Emergency Management

of
Severe Burns
THE EDUCATION COMMITTEE OF
AUSTRALIA AND NEW ZEALAND BURN ASSOCIATION LTD

Published by : KOLEGIUM ILMU BEDAH INDONESIA

Translated by : DR Yefta Moenadjat, dr, SpBP(K)

 The Education Committee
of

The Australian and

New Zealand Burn Association Limited
ACN 054 089 520

Emergency Management of Severe Burns

(EMSB)

COURSE MANUAL
17th edition
Feb 2013

ISBN 0-9775182-0-5

Australia and New Zealand Burn Association Ltd 1996

This manual is copyright. No part of the publication may be reproduced, stored in a retrieval system, or transmitted in any
form or by any means, electronic, mechanical, photocopying, recording or otherwise without the express written
permission of the Australian and New Zealand Burn Association Limited.

ANZBA, PO Box 550, Albany Creek, Qld 4035.

Ph: 0011 61 7 3325 1030 / Email: [email protected]

© ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd.

www.anzba.org.au

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CONTENTS
Prologue and Acknowledgements ................................................................................ 5

Course Program - Outline and Timeline .................................................................. 7

Chapter 1: Introduction - Epidemiology and Aetiology .......................................... 8

Chapter 2: Emergency Examination and Treatment ...............................................15

Chapter 3: Local and General Response to Burn Injury ........................................ 24

Chapter 4: Inhalation Injury ................................................................................... 28

Chapter 5: Burn Wound Assessment .................................................................... 36

Chapter 6: Burns Shock and Fluid Resuscitation ......................................................43

Chapter 7: Management of the Burn Wound ....................................................... 48

Chapter 8: Indications and Procedures for Referral ................................................54

Chapter 9: Burns in Children .......................................................................................59

Chapter 10: Electrical Injuries ................................................................................ 67

Chapter 11: Chemical Burns .......................................................................................75

Chapter 12: Management of the Burn Patient After the First 24 Hours .............. 81

Chapter 13: The Outpatient Management of the Minor Burn ...............................91

References ............................................................................................................... 97

Appendices:

Neurological Assessments .........................................................................................101

Tetanus Protocol ................................................................................................... 102

Escharotomy Diagrams ..............................................................................................103

Selecting an Appropriate Dressing ....................................................................... 104

© ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd.

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Daftar Isi
Bab 1: Introduksi: Epidemiologi dan Etiologi ...........................................................107

Bab 2: Penilaian dan Tatalaksana Emergensi ..........................................................115

Bab 3: Respon Lokal dan Sistemik pada Luka Bakar ...............................................125

Bab 4: Cedera Inhalasi .......................................................................................... 129

Bab 5: Asesmen Luka ............................................................................................ 138

Bab 6: Syok Luka Bakar dan Resusitasi Cairan ..................................................... 144

Bab 7: Tatalaksana Luka ....................................................................................... 150

Bab 8: Indikasi dan Prosedur Rujukan.................................................................. 156

Bab 9: Luka Bakar pada Anak ............................................................................... 161

Bab 10: Luka Bakar Listrik..................................................................................... 171

Bab 11: Luka Bakar Kimia ..................................................................................... 180

Bab 12: Manajemen Penderita Luka Bakar setelah 24 Jam Pertama ...................187

Bab 13: Manajemen Rawat Jalan pada Luka Bakar Ringan ...................................199

Referensi .......................................................................................................................197

Lampiran:

Penilaian Neurologik.............................................................................................. 210

Tetanus Protocol.................................................................................................... 211

Rekomendasi untuk Sayatan Eskarotomi .............................................................. 212

Selecting an Appropriate Dressing ........................................................................ 213

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PROLOGUE

The Australian and New Zealand Burn

Association Limited
The Association was formed in 1976 by a group of medical and nursing staff who were drawn
together by their common interest in improving the quality of care that their burn patients received.

Since then this group has expanded to now include a truly multidisciplinary group of burn care
professionals who are interested in teaching, care, research, and prevention of burn related
problems.

The multidisciplinary nature of the Association is an extension of every day burn care philosophy, as
practiced in burn units throughout Australia and New Zealand.

The Association has an important role in the promotion of the Minimum Standards of Burn Care in
Australia and New Zealand and it is in this context that this publication and the related EMSB course
have been developed. It is hoped that this initiative will improve standards of burn care for the
severely burnt patient.

