 5 3 . 1C o

ntrac tio ns

Contractions are often described as intermittent waves of pain reaching a crescendo and then tapering, with a period of little or no pain in between. The frequency of contractions is measured from the beginning of one contraction until the beginning of the next and is described in one of two ways: (1) by how often they come (i.e. 3 minutely, 5 minutely, 10 minutely); and (2) by how often they occur in a 10-minute period (i.e. 3 in 10 minutes, 2 in 10 minutes or 1 in 10 minutes). The length of a contraction is measured from the beginning of that contraction until the end (i.e. 20 seconds, 30 seconds, 45

seconds and 60 seconds). In normal labour contractions rarely last longer than a minute or the baby would be compromised (Stables & Rankin, 2010). With the mother ’s permission to feel for a contraction, the paramedic should place one hand on the uterine fundus. The abdomen will become increasingly more tense for a period of time, usually no longer than 60 seconds, and then it will relax for a period of time before becoming tense again.

Each labour will have unique characteristics depending on several factors, including the number of previous babies the woman has had, the position and presentation of this baby, the gestation in weeks and whether there are other obstetric or medical complications. Labour is a dynamic process during which the contractions increase in strength, duration and frequency. A patient may describe the frequency of contractions by how many minutes apart they are but it is important that the paramedic is also aware of the length. Assessing the contractions accurately will assist in determining the appropriate form of pain relief. As the labour progresses, the contractions may come three times in 10 minutes and last up to 60 seconds. This often signifies that the woman is in active labour. Even so, the birth could still be several hours away. If the patient is very distressed and demanding, it is likely that she has entered the transitional phase but that does not always rule out the opportunity to transport. In this case the patient’s calm presentation, the timing of the contractions and the lack of an urge to push during the contractions suggest that birth is not imminent.

Vaginal discharge Assessing the vaginal discharge during labour will assist paramedics to gauge the wellbeing of both the mother and the baby as well as assisting in decision making. Vaginal discharge can include the expelled mucus plug as the cervix dilates, amniotic fluid and any vaginal bleeding. In this case, the discharge appears normal and does not indicate any urgency.

Signs of imminent delivery As the second stage can take up to an hour to complete, there is often enough time to transport the patient to hospital but paramedics should consider the circumstances in which they have been requested. Most mothers have a plan for the birth and requesting an ambulance may suggest that events are occurring faster than anticipated, which could indicate a rapid progression of labour. An uncontrollable urge to push or bear down, uncontrollable grunting and an urge to defecate should all be considered as imminent signs of birth. As the baby descends through the pelvis, this will progress to anal pouting or puckering, perineal bulging and the presenting part becoming visible. It is worth noting that the rate of progression can slow or even halt and concurrent preparation for transport is always advisable. More often than not, the births

that paramedics attend progress quickly and may require the paramedics to support the mother through the birth. In this case there are no signs of imminent delivery.

T he baby’s wellbeing One of the key assessments of fetal wellbeing is to monitor the fetal heart rate (FHR) through labour and especially in relation to the contractions. Paramedics do not commonly have the equipment to monitor the FHR, however, so assessing fetal wellbeing is difficult in this setting. Enquiring about the last fetal movements provides a small amount of information about the baby’s wellbeing, but babies do not continually move in utero so a lack of movement does not necessarily indicate a problem. This patient says she felt her baby kick 15 minutes before she called for the ambulance. As her membranes have ruptured and the fluid appears clear, there is no suggestion that the baby is distressed.

Signs of the second stage of labour and an imminent delivery While this patient’s heart rate may be higher than that of a non-pregnant woman of her age, it is not unexpected in pregnancy and especially during labour. Her respiratory rate is within normal limits but respiratory hyperventilation is common in the first stage of labour. The patient is having two strong contractions every 10 minutes and they are lasting for 50 seconds. She is panting through the contractions and is relatively pain-free between them.

P RACT ICE T IP Most patients have a pre-arranged obstetric plan, including their hospital of choice. If the patient progresses rapidly, delivery at an alternative hospital with midwifery facilities is better than delivery in the back of an ambulance.

The crew make the sound decision that the patient is in the active phase of the first stage of labour and can be transported the estimated 20 minutes to hospital.

T REAT Emergency management Safety While the patient is in her own home, she should be allowed to remain in a position of comfort until the initial assessments and evaluations have been

completed. For safety reasons, she should be transported in either a semirecumbent or a lateral position to avoid supine hypotensive syndrome. If her membranes ruptured on the floor, check that there are no slip hazards. Last micturition As the baby descends into the pelvis, the bladder is vulnerable to traumatic damage (Fraser & Cooper, 2003). In addition, a full bladder can delay the progress of the baby’s head as it descends during the second stage (Stables & Rankin, 2010). Prior to transport, the paramedics should encourage the woman to pass urine, as there will be little chance until they arrive at the hospital. Vaginal discharge A maternity pad placed at the labia will enable the crew and the receiving hospital to accurately describe and measure vaginal loss. Analgesia Regular contractions can be very painful. The possibility of not giving birth in the intended place, with the expected carers, can be extremely stressful and exacerbate the patient’s discomfort (Pairman et al., 2010). If the patient requires analgesia, the use of numerical scores as an assessment tool for pain is not recommended for a woman in labour (National Institute for Health and Care Excellence, 2007). The intermittent nature of contraction pain makes it difficult to manage and fast-acting inhaled analgesics are better suited than long-lasting IV agents such as opioids, which can have a sedative effect between contractions. Opiates also cross the placental barrier and so their use in late labour risks producing respiratory depression in a newborn infant and even drowsiness for several days after birth, which can affect the baby’s breastfeeding (National Institute for Health and Care Excellence, 2007). When paramedics have no option but to administer an opioid analgesic, it is important that they assess the mother completely to ensure that they are satisfied she is not near the second stage. Philosophically, the management of pain for a woman in labour is very different from many of the other cases paramedics manage. The woman in labour should be treated as a ‘normal’ or ‘well’ event not an ‘emergency’ or ‘ill’ event. Certainly as the prehospital context is unplanned and the usual in-hospital or home birth resources are unavailable, there is some risk. But most unplanned births are uncomplicated and occur without undue incident. While paramedics cannot provide the continuity of care that has been shown to be a key element of successful progress in labour, they can provide a calm and reassuring environment for the mother. Building rapport and trust with the mother will reassure her that she is safe and is essential for delivering safe but adequate pain relief. Oxygen Physiological anaemia is commonly experienced in late pregnancy, but labour is a normal process so oxygen is not required in this situation. Although oxygen may be administered during obstetric emergencies, it is important to note that there is no recent quality evidence to support the effectiveness or not of this practice (Pairman et al., 2010). Although the flow of oxygen to the placenta is reduced in normal labour, the normal-term fetus adapts well by redistributing

the flow of blood to protect vital organs such as the heart and brain, so overall the fetal circulation is unaffected by the pressure of the contractions (Steer & Flint, 1999). Preparation for an emergency birth Although many of the women in labour attended to and transported by paramedics do not actually give birth prior to arrival at hospital, it is wise for the crew to prepare for emergency birth. This includes arranging to rendezvous with another crew en route, as it can take more than two crew members to manage both the mother and the infant if problems arise. The majority of babies are born without incident, but crews should also routinely prepare the scene for neonatal resuscitation (see Ch 54). 1116 hrs: After travelling for 12 minutes, the patient becomes very distressed and commences a guttural groaning. She tells the paramedics that she needs to push. Upon visual inspection, the paramedics notice anal pouting and perineal bulging. The decision to pull over for delivery is difficult. However, the paramedics have to set up not only for delivery but also for potential resuscitation of the newborn in a very tight environment. Comfort/analgesia Often a woman feels relief when she pushes according to her own natural urges during the second stage (Fraser & Cooper, 2003; Pairman et al., 2010; Stables & Rankin, 2010). As well as assessing the frequency, length and intensity of the contractions, the paramedics should assess how the woman pushes during the contractions. It can be normal for a woman to have several short 5second pushes in one contraction. The imminent signs of delivery Once the baby has descended, the bobbing of the presenting part on the perineum should be visible to the paramedics. If the rate of progression appears to halt or slow, the paramedics will need to consider recommencing transport, as this could be a sign that there may be an unexpected problem. They also need to ensure that the mother does not progress too rapidly and have an explosive birth. They can prevent this by coaching her on her breathing throughout the contractions. Provided the baby does not become stuck, the head should be delivered within a few minutes of it being visible between the labia. The paramedics want the baby’s head to be delivered, but not so rapidly that it causes damage to the baby and to the perineum, hence this is the phase where they will instruct the patient to pant in an effort to control the rate of delivery. Vaginal discharge The paramedics should continue to assess the colour and amount of vaginal discharge. Often, as the cervix dates fully, a more heavily blood-stained ‘show’ will be discharged. While this is normal, any frank bleeding should be considered abnormal (Fraser & Cooper, 2003; Pairman et al., 2010; Stables & Rankin, 2010). If the membranes have not already ruptured, they will usually rupture at the commencement of the second stage but this cannot be guaranteed (Fraser & Cooper, 2003).

Fetal wellbeing As the baby descends, fetal oxygenation is threatened due to cord or head compression, so the paramedics need to continue to monitor the amniotic fluid, looking for meconium staining. It is not unusual for fetal movements to be reduced or difficult to detect during the second stage. Position Usually during the second stage a woman should be able to assume any position where she feels the most comfortable. Squatting, kneeling on all fours or standing positions all produce a 28% increase in the outlet compared to supine or semi-recumbent positions. However, the back of the ambulance can be restrictive and may limit the amount of freedom the woman has, especially when moving. The birth process The paramedics should allow the mother to follow her instincts and push as she wants. There is no evidence to support the practice of instructing the mother to push (Valsalva manoeuvre) and it has been suggested that this could cause problems for both mother (Stables & Rankin, 2010) and baby (Pairman et al., 2010). Initially, with contractions the baby’s head will advance and recede: this slowly stretches the perineum to allow it to accommodate the baby’s head (see Fig 53.7). Once the baby’s head remains on the perineum and does not recede (crowning), the mother may complain of a burning sensation as the perineum stretches. During this time, the paramedics can encourage the mother to pant to minimise the possibility of perineal damage associated with a rapid birth. While the mother is pushing, she may defecate. This is quite normal. Placing a pad over the rectum will enable the paramedics to keep the area clean. Most babies will birth spontaneously with minimal or no hands-on assistance. However, rapid descent of the head has been associated with an increase in maternal perineal tears. Lightly placing fingers on the descending head can provide support in a rapid birth and prevent perineal tears (Pairman et al., 2010). However, it is important not to place too much pressure on the head so that its progress is hindered. Once the baby’s head is born, there is a rest period between contractions. Traditionally at this time the baby is checked to see whether the cord is wrapped around the neck and to identify whether it needs to be cut to relieve pressure. For the mother this is an awkward procedure and many women find it uncomfortable or even painful. Most babies birth through the cord, so cutting the cord at this stage needs careful consideration as it will remove the only source of oxygen the baby receives and could cause further distress (Pairman et al., 2010). Paramedics should avoid cutting the cord unless it is obstructing the descent of the baby through the pelvis. As the baby is born the paramedics should still be assessing the amniotic fluid for any change in colour. With the next contraction the baby’s shoulders enter the pelvis and rotate into the anterior-posterior diameter of the outlet position. This rotation of the shoulder is observed externally as the baby’s head restitutes to come into alignment with the shoulders. This is a natural movement and should not be forced. With the next contraction the woman may need to be encouraged to

give another push and the anterior shoulder should deliver. If it does not deliver spontaneously, the paramedic may need to apply some gentle upward traction if she is on all fours. Following the birth of the anterior shoulder, some gentle downward traction will deliver the posterior shoulder. Immediately the rest of the baby will follow. The time of birth should be noted. Care of the baby 1132 hrs: Immediate care of the baby commences (see Ch 54). One paramedic takes responsibility for the baby and the other cares for the mother. They assist the patient to roll over so that she can hold her baby. With the patient’s permission, the paramedics place the baby skin to skin on her abdomen and they wrap both mother and baby in a blanket to keep them warm. While paramedics should not force breastfeeding, it often occurs naturally with mother and baby in this position. This will stimulate the release of oxytocins, which aid in the completion of the third stage. Many ambulance services have operating instructions requiring all patients to be secured appropriately in a moving vehicle that would (taken literally) include a newborn baby. Paramedics have to balance the very real risk of hypothermia that is easily prevented with skin-to-skin contact (in the absence of a heated cot in the ambulance) with the risk of injury associated with an ambulance crash. The birth of the baby signals the end of second stage of labour and the commencement of the third stage. The third stage Contractions/pain The uterus continues to contract after the birth of the baby, but usually this does not cause any undue distress. Rarely, a woman may experience painful ‘after pains’ and require analgesia. Increasing pain could be a sign of trauma (uterine rupture for instance) and while reassuring the patient the paramedics should be re-evaluating for any signs of peritonism. Vaginal discharge The paramedics need to check for any vaginal discharge at the end of the second stage and the beginning of the third stage. While there is a slight possibility that signs of meconium as the baby is born could indicate that the baby was stressed, it is more likely to be a normal bowel action (see Ch 54). A gush of blood can be a sign of normal placental separation, but other causes should be considered. If there is continual bleeding, especially greater than 500 mL, the paramedics should manage this postpartum haemorrhage by controlling obvious sources of haemorrhage with direct pressure and instituting volume replacement as usual. Perineal damage The perineum should be assessed for tearing or trauma and managed if required. Applying a combined dressing or maternity pad has two benefits: (1) it provides pressure to arrest bleeding and (2) it aids assessment of any further bleeding. Position

For transport during the third stage the mother can assume a position of comfort. But the paramedics need to continually assess for signs of separation and descent, as they may need to stop the ambulance to deliver the placenta. The best position for delivery of the placenta is an upright position (Coad & Dunstall, 2011), which is not optimum in a moving vehicle. Last void The paramedics should document the last time the patient voided as a full bladder can delay completion of the third stage and contribute to postpartum haemorrhage (Coad & Dunstall, 2011; Pairman et al., 2010). This information will be useful to pass on to the midwifery staff. Management The third stage is a vulnerable period in the prehospital setting with an increased risk of postpartum haemorrhage (Coad & Dunstall, 2011; Stables & Rankin, 2010). Crews need to weigh the benefits of the physiological third stage against the possible need to manage complications. As the physiological third stage can take up to an hour, the paramedics should resume transport while continually assessing for signs of separation and descent. There is no need to pull the cord or manipulate the uterus at any time. Unless neonatal resuscitation is required or transferring the mother to the stretcher proves problematic, the cord should remain intact during transport to facilitate the physiological third stage (Fraser & Cooper, 2003; Pairman et al., 2010; Stables & Rankin, 2010). If the cord has been clamped or cut during the birth or before it stops pulsating, the physiology of the third stage is altered and active management is required (Pairman et al., 2010). In the prehospital setting physiological management of the third stage must be considered the most appropriate option but it depends on the circumstances. For a birth at term, leaving the cord intact until it ceases pulsation is sensible. Unfortunately, unplanned births before arrival (BBAs) at hospital have a greater risk of maternal and neonatal complications (McLelland et al., 2011) so it may not always be possible to physiologically manage the third stage. That said, true active management of the third stage can prove difficult in the prehospital setting. Use of prehospital pharmacology depends on the availability of the drugs and the ambulance service guidelines but may include intramuscular Syntocinon or oral Misoprostol. If the ambulance service guidelines recommend pharmacology only with postpartum haemorrhage, the paramedics should be alert to the increased risk of bleeding once the umbilical cord has been cut. With good reason, many prehospital guidelines (Woollard et al., 2008) advise against paramedics practising controlled cord traction, but this technique may be necessary if there is a postpartum haemorrhage (see case study 5 and Box 53.3). B O X 5 3 . 3C o

ntro lled c o rd trac tio n

In the prehospital setting controlled cord traction should be undertaken only if absolutely necessary for postpartum haemorrhage

and if oxytocic medication has been administered.