Contributors to this Manual

The following, who are members of the Education Committee of the Australian and New Zealand
Burns Association, have generously given of their time and expertise in the initial creation and
development of this course:
Lynne Brodie, New South Wales
Robert K. Brodribb, Tasmania
Diana Dickson, New South Wales
Norman Farey, Victoria
Di Mandeno, New Zealand
Ian Leitch, South Australia
Hugh C.O. Martin, New South Wales
Michael M. Muller, Queensland
Fiona Wood, Western Australia.
Peter Hodgkinson, South Australia.
Mark Magnusson, Queensland.
Mrs Jill Martin, New South Wales
George Skowronski, New South Wales.
Mrs Diedre Stone, South Australia
Peter Widdowson, New Zealand
Jill Clausen, South Australia

A special thanks is owed to Mani M. Mani, M.D., Kansas USA

The Course was reviewed and updated in 2012, and thanks is extended to:

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Lynne Brodie, New South Wales
Peter Campbell, New South Wales
Nicholas Cheng¸ New South Wales
Siobhan Connolly, New South Wales
Anne Darton, New South Wales
Diane Elfleet, New South Wales
John Harvey, New South Wales
Andrew Ives, Victoria
Simon Jensen, Queensland
Chris Johnstone, Queensland
Peter Maitz, New South Wales
Hugh Martin, New South Wales
David Milliss, New South Wales
Alison Mustapha, Northern Territory
Stephen O’Donaghue, Queensland
Melinda Pacquola, Victoria
Chris Parker, New South Wales
Kelly Waddell, New South Wales
Alwena Willis, Western Australia
Richard Wong She, New Zealand

The EMSB Course has now been established in the following countries:

Australia, New Zealand, Great Britain, The Netherlands, South Africa and Bangladesh. Each of these
countries has a license to provide the EMSB Providers’ Courses and the EMSB Instructors Course in
their area under supervision of ANZBA. The course is also taught by a mixture of visiting and local
faculty in Papua New Guinea, The Pacific Islands, Malaysia, Hong Kong, India and Sri Lanka. The
EMSB Manuals and Courses have been adapted to address country specific circumstances, whilst
retaining standardized examination processes and pass marks throughout the world. In addition,
ANZBA has organised several courses in differing countries with a multinational faculty and ANZBA
will endeavour to continue this approach. An EMSB certificate is therefore valid worldwide and is an
expression that the recipient is knowledgeable in the initial treatment of burn injuries.

Since the original course was written and in accordance with this being a consensus course,
repeated updates and refinements have been made by numerous members of the teaching
faculty, and some candidates.

For suggestions please contact :

The Chairman of the Education Committee Prof. Peter Maitz via the Secretariat of the Australian &
New Zealand Burns Association [email protected]

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 Kata Pengantar

Puji syukur kehadirat Allah SWT yang telah memberi kesempatan terselenggaranya kursus
manajemen awal luka bakar kritis (Early Management of Severe Burn, EMSB) yang merupakan
kerjasama Kolegium Ilmu Bedah Indonesia dengan Australian–New Zealand Burn Association
(ANZBA) setelah diinisiasi lebih sepuluh tahun lamanya.

Kursus ini memuat pengetahuan dasar dan tatalaksana luka bakar kritis pada kesempatan awal yang
perlu diketahui oleh setiap tenaga medik yang dihadapkan pada kasus luka bakar; khususnya luka
bakar kritis.

Di negara maju seperti Amerika Serikat, tatalaksana awal luka bakar diterapkan secara konsisten
mengacu pada petunjuk praktis (practice guidelines) yang ditetapkan oleh American Burn
Association (ABA). Di negara tetangga kita, di Australia dan New Zealand, tidak berbeda halnya. Para
tenaga medis dididik untuk menangani kasus sejak awal melalui kursus dimaksud. Di Amerika
Serikat, kursus ini disebut Advanced Burn Life Support (ABLS) yang serupa dengan Advanced Trauma
Life Support (ATLS), sedang di Australia disebut Early Management of Severe Burn, EMSB.
Penyelenggaraan kursus–kursus ini, sebagaimana halnya ATLS tercatat telah membawa dampak
penurunan angka mortalitas luka bakar di dunia internasional.

Kursus ini memberi dampak melalui tertatanya sistem penanganan kasus luka bakar fase akut, bukan
hanya prioritas ABC traumatologi, namun dalam suatu sistem penanganan emergensi (emergency
medical system, EMS) yang baik. EMS yang tertata baik dan dilaksanakan oleh berbagai pihak
membawa kasus luka bakar pada penanganan definitif yang tepat sehingga angka mortalitas dapat
ditekan.