Unless the third stage is complicated by excessive bleeding, there is no rush to deliver the placenta in the prehospital setting and so active management is not often necessary. Sometimes the mother may have a desire to push again and will spontaneously deliver the placenta. Otherwise, it is wisest to allow the placenta to remain in situ and leave management of third stage to the maternity staff. If the placenta is delivered during transport, it should be placed in a plastic bag and taken to hospital. The paramedics can check that the placenta is complete but this will be done again in the maternity unit.

Hospital admission Ideally, the paramedics should transport the patient to the hospital that she has booked into as it will have a record of her obstetric history and medical history, including her blood group. A common exception to this is if the baby is premature and requires a special care nursery (SCN) or neonatal intensive care unit (NICU). Other possible exceptions include that the hospital is too far away. There are a variety of models of care available to pregnant women. The patient could be under the care of a midwife or a medical practitioner such as an obstetrician. Even if the baby was born outside the hospital, the primary carer will oversee the overall management. On admission to the hospital, management will depend on the patient’s condition. If the placenta has not been delivered, she will be admitted to the birthing suite; if it has been delivered, she will be admitted into postnatal care. Any perineal or vaginal lacerations will be repaired; and twice per day the involution of the uterus will be checked to ensure that it is descending as required and her vaginal loss (lochia) and any sutures will be checked for signs of infection. As much as possible mother and baby will remain together unless the baby needs to be admitted to SCN or NICU. A normal, healthy term baby will room in with the mother and she will be encouraged to breastfeed as soon as possible. The length of hospital stay varies from 2 to 5 days for a normal birth. Even if the baby is in SCN or NICU, most women will be discharged within this timeframe.

Investigations Any required investigations depend on the woman’s condition; often, for a normal birth no investigations are required. If the mother is a negative blood group, the baby’s blood group will be checked; if the baby is a positive blood group, the mother will receive anti-D within 72 hours of the birth. This will prevent the mother forming antibodies against the blood type of any subsequent babies she may carry. If the woman has suffered excessive bleeding, her haemoglobin and blood group will be checked.

Follow-up Discharge follow-up for a normal birth is largely dependent on the model of care chosen by the woman. In the caseload model, the woman will continue to be cared for by the midwife or midwives of that team. Women not in the caseload model will be visited by the hospital domiciliary midwife for up to a week after the birth. The number of visits made depends on the length of the woman’s stay in hospital: the shorter the stay, the more visits. Women in the medical model will visit their medical practitioner approximately 6 weeks after discharge. Once the woman has been discharged from the services provided by the hospital, the maternal child and health nurse will usually make at least one visit to the woman’s home. Thereafter, the woman will usually go to the maternal child and health centre to have her baby’s health monitored.

CA SE ST U DY 2 Case 11121, 2245 hrs. Dispatch details: A 25-year-old female, who is 34 weeks’ pregnant, is in labour with her second child. Initial presentation: The ambulance crew find the patient lying in a left lateral position on her bed. She tells them that she thought the contractions would stop but they have got stronger since her membranes ruptured.

ASSESS 2258 hrs History: She says that her contractions started at 6 tonight and she is now having 3 contractions in 10 minutes. Her membranes ruptured an hour ago and the amniotic fluid has been clear. She also had a show earlier in the day. Her husband does not have a driver ’s licence and they have no-one to drive her to hospital. She has had the urge to push during the last few contractions. This is her second pregnancy and she has had one live birth. 2300 hrs Examination: The patient has anal pouting and perineal bulging. As the paramedics prepare to assist with the birth, they observe fresh meconium when she pushes. With the next push, they realise that the presenting part is the baby’s buttocks.

Breech presentation In a breech presentation the presenting part of the baby is the sacrum, foot or knee. There are four types of breech presentation (see also Fig 53.11):

FIGURE 53.11 Types of breech presentation. A Complete. B Frank or extended. C Footling (keeling). D Footling (single). Source: Pairman et al. (2014).

• Extended, frank or incomplete breech occurs in 45–50% of breech presentations, usually in women who are having their first baby. The baby’s thighs are flexed with the legs extended at the knees so the feet lie adjacent to the baby’s head. • Complete or flexed breech occurs in 10–15% of breech presentations, usually in women who have previously had babies. The baby’s thighs are flexed and crossed, with the feet close to the buttocks. • Footling breech is rare and occurs more commonly in premature births, usually before 34 weeks (Fraser & Cooper, 2003). One or both of the hips and knees are extended and the feet present below the buttocks. • Knee breech is the rarest breech presentation with one or both hips extended and the knees flexed, presenting below the buttocks. The proportion of breech presentations decreases as the gestational age of the baby increases, from 25% at 35 years old • maternal BMI >30

• short maternal stature • post-maturity • previous history of shoulder dystocia • prolonged active first and second stages of labour. However, it is often unpredictable with no predisposing factors. Warning signs of shoulder dystocia In the prehospital setting early recognition of probable shoulder dystocia is the most effective management. Given that shoulder dystocia has been shown to be associated with a prolonged second stage (Alhadi, Byrne & McKenna, 2001), if the woman is not progressing well in the second stage the paramedics should transport her to the nearest obstetric facility. If transport is not an immediate option (due to location or distance to hospital), shoulder dystocia presenting with an obstructed second stage may respond to a manoeuvre that changes the angle of the pelvis relative to the spine, creating a little more room for the anterior shoulder to slip under the symphysis pubis at the front of the pelvis. There are a number of positions, all of them with esteemed individuals’ names, but they are all a combination of changing the angle of the pelvis and applying a little downward traction to help the shoulder slip under the symphysis pubis. If these techniques do not work, the patient needs to be in expert hands as soon as possible. Recognition of shoulder dystocia Signs of shoulder dystopia as the head is birthing include: • difficulty with progress of the head and chin • the head burrows into the perineum (‘turtle neck’ sign) • restitution of the head does not occur, a sign that the shoulders have not entered the pelvis. Do not to confuse ‘bed’ dystocia or ‘snug shoulders’ with ‘mild’ dystocia (Pairman et al., 2010). ‘Bed’ dystocia occurs when a woman lies in the semiFowler ’s or semi-recumbent position and the baby’s head is born into the mattress of the bed. The shoulders are not impacted behind the pubis symphysis. While progress of the head may be slow, the ‘turtle neck’ sign does not occur. This is easily managed by changing the woman’s position to all fours, standing or rolling to the left lateral (Pairman et al., 2010).

T REAT As shoulder dystocia is often unexpected, paramedics should know the basic manoeuvres used to manage this obstetric emergency. It is advisable to request a second ambulance, especially as there is an increased likelihood of the baby requiring supportive measures after this type of delivery. Management requires at least two paramedics and may even need the assistance of any available bystanders to employ the following manoeuvres: • Continue to use downward traction to deliver the baby’s head but do not twist the head or use excessive force.

• As quickly as possible the mother should be placed in a semi-recumbent position on one pillow. Her knees should be pulled to her chest, slightly abducting, in the McRobert’s manoeuvre (see Fig 53.14 and Box 53.2). If the mother is very tired she may need some assistance with this. Attempt to birth the baby again by applying gentle downward traction to the baby. B O X 5 3 . 2L i m i t a t i o

se

ns in the pr eho spital

ing

In a hospital or home birth, procedures such as episiotomy and internal manoeuvres are used for shoulder dystocia. However, the value of an episiotomy in shoulder dystocia is often debated (Baston, 2006) and internal manoeuvres can be complicated. While paramedics are limited by the procedures they can perform in the prehospital setting, 58% (Gherman et al., 2006) to 90% (Carlin & Alfirevic, 2006) will be successfully managed by using the McRobert’s, Rubin 1 or Gaskin manoeuvre. The McRobert’s manoeuvre has benefits for both the mother and the baby. This position rotates the sacrum backwards, straightening it relative to the lumbar vertebrae and allowing the pelvic inlets to open to the maximum diameter possible. This enables the symphysis pubis to rotate over the top of the anterior shoulder. Simultaneously the fetal spine straightens, facilitating the posterior shoulder passing over the sacral promontory into the hollow of the sacrum (Carlin & Alfirevic, 2006; Pairman et al., 2010; Stables & Rankin, 2010). In the Rubin 1 manoeuvre the second paramedic should attempt to identify the baby’s back by checking which way the baby is trying to face. Remember, although restitution will not have occurred completely at this stage, the baby will be trying to turn one way rather than the other. Once the back is identified, the second paramedic should stand on that side of the mother. With both hands interlocked but using the heel of one hand (external compression style), the second paramedic with moderate pressure should push down and away on the anterior shoulder (Carlin & Alfirevic, 2006; Pairman et al., 2010; Stables & Rankin, 2010). In the Gaskin manoeuvre the woman is placed in the ‘all fours’ position. In reality, this is an upside-down McRobert’s manoeuvre. The flexible sacroiliac joint opens, increasing the anteroposterior diameter by a further 1–2 cm and allowing sufficient room to deliver the posterior shoulder (Carlin & Alfirevic, 2006; Pairman et al., 2010; Stables & Rankin, 2010).

• If the McRobert’s manoeuvre is unsuccessful, the mother should continue to

remain in that position. The second paramedic should apply suprapubic pressure to the anterior shoulder and perform the Rubin 1 manoeuvre (see Box 53.2). Initial continuous pressure should be applied for 30 seconds but if this is not successful, the second paramedic should rock back and forth on the heel of the hand for a further 30 seconds. During this procedure the paramedic assisting should continue to apply gentle downward traction. • If the above manoeuvres are unsuccessful, the mother should be placed on all flours or in the Gaskin position with her head as low as possible, her pelvis as high as possible and her hips well flexed (see Box 53.2). Apply gentle downward traction to the posterior shoulder (i.e. nearest to the mother ’s back). • If this is not successful, the mother should be placed in the ambulance and transported to the nearest obstetric facility. The receiving hospital should be notified of the problem and the impending arrival. • En route apply oxygen to the mother and if able insert an intravenous therapy line. Do not stay on scene to do this as this is a true emergency. • If the baby is born during any of this procedure the neonate should be managed as per the neonatal resuscitation guidelines (see Ch 54). The mother should be managed as per the third stage. She will be at greater risk of postpartum haemorrhage due to perineal trauma and an atonic uterus.

CA SE ST U DY 4 Case 11834, 1420 hrs. Dispatch details: A 34-year-old woman, who is 35 weeks’ pregnant, in labour, membranes broken. Initial presentation: The ambulance crew find the patient sitting in a chair in the manager ’s office of the local supermarket, in labour with her sixth child.

ASSESS 1435 hrs History: The patient says was doing the weekly shopping when she felt a gush of clear fluid from her vagina. She has been having slight pains all morning but they have become more frequent since her membranes ruptured. She says that she can feel something in her pants but has been too scared to look.

1438 hrs Examination: On inspection the paramedics see part of the umbilical cord hanging from her vagina. There are no signs of the second stage.

Cord prolapse In cord presentation the baby’s umbilical cord lies in front of the presenting part but the membranes have not ruptured. When the membranes have ruptured this becomes cord prolapse (see Fig 53.15). An occult cord prolapse lies adjacent to the presenting part and an overt cord prolapse lies below the presenting part. Cord prolapse may occur if a woman is not in labour, or is in the first stage or third stage. As paramedics do not have the equipment to monitor the fetal heart it is not possible for them to diagnose and therefore manage either a cord presentation or an occult cord prolapse. The incidence of cord prolapse is around 0.2–0.4% of all births (Carlin & Alfirevic, 2006).

FIGURE 53.15 In cord presentation the baby’s umbilical cord lies in front of the presenting part and the membranes have not ruptured. When the membranes rupture this becomes cord prolapse. Source: Pairman et al. (2014); Henderson & Macdonald (2004). Predisposing factors include: • a high presenting part

• multigravida • malpresentation (e.g. breech, shoulder, face or brow; transverse or oblique lie) • prematurity or birth weight 18 hours before birth of the baby • Chorioamnionitis (a bacterial infection of the membranes surrounding the fetus: associated with preterm labour) • Bleeding during the second trimester of pregnancy • Previous stillbirth or neonatal death

Fetal risk factors • Twins, triplets or higher order multiples • Preterm labour (especially less than 35 weeks’ gestation) • Post-term birth (after 42 weeks’ gestation) • Large for dates (birth weight >90th centile) • Fetal growth restriction • Fetal anaemia or Rh isoimmunisation • Polyhydramnios (excessive amniotic fluid) • Oligohydramnios (deficiency of amniotic fluid) • Breech or any other presentation other than cephalic (head down) • Reduced fetal movement before the onset of labour • Thick meconium in the amniotic fluid

Prior to birth and/or during labour, any event that compromises placental function or

blood flow through the umbilical cord can lead to fetal hypoxia. The fetus compensates in response to hypoxia by initiating the ‘diving reflex’ (similar to that seen in diving mammals) to preferentially redistribute blood to the brain, adrenal glands and heart and away from the lungs, liver, spleen, intestines and kidneys (Merrill & Ballard, 2005). The fetus is also capable of switching to anaerobic metabolism, using the glycogen stores in the liver for glycolysis. As most glycogen stores are laid down in the third trimester of pregnancy, preterm babies and growth-restricted babies may not have sufficient glycogen stores to maintain anaerobic metabolism for a prolonged period of time. Events that can compromise uterine, placental or umbilical blood flow before and during labour include: • antepartum haemorrhage • placental abruption • cord prolapse • cord compression • a true knot or a nuchal cord (cord wrapped tightly around the baby’s neck) • maternal pre-eclampsia or eclampsia At birth, lung aeration is central to the transition to extrauterine life. If breathing is not established, PVR will remain high and the ductus arteriosus will remain open. Deoxygenated blood will continue to bypass the pulmonary circulation and enter the systemic circulation. The failure of PVR to decrease is known as persistent pulmonary hypertension of the newborn (PPHN). Conditions associated with PPHN include meconium aspiration syndrome, sepsis, pneumonia, asphyxia and respiratory distress syndrome (Lucas & Ginsburg, 2003). This can progress to a vicious cycle of worsening tissue hypoxia, ischaemia and metabolic acidosis, ultimately causing irreversible organ damage or death.

Failure to breathe effectively at birth There are various reasons why a newborn baby may not breathe at birth or fail to breathe effectively despite efforts to do so. These include: • respiratory depression secondary to hypoxia (before or during birth) • failure to generate sufficient pressure during inspiration to force lung liquid from the alveoli and allow air to enter the alveoli—this is more common in very premature babies who have weaker respiratory muscles, a possible lack of surfactant and reduced drive to breathe (ARC/NZRC, 2010) • the effects of maternal drugs, especially narcotics used within 4 hours of giving birth (including opiates given therapeutically by clinicians) • meconium (or blood) blocking the airway • a structural abnormality affecting the airways (rare).