Berbeda halnya dengan situasi di Indonesia. Pengetahuan mengenai luka bakar dirasakan minim,
khususnya pengetahuan mengenai tatalaksana awal. Pengetahuan mengenai hal ini kurang
disosialisasikan sehingga banyak petugas medis tidak mengetahui prioritas dan urgensi merujuk
penderita kritis. Disamping kondisi geografis yang tidak mendukung, kondisi sosial– budaya dan
ekonomi masyarakat belum memungkinkan terujudnya suatu tatanan yang baik dalam manajemen
kasus luka bakar sebagaimana diselenggarakan di negara–negara maju.

Penatalaksanaan kasus luka bakar kritis di Indonesia selama ini mengacu pada protokol kaku
berdasarkan pengetahuan yang diperoleh selama masa pendidikan untuk selanjutnya diwarnai
pengetahuan otodidak dan pengalaman klinis individu–individu yang bervariasi dan mengacu pada
kondisi di lapangan.

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Namun, di era kemajuan zaman ini, untuk mendapatkan hasil optimal di tingkat nasional kiranya
masih terlalu banyak hal perlu dibenahi, terutama konsep tatalaksana awal. Karenanya, pada
kesempatan ini perkenankan kami menyelenggarakan kursus Early Management of Severe Burn
yang diharapkan agar setiap insan yang dihadapkan pada penatalaksanaan kasus luka bakar kritis
memiliki kompetensi standar internasional.

Untuk mempermudah pengertian dan menghindari salah persepsi, kami berusaha menerjemahkan
buku pegangan kursus ini ke dalam bahasa Indonesia yang dihadirkan mendampingi bahasa aslinya;
tanpa mengurangi rasa hormat kami pada mereka yang fasih dalam berbahasa Inggris.

Selamat mengikuti kursus.

DR Yefta Moenadjat, dr, SpBP(K)

© ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd.

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 COURSE PROGRAM
EMSB Course - Outline and Timeline
Part One – Lectures
08:00–08:10 Welcome & Introduction (10 min) Faculty
08:10–08:20 Local & General Response to Burn Injury (10 min) Faculty
08:20–08:45 Emergency Examination & Treatment (25 min) Faculty
08:45–08:50 Short Break ( 5 min)
08:50–09:05 Airway Management & Inhalation Injury (15 min) Faculty
09:05–09:20 Burn Wound Assessment (15 min) Faculty
09:20–09:35 Shock & Fluids (15 min) Faculty
09:35–09:40 Short Break ( 5 min)
09:40–09:55 Burn Wound Management (15 min) Faculty
09:55–10:05 Documentation & Transfer / Review (10 min) Faculty

10:05–10:20 Morning Tea (15 min)

Part Two – Skill Stations(20 min + 2 min turnover) Timekeeper:Faculty

10:20–10:40 Burn Area & Fluid Requirements (20 min) Faculty
ROTATE
ROOMS

10:42–11:02 Documentation & Transfer (20 min) Faculty

11:04–11:24 Escharotomy (20 min) Faculty
11:26–11:46 Wound Assessment &Mx (20 min) Faculty
11:48–12:08 Airway Management (20 min) Faculty
12:10–12:40 Lunch (30 min)

Part Three – Interactive Discussion Groups(20 min + 2 min turnover) Timekeeper:Faculty

ROTATE

12:40–13:00 Paediatric (20 min) Faculty

ROOMS

13:02–13:22 Chemical (20 min) Faculty

13:24–13:44 Electrical (20 min) Faculty
13:46–14:06 Multiple Injuries (20 min) Faculty

14:10–14:45 Demonstration of Simulation + Break (20 + 15 min)

Part Four – Multiple Choice Exam & Simulations Timekeeper:Faculty

14:45–15:50 Group A MCQ Exam Faculty
Group B Simulations
st
14:45–15:00 – simulation practice 1 (1 Patient as a Group) (15 min)
nd
15:02–15:14 – simulation practice 2 (2 Patient as a Group) (12 min) Pt A Faculty / Faculty
rd
15:16–15:26 – simulation test 1 (3 Patient Individually) (10 min) Pt B Faculty /Faculty
15:28–15:38 – simulation test 2 (3rd Patient Individually) (10 min) Pt C Faculty / Faculty
rd
15:40–15:50 – simulation test 3 (3 Patient Individually) (10 min) Pt D Faculty / Faculty

15:50–16:00 Break & Turnover (10 min)

16:00–17:05 Group B MCQ Exam
Group A Simulations
st
16:00–16:15 – simulation practice 1 (1 Patient as a Group) (15 min)
nd
16:17–16:29 – simulation practice 2 (2 Patient as a Group) (12 min)
rd
16:31–16:41 – simulation test 1 (3 Patient Individually) (10 min)
rd
16:43–16:53 – simulation test 2 (3 Patient Individually) (10 min)
rd
16:55–17:05 – simulation test 3 (3 Patient Individually) (10 min)
th
17:05– Re-sits of Simulations if required (with 4 Patient individually as required)
–18:00 Summation and Presentations