Meconium blocking the airway Meconium is the first faeces passed by the baby and contains amniotic fluid, mucus, lanugo (hair shed from the fetal skin), epithelial cells, bile and water. It is odorous, black or dark green and viscous. If the fetus becomes distressed in utero, it can pass meconium into the amniotic fluid. Placental insufficiency (especially in post-term babies), maternal hypertension, pre-eclampsia or maternal drug use can all cause fetal distress in utero. As the fetus becomes more hypoxic, the anal sphincter relaxes and meconium is passed into the amniotic fluid. In response to continued hypoxia, the fetus begins to gasp, leading to inhalation of the meconium into the fetal lungs before birth. This can cause meconium aspiration syndrome after birth—a complex interplay of chemical pneumonitis, surfactant dysfunction and partial or complete obstruction of the airway leading to gas trapping, alveoli collapse and atelectasis (see Fig 54.2). As the disease progresses, the baby becomes increasingly acidotic, hypoxic and hypercapnic and may develop PPHN. Clinically, the baby may have meconium staining (especially of the umbilical cord, skin and fingers) and develop early-onset respiratory distress.

FIGURE 54.2 The pathophysiology of meconium aspiration syndrome. Source: Kliegman (2011). The incidence of meconium aspiration syndrome is 1.5 per 1000 births in Australia (Bowman & Fraser, 2010b). Meconium aspiration syndrome is rare in newborns before 34 weeks’ gestation and is more common in term and post-term infants. In a baby who is breech, meconium in the amniotic fluid can be a normal occurrence and does not necessarily indicate fetal distress.

CA U T ION! Never administer naloxone to the baby of a mother suspected of using opiates. Naloxone can cause an acute withdrawal and seizures in the newborn.

Look for! • Hyperinflated (barrel-shaped) chest • Nasal flaring • Retraction and recession (in-drawing) of the lower ribs and sternum • Respiratory rate >60 BPM • Worsening cyanosis

Listen for! • Widespread ‘wet’ inspiratory crackles

Structural abnormalities affecting the airways Newborn babies are preferential nose breathers up to 8 weeks of age. If there is a structural blockage of the airway, a baby will not be able to establish effective breathing. Structural malformations of the airway are very rare. If diagnosed during pregnancy, any plans for a home birth should be abandoned. Although rare, it is important to consider a structural abnormality as a differential diagnosis in a newborn baby who is making efforts to breathe but remains cyanosed and has limited, unilateral or no chest wall movement. Some of the structural airway abnormalities in newborn babies include: • Choanal atresia. A narrowing or blockage of the nasal airway by tissue or bony cartilage. May be unilateral or bilateral. Incidence: 1.5 per 10,000 births in Australia (Riley & Halliday, 2008). • A pharyngeal airway malformation (e.g. Pierre Robin sequence). Small mandible, cleft palate and a large tongue that falls back into the pharynx obstructing the airway when the baby is lying supine. Incidence: 1.6 per 10,000 births in Australia (Riley & Halliday, 2008). • Diaphragmatic hernia. The abdominal contents (intestines ± the liver) have herniated through a hole in the diaphragm, causing a hypoplastic lung on the affected side. Incidence: 2.8 per 1000 births in Australia (Riley & Halliday, 2008). • Pneumothorax. May occur spontaneously at birth with the pressures exerted during the first breaths of life (incidence: 1–2 per 100 births) or as a result of use of excessive pressure during bag-valve-mask (BVM) ventilation.

Look for! • Persistent cyanosis despite efforts to breathe

• Nasal flaring • Retraction and recession (in-drawing) of the lower ribs and sternum • Respiratory rate >60 BPM

Listen for! • Decreased or absent breath sounds: unilateral or bilateral • Bradycardia (HR 100 BPM Grimace Crying Activity Moving all limbs Respiratory effort Crying and breathing D: There is no environmental danger to the mother, baby or the crew.

R: Crying. A: The baby’s airway appears clear and has not been contaminated by meconium. B: The baby’s respiratory function is currently normal. C: The baby’s heart rate is >100 BPM. Although the baby initially appears cyanosed the heart rate and muscle tone are good. While cyanosis is a critical sign in adults, it is common in newborns in the first few minutes after birth. The entire clinical picture needs to be considered.

CONFIRM The mother has told the paramedics that she is 39 weeks’ gestation and expecting one baby. Twins would confound this clinical scene. The paramedics would need to call for immediate back-up if this mother was giving birth to twins, as then there would be three patients to stabilise and transport. The paramedics have seen that the amniotic fluid is clear of meconium. The baby is crying and has good tone, which would indicate that her heart rate is likely to be above 100 BPM. Although the baby appeared cyanosed at birth, this is a normal finding in the first minute after birth and does not require intervention if the baby is breathing, moving and has a heart rate above 100 BPM. The paramedics perform a set of initial observations on the baby to confirm: • Is the baby’s heart rate above 100 BPM when auscultated with a stethoscope over the apex? • Is the baby continuing to breathe at a rate of 30–60 BPM? • Is the baby’s breathing effortless? (No nasal flaring, chest recession or expiratory grunting) • Is the baby becoming centrally pink over the first minutes after birth? (Pink gums, mucous membranes and chest) As they make their initial assessment of the baby, the paramedics need to reassure the mother that her baby looks healthy. She will want to know (or confirm) what gender her baby is and that her baby has no obvious abnormalities. The paramedics should look for any other obvious congenital abnormities of the head, neck, face, limbs, spine and genitalia. The paramedics should note and document the time of birth. They also need to allocate the baby a 1-and a 5-minute Apgar score (see Table 54.2). The Apgar score is not used to guide the resuscitation process: rather, it is assigned retrospectively to summarise the newborn’s transition to extrauterine life and to quantify the newborn’s response to any resuscitation interventions. Bear in mind that a non-vigorous newborn requires immediate intervention at birth, well before the 1-minute Apgar score is assigned. Conversely, a vigorous newborn can score ‘0’ for colour at 1 minute, but not require resuscitation. Heart rate is the most important of the five signs and colour is the least useful

(Australian Resuscitation Council, 2006). Initial assessment of the baby is therefore based on assessment of breathing, muscle tone and heart rate. Subsequent assessment is based on breathing, heart rate, muscle tone and colour. Assessment of the baby’s temperature is also important before and during transport to hospital to detect hypothermia. (Aim for normothermia: a rectal or per axilla temperature of 36.5–37.2°C.) Use a digital thermometer to assess the baby’s temperature. A newborn baby’s external auditory canal is usually too small to obtain an accurate temperature using a tympanic membrane thermometer. TABLE 54.2 Apgar score

T REAT Emergency management Safety This baby has been born in her mother ’s kitchen. If there had been time, it would have been ideal to move the mother to her bed for the birth, then an area on the floor beside the bed could have been set up with warm blankets and towels to receive the baby. The paramedics needed to be ready to ‘catch’ this baby, ideally with warm towels ready, to prevent her from being born onto the cold hard floor of the kitchen. As a minimum, the crew should have the obstetric kit and newborn BVM ventilation device on hand. Warmth As this baby is vigorous, she should be dried quickly and placed on her mother ’s chest, skin-to-skin to maintain warmth. A warm blanket should be placed over both of them and a hat (or the corner of a warm towel) placed on the baby’s head. This is important as newborn babies can lose heat quickly due to the large surface area of their head. Many ambulance service operating instructions require all patients to be secured appropriately in a moving vehicle, which

taken literally would include a newborn baby. Paramedics need to balance the very real risk of hypothermia, which is easily prevented with skin-to-skin contact with the mother, with the risk of injury associated with an ambulance crash. If a baby is not vigorous at birth, the baby should be placed supine onto warm towels and blankets on the floor beside the mother (or on the end of the stretcher if in the ambulance). The baby should be dried quickly, especially the head, and the wet towel removed and replaced with a clean warm one. A hat should be placed on the baby’s head and a piece of bubble wrap placed over the baby’s body, up to the neck, leaving the head exposed. This will allow the paramedics to continue to assess and treat the baby, while maintaining warmth.

EVALUAT E Continue to assess the newborn: • Is the baby breathing effectively? • Is the baby’s heart rate >100 BPM? • Is the baby pinking up over the first few minutes after birth? If yes, the baby should be nursed skin-to-skin with the mother en route to hospital. If not, the baby will require the next steps of resuscitation: ensuring a clear airway and initiation of positive pressure ventilation if the heart rate is 100 BPM) and there is no obvious meconium in the mouth, suctioning is not indicated. • If there is meconium visible in the mouth, suction the oropharynx, followed by the nares (only if necessary). • If the baby is not vigorous (not breathing, flaccid and HR 2000 g or >34 weeks’ gestation.

Intravenous or IO access Since so few babies require the administration of drugs following birth, paramedics will most likely be unfamiliar with gaining access to the intravascular space. Compared with adults, using IO devices may be faster and more reliable. The IO route is quickly becoming the preferred method of establishing access in the prehospital environment. The preferred site is the proximal tibia. Aim to enter a few centimetres below the tibial tuberosity at the centre of the flat anteromedial surface. Direct the needle caudally away from the upper tibial epiphysis (Bowman & Fraser, 2010d). The distal anterolateral surface of the tibia is an alternative site. The distal femur and sternum should not be used in babies (Bowman & Fraser, 2010d). An 18-gauge IO needle is preferable to using an IO gun in a premature baby (ARC/NZRC, 2010). An IO gun should be used with extreme caution in a premature baby, especially one weighing less than 1500 g due to the fragility of the baby’s small bones and the small IO space. Umbilical venous catheterisation (UVC) is not a supported procedure in paramedic practice. There is a risk of cannulating the umbilical artery and inadvertently administering vasoactive drugs into the artery (e.g. adrenaline). Complications include bleeding, infection, perforation, clot formation, cardiac arrhythmias, hepatic necrosis and portal hypertension (Bowman & Fraser, 2010c). Peripheral cannulation (IV) is extremely difficult in a newborn who is shocked or collapsed. Since it is also time-consuming it is better to proceed with patient transport.

Medications and fluid administration The priority during advanced resuscitation of a newborn baby is to ensure that the continuity and technique of external chest compressions and positive pressure ventilation is not compromised. However, if external chest compressions with positive pressure ventilation in 100% oxygen fail to restore the heart rate and circulation, then adrenaline may be required. Adrenaline is indicated if the heart rate is below 60 BPM after at least 30 seconds of external chest compressions with BVM ventilation in 100% oxygen (and at least 30 seconds of effective BVM ventilation in air before ECC is commenced). Adrenaline should preferably be administered intravenously (ARC/NZRC, 2010; Perlman et al., 2010). Inserting a peripheral line in a shocked or collapsed newborn is extremely difficult. An IO needle can be used as an alternative if there is no IV access (ARC/NZRC, 2010). If there is no IV or IO access, adrenaline can be administered via an endotracheal tube, in which case up to 10 times the IV dose is recommended (50–100 mcg/kg) although this practice is no longer recommended in the adult resuscitation area and is being questioned for newborns (ARC/NZRC, 2010). Volume expanders may be indicated in a baby in whom hypovolaemia secondary to fetal blood loss or septic shock is suspected. Normal saline is the volume expander of choice in the pre-hospital setting—0.9% sodium chloride for volume expansion is indicated if:

• blood loss is suspected and the baby appears shocked: pale, capillary refill >4 seconds, poor perfusion, weak femoral pulses • the baby is not responding to resuscitation measures with an improvement in heart rate. Consideration should be given to preventing and treating hypoglycaemia in all babies, especially those who have required resuscitation at birth. Adverse neurological outcomes have been demonstrated in newborns with hypoglycaemia following a hypoxic ischaemic insult (Salhab et al., 2004; Perlman et al., 2010). Although the optimal range of blood glucose concentration to minimise brain injury is still to be defined, aim to maintain the baby’s blood glucose level ≥2.6 mmol/L (ARC/NZRC, 2010). IM glucagon can be administered if IV or IO access is not available for a continuous 10% glucose infusion. Glucagon acts by mobilising glycogen from the liver. If the baby has inadequate stores of glycogen (e.g. extremely preterm baby or growth-restricted baby), glucagon treatment may not be as effective. The following drugs are not indicated in newborn resuscitation: • Lignocaine, atropine, calcium, magnesium, potassium, vasopressin and amiodarone are not indicated in the resuscitation of a newborn baby at any time. • Sodium bicarbonate. Level 1 evidence from two human trials has failed to demonstrate a beneficial impact on survival, neurological outcome or acid–base balance in asphyxiated babies (Lokesh et al., 2004; Murki et al., 2004). The known side effects include depressed myocardial function, exacerbation of intracellular hypercarbia, paradoxical intracellular acidosis, reduced cerebral blood flow and increased risk of intraventricular haemorrhage in preterm babies. • Naloxone. This is not indicated in initial newborn resuscitation as there is no evidence of benefit and substantial evidence of risk (myocardial depression, cardiac arrhythmias, exacerbation of cerebral white-matter neuro-histological injury; Van Woerkom et al., 2004). The first priority is to provide BVM ventilation if the baby is not breathing. If there is any suspicion that the mother is an intravenous drug user, naloxone is absolutely contraindicated in the baby, as it can cause an acute withdrawal and seizures.

Documentation The paramedics should document the following whenever a birth occurs in the prehospital setting: • time of birth (this is not always possible if the birth occurred prior to the paramedics’ arrival) • time of first spontaneous breath • resuscitation interventions, timing and response (including BVM ventilation, use of 100% oxygen, external chest compressions, adrenaline or sodium chloride administration) • heart rate, respiratory rate, respiratory effort, perfusion, tone and colour every 15 minutes during transport • temperature (per axilla or rectal) • blood glucose level (if possible) • Apgar score at 1 and 5 minutes (and assessed every 5 minutes until the score is 7 or greater).

Birth during transport Delivering a baby during transport adds a layer of complexity to the care of both mother and baby. Space (or lack thereof ) is a significant issue. This will be a highly emotional and potentially chaotic situation, even if the baby is born in a healthy condition. If the baby requires resuscitation, this will have to be performed on the end of the stretcher at the mother ’s feet, in her full view. Even if the mother has a support person with her in the ambulance, that person will need to sit in the front passenger seat to give the paramedics room to work in the rear of the ambulance. All aspects of resuscitation and subsequent care of the baby are further complicated by the limitations of suitable equipment for sick newborns in the pre-hospital environment, including monitoring equipment, umbilical catheters for intravenous access, an incubator for thermoregulation and assisted ventilation devices. If the mother experiences complications during the birth (e.g. shoulder dystocia) or following the birth (e.g. postpartum haemorrhage), the paramedics will be further stretched. Back-up assistance from a second crew is highly desirable if the birth is complicated or the baby is premature or compromised. Where possible, mother and baby should not be separated and each should have their own paramedic, but this may not be possible in some rural and remote areas. Ideally, a paramedic from the second crew can drive the ambulance while the two paramedics from the first crew care for the mother and her baby. Paramedics are strongly advised to consult with a neonatologist from their local Newborn and Paediatric Emergency Transport Service or equivalent regarding ongoing emergency management of any baby requiring resuscitation and for all premature babies. The consultant can direct the paramedic crew to the most appropriate receiving hospital, which may not necessarily be the closest hospital, en route. The consultant may also activate a neonatal team to proceed to the receiving hospital to continue management of the baby and to transfer the baby to a tertiary hospital with a neonatal intensive care unit. There will be times when a baby is too premature or too severely asphyxiated to survive, despite the best efforts of the paramedics. If a baby has been stillborn or has died despite resuscitation efforts, the paramedics will find themselves in one of the most difficult situations they will face in their career. The death of a baby is devastating for all involved. Encourage the mother (and father, if he is present) to see their baby and allow one of the parents to hold the baby during transport to hospital if they wish. The hospital will arrange for SANDS (the Stillbirth and Neonatal Death Support Association) to contact the parents and offer counselling to the family. It is equally important that the paramedics are provided with an opportunity to debrief and receive counselling following the death of a baby in their care.

Discontinuing resuscitation The Australian Resuscitation Council guidelines (ARC/NZRC, 2010) and international guidelines state that it is reasonable to discontinue resuscitation of a newborn baby if there is no measurable heart rate after 10 minutes of maximal resuscitation (ARC/NZRC, 2010; Kattwinkel et al., 2010; Perlman et al., 2010). Both survival and quality of survival deteriorate rapidly beyond this time and there is a very high risk of severe neurological disability if the baby does survive (Casalaz, Marlow & Speidel, 1998; Haddad et al., 2000). Where early death is inevitable, resuscitation is not indicated. This may be the case in babies born at the limits of viability (4 seconds, temperature 34.6°C (per axilla). Respiratory status: 88 BPM, equal air entry bilaterally, nasal flaring and grunting with each breath, marked intercostal and substernal retraction. Conscious state: The baby has her eyes closed. She is lying in an extended posture.

CONFIRM In many cases paramedics are presented with a complex situation involving more than one patient. A critical step in the treatment plan is to determine who should receive priority in this situation. The mother is conscious with no obvious haemorrhage but the newborn is clearly extremely preterm and is unable to breathe effectively. The paramedics’ visual assessment confirms that the baby is experiencing the problems associated with preterm birth that they anticipated.

T REAT

Emergency management The first priority for the paramedics is to move this mother and her baby to a safer, warmer place than a cold bathroom floor. Simultaneously, they need to rapidly assess the baby’s heart rate, work of breathing, tone and oxygenation (if possible). They also need to call for back-up from an intensive care paramedic crew, as it is highly likely that this baby will require respiratory support before transport to hospital. At 26 weeks’ gestation, early-onset respiratory distress and respiratory failure are inevitable. Preterm babies have the following anatomical and functional problems that result in an inability to support ventilation and oxygenation: • underdeveloped alveolar saccules with limited surface area for gas exchange • lack of pulmonary surfactant so alveoli collapse on expiration and functional residual capacity (FRC) is not established • low compliance in the lung (small changes in volume in response to application of high pressures). The lack of surfactant and decreased lung compliance lead to increased work of breathing, fatigue, atelectasis and a ventilation/perfusion (V/Q) mismatch (Gardner, Enzman-Hines & Dickey, 2011). Clinically the baby will be tachypnoeic (respiratory rate >60 BPM), with grunting, nasal flaring and chest recession, and may be centrally cyanosed. One paramedic clamps and cuts the umbilical cord while the other prepares an area in the bedroom to treat the baby. Having laid down a warm towel on top of two blankets, the paramedic cuts a hole in a 28 × 38 cm zip-lock bag. The baby is carried into the bedroom and laid supine on the warm towel, then placed with her body completely in the bag and her head outside of the bag. The paramedic zip locks the bag at the bottom and places a warm blanket over the bag. He dries the baby’s head and uses a corner of a second towel to cover the top of her head. 1822 hrs: Perfusion status: HR 90 BPM (auscultation), skin slightly centrally cyanosed. Respiratory status: No respiratory effort. Conscious state: The baby has her eyes closed and is floppy. 1826 hrs: The paramedics commence BVM ventilation at a rate of 60 BPM. This rate is appropriate for a baby of 26 weeks’ gestation with respiratory distress as she is likely to be hypercapnic. Her heart rate improves quickly with BVM ventilation to 130 BPM, but she remains cyanosed. As her colour is not improving and she has signs of marked respiratory distress, the paramedics BVM ventilate her using 100% oxygen. If the respiratory distress remains severe, intubation should be considered according to local guidelines and the baby ventilated at 60 BPM, aiming for a tidal volume of 4–6 mL/kg. The insertion of a UVC is not generally supported in paramedic practice. The risk of haemorrhage, inadvertent cannulation of the umbilical artery, drug or fluid administration into the artery, air embolism and infection are too great. While insertion of an IO needle is easier and quicker than peripheral venous cannulation of a newborn baby in the pre-hospital setting, there is no IO needle small enough to safely cannulate a baby of 26 weeks’ gestation. The crew will

not be able to gain IV access on this baby. Furthermore, such a procedure would only delay transport to hospital, which is a priority in this case.

EVALUAT E In hospital umbilical venous and arterial lines were inserted. A chest x-ray revealed respiratory distress syndrome. Surfactant replacement therapy was given intratracheally, maintenance fluids of 10% glucose were commenced, and IV penicillin and gentamicin were given for 7 days. A dobutamine infusion was also required to treat hypotension. The baby required high-frequency ventilation for 14 days and then extubation to nasal CPAP and remained on nasal CPAP for a further few weeks. She was discharged home after 14 weeks on low-flow oxygen of 100 mL/min.

Long-term role Complications of prematurity and peripartum asphyxia can have lifelong effects. Extremely low birth weight babies (500–999 g birth weight) have increased rates of adverse neurodevelopmental outcomes such as cerebral palsy, deafness, blindness and severe developmental delay (Doyle et al., 2011). The rates of disability increase with decreasing gestational age. Babies with moderate or severe HIE are also at risk of developing adverse neurodevelopmental outcomes as a result of hypoxic ischaemic damage to their brain such as cerebral palsy, cognitive delay and memory difficulties. At least 25% of survivors will have significant long-term major neurosensory problems (Jacobs & Tarnow-Mordi, 2010).

CA SE ST U DY 3 Case 10306, 0430 hrs. Dispatch details: A 26-year-old female who is 41 weeks’ pregnant is in labour for a planned home birth. There is thick meconium in the amniotic fluid. The midwife assisting with the home birth has requested transport to hospital. Initial presentation: The paramedics are met by the woman’s husband. He takes them into the lounge room where they find the woman on all fours over a fit ball. The midwife is listening to the fetal heart rate with a fetal Doppler monitor.

ASSESS 0444 hrs Primary survey: The woman is alert. She has just had a strong contraction lasting 1 minute. The fetal heart rate was 80 BPM during and for 30 seconds after the contraction. 0445 hrs Chief complaint: The midwife shows the crew a sanitary pad covered in thick meconium.

P AT I E NT HI ST ORY Ask!

• When did your membranes (‘waters’) rupture? • What colour was the amniotic fluid when your membranes ruptured? • Has the colour of the amniotic fluid changed? If so, has it become darker or lighter? • Has the consistency of the amniotic fluid changed? If so, has it become thicker or thinner? • Is your baby positioned head down or breech?

0446 hrs Pertinent hx: The midwife informs the crew that the woman was 8 cm dilated when she performed a vaginal examination 15 minutes ago. It was at this time that the membranes ruptured and she saw meconium in the amniotic fluid. The woman is 41 weeks and two days pregnant. This is her first pregnancy. The woman has been in labour for 12 hours. If this baby is breech, this could explain the meconium in the amniotic fluid. Meconium in a breech baby can be a normal finding that is not necessarily indicative of fetal distress. However, the fetal heart rate dropping to 80 BPM during and after a contraction is a sign that the fetus is distressed in utero. 0447 hrs Reassessment: The mother has another strong contraction and grunts, ‘I need to push!’ 0448 hrs Management: With the next three contractions, the midwife delivers the baby. He is floppy, not moving and not making any effort to breathe. His umbilical cord, fingers and toes are meconium-stained. The paramedics quickly suction the baby’s oropharynx of meconium and then suction the nares. They dry the baby and stimulate him to breathe by rubbing his back and head with the towel. Then they remove the wet towel and replace it with a warm, dry towel. 0451 hrs Vital signs survey: Perfusion status: HR 78 BPM (auscultation), regular; skin warm, cyanosed. Respiratory status: No respiratory effort following airway clearance. Conscious state: Not moving and floppy.

CONFIRM In this particular case, the fact that the baby is not breathing is not in dispute. However, the paramedics need to consider their management strategy given this is a neonate. The first priority is to ventilate the baby. The baby should be resuscitated in room air initially. Using 100% oxygen may further delay the time taken for him to take his first breath. The crew may need to provide supplementary oxygen if his heart rate does not improve with BVM ventilation. The first step is to provide BVM ventilation at a rate of 40–60 BPM in air (21%) for at least 30 seconds, then reassess the baby’s heart rate and

breathing effort. If the heart rate is 60–100 BPM, BMV ventilation should be continued and supplemental oxygen provided until the heart rate is above 100 BPM and the baby is breathing effectively. If the heart rate is below 60 BPM, chest compressions and 100% oxygen are now indicated.

T REAT 0452 hrs: The paramedics provide BVM ventilation at a rate of 30 BPM. This slower rate of ventilation is recommended because meconium aspiration is associated with gas trapping. Slowing the BVM rate enables a longer expiratory time. The paramedics aim for 0.5 seconds for inflation and 1.5 seconds for exhalation (2 seconds per inflation = 30 BPM). After 30 seconds of effective BVM ventilation, the baby starts to move and opens his eyes. He also takes some breaths on his own. 0453 hrs: Perfusion status: HR 110 BPM (auscultation), skin cyanosed but becoming pink. Respiratory status: 20 BPM, equal air entry bilaterally. Conscious state: The baby has opened his eyes and is moving his legs. His arms remain extended. 0454 hrs: The paramedics stop BVM ventilation as the baby is breathing spontaneously and his heart rate is >100 BPM. However, the baby develops signs of respiratory distress over the next few minutes. 0456 hrs: Perfusion status: HR 140 (auscultation), skin centrally cyanosed. Respiratory status: 60 BPM, equal air entry bilaterally, barrel-shaped chest, nasal flaring and grunting with each breath. Conscious state: The baby is lying with his eyes closed. He is flexed but does not resist extension of his limbs. 0457 hrs: The paramedics commence oxygen at 2 L/minute via nasal cannula. 0500 hrs: The paramedics prepare to load the mother and baby for transport to hospital and document the events to date. The mother is assisted to the patient stretcher for transport. The baby is placed skin to skin with her.

EVALUAT E Evaluating the effect of any clinical management intervention can provide clues to the accuracy of the initial diagnosis. Some conditions respond rapidly to treatment so patients should be expected to improve if the diagnosis and treatment were appropriate. A failure to improve in this situation should trigger the clinician to reconsider the diagnosis. In this case although the complexities of the transition to extrauterine life

can lead to increasing respiratory distress the paramedics have few treatment options. This baby is at risk of respiratory failure secondary to peripartum hypoxia-ischaemia and meconium aspiration. Consideration should be given to securing an airway in this baby for transport to hospital. The paramedics should consult with the neonatal emergency transport team to discuss the need for intubation and for an appropriate destination hospital. Back-up from an intensive care ambulance team should be considered. The baby required intubation shortly after arrival at the receiving hospital for worsening respiratory distress. His chest x-ray was consistent with meconium aspiration syndrome. He required ventilation for 48 hours and oxygen therapy for a further 4 days. He received IV antibiotics for 7 days. He was discharged home fully breastfeeding on day 9.

CA SE ST U DY 4 Case 11008, 0500 hrs. Dispatch details: A 31-year-old female who is 38 weeks’ pregnant has ruptured her membranes and is having regular contractions. She has gestational diabetes. Initial presentation: The paramedics are met at the front door by the patient. They estimate her weight to be 120 kg. She tells them she has been having regular contractions since midnight. She is home alone as her husband is working a night-shift and is due home at 7. She phoned for an ambulance when her membranes ruptured.

ASSESS 0517 hrs Pertinent hx: The woman informs the paramedics that she was diagnosed with gestational diabetes at 28 weeks’ gestation. She is on a controlled diet. She was booked for a planned induction in 2 days’ time as the baby is large for dates on ultrasound. This is her first baby. She has a strong contraction lasting 1 minute and becomes distressed with the pain. The paramedics need to determine whether there are any additional factors placing this baby at risk of requiring resuscitation. They establish that this is a term fetus and that the amniotic fluid was clear of meconium. They ascertain that her membranes ruptured less than 18 hours ago.

0524 hrs Treatment: The paramedics decide to assist the mother into the ambulance and proceed to the nearest maternity hospital, which is 35 km away. On the way, her contractions become closer and last longer. 0545 hrs Treatment: Approximately 30 km into the journey, she becomes extremely distressed with the pain and tells the paramedics she has a strong urge to push. They pull over to the side of the road in a truck stop. With the next four contractions, the baby’s head is delivered, but the baby’s shoulders are stuck. The baby’s head is on the perineum for 6 minutes. They perform the McRobert’s manoeuvre (see Ch 53) and the baby’s body is born. The baby boy is floppy. He is not moving or making any effort to breathe. There is no blood or meconium in the amniotic fluid. 0600 hrs Vital signs survey: Perfusion status: HR 40 BPM (auscultation), skin cyanosed. Respiratory status: No respiratory effort. Conscious state: The baby is floppy.

CONFIRM In many cases paramedics are presented with a collection of signs and symptoms that do not appear to describe a particular condition. A critical step in determining a treatment plan in this situation is to consider what is the most likely cause for the baby’s poor condition at birth. The mother is conscious with no obvious uncontrolled haemorrhage but the baby is not active. Given the length of time the baby’s head was stuck on the perineum, the most likely problem is a hypoxic-ischaemic insult.

T REAT Emergency management The paramedics quickly dry the baby and stimulate him to breathe by rubbing his back and head with a towel. They wipe the secretions from the corner of his mouth and nose with a corner of the towel. They remove the wet towel and replace it with a warm, dry towel, and cover the baby’s head with a corner of the clean towel. They then position him supine on the end of the stretcher with his head in a neutral position and place a small rolled towel under his shoulders to help maintain his head in this position. 0602 hrs: The paramedics provide BVM ventilation at a rate of 60 BPM in air. They are achieving good chest wall rise with each BVM inflation. After 30 seconds of effective BVM ventilation, they re-evaluate the baby’s heart rate, respiratory effort and muscle tone. There is no change. 0603 hrs: They connect the BVM to 100% oxygen. While one paramedic

ventilates at 60 inflations per minute, the second auscultates the baby’s heart rate again. There is still no change. It is not routine practice to assess for a shockable arrhythmia in a newborn baby. Bradycardia occurs secondary to hypoxaemia, not because of cardiac arrhythmias such as ventricular fibrillation. However, as this baby is a largeterm newborn, the ECG electrodes (‘dots’) can be safely applied to his chest and abdomen and will provide the paramedics with an accurate and continuous reading of his heart rate via the vital signs monitor. A continuous heart rate reading will be extremely valuable in guiding ongoing resuscitation interventions. 0604 hrs: The paramedics commence external chest compressions using the hand encircling technique with BVM ventilation at a ratio of 3:1, using 100% oxygen. After 30 seconds of external chest compressions and BVM ventilation in 100% oxygen, the baby’s heart rate is still 50 BPM. They contact the clinician and continue CPR. If the baby’s heart rate is >60 BPM but 100 BPM and the baby is breathing spontaneously. If the baby’s heart rate is 4000 g birth weight) and/or large for gestational age (>90th percentile). This increases their risk of shoulder dystocia, birth injury, brachial nerve plexus and perinatal asphyxia. Surfactant synthesis can be delayed or inhibited in the fetus because of elevated fetal serum insulin levels, placing the newborn at increased risk of developing respiratory distress (McGowan et al., 2011).