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 CHAPTER 1

Introduction
Epidemiology and Aetiology

Introduction
The patient with burns presents a difficult challenge to most health care personnel. Apart from the
serious nature of the injury and immediate discomfort, there are also potentially permanent changes
to appearance, function and independence, loss of income and compromise of their employment
futureas well as a general uncertainty about the future. All of this is distressing not only for the
patient, but also for their families and for those caring for them. The well known surgical maxim that
the trauma patient who is seen, assessed and treated early by skilled personnel heals more quickly
than the patient whose treatment is delayed, is as true for the burn victim as it is for any other
trauma patient[1]. It is important that the right treatment is instigated quickly not only to save a
person’s life, but also their future.

This course is based on the principle that timely emergency assessment, resuscitation and transfer
provide the best chance of recovery[2]. Ultimately, the patient that we will be called upon to
manage with burns, and perhaps with associated severe injuries, willbenefit from this course.

The aim of this course is to provide sufficient factual information regarding the presentation,
diagnosis and initial management of the patient with severe burns, to enable medical and nursing
practitioners to deal competently with this urgent and often life threatening problem.

This course was written by members of the ANZBA Education Committee, with each individual
chapter being written from members’ personal (and considerable) experience in different areas of
burn care. All the contained material is original material that has not been published in this form
before.

The course follows the trauma management protocols as taught by the Royal Australasian College of
Surgeons in their Emergency Management of Severe Trauma course (EMST), as this course is the
accepted trauma management teaching system for medical practitioners in Australia and New
Zealand.

The Emergency Management of Severe Burns (EMSB) course provides trauma management
guidelines and protocols specific to burns, that are additive in content to EMST. While EMSB is
designed to be a “Stand Alone Course”, which provides sufficient information to define the
Minimum Standards of Emergency Burn Care (of the Australian and New Zealand Burn Association),
the course can also be taught in conjunction with the EMST, providing extra information specific to
the management of burns.

EMSB covers the principles of the emergency management of severe burns in Australia and New
Zealand. The course is appropriate for medical and nursing practitioners working anywhere in the
© ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd.
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field of burn care, from members of the burn unit, to medical and nursing staff in isolated areas.
Apart from teaching the material contained, the course seeks to emphasise the benefits of all
emergency care givers having knowledge of the same protocols of emergency burn care, as this
facilitates primary care and appropriate referral; the ultimate beneficiary of this approach being our
patient with burns.

The information is taught in six separate and complimentary sections:

1. Course Manual

This manual contains the complete syllabus and is sent to all students before each course. Students
are expected to read the manual, twice if possible, before attending the course. The ‘Structure of the
EMSB’image (page 15) is included to assist in the recognition of the most important aspects of the
course.

2. Formal Lectures

These take place at the beginning of the course. They will outline the course proper, and will
reinforce your reading of the manual. They are not a
substitute for the manual, and will vary to include the individual clinical experience of the lecturers.

3. Skill Stations

These will teach important practical aspects of the course and provide students with the opportunity
to apply the knowledge they have gained from the manual and lectures.

4. Interactive Discussion Groups

This section will teach special areas of burn management in an interactive small group environment
to maximise the opportunities for students to discuss these topics, and to use their own clinical
experience, at their own level, to explore these topics.

5. Simulated Burn Cases

In this section, volunteers who have been moulaged to simulate clinical cases of burns will be used
to give students some practical experience of management of the severe burn. This section will tie
the course together, and make it clinically relevant.

6. Examination and Clinical Test

At the end of the course, students will be asked to take a multiple choice exam paper, as well as a
clinical case test, (using a moulaged simulated burn case), to test students level of knowledge and
the effectiveness of our teaching.

Successful students will receive an official certificate from the Australian and New Zealand Burn
Association.

© ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd.

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The Team Concept of Burn Care
Since the Second World War, significant advances in burn care have resulted in the gradual decrease
in mortality and morbidity from severe burns[2].

Intravenous resuscitation, improved nutrition, the introduction of topical antimicrobials, and the
introduction of protocols for surgery that promote early closure of the burn wound have all
contributed to this remarkable improvement in survival[2].

Burn Units

With these improvements in burn management has come the realisation that specially trained staff
are able to operate more effectively within a purpose built acute facility[2]. These facilities allow
higher quality care to be available even for minor burns than is available outside a burn unit.

The concentration of specialist team members within one facility has the added advantage of being
more cost effective, and the sharing of knowledge in a team environment allows the development of
high levels of expertise by individual team members[2]. This ensures that patients receive the best
care possible. The support that team members give each other during times of stress contributes to
staff morale, and maximises staff retention.

Burn Team

The Burn Team consists of a multidisciplinary group whose individual skills are complementary to
each other. Team members recognise the benefits of interdisciplinary cooperation in providing the
best quality care to the patient with burns[2, 3].

Pre-hospital Clinicians

Ambulance personnel and Retrieval services provide essential pre-hospital care for burn patients by
establishing fluid resuscitation, airway stabilisation and transferring the patient. The early
management provided pre-hospital assists the burn patients’ chance of survival and optimal
outcome.

Emergency Department

Many burn patients will be assessed and receive their initial treatment in an Emergency Department,
whether in a burn unit hospital, or rural or metropolitan hospital. A high quality working relationship
between the burn unit and Emergency Department is essential to provide top quality care.

Surgeons

Burn Surgery has become a sub-specialty of Plastic Surgery, General Surgery, and Paediatric Surgery.
Burn Surgeons have a particular interest in the management of the seriously injured burn patient, in
wound healing, rehabilitation, and related research[2].

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Nurses

The Burn Nurse is the lynch pin of the team, providing day to day continuity of care. Burn nurses
have specialist expertise in wound care, skin graft care, intensive care of the severely burnt patient,
psychiatric nursing and discharge planning[2].

Anaesthesia

Burn surgery requires specialised anaesthetic techniques to assist the surgeon in treating the
severely ill patient, managing severe blood loss, and maximising the area of burn wound surgery that
can be treated at any one time[2]. This contributes to early burn wound closure.

Intensive Care

Many severely burnt patients will be cared for at some stage of their hospitalisation in Intensive
Care. A high quality working relationship between the Burn and Intensive Care units is essential to
provide top quality care.

Physiotherapist, Occupational Therapist

Therapists play an indispensable role in the care and rehabilitation of the burn patient[2]. This
begins at the time of admission to the burn unit, and continues well into the outpatient treatment
after discharge. Burn therapy is a specialised sub-discipline and is not usually available to patients
outside burn units.

Speech Pathologist

The burn unit Speech Pathologist provides comprehensive clinical assessment and management of
severe burn patients with swallowing, voice and communication disorders as a result of the burn
injury or secondary complications including sepsis, debility, oro-facial contractures or presence of a
tracheostomy

Dietitians
Optimal nutrition is necessary to counteract the extreme catabolic response that occurs with
burns[2]. For this reason burn units have specialised dietetic staff.

Psychosocial

Social Workers, Psychiatrists, Psychologists and Chaplains form part of the burn team, providing
necessary support and treatment for the wide variety of psychosocial problems that burn patients
commonly have. Special expertise is required to manage these difficult problems[2]. The patient’s
ability to function in society in the long term is as dependent on this psycho-social adjustment as it is
on the quality of the physical result.

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Rehabilitation

Post burn rehabilitation begins at the time of admission[2], and in the minor burn can usually be
managed as part of outpatient care. Severely burnt patients may require much more intensive
rehabilitation to enable the attainment of maximum function, allowing return to daily living activities
and employment. A close relationship with rehabilitation personnel facilitates this.

The burn team provides optimal quality of care utilising shared management protocols which
provide individual support for team members, optimise professional attainment, and provide the
highest quality of care for the patient with burns[2].

The Epidemiology and Aetiology of Burns

A. Epidemiology
Burns are a common form of trauma [2, 4-6]. Some burns occur as genuine accidents, but most are
caused by carelessness or inattention, pre-existing medical conditions (the presentation of which
may be a collapse), or they may follow alcohol or drug abuse. (See Table 1)

Approximately 1% of the population of Australia and New Zealand (220,000) suffer a burn requiring
medical treatment each year. Of those, 10% will require hospitalisation, and 10% of those
hospitalised will be burnt sufficiently severely for their life to be threatened. 50% of all those burnt
will suffer some daily living activity restriction. (Source 2001 Australian National Health Survey)

A 70% TBSA burn may cost $700,000 for acute hospital treatment, to this figure must also be added
the additional costs of rehabilitation, time off work, and loss of earning represent a substantial cost
to the community.

In both adults and children, the commonest place to be burned is the home [1, 7]. In children, over
80% of accidents occur in the home. The most dangerous places in the home are the kitchen and the
bathroom, as most scalds in children and the elderly occur in these two rooms. In addition, the
laundry contains dangerous chemicals, and the garage or of accidents occur in the home. The most
dangerous places in the home are the kitchen and the bathroom, as most scalds in children and the
elderly occur in these two rooms. In addition, the laundry contains dangerous chemicals, and the
garage or garden shed contains chemicals and dangerous flammable liquids.