Future research The survival rate for extremely preterm babies plateaued in the middle of the first decade after 2000 (Doyle et al., 2011). As it is unlikely that the lower limits of survival will be reduced beyond 22–23 weeks’ gestation, the focus is on improving the long-term outcomes of extremely premature babies. For example, since 2010 magnesium sulfate has been routinely given to mothers at risk of preterm birth before 30 weeks’ gestation because of its neuroprotective effects for the fetus (Doyle, Crowther & Middleton, 2009). Therapeutic hypothermia is offering hope to parents whose babies have moderate or severe HIE. If commenced within 6 hours of birth, therapeutic hypothermia can reduce rates of cerebral palsy and cognitive impairment (Jacobs & Tarnow-Mordi, 2010). However, babies must meet strict criteria before this therapy is considered. Paramedics should not commence therapeutic hypothermia in the pre-hospital environment because of its side effects of deep brain and body hypothermia. Current research is focusing on hypothermia in combination with various therapies, including the use of erythropoietin (Levene, 2010), xenon (a noble anaesthetic gas) and topiramate (an anticonvulsant).

Summary Newborn babies rarely require resuscitation at the time of their birth: most newborns make vigorous efforts to inhale air into their lungs at birth and clear their own airway very effectively. Cyanosis is common immediately after delivery and heart rate, breathing and muscle tone are the three criteria that should be used to assess the newborn at birth to determine the need for ongoing resuscitation interventions. If the newborn does not start breathing or has a heart rate below 100 BPM after being dried and stimulated, BVM ventilation is indicated. When performed correctly, BVM ventilation will reliably result in a rapid improvement in heart rate, usually without the administration of supplementary oxygen. Air (21% oxygen) should be used initially, with 100% oxygen reserved for those babies who do not respond to BMV ventilation in the first few minutes of life. Newborn babies lose heat very quickly and pre-hospital interventions to manage hypothermia should be instigated as part of the resuscitation process. Prematurity is associated with an increased risk of mortality and morbidity. Transferring the woman with threatened preterm labour to a tertiary perinatal centre before the birth of her baby increases the baby’s chance of survival and quality of life.

References Australian Resuscitation Council (ARC), the New Zealand Resuscitation Council (NZRC). Section 13. Neonatal Guidelines. Retrieved 3 November 2011 from www.resus.org.au, 2010. Björklund, L. J., Ingimarsson, J., Curstedt, T., John, J., Robertson, B., Werner, O., Vilstrup, C. T. Manual ventilation with a few large breaths at birth compromises the therapeutic effect of subsequent surfactant replacement in immature lambs. Pediatric Research. 1997; 42(3):348–355. Bowman, E., Fraser, S., Blood pressure. Neonatal Handbook 2010; . Retrieved 3 November 2011 from www.rch.org.au/nets/handbook/index.cfm?doc_id=450 Bowman, E., Fraser, S., Meconium aspiration syndrome. Neonatal Handbook 2010; . Retrieved 3 November 2011 from www.rch.org.au/nets/handbook/index.cfm?doc_id=723 Bowman, E., Fraser, S., Umbilical venous catheterisation. Neonatal Handbook 2010; . Retrieved 9 November 2011 from www.netsvic.org.au/nets/handbook/index.cfm? doc_id=891 Bowman, E., Fraser, S., Intraosseous needle insertion. Neonatal Handbook 2010; . Retrieved 10 November 2011 from www.netsvic.org.au/nets/handbook/index.cfm?doc_id=455 Casalaz, D. M., Marlow, N., Speidel, B. Outcome of resuscitation following unexpected stillbirth. Archives of Disease in Childhood, Fetal and Neonatal Edition. 1998; 78:F112–F115. Chow, S. S.W. Report of the Australian and New Zealand Neonatal Network 2011. Sydney: Australian and New Zealand Neonatal Network, 2013; 1–78. Crossley, K. J., Allison, B. J., Polglase, G. R., Morley, C. J., Davis, P. G., Hooper, S. B. Dynamic changes in the direction of blood flow through the ductus arteriosus at birth. The Journal of Physiology. 2009; 587(19):4695–4704. Davis, P. G., Tan, A., O’Donnell, C. P.F., Schulze, A., Resuscitation of newborn infants with 100% oxygen or air: a systematic review and meta-analysis. Lancet. 2004;364(9442):1329– 1333 Dawson, J., Kamlin, C., Vento, M., Wong, C., Cole, T. J., Donath, S. M., Morley, C. J., Defining the reference range for oxygen saturation for infants after birth. Pediatrics.

2010;125(6):e1340–e1347, doi: 10.1542/peds.2009–1510. Dawson, J., Kamlin, C., Wong, C., te Pas, A., Vento, M., Cole, T., et al, Changes in heart rate in the first minutes after birth. Archives of Disease in Childhood: Fetal and Neonatal Edition. 2010;95(3):F177–F181, doi: 10.1136/adc.2009.169102. Doyle, L. W., Crowther, C. A., Middleton, P. Antenatal magnesium sulphate and neurologic outcome in preterm infants: a systematic review. Obstetrics & Gynecology. 2009; 113:1327–1333. Doyle, L. W., Roberts, G., Anderson, P. J., for the Victorian Infant Collaborative Study Group, Changing long-term outcomes for infants 500–999 g birth weight in Victoria, 1979– 2005. Archives of Disease in Childhood: Fetal and Neonatal Edition. 2011;96(6):F443–F447, doi: 10.1136/adc.2010.200576. East, C. E., Colditz, P. B., Begg, L. M., Brennecke, S. P., Update on intrapartum fetal pulse oximetry. Australian and New Zealand Journal of Obstetrics and Gynaecology. 2002;42(1):23–28, doi: 10.1111/j.0004–8666.2002.00023.x. Gardner, S., Carter, B., Enzman-Hines, M., Hernandez, J. Merenstein & Gardner ’s Handbook of Neonatal Intensive Care, 7th ed. St Louis: Mosby, 2011. Gardner, S. L., Enzman-Hines, M., Dickey, L. A. Respiratory diseases. In Gardner S.L., Carter B.S., Enzman-Hines M., Hernandez J.A., eds.: Merenstein and Gardner’s Handbook of Neonatal Intensive Care, 7th ed., St Louis: Mosby, 2011. Haddad, B., Mercer, B. M., Livingston, J. C., Talati, A., Sibai, B. M. Outcome after successful resuscitation of babies born with Apgar scores of 0 at both 1 and 5 minutes. American Journal of Obstetrics and Gynecology. 2000; 182:1210–1214. Hageman, J. R., Slotarski, K., Casserly, G., Hawkins, H.Goldsmith J.P., Karotkin E.G., eds. Assisted Ventilation of the Neonate. 4th ed. Elsevier, 2003:91–105. Hilder, L., Zhichao, Z., Parker, M., Jahan, S., Chambers, G. M. Australia’s Mothers and Babies 2012. Canberra: AIWH, 2014; 1–127. [Perinatal Statistics Series No. 30. Cat no. PER 69]. Jacobs, S. E., Tarnow-Mordi, W. O., Therapeutic hypothermia for newborn infants with hypoxic–ischaemic encephalopathy. Journal of Paediatrics and Child Health. 2010;46(10):568–

576, doi: 10.1111/j.1440–1754.2010.01880.x. Kamlin, C. O.F., O’Donnell, C. P.F., Everest, N. J., Davis, P. G., Morley, C. J., Accuracy of clinical assessment of infant heart rate in the delivery room. Resuscitation. 2006;71(3):319– 321, doi: 10.1016/j.resuscitation.2006.04.015. Kattwinkel, J., Perlman, J. M., Aziz, K., Colby, C., Fairchild, K., Gallagher, J., et al, Special Report. Neonatal Resuscitation: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Pediatrics. 2010;126(5):e1400–1413, doi: 10.1542/peds.2010–2972E. Kliegman, R. M., et al. Nelson Textbook of Pediatrics, 19th ed. Philadelphia: Saunders, 2011. Lantos, J. D., Miles, S. H., Silverstein, M. D., Stocking, C. B. Survival after cardiopulmonary resuscitation in babies of very low birth weight. Is CPR futile therapy? New England Journal of Medicine. 1988; 318:91–95. Laws, P. J., Li, Z., Sullivan, E. A. Australia’s Mothers and Babies 2008. Australian Institute of Health and Welfare and the University of New South Wales, Sydney, 2010. Retrieved from www.npsu.unsw.ed.au Levene, M. I., Cool treatment for birth asphyxia, but what’s next? Archives of Disease in Childhood: Fetal and Neonatal Edition. 2010;95(3):F154–F157, doi: 10.1136/adc.2009.165738. Lokesh, L., Kumar, P., Murki, S., Narang, A., A randomized controlled trial of sodium bicarbonate in neonatal resuscitation—effect on immediate outcome. Resuscitation. 2004;60(2):219–223, doi: 10.1016/j.resuscitation.2003.10.004. Lucas, V. W., Ginsburg, H. G. Cardiovascular aspects. In Goldsmith J.P., Karotkin E.H., eds.: Assisted Ventilation of the Neonate, 4th ed., Philadelphia: Saunders, 2003. Mariani, G., Dik, P. B., Ezquer, A., Aguirre, A., Esteban, M. L., Perez, C., Fustiñana, C., Preductal and post-ductal O2 saturation in healthy term neonates after birth. The Journal of Pediatrics. 2007;150(4):418–421, doi: 10.1016/j.jpeds.2006.12.015. McGowan, J. E., Rozance, P. J., Price-Douglas, W., Hay, W. W. Glucose homeostasis. In Gardner S.L., Carter B.S., Enzman-Hines M., Hernandez J.A., eds.: Merenstein and Gardner’s Handbook of Neonatal Intensive Care, 7th edn., St Louis: Mosby, 2011.

Merrill, J. D., Ballard, R. A. Care of the high risk infant. In: Avery G.B., ed. Avery’s Diseases of the Newborn. Philadelphia: Saunders, 2005. Murki, S., Kumar, P., Lingappa, L., Narang, A. Effect of a single dose of sodium bicarbonate given during neonatal resuscitation at birth on the acid–base status on first day of life. Journal of Perinatology. 2004; 24(11):696–699. Niermeyer, S., Clarke, S. Delivery room care. In Gardner S.L., Carter B.S., Enzman-Hines M., Hernandez J.A., eds.: Merenstein and Gardner’s Handbook of Neonatal Intensive Care, 7th edn., St Louis: Mosby, 2011. O’Donnell, C. P.F., Kamlin, C. O.F., Davis, P. G., Carlin, J. B., Morley, C. J., Clinical assessment of infant colour at delivery. Archives of Disease in Childhood: Fetal and Neonatal Edition. 2007;92(6):F465–F467, doi: 10.1136/adc.2007.120634. Pairman S., Pincombe J., Thorogood C., Tracy S., eds. Midwifery Preparation for Practice, 3rd ed., Sydney: Elsevier, 2014. Perlman, J. M., Wyllie, J., Kattwinkel, J., Atkins, D. L., Chameides, L., Goldsmith, J. P., on behalf of the Neonatal Resuscitation Chapter Collaborators, Special Report: Neonatal Resuscitation. 2010 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science with Treatment Recommendations. Pediatrics. 2010;126(5):e1319–1344, doi: 10.1542/peds.2010–2972B. Riley, M., Halliday, J.Birth Defects in Victoria, 2005–2006. Melbourne: Victorian Government Department of Human Services, 2008. Salhab, W. A., Wyckoff, M. H., Laptook, A. R., Perlman, J. M. Initial hypoglycemia and neonatal brain injury in term infants with severe fetal acidemia. Pediatrics. 2004; 114(2):361–366. Siew, M. L., te Pas, A. B., Wallace, M. J., Kitchen, M. J., Lewis, R. A., Fouras, A., et al, Positive end-expiratory pressure enhances development of a functional residual capacity in preterm rabbits ventilated from birth. Journal of Applied Physiology. 2009;106(5):1487– 1493, doi: 10.1152/japplphysiol.91591.2008. South, M., Isaacs, D.Practical Paediatrics. London: Churchill Livingstone, 2012. Snell R.S., Smith M.S., eds. Clinical Anatomy for Emergency Medicine. St Louis: Mosby,

1993. The Consultative Council on Obstetric and Paediatric Mortality and Morbidity Annual Report for the Year 2007, Incorporating the 46th survey of perinatal Deaths in Victoria. Victorian Government Department of Health, Melbourne, 2010. Retrieved from www.health.vic.gov.au/ccopmm Van Woerkom, R., Beharry, K. D., Modanlou, H. D., Parker, J., Rajan, V., Akmal, Y., Aranda, J. V. Influence of morphine and naloxone on endothelin and its receptors in newborn piglet brain vascular endothelial cells: clinical implications in neonatal care. Pediatric Research. 2004; 55:147–151. Vento, M., Asensi, M., Sastre, J., García-Sala, F., Pallardó, F. V., Viña, J. Resuscitation with room air instead of 100% oxygen prevents oxidative stress in moderately asphyxiated term neonates. Pediatrics. 2001; 107(4):642–647. Vento, M., Asensi, M., Sastre, J., Lloret, A., Garcia-Sala, F., Minana, J. Hyperoxemia caused by resuscitation with pure oxygen may alter intracellular redox status by increasing oxidized glutathione in asphyxiated newly born infants. Seminars in Perinatology. 2002; 26(6):406–410. Wood, F. E., Morley, C. J., Dawson, J. A., Kamlin, C. O.F., Owen, L. S., Donath, S., Davis, P. G., Improved techniques reduce face mask leak during simulated neonatal resuscitation: study 2. Archives of Disease in Childhood: Fetal and Neonatal Edition. 2008;93(3):F230–F234, doi: 10.1136/adc.2007.117788.

PA R T 3

ESSENTIAL KNOWLEDGE O U TL I N E INTRODUCTION TO ESSENTIAL CONCEPTS OF PARAMEDIC PRACTICE CHAPTER 55: Perfusion CHAPTER 56: The autonomic response CHAPTER 57: The inflammatory response

SECTION 18

ESSENTIAL CONCEPTS OF PARAMEDIC PRACTICE O U TL I N E INTRODUCTION TO ESSENTIAL CONCEPTS OF PARAMEDIC PRACTICE CHAPTER 55: Perfusion CHAPTER 56: The autonomic response CHAPTER 57: The inflammatory response

INTRODUCTION TO ESSENTIAL CONCEPTS OF PARAMEDIC PRACTICE IN THIS SECTION Chapter 55 Perfusion Chapter 56 The autonomic response Chapter 57 The inflammatory response

A number of essential physiological concepts underpin paramedic practice and are common to a wide range of diseases and injuries. Perfusion, the autonomic nervous system and inflammation are concepts that all paramedics must understand if they are to make safe and effective clinical decisions. These homeostatic responses are common across nearly all of the conditions that paramedics confront and the importance of understanding how they integrate into the disease process cannot be overemphasised. However, these chapters are by no means sufficient in depth or breadth to fully provide the understanding that paramedics need: consider them instead as a quick reference to aid in understanding. For more detailed discussions, refer to a specialist pathophysiology text.

CHAP TER 55

Perfusion By Matt Johnson and Kathryn Eastwood

Introduction One of the consequences of working in an environment subject to time pressures and few diagnostic tools is paramedics’ propensity to summarise complex physiological responses into axioms that can be used as rules to assist in decision making. Viewed from outside the profession, these axioms may appear rather unsophisticated, but they are rarely incorrect. For example: ‘The first two rules of ambulance care: (1) the air must go in and out; and (2) the blood must go around and around.’ Simplistic certainly, but this saying holds a truth that is not only reinforced by the primary survey (A, B, C) but is also the basis of sustaining life: no cell can survive without an adequate supply of nutrients. This concept is central to homeostasis, as well as in determining how you as a clinician are going to correct disturbances caused by illness or injury. Without an understanding of the concept of perfusion, you risk simply treating the patient’s symptoms rather than managing the underlying cause.