TABLE 1
Children’s Place of Burning (%)
Home 82%
Outdoors 12%
Roadway 3%
Work 1%
Institutions/School 1%
Other 1%
(ANZBA Bi-NBR Annual Report 2011[8])
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TABLE 2
Adult’s Place of Burning (%)
Home 56%
Work 17%
Roadway 11%
Outdoors 11%
Institutions 3%
Other 2%
(ANZBA Bi-NBR Annual Report 2011[8])

Injuries caused at work often involve carelessness, and are caused occasionally by unsafe work
practices, particularly the careless handling of flammable liquids. Attention to occupational health
and safety policies has the potential to make these become less frequent.

Military burns

Approximately two thirds of military burns are non battle related casualties[2]. These occur in the
same manner as they do in civilian life.

Burns as battle casualties comprise 10% of total battle related casualties. Military burns with a blast
component have a high risk of producing an inhalation injury as well as a skin injury. Multiple trauma
is likely to coexist.

The contingencies of battle, the evacuation plan and the casualty holding policy at the time, together
with the logistics of re-supply, may impose very different management protocols on burns in
wartime compared with the optimal treatment in peacetime.
70% TBSA

B. Aetiology
Tables3 and 4 lists those factors that caused burns in both children and adult patients admitted to a
burn unit in Australia or New Zealand from 2009 to 2010.

TABLE 3
Causes of Children’s Burns (%)
Scalds 55%
Contact 21%
Flame 13%
Friction 8%
Electrical 1%
Chemical 1%
Other 1%
(ANZBA Bi-NBR Annual Report 2011[8])

TABLE 4
Causes of Adult’s Burns (%)
Flame 44%
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Scald 28%
Contract 13%
Chemical 5%
Friction 5%
Electrical 2%
Other 3%
(ANZBA Bi-NBR Annual Report 2011[8])

The causes of burns in adults and children differ in that fire is the most common cause in adults, and
scalds are the most common cause in children. As children become older so their patterns of burn
causation become more like the adult.

As adults age, their patterns of injury also change. The elderly are particularly at risk of injury from
scalds at home, or as residents of care institutions.

All age groups are likely to be injured in conditions of social disharmony or disruption. This is
particularly true of children, especially infants and toddlers, who are dependent on surrounding
adults for care and security. Injuries from carelessness, inattention, poor parenting, and
unfortunately from assault (burning is a common method of child abuse) occur frequently, and need
investigation when suspected.

Summary

© ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd.

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 CHAPTER 2

Emergency Examination
And Treatment
Introduction
When the survivor of a burn injury is first seen by medical personnel, rapid assessment and
treatment can be life saving [9]. While most patients with minor burns will not have associated
injuries, such injuries are more likely in patients with major burns. Whatever the size of the burn, the
patient will fall into one of two categories; those whose non-burn injuries are obvious, and those
whose other injuries are concealed. Patients who have minor burns with non-burn injuries usually
fall into the first category. However, it is common for life-threatening injuries to be missed when a
significant burn is present because the obvious burn injury catches the attention of the treating
doctor [9].

The history should alert the medical personnel to the possibility of co-existing injuries [9]:

 road traffic accident, particularly with ejection or at high speed

 blast or explosion
 electrical injury, especially high voltage
 jump or fall while escaping

Non-communicative patients, whether unconscious, intubated, psychotic, or under the influence of

substances, should be regarded as potentially multiply injured and treated accordingly.

After immediate first aid has been given, the principles of primary and secondary survey and
simultaneous resuscitation should be followed[2].

Staff should don personal protective equipment (PPE) such as gloves, goggles and gowns prior to
attending any patient [2].

First Aid
First aid consists of :
 stopping the burning process
 cooling the burn wound
It is effective within the first threehours from the time of burn (see Chapter 7).

© ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd.

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 Structure of EMSB
A B C D E A.M.P.L.E.
L I R I I X FLUIDS History
O R E R S P
W A C A O
O A T U B S ANALGESIA Head to Toe
Y H I U Examina on
K L
I A L R
N T I E
TESTS Tetanus
G I T
O Y TUBES
N
D
C AVPU
O2 control
spine & Pupils Control Support
I.V.

First
©EMSB
Aid Survey

Primary Survey
Immediately life threatening conditions are identified and emergency management begun [9, 10].
Do not get distracted by the obvious burn injury.