What is perfusion? Definitions of perfusion often focus on the movement of fluid through a capillary but to apply the concept to emergency health settings paramedics need to include more than simply fluid in their understanding of this concept. If we refer back to rule 2, the blood must circulate because cells require a constant supply of nutrients (and the removal of waste products) if they are to function normally and it is the blood that carries these nutrients. Oxygen and glucose are the primary nutrients required by cells and under normal circumstances the lungs and gastrointestinal tract, respectively, load sufficient amounts of each of these into the blood. Including the amount of oxygen and glucose delivered to the cells in the definition of perfusions adds the notion that a cell can be adequately supplied with blood but still be poorly perfused if that blood does not carry sufficient oxygen or glucose. Perfusion is therefore a product of the interaction between various systems. This includes not only the cardiovascular system (see Box 55.1), but also the respiratory and gastrointestinal systems. A flaw in any of these systems can result in alterations to perfusion and cellular function. Figure 55.1 outlines the interactions between the systems that create perfusion and demonstrates the dependent nature of these components. In practice, the term perfusion is often used synonymously with the term ‘pressure’ but when the system is considered as a whole, ‘pressure’ is only one component of perfusion (see Box 55.2). B O X 5 5 . 1P

relo ad and afterlo ad

Two common terms used when discussing perfusion are preload and afterload. Preload is the pressure of blood that fills the heart during diastole. The greater the volume of blood filling the ventricles, the more the walls of the ventricles are stretched and the stronger the contraction. Paramedics are primarily concerned with situations where preload is too low (the heart cannot pump what it does not receive) as this will generally result in low cardiac output and poor perfusion. A lack of blood volume and widespread vasodilation (e.g. anaphylaxis) are common causes of low preload, but it can also occur when the right ventricle is unable to supply the left ventricle with sufficient blood. A blockage in the blood vessels supplying the right ventricle or in the pulmonary blood vessels leading to the left side of the heart can cause this situation. Afterload refers to the amount of pressure in the aorta that the left ventricle must overcome to eject its volume of blood. High afterload pressure will make it more difficult for the left ventricle to eject its contents, but there needs to be sufficient afterload to force the blood already in the aorta to move along the arteries and towards the cells.

B O X 5 5 . 2O v e r p e r f u s i o

n and under per f usio n

The terms overperfusion and underperfusion do not refer to the quality of perfusion but to tissues receiving more (or less) blood than would be expected to meet their metabolic needs. For instance, the skin is often overperfused with the extra blood directed there to dissipate heat. Other organs, such as the heart and lungs, receive more blood than they need for their own metabolic purposes and as such can survive unharmed for a period of underperfusion.

FIGURE 55.1 The perfusion pathway. Perfusion is too often considered to be just another term for ‘blood pressure’ when it actually describes the ability of the body to supply cells with the environment they need to

function normally.

The basics of normal perfusion The l ungs With each breath, oxygen is drawn into the alveoli of the lungs. Simultaneously, the lungs receive all the deoxygenated blood from the right side of the heart. As the blood passes through the capillaries, oxygen diffuses from the alveoli into the blood. It takes a red blood cell (RBC) approximately 0.75 seconds to pass through the capillary at rest, but only 0.25 seconds for diffusion to occur (West, 2011).

The blood Once oxygen diffuses into the blood it passes into RBCs and binds with haemoglobin (Hb). The amount of oxygen capable of being carried in the blood is dependent on the amount of Hb. Normally, 100 mL of blood carries 20 mL of oxygen when 100% saturated.

The blood vessels Arteries carry oxygenated blood from the heart via arterioles to the capillary beds; the porous walls of the capillaries allow nutrients and wastes to diffuse easily. Veins carry deoxygenated blood back to the heart.

The heart The right ventricle pumps deoxygenated blood to the lungs to be replenished. The left ventricle pumps oxygenated blood to the organs. The efficiency of the pumps determines how much blood is forced into the vessels.

The liver The liver receives blood from the systemic circuit but also from the gastrointestinal system when it processes the wide range of chemicals absorbed in the gut (Craft, Gordon & Tiziani, 2011). Responding to hormones released by the pancreas, the liver can extract glucose from the blood and store it for later use or release stored glucose into the blood for cell metabolism.

The cells Cells require a constant supply of oxygen, glucose and other nutrients and a constant adequate blood flow is the means by which they are supplied.

Disturbances of perfusion The l ungs The ability of the lungs to present fresh supplies of oxygen to the blood passing through the lung capillaries is an essential component of maintaining normal cell function. Disturbances to oxygenation can occur because of problems with ventilation, external respiration, or both. Causes of problems with ventilation (the process of air moving in and out of the lungs) include: • choking and airway obstruction (see Ch 16) • asthma (see Ch 17), croup (see Ch 23) and anaphylaxis (see Ch 27) • damage to the chest wall or diaphragm—can reduce ventilation (see Ch 33) • spinal cord injury—can cause paralysis of the diaphragm (see Ch 35). Causes of problems with external respiration (the movement of oxygen from the alveoli to the blood) include: • chronic obstructive pulmonary disease (see Ch 19) • acute pulmonary oedema (see Ch 18) • pulmonary embolism (see Ch 21) • changes to atmospheric pressure that occur with diving and aviation (see Ch 39).

The blood Changes to the blood that result in poor perfusion can be categorised as either insufficient volume (hypovolaemia) or insufficient haemoglobin to carry adequate supplies of oxygen (anaemia). Causes of hypovolaemia include: • injuries that cause significant bleeding (burns, see Ch 36; musculoskeletal injuries, see Ch 34; post-partum haemorrhage, see Ch 45) • conditions that promote movement of fluid from the intravascular space to the interstitial space and so result in a loss of circulation volume (burns, see Ch 36; anaphylaxis, see Ch 27). Causes of anaemia include: • diseases that cause a decrease in RBCs (kidney disease, B12 deficiency, iron deficiency) • a slow undetected haemorrhage such as a persistent bowel bleed—this is not uncommon and it is difficult for patients to detect as the digestive process turns red blood into black and tarry stools.

The blood vessels The layer of smooth muscle in arteries, arterioles and veins provides a mechanism by which the volume of the blood vessels can be altered (McCance & Huether, 2012). Contracting the muscle allows the vessel to reduce in diameter and maintain pressure when there is a loss of fluid (blood). Relaxation of the smooth muscle layer causes the opposite effect. The smooth muscle layer is innervated by the autonomic nervous system

(see Ch 56). The muscle is also responsive to hormones such as adrenaline and substances released during the inflammatory process (see Ch 57). Causes of vasoconstriction (a decrease in vessel diameter) include: • sympathetic nervous system innervation • adrenaline, noradrenaline • high levels of oxygen (except in the pulmonary circulation). Causes of vasodilation (an increase in vessel diameter) include: • parasympathetic nervous system innervation • inflammatory substances such as histamine (anaphylaxis, see Ch 27) and nitric oxide • drugs such as glyceryl trinitrate and morphine (see Ch 24) • low levels of oxygen and/or high levels of CO2 in the systemic system, and high levels of oxygen in the pulmonary system.

The heart Disturbances of rate Bradycardia: Rates that are too slow do not eject sufficient blood into the systemic system to deliver the oxygen and glucose that cells require. The shorter pulmonary circuit is less affected by bradycardia. Tachycardia: As the heart rate approaches 200 BPM the ventricles may not have sufficient time to fill before they contract and eject blood into the systemic circuit. This can result in a decrease in cardiac output and cell perfusion (see Ch 25).

Disturbances of rhythm The heart relies on a coordinated contraction to maximise efficiency (see Ch 25). Injury to the tissues of the heart that control its regular rate and rhythm can result in disturbances to the normal rhythm of the heart and lead to decreased cardiac output (e.g. atrial fibrillation, atrial flutter).

Ej ection fraction When the left ventricle contracts, it forces blood into the systemic circulation. As such, it has the highest workload of any of the chambers of the heart and accordingly makes up 75% of the muscle mass of the heart. In the instant before it contracts, the left ventricle normally holds about 120 mL of blood (in a 70-kg male). Upon contracting it ejects about 70 mL of blood (McCance & Huether, 2012). The blood ejected is referred to as the stroke volume. The percentage of blood ejected is referred to as the ejection fraction: this is normally 55–70% (McCance & Huether, 2012). Damage to the muscle of the left ventricle can result in a less forceful contraction and less blood being forced into the systemic circuit.

Preload Blood returning to the heart fills the heart. This blood is at a low pressure and changes in that pressure affect the blood’s ability to fill and stretch the heart. A normal preload (around 5–10 cm of water pressure above the right atria) is sufficient to adequately fill and stretch the heart. A reduction in preload pressure results in a reduction in both stroke

volume and force of contraction. An increase in preload pressure conversely improves stroke volume and force of contraction up to the point of failure (Craft, Gordon & Tiziani, 2011).

The liver In combination with the pancreas and the gastrointestinal system, the liver plays a vital role in maintaining normal cell function by ensuring a normal glucose level in the blood. However, injury or disease affecting any one of these three organs can result in disturbances of glucose levels. Hormones (glucagon and insulin) secreted by the pancreas determine the uptake and release of glucose by the liver. Diabetes and pancreatitis affect the amount of glucagon and insulin released but also tissue sensitivity to these hormones. Intentional or accidental mismanagement of diabetic medications can cause hypoglycaemia. Chronic liver and GIT diseases do not commonly present as health emergencies but they may complicate the diagnosis and management of other health emergencies. Chronic liver disease may also restrict the ability of patients to compensate for other health problems.

Assessment of perfusion The body’s ability to compensate for poor perfusion poses a number of problems for the paramedic. At the extreme end of the scale—no perfusion—the clinical picture is clear: the patient will be unconscious, pulseless and cool to touch. The speed at which this state develops, however, and the range of symptoms that present as the patient passes from adequate to no perfusion are far less clear. Nearly all perfusion assessment tools use a combination of heart rate, blood pressure, skin and conscious state to categorise the severity of the condition. Of all of these, blood pressure can be the least reliable indicator of perfusion status. Patients who are normally hypertensive can be suffering poor perfusion when their systolic and diastolic values would be considered to be within the normal range. Without a pre-event measure of normal blood pressure, it can be difficult to evaluate the significance of a reading during a health crisis. (However, it is very useful in setting a baseline with which subsequent measurements can be compared.) The body’s response of raising the heart rate and restricting blood flow to essential organs also ‘protects’ the blood pressure until there is no more capacity for compensation. Hypotension is therefore generally considered a late sign of poor perfusion. An early sign of poor perfusion is often an increased heart rate (Craft, Gordon & Tiziani, 2011). In response to sympathetic nervous system (SNS) innervation, the increase in heart rate supports cardiac output despite a decreased blood volume (cardiac output = heart rate × stroke volume). In the field, this tachycardia needs to be distinguished from anxiety and a response to pain—which is why matching it to the broader clinical picture is important. The earliest sign, the vasoconstrictor effect of the SNS on the vessels leading to non-essential organs, is a strong indication that the tachycardia is not simply a response to pain and is reliably measured by assessing the skin. Cool, pale and clammy skin indicates shunting of the blood and a state of inadequate perfusion. Conscious state is the last of the four perfusion indicators usually assessed. In the setting of hypovolaemia, an altered conscious state is a late indicator, as the brain preferentially receives blood as the body responds to blood loss. However, the brain is far more susceptible to hypoxia and hypoglycaemia. Changes in these parameters often alter the conscious state long before changes occur to the skin. Remember, however, that the body is adept at maintaining its perfusion and the progression from normal to extremely ill may not be apparent in a single assessment. It will, however, become obvious if a series of accurate assessments are performed over time. This highlights the importance of undertaking sequential observations for any patient you suspect could develop perfusion problems.

Principles of medical management of perfusion Having an understanding of the causes of poor perfusion combined with an accurate patient assessment, paramedics should be able to effectively identify and manage patients with poor perfusion.

Ventilate As per rule 1 and the primary survey, always ensure the patient is ventilating adequately before you starting looking for other issues. Hypoxia will initially raise the heart rate, affect the conscious state and, if prolonged, eventually slow the heart rate and concurrently reduce perfusion. Ensuring adequate ventilation can be as simple as positioning the patient or providing jaw support, or it can be as complex as decompressing a tension pneumothorax with a wide-bore needle or pneumocath. Do not move to the circulation (C) until you have resolved any issues with airway (A) and breathing (B).

The heart Disturbances of heart rate and rhythm should be identified during the vital signs survey and, if associated with inadequate perfusion, managed as a priority. Intensive care paramedics across Australia and New Zealand carry a range of antiarrhythmic medications such as atropine, adrenaline, verapamil, amiodarone and adenosine. The use of external defibrillators to electrically revert dangerous arrhythmias and conduct external pacing is also common practice. In addition, intensive care paramedics administer a range of medications to improve ventricular contractility. This group of medications (known as inotropes) can increase the ejection fraction and improve cardiac output.

The liver The brain has a high metabolic demand and no mechanism for storing significant amounts of glucose or oxygen (McCance & Huether, 2012). As a result, the conscious state decreases rapidly if supplies of either are compromised. It is unusual for inadequate blood supply to be the cause of the problem when a patient is unconscious but has palpable distal pulses. If you have resolved any ventilation issues and have an unconscious patient with distal pulses, consider whether the blood being delivered to the brain is not carrying sufficient glucose.

Volume, inotrope, pressor (VIP) Restoring lost blood volume with intravenous fluids is widely supported by ambulance guidelines across Australia and New Zealand. If other causes of poor perfusion have been eliminated or treated and the patient remains poorly perfused, replacing lost volume is the

first step in managing poor perfusion. In most settings an initial dose of 20 mL/kg of isotonic crystalloid is recommended, followed by a repeat if the patient remains poorly perfused. The aim is to restore preload to an optimum level, thus ensuring that the heart receives optimum filling and stretch pressures. If the patient remains poorly perfused despite optimum filling and pressures, the standard treatment is to commence inotrope therapy. Adrenaline, noradrenaline or dopamine all promote varying degrees of vasoconstriction and increase circulatory pressures but should not be commenced until normal intravascular volumes have been restored. In patients with low or absent vascular tone, normal preload will not be restored by volume alone and vasopressors (adrenaline, noradrenaline or even metaraminol) have to be used to improve venous return. This ‘fill then squeeze’ approach aims to ensure there is sufficient circulating volume before vasoconstriction restricts blood flow to some organs. Paramedics in Australia and New Zealand don’t commonly use selective pressors such as metaraminol. Unlike the inotrope family of drugs which have effects on both the heart and the blood vessels, the pressors produce only potent vasoconstriction. There are a number of controversies surrounding the best fluid to use to restore perfusion (isotonic, hypertonic, crystalloid, colloid), how much should be administered and even whether it should be administered if there is a suspicion the patient may still be bleeding. This area is likely to see significant changes in guidelines over the next decade as data is collected and assessed.

Summary The term ‘perfusion’ describes the ability of the cardiovascular system to supply cells with adequate nutrition and removal of wastes. It is often used synonymously with the term ‘pressure’ but ‘pressure’ is only one component of perfusion. There is no heart rate or blood pressure that describes adequate perfusion, as individual anatomy and physiology can alter the delivery of nutrients to cells as pressures fluctuate. Rates and pressures outside the normal range should always be considered as pathological until proven otherwise. Assessing perfusion involves a number of factors including heart rate, blood pressure, conscious state and circulation to the skin. Poor perfusion (regardless of cause) usually triggers a sympathetic nervous system response. The role of oxygen and glucose in providing adequate cellular perfusion is often overlooked.