A. Airway maintenance with cervical spine control

B. Breathing and ventilation

C. Circulation with haemorrhage control

D. Disability - neurological status

E. Exposure + environmental control

A. Airway Maintenance with Cervical Spine Control

 Check for a patent airway, easiest by speaking to the patient. If the airway is not patent, clear the
airway of foreign material and open the airway with chin lift/jaw thrust. Keep movement of the
cervical spine to a minimum and never hyperflex or hyperextend the head and neck[2, 9].
 Control cervical spine (best with rigid collar). Injuries above the clavicle, such as facial injuries or
unconsciousness, are often associated with cervical fractures.

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B. Breathing and Ventilation

 Expose the chest and ensure that chest expansion is adequate and equal[2].
 Always provide supplemental oxygen –100% high flow(15 l/min) via a non-rebreather mask[2, 9].
 If required ventilate via a bag and mask or intubate the patient if necessary.
 Carbon monoxide poisoning may give a cherry pink, non-breathing patient.
 Beware a respiratory rate <10 or >30 per minute.
 Beware circumferential chest burns - is an escharotomy required?

C. Circulation with Haemorrhage Control

 Apply pressure to point of haemorrhage

- Pallor occurs with 30% loss of blood volume.
- Mental obtundation occurs with loss of 50% of blood volume.
 Check the central pulse – is it strong or weak?
 Check blood pressure
 Capillary refill (centrally and peripherally)– normal return is ≤2 seconds. Longer indicates
hypovolaemia or need for escharotomy on that limb; check another limb.
 Insert 2 large bore, IV lines preferably through unburned tissue
 Take blood for FBC/U&E/LFT/Coags/β-hCG/Cross Match /Carboxyhaemoglobin[2, 9].
 If the patient is shocked commence fluid resuscitation with Hartmann’s boluses to attain a radial
pulse.

The early appearance of clinical signs of shock is usually due to another cause. Find it and treat it.

D. Disability: Neurological Status

 Establish level of consciousness:

A- Alert
V- Response to Vocal stimuli
P- Responds to Painful stimuli
U- Unresponsive

 Examine the pupil’s response to light. They should be brisk and equal.
 Be aware that hypoxaemia and shock can cause restlessness and decreased level of
consciousness[9].

E. Exposure with Environmental Control

 Remove all clothing and jewellery including piercings and watches[2]

 Log roll the patient to visualise posterior surfaces
 Keep the patient warm[7, 9]
 Area burned is estimated by using the Rule of Nines or palmar (Rule of One’s) methods

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Fluids, Analgesia, Tests and Tubes
The ‘FATT’ between the primary and secondary survey.

Fluid Resuscitation
(See Chapter 6)

 Fluids are given initially as per Modified Parkland formula [7, 11-19]:

3–4mls x weight (kg) x % burn TBSA

+ maintenance for children.
 Crystalloids (e.g. Hartmann's solution) are the recommended fluid
 Half of the calculated fluid is given in the first eight hours; the rest is given over the next sixteen
hours [3, 12, 15, 19].
 The time of injury marks the start of fluid resuscitation [7].
 If haemorrhage or non-burn shock treat as per trauma guidelines.
 Monitor adequacy of resuscitation with [3, 7, 11, 14, 18, 20]:
- Urinary catheter with hourly output measured
- ECG, pulse, blood pressure, respiratory rate, pulse oximetry and arterial blood gas
analysis as appropriate
 Adjust resuscitation fluids as indicated.

Analgesia[9]
 Burns hurt – give intravenous morphine 0.05–0.1mg/kg
 Titrate to effect – smaller frequent doses are safer.

Tests
 X-Ray
- Lateral cervical spine
- Chest
- Pelvis
- Other imaging as clinically indicated

Tubes
 Nasogastric tube
Insert nasogastric tube for larger burns (>10% in children; >20% in adults), if associated injuries,
or to decompress stomach for air transfer. Gastroparesis is common.

Secondary Survey
This is a comprehensive, head to toe examination that commences after life threatening conditions
have been excluded or treated[2].

History: A – Allergies
M – Medications
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 P – Past illnesses
L – Last meal
E – Events / Environment related to injury

Mechanism of Injury

As much information regarding the interaction between the person and their environment should be
obtained:

Burn[9]
Duration of exposure
Type of clothing worn
Temperature and nature of fluid if a scald
Adequacy of first aid measures.