References Craft, J., Gordon, C., Tiziani, A.Understanding Pathophysiology. Sydney: Elsevier, 2011. McCance, K., Huether, S. Pathophysiology: The Biologic Basis for Disease in Adults and Children, 6th ed. Philadelphia: Mosby, 2010. West, J. B. Respiratory Physiology, 9th ed. Philadelphia: Wolters Kluwer, 2011.

Suggested reading McGloin, S.Advanced Practice in Critical Care. Sydney: Wiley-Blackwell, 2010. Patton, K.T., Thibodeau, G. Anatomy and Physiology, 7th ed. St Louis: Mosby, 2009.

CHAP TER 56

The autonomic response By Leanne Boyd

Introduction Paramedics need to have an understanding of the nervous system because it regulates, coordinates and oversees all other body systems. The nervous system actually functions as a whole but it can be subdivided to enhance understanding, as illustrated in Figure 56.1. The primary division is the central nervous system and the peripheral nervous system. The central nervous system consists of the brain and the spinal cord. The peripheral nervous system consists of the cranial and spinal nerves and the peripheral components of the autonomic nervous system. While all elements of the nervous system are important, it is the autonomic nervous system that most impacts on paramedic practice and therefore provides the focus of this chapter.

FIGURE 56.1 Subdivisions of the nervous system. Source: Craft, Gordon & Tiziani (2011).

What is the autonomic nervous system? The autonomic nervous system is made up of two divisions: the sympathetic nervous system and parasympathetic nervous system. These systems govern involuntary functions of cardiac muscle, smooth (involuntary) muscle and glands (Brown & Edwards, 2012). Both divisions function to maintain homeostasis, albeit in totally different ways. For example, the sympathetic nervous system speeds up the body and prepares it for action, particularly in moments of acute stress (‘fight or flight’). In contrast, the parasympathetic nervous system is active during periods of rest and recovery and tends to slow the body down (rest and digest). Figure 56.2 summarises parasympathetic and sympathetic effects. Under normal circumstances, there is underlying neurological tone (sympathetic or parasympathetic) for many of our tissues and organs, as illustrated in Table 56.1. An understanding of each system is important for paramedics, as both systems can negatively impact on patient outcomes if the innervation of one system dominates inappropriately. TABLE 56.1 Underlying neurological tone Site Predominant tone Ciliary muscle Parasympathetic Iris Parasympathetic Sinoatrial node Parasympathetic Arterioles Sympathetic Veins Sympathetic Gastrointestinal tract Parasympathetic Uterus Parasympathetic Urinary bladder Parasympathetic Salivary glands Parasympathetic Sweat glands Sympathetic

FIGURE 56.2 Summary of the effects of the parasympathetic and sympathetic nervous systems. Source: Bryant & Knights (2011).

The parasympathetic nervous system The main function of the parasympathetic nervous system is to conserve and restore energy. The preganglionic cell bodies of the parasympathetic nervous system are located in the brainstem and the sacral spinal segments (S2–S4). The parasympathetic ganglia are located in or near the structures that they innervate (Brown & Edwards, 2012). Parasympathetic nerves arising from nuclei in the brainstem travel to the viscera of the head, thorax and abdomen within cranial nerves, such as the oculomotor (III), facial (VII), glossopharyngeal (IX) and vagus (X) nerves.

The sympathetic nervous system The sympathetic nervous system activates energy stores in times of need and is referred to as the coordinator of the ‘fight or flight’ response. You have probably experienced this response in some form: for example, a near-miss in the car or an unexpected loud noise, which results in symptoms such as a rapid heart rate and dry mouth. The sympathetic division is innervated by cell bodies located from T1 to L2. The preganglionic axons of the sympathetic division form synapses shortly after leaving the cord in the sympathetic ganglia or chain. At the sympathetic ganglia, most preganglionic neurons then synapse with their respective postganglionic neuron, which innervates target organs throughout the body, as illustrated in Figure 56.3. Some preganglionic sympathetic neurons innervate the cells of the adrenal medulla, which produce adrenaline and noradrenaline. When these substances are released by the adrenal medulla into the bloodstream, they are hormones; however, when they are released by neurons and travel across the synapse, they are neurotransmitters (despite being exactly the same substance). The effect of neurotransmitters is short term, whereas some substances such as hormones have longerlasting, possibly detrimental effects at the target organs (Craft, Gordon & Tiziani, 2011).

FIGURE 56.3 Sympathetic and parasympathetic neurotransmitters and receptors. Source: Craft, Gordon & Tiziani (2011).

Neurotransmitters and receptors The sympathetic and parasympathetic nervous systems both release chemicals called neurotransmitters. These chemicals relay the nerve’s electrical signal across the gaps created when the nerve connects to cells, organs or other nerves. These chemical neurotransmitters then attach to sympathetic or parasympathetic receptors to cause an effect, as illustrated in Figure 56.3.

Sympathetic neurotransmitters and receptors Adrenaline and noradrenaline are the neurotransmitters for the sympathetic nervous system and are collectively referred to as catecholamines. They stimulate two major classes of adrenergic receptors: • alpha-adrenergic receptors (α1 and α2) • beta-adrenergic receptors (β 1, β 2 and β 3). The cells of the effector organs have particular types of adrenergic receptors located on their surfaces and a cell may actually have more than one type of adrenergic receptor. The effects of the sympathetic nervous system on target organs are summarised in Table 56.2.

TABLE 56.2 The stimulation effects of the sympathetic and parasympathetic nervous systems

Source: Craft, Gordon & Tiziani (2011).

Parasympathetic neurotransmitters and receptors The neurotransmitter for the parasympathetic nervous system is acetylcholine and parasympathetic neurons are collectively referred to as cholinergics. Acetylcholine works through cholinergic receptors, which are broadly categorised into nicotinic and muscarinic receptors. Nicotinic receptors are located at the first synapse (at the ganglia) of both the sympathetic and the parasympathetic nervous systems. Muscarinic receptors are found on all effector cells that are stimulated by the postganglionic cholinergic neurons of either the parasympathetic nervous system or the sympathetic system. The effects of the parasympathetic nervous system on target organs are summarised in Table 56.2.

Intracellular second messengers An awareness of the intracellular second messengers associated with the sympathetic nervous system in particular is relevant to paramedic practice. The second messenger mechanism is usually slower and longer-lasting than the direct mechanism. Using intracellular messengers it can regulate other cellular processes, such as cytoskeleton movement, gene expression and shuttling of proteins along the axonal transport system

(Patton & Thibodeau, 2010). When a β 1 sympathetic receptor is stimulated, this results in activation of the enzyme adenyl cyclase, whose role is to create cyclic adenosine monophosphate (cAMP) from adenosine triphosphate. In the heart, increased levels of cAMP are responsible for the changes to free intracellular calcium associated with the increased force of contraction and for the decreased membrane stability that results in an increased heart rate and, if in excess, ectopic beats and eventually ventricular tachycardia/ventricular fibrillation (Bryant & Knights, 2011). In the lungs, stimulation of a β 2 receptor produces an increase in cAMP that is responsible for bronchodilation. Stimulation of the parasympathetic system in the lungs produces an increase in cyclic guanine monophosphate (cGMP), which has an opposite effect to cAMP. A balance in effect between cAMP and cGMP is involved in governing many cellular responses to the autonomic nervous system. Peripheral blood vessels responding to sympathetic stimulation have a different intracellular second messenger, inositol triphosphate, which produces vasoconstriction by actions on the smooth muscle. This is opposed by intracellular levels of cGMP, which is formed in response to nitric oxide stimulation of the blood vessel. The relevance of this to paramedic practice is that glyceryl trinitrate (GTN) acts by stimulating the production of cGMP, causing vasodilation. A potentially hazardous drug interaction exists between GTN and the erectile dysfunction drugs that work by blocking the breakdown of cGMP: this is the reason behind the relative contraindication of GTN in the presence of these drugs (Bryant & Knights, 2011). The effect of glucagon on liver cells is to promote the breakdown of glycogen. Glycogen shares the intracellular second messenger cCAMP with the sympathetic system. This explains the ability of adrenaline to produce an increase in blood glucose and the ability of glucagon to increase the heart rate. Glucagon’s ability to increase the heart rate means it can be used as an alternative treatment when a patient is suffering from an overdose of beta-blockers.

Assessment of autonomic nervous system function S ym pa the ti c Most of the patients paramedics encounter will be experiencing some level of sympathetic nervous system response. Paramedics are usually called when an adverse health event exceeds the coping mechanisms or resources of the patient or their family. This indicates that there is a high likelihood the sympathetic ‘fight or flight’ response is in action. This will most likely affect the patient’s physiological parameters and it is almost impossible to distinguish whether the vital signs you are recording are purely related to a pathophysiological state or are augmented/led by sympathetic stimulation. An example of the sympathetic effect on cardiac output is illustrated in Figure 56.4.

FIGURE 56.4 The effect of sympathetic and parasympathetic stimulation on cardiac output. Source: Hall (2011). To illustrate this complexity, imagine that a patient has cut his finger with a butcher ’s

knife and lost a significant amount of blood. He presents as tachycardic, cool, pale and clammy. The injury will result in sympathetic innervation, which will increase his heart rate. This increase in heart rate will support cardiac output for a period of time despite the decreased blood volume from the bleed (cardiac output = heart rate × stroke volume). The paramedic must determine whether the tachycardia is purely an expected sympathetic response or because of pain or other pathophysiology. The vasoconstrictor effect of the sympathetic response on the vessels leading to non-essential organs is a strong indication that the tachycardia is not simply a response to pain and is reliably measured by assessing the skin. Cool, pale and clammy skin indicates shunting of the blood and a state of inadequate perfusion. This simplistic case demonstrates the interconnectedness between the sympathetic response and the patient’s presentation. Critical illness is a potent stimulus of the sympathetic nervous system and, if prolonged, can have increasingly detrimental effects. Several organ systems may be affected. The heart seems to be most susceptible to sympathetic overstimulation. Detrimental effects include impaired diastolic function, tachycardia, tachyarrhythmia and myocardial ischaemia. Adverse effects have also been observed in other organs such as the lungs (pulmonary oedema, elevated pulmonary arterial pressures), the coagulation system (hypercoagulability, thrombus formation), the gastrointestinal system (hypoperfusion, inhibition of peristalsis), the endocrine system (decreased prolactin, thyroid and growth hormone secretion), the immune system (immunomodulation, stimulation of bacterial growth), metabolism (increase in cell energy expenditure, hyperglycaemia and electrolyte changes), bone marrow (anaemia) and skeletal muscles (apoptosis) (Dünser & Hasibeder, 2009).

Parasympathetic The effects of parasympathetic stimulation are evidenced in everyday life and ordinary circumstances. The parasympathetic system is the ‘relax, restore and maintain’ system. Given this, it doesn’t normally present a problem in patient assessment for paramedics: reflex responses are rarely evaluated in the pre-hospital setting. However, some abnormal responses are easily observed and they may indicate autonomic nerve injury. These responses include loss of temperature control, hypotension (in the absence of volume loss), bradycardia (in the absence of hypoxia) and priapism (Sanders, 2007) and they are often found in patients with a relatively high-level spinal cord injury. Normally, sympathetic stimulation maintains the muscle tone that keeps blood vessels at their usual diameter. If sympathetic stimulation is disrupted by an injury to the spinal cord or medulla, neurodepressive drugs, emotional stress or some other factor, the blood vessels dilate significantly. Widespread vasodilation reduces blood pressure, thus reducing blood flow (Patton & Thibodeau, 2010). Bradycardia results because parasympathetic innervation to the heart dominates.

Principles of management Potential therapeutic options to manage excessive sympathetic reactions comprise temperature control, adequate use of sedative/analgesic drugs, aiming for reasonable cardiovascular targets, adequate fluid therapy and use of medications such as steroids and antibiotics to reduce underlying inflammatory or infective responses (Dünser & Hasibeder, 2009). Potential therapeutic options to manage inadequate sympathetic response comprise administration of IV fluids and adrenergic agonists. The patient with a spinal cord injury will also need to be monitored for hypothermia due to hypothalamic dysfunction (Brown & Edwards, 2012).

Summary The autonomic nervous system has two divisions: the sympathetic nervous system and the parasympathetic nervous system. These systems govern involuntary functions of cardiac muscle, smooth (involuntary) muscle and glands. The sympathetic nervous system responds to stress and prepares the body for action (‘fight or flight’), while the parasympathetic nervous system dominates during periods of rest and recovery and tends to slow the body down. Poor perfusion, hypoglycaemia, pain and other noxious stimuli can all trigger the sympathetic nervous system and the signs of sympathetic innervation can help identify the underlying illness or injury. A number of illnesses or injuries can trigger a widespread parasympathetic response and recognising this ‘pattern’ can assist in determining the cause.

References Brown, D., Edwards, H. Lewis’s Medical–Surgical Nursing, 3rd ed. Sydney: Elsevier, 2012. Bryant, B., Knights, K.Pharmacology for Health Professionals. Sydney: Elsevier, 2011. Craft, J., Gordon, C., Tiziani, A.Understanding Pathophysiology. Sydney: Elsevier, 2011. Dünser, M., Hasibeder, W. Sympathetic overstimulation during critical illness: adverse effects of adrenergic stress. Journal of Intensive Care Medicine. 2009; 24(5):293–316. Hall, J. E. Guyton and Hall Textbook of Medical Physiology, 12th ed. Philadelphia: Saunders, 2011. Patton, K., Thibodeau, G. Anatomy and Physiology, 7th ed. St Louis: Mosby, 2010. Sanders, M. Mosby’s Paramedic Textbook, 3rd ed. St Louis: Mosby, 2007.

CHAP TER 57

The inflammatory response By Matt Johnson

Introduction Chapter 55 established how a constant supply of nutrients to cells is essential to homeostasis. But accidental exposure to pressure, heat, cold, microbes, chemicals and radiation will quickly injure and kill the cells that make up human tissue. In fact, when you consider the number of potential diseases and accidents that can befall any one of us, the body’s ability to locate and heal damaged tissue is as essential to health as its more immediate needs for oxygen or glucose. Despite the vast number of different causes of cell damage, the method by which the body responds is remarkably consistent. This inflammatory response is extremely sensitive and finely balanced but in some circumstances the complex interactions between the numerous chemicals and compounds that drive the inflammatory response can spread beyond the area of damaged tissue. Ironically, when this occurs the inflammatory response can harm healthy tissue, particularly if the response is inappropriate or prolonged. The detrimental effects of an uncontrolled or misdirected inflammatory response have long been recognised as the cause behind chronic diseases such as rheumatoid arthritis, lupus, coeliac disease and multiple sclerosis, but they also drive acute events such as asthma, anaphylaxis, sepsis, burn shock and secondary head injury. Research has found that even cardiovascular disease is driven by an abnormal response to tissue injury (Koenig, 2000). The notion that the process of repair and healing can actually cause harm is counterintuitive, but it is something that paramedics must understand because it impacts on the chronic and acute conditions they are required to recognise and treat. Thankfully, as complex as the inflammatory response can be when examined in detail, the inflammatory principles are relatively easy to understand, are predictable and can often be managed in the emergency setting. This chapter provides an introduction to the inflammatory process, but does not go into the detail needed to understand many of the complex interactions surrounding the inflammatory response. The reader is strongly encouraged to study this important area in more depth using specific physiology and pathophysiology textbooks on the subject.

What is inflammation? Inflammation is the name given to the syndrome that results when the body detects injured or destroyed cells (Patton & Thibodeau, 2010). It results from a cascade of chemical and biological reactions that drive further chemical responses. The inflammatory response is triggered to prevent infection, minimise further injury to the body and promote healing. The two most common triggers of inflammation are infection and direct tissue injury. Generally these produce an inflammatory response that is restricted to the site of damaged tissue but occasionally this response can cascade out of control and begin to affect tissues far from the original site of injury or infection, and can even evolve into a life-threatening condition. In addition to the classic instigators of tissue injury and infection, there are a range of adverse conditions that initiate the inflammatory response (see Box 57.1). These include ischaemia, defects in genetics or immunity, temperature extremes, chemical agents, nutrient deprivation and radiation (Trask, Rote & Huether, 2010). B O X 5 7 . 1C a u s e s

o f ac ute inflammatio n

• Trauma: pressure, abrasion, laceration • Thermal injury: burns, frostbite • Tissue necrosis from hypoxia or poor perfusion • Infections (bacterial, viral, parasitic) • Microbial toxins • Immune reactions • Irradiation and chemical agents

The basics of normal inflammation The key to understanding the inflammatory response is to remember that it is designed to minimise further injury, clean the area of damaged tissue and promote new cell growth. Accordingly, the primary action of the inflammatory process can be summarised as increasing blood flow to the area of injury. In addition to nutrients, this blood will bring the specialised white blood cells (leucocytes) required to remove dead tissue and fight infection (see Fig 57.1). Of course, open wounds can result in large amounts of blood loss, so the inflammatory response also plays a role in blood clotting.

FIGURE 57.1 The inflammatory response to minor injury. Source: McCance & Huether (2014). When the body receives a minor injury, inflammation provides increased blood supply to the site of injury and is the first stage of the healing process. Tissue damage from trauma, hypoxia or infection stimulates mast cells to release their intracellular granules (inflammatory mediators), which triggers three main processes: vasodilation, increased vascular permeability (cells of the capillary membrane move apart to allow access from the blood to the tissues) and chemotaxis (chemical attractor of inflammatory cells; see Box 57.2 and Fig 57.2). Collectively, this allows inflammatory cells to move to the site and stimulates the release of other pathways (complement, kinin and clotting) that limit the effect of the foreign substance, allowing time for the immune response (see Fig 57.3).

B O X 5 7 . 2T

he inflam m ato r y r espo nse

The inflammatory response involves three key processes: 1. vasodilation, resulting in increased blood flow to the damaged area 2. increased vascular permeability, as plasma leaks from blood vessels into the damaged area (refer to Fig 57.2) 3. chemotaxis—emigration of white blood cells and plasma proteins from blood into the damaged area.

FIGURE 57.2 Mast cells play an integral role in the inflammatory process. These specialised cells synthesise factors that generate pain, trigger vasodilation and promote coagulation. The breakdown of mast cells causes vasodilation, but also attracts white blood cells to the area. Source: Craft, Gordon & Tiziani (2011).

FIGURE 57.3

The inflammatory pathway. Source: Craft, Gordon & Tiziani (2011).

In more detail, the inflammatory process can be viewed as occurring over four stages.

Stage 1: injury A fit, healthy male has fallen from his bicycle and has a deep abrasion to his forearm. As his arm was compressed against the concrete gutter and his momentum forced it to slide across the rough surface, the skin was scoured away and the softer connective tissue underneath suffered a mix of compression, abrasion and heat. As a result, individual cell membranes were damaged and substances usually only found inside cells were released into the interstitial space.

Stage 2: detection The release of intracellular contents (particularly K+ ions, proteins and uric acid) into the extracellular space is the usual trigger for the inflammatory response that occurs after trauma. Once released into the extracellular space these foreign substances are detected by specialised cells that reside under the skin. These cells (macrophages and lymphocytes) act as an early detection system and are commonly found in tissues that are subject to injury or exposed to infective agents (e.g. the skin and the lining of the lungs and gastrointestinal system). They can also be found in the blood. Inflammatory mediator release can also be

triggered by hypoxia or other cell damage or in response to other inflammatory mediators from other cells elsewhere in the body.

Stage 3: response and recruitment As pathologists explore the inflammatory process in increasing detail they are unravelling what appears to be a never-ending string of precursor chemicals that trigger subsequent reactions that drive the inflammatory response forwards. For this chapter we deal with just the primary drivers involved in the process: if you are interested in learning more about the structure and function of the immune system, see Chapter 12 in Craft, Gordon and Tiziani (2011). Mast cells and granulocytes are cells that release inflammatory mediators to activate the main inflammatory response. Once the mast cells are activated, they release substances that drive the inflammatory process forwards. Some of these substances (such as histamine and serotonin) are active on their release, while others circulate in the blood in an inactive form and only become active when they contact other inflammatory mediators or intracellular contents (cytokines, chemokines, amines and eicosanoids). Inflammatory mediators can be divided into seven groups but the primary and most immediate effect of most of them is to alter blood flow in the region of the injury. They cause this change through two mechanisms: vasodilation and increased vessel permeability. Inflammatory mediators are very vasoactive (meaning they act on blood vessels): they increase blood flow to the area and allow plasma proteins and leucocytes (mainly neutrophils) that are normally trapped within the circulatory system to escape into the extracellular space (Medzhitov, 2008). The neutrophils attack foreign bodies or damaged tissue by releasing a number of powerful toxins, while the plasma proteins prolong vasodilation but also act to scavenge foreign cells and promote clotting (see below). In addition, the presence of the plasma proteins in the interstitial space creates an osmotic pressure that draws plasma from the intravascular space. This increase in blood flow and fluid leakage from the vessels results in two of the classic signs of inflammation: redness and swelling (see Fig 57.4). Inflammatory mediators cause rapid dilation of the postcapillary venules, which results in increased blood flow into the microcirculation. Histamine also causes increased vascular permeability resulting from retraction of endothelial cells lining the capillaries. The movement of fluid from the intravascular to the interstitial space challenges the lymphatic system, which may not be capable of draining all the exudate from the area (see Box 57.3). B O X 5 7 . 3T

h e lym p h a tic syste m a n d

inflammatio n The role of lymphatic vessels is to drain interstitial fluid and return it to the main circulatory system. The fluid in the lymph system passes through lymph nodes where immune cells (B cells) produce antibodies specific to the bacteria that is detected. Once matured, the antibodies bind to the bacteria and identify them for macrophages. Lymph nodes that drain injured or infected limbs will appear swollen and painful as a result of this process.

FIGURE 57.4 Capillary changes due to inflammation. Source: Craft, Gordon & Tiziani (2011).

The role of plasma proteins in inflammation The relationship between inflammation and healing is demonstrated by the activation of various plasma proteins. The tissue damage and subsequent vasodilation and increased vessel permeability triggered by the release of the inflammatory mediators attracts plasma proteins from three interrelated systems to the site of the injury. These proteins are integral to the inflammatory response and are classified as belonging to the complement, kinin or

clotting groups: • The complement group. Of the 20 proteins in this group all are inactive in the plasma until an injury or infection occurs. In reality, many of the group’s proteins simply form enzymes that drive the formation of other proteins within this system to promote vasodilation and histamine release, but several form potent chemical compounds that attack the cell membranes of foreign cells. Others attach to foreign or damaged cells and act as ‘chemical beacons’ to attract neutrophils and monocytes. • The clotting group. The clotting system is activated by a group of plasma proteins when they are exposure to damaged tissue (collagen, to be precise). This can occur when connective tissue and vessels are damaged by trauma; once activated, the plasma proteins in this group not only promote coagulation, they also release pro-inflammatory substances. In this way, inflammation and clotting are intrinsically connected. • The kinin group. The kinin and coagulation groups are intertwined with one of the plasma proteins involved in coagulation (factor XII), converting the inactive kinin protein (prekallikrein) into its active form. Once activated, most of the potent kinin proteins cause vasodilation and increased vessel permeability, but they also promote coagulation (activates Hageman factor) and the conversion of at least one of the complement plasma proteins (C5) to its active form.

Stage 4: resolution and repair The numerous chemicals that drive the inflammatory pathways are part of a finely balanced cascade: many of these chemicals stimulate the production of some inflammatory chemicals while simultaneously suppressing the production of others. When it works perfectly, the process initially drives the inflammatory response forwards, but eventually the change in the affected tissues starts to retard the progression. At a cellular level the neutrophils (and their toxic effects) are replaced by monocytes, which remove dead cells and initiate tissue growth (Serhan & Savill, 2005).

Alternative trigger: infection Apart from direct injury by trauma, the introduction of pathogens into the interstitial space also triggers the inflammatory process. In some cases the pathogen is recognised directly by inflammatory cells, while in other instances the activity of the pathogen triggers the inflammatory response. Foreign substances such as silica are not necessarily infective but are known to produce an aggressive inflammatory response.

Abnormal inflammation There are a number of conditions where the delicate balance between pro-and antiinflammatory mediators that normally promote healing becomes disrupted and the response actually leads to more tissue damage. At their most severe, these abnormal reactions can lead to acute life-threatening episodes of anaphylaxis and asthma (see Fig 57.5), although there are conditions such as arthritis where the effects are less acute but they are persistent and cause structural changes to tissues.

FIGURE 57.5 Inflammatory effects in asthma. Asthma is a disease driven by the inflammatory response in both the acute and the chronic phases. Inhaled antigens (1) bind to immunoglobulin E (IgE) on mast cells and trigger the mast cells to degranulate (2) and release mediators such as histamine, leukotrienes, prostaglandin D2, interleukins and platelet-activating factor. Combined, these mediators (3) induce bronchospasm and oedema from increased capillary permeability and trigger goblet cells to secrete mucus. The antigens are also detected by dendritic cells (4) that process and present them to Th2 cells (5). This produces interleukin-4 (IL-4), which promotes B cells to form more IgE. Th2 cells also produce interleukin-5 (IL-5) (6), which activates eosinophils. Eosinophil products damage the respiratory epithelium, leading to more inflammation and damage. Other inflammatory cells, including neutrophils (7), also contribute to the inflammatory process. Source: McCance & Huether (2014). The effects of abnormal inflammation depend on the degree of insult and the organs

affected, but the process is consistent with that of normal inflammation, starting with cellular or tissue damage and leading to varying degrees of a local or systemic response. In many conditions the acute phase will not completely subside and instead becomes chronic.

Step 1: tissue damage/infection The introduction of particular types of antigens (e.g. immunoglobulin E) or the destruction of a large amount of tissue (e.g. from burns) can cause the release of massive amounts of pro-inflammatory mediators that can cascade out of control, spreading away from the initial site of injury and causing systemic effects. In addition to causing vasodilation and increased vessel permeability, most inflammatory mediators cause small muscle constriction in the muscles lining the bronchioles of the lungs and the walls of the gastrointestinal system.

Step 2: systemic manifestations Hypotension Widespread small vessel dilation allows blood to pool and decreases venous return to the heart. Combined with a shift of plasma from the intravascular space to the interstitial space this can rapidly reduce cardiac output. As cellular perfusion deteriorates cells start to die, releasing their contents into the interstitial space and driving the inflammatory process further forwards. Signs: Hypotension, tachycardia, warm red skin (due to blood pooling in the capillaries), oedema (due to plasma pooling in the interstitial space).

Hypoxia If a severe inflammatory response is triggered in the lungs, spasm of the smooth muscle in the bronchioles reduces the airway diameter and impedes ventilation. This can be further complicated by the stimulation of mucus-producing cells. In extreme cases, the change in vessel permeability can cause airway swelling that can lead to further airway occlusion. Signs: Wheeze (bronchoconstriction), cough (mucus production), stridor (laryngeal oedema).

Fev er Elevations in body temperature are commonly associated with the inflammatory process, and especially to responses to infection (Kumar et al., 2009). This is caused by cytokines (produced as a part of the inflammatory response) being converted to prostaglandins that affect the hypothalamus (see Box 57.4). Medications that inhibit prostaglandin synthesis (aspirin, ibuprofen) are effective in reducing fever. It is theorised that increased body temperature may improve the response of lymphocytes to microbial agents (Kumar et al., 2009).

B O X 5 7 . 4P

la yin g with p r o sta g la n d in s

Derived from arachidonic acid, prostaglandins are important mediators in the inflammatory process and cause increased vascular permeability, neutrophil chemotaxis and pain by direct effects on nerves. Activation of phospholipase A2 by hypoxia, cell damage and the inflammatory cascade is the first step in the cellular response. Phospholipase A2 breaks down phospholipids to release arachidonic acid, the raw material for the production of prostaglandins (via the cyclo-oxygenase enzyme system, COX) and leukotrienes (via the lipoxygenase enzyme system). A number of anti-inflammatory drugs (aspirin and NSAIDs) are specifically aimed at inhibiting prostaglandin production acting on the COX enzymes to reduce pain and fever. The intrinsic link between inflammation and coagulation (thromboxanes involved in platelet aggregation are also created via the COX system) is evidenced by the effects these drugs have on increasing bleeding time. Other anti-inflammatory drugs have been shown to cause increased coagulability and have led to an increased risk of heart attack or stroke (Bryant & Knights, 2011).

Signs: Temperature >38°C or 10 mmHg during inspiration, resulting in a loss of radial pulse detection for the affected beats. purulent. Containing, causing or discharging pus. pyrexia. Fever or elevated temperature. pyrogen. A fever-inducing substance. rapid sequence intubation (RSI). The rapid induction of a patient using a combination of

anaesthetic and paralysing agents given in quick succession to allow for the intubation of the airway. recipient. A person who receives organs and/or tissues from another person (the donor). refeeding syndrome. May occur in patients who have not received nutritional support for some time; involves life-threatening fluid and electrolyte shifts after initiation of aggressive nutritional support therapies. rejection. Destruction of the allograft due to the body’s ability to identify self from nonself. renal replacement therapy (RRT). Any treatment that replaces renal function; includes intermittent haemodialysis and peritoneal dialysis. research. Systematic, rigorous investigation to establish facts, principles and new knowledge. research participant. Individual about whom a researcher obtains data through intervention or interaction with that person or their identifiable private information. respect for person. Has two fundamental aspects: (1) respect for the autonomy of those individuals who are capable of making informed choices and respect for their capacity for self-determination; and (2) protection of persons with impaired or diminished autonomy—that is, those individuals who are incompetent or whose voluntary capacity is compromised. resuscitation. The preservation or restoration of life by establishing and/or maintaining airway, breathing and circulation and related emergency care. retrieval. The removal of organs and/or tissues from a donor for the purposes of transplantation into another person. return of spontaneous circulation (ROSC). The resumption of sustained cardiac activity; signs include breathing (more than a few gasps), coughing, a palpable pulse or a measurable blood pressure. rhabdomyolysis. The breakdown of muscle tissue due to a direct or an indirect muscle injury that results in the release of the contents of muscle fibres and cells. rhinorrhoea. Discharge of mucus through the nose (i.e. a runny nose). risk. The function of the magnitude of a harm and the probability of its occurrence. root cause analysis. A structured process of analysing each step in a chain of events that led to a mistake or an error. Commonly applied to the health setting, where a team of unbiased experts are called on to dispassionately investigate how and why an error might have been caused by looking more at the system problems that emerged than at individual negligence. scavenger system. A system that removes gas following exhalation from the patient or a device close to the patient through which medication is being delivered; its function is to avoid the environment and those other than the patient receiving the medication.

sensory overload. A prolonged overstimulus of the senses that can result from excessive or prolonged periods of noise, light, odours and touch from both equipment and personnel. sepsis. A systemic inflammatory response to infection. sepsis-induced hypotension. A systolic blood pressure