Penetrating
Velocity of missile
Proximity
Direction of travel
Length of knife blade, distance inserted, direction

Blunt
Speed of travel and angle of impact
Use of restraints
Amount of damage to passenger compartment
Ejection?
Height of fall
Type of explosion or blast and distance thrown

Examination

Head
Eyes… penetrating injuries are often missed
check visual acuity
Scalp… lacerations, boggy masses

Face
Stability of mid-face
Check for missing teeth / malocclusion
CSF leak from nose, ears or mouth
Soot, blisters, oedema of the tongue or pharynx

Neck
Inspect, palpate, x-ray. Always suspect cervical fracture
Lacerations deep to platysma– operating theatre or angiography

Chest
Examine whole chest – front and back

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Ribs, clavicles and sternum
Check breath sounds and heart sounds
Circumferential burns may need escharotomy if restricting ventilation
Cough productive of soot
Altered voice or brassy cough

Abdomen
Requires frequent re-evaluation especially for increasing tenderness and distension
If there is a seat belt bruise, assume intra-abdominal pathology such as ruptured viscus
If assessment of the abdomen is unreliable, equivocal or impractical, for example in the presence of
an extensive abdominal burn, then further investigation with a CT scan, or Focused Assessment with
Sonography for Trauma (FAST) scan is mandatory in multiply injured patients.

Perineum
Bruising, meatal blood

Rectal
Blood, lacerations, sphincter tone, high riding prostate

Vaginal
Foreign bodies, lacerations

Limbs
Contusion, deformity, tenderness, crepitus
Assess extremity pulses regularly. In constricting circumferential extremity burns with developing
oedema, the eschar initially obstructs venous return which in turn embarrasses arterial inflow
producing tissue ischaemia. This may produce the classic signs of decreasing limb perfusion of pain,
paraesthesia (or numbness), pulselessnessand paralysis. When venous return from an extremity is
obstructed by oedema, an escharotomy is indicated to restore adequate circulation. (see Chapter 7)

Pelvis
Rapid access to radiology in most emergency departments/trauma units precludes the need to test
pelvic stability by springing the pelvis with the heel of the hand on the symphysis pubis and the
wings of the ilium anteriorly. If radiology not readily available this should be done once only by a
senior clinician.

Neurological
Glasgow Coma Scale (see appendix)
Motor and sensory assessment of all limbs
Paralysis or paresis indicates a major injury and immobilisation with spinal boards and semi-rigid
collars is indicated.

Note: In burned patients, paresis of a limb may be due to vascular insufficiency caused by rigid
eschar for which escharotomy is necessary.

Decreased level of consciousness could be due to:

- hypovolaemia from undiagnosed bleeding or under resuscitated burn shock
- hypoxaemia

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- intracranial expanding space occupying lesion.

Documentation
Take notes
Seek consent for photography and procedures
Give tetanus prophylaxis if required (see appendix) [21]

Re-evaluate
Re-evaluate Primary Survey – particularly
- respiratory compromise
- peripheral circulation insufficiency
- neurological deterioration
- adequate fluid resuscitation
- review imaging
- Note urine colour for haemochromogens
Laboratory investigations:
- Haemoglobin / haematocrit
- Urea / creatinine
- Electrolytes
- Urine microscopy
- Arterial blood gases
- Carboxyhaemoglobin (if available)
- Blood sugar level
- Drug screen (may be required by Police)

Chest x-ray
Electrocardiogram

Emergency Burn Wound Care

(see Chapter 7)

As most burn wounds are sterilised at the time of burning, extensive burn wound care involving
complicated dressings is unnecessary and causes unwarranted delays. The appropriate treatment of
the burn is to cover the wound with plastic cling wrap or a clean sheet and arrange for evacuation
[22]. If the referral of the patient is delayed more than 8 hours, or if the wound has been extensively
contaminated with polluted water or industrial waste, then a topical antimicrobial should be used.
Clean the wound and contact the receiving burn unit regarding advice on which dressing to apply.
They will often recommend an antimicrobial dressing such as a silver or Silver Sulphadiazine cream.

Do not constrict limbs with compromised circulation by using tight dressings. Dressings should be
checked frequently to exclude constriction.

Electrical Injuries
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(see Chapter 10)

Conduction of electrical current through the chest may cause transient cardiac arrhythmias or
cardiac arrest, though this is rare in low voltage injuries (<1000 V). Patients who have been
electrocuted may require 24 hours of ECG monitoring if they have suffered a high voltage injury, loss
of consciousness or have an abnormal ECG on arrival at the hospital [23]. Dysrhythmias are more
likely to occur if the patient has pre-existing myocardial disease which may be aggravated by small
amounts of current damage.

Remember that small entrance or exit wounds may be associated with severe deep tissue damage.

Chemical Burns
(see Chapter 11)

While there is residual chemical on the skin, burning continues. Therefore contaminated clothing
should be removed and the burn washed with copious amounts of water for a long time [24]. Seek
advice for special chemicals from Poisons Information Australia (13 11
26) or New Zealand National Poisons Centre (0800 764 766).

Chemical burns to the eye require continuous flushing with water. Swelling of the eyelids and eyelid
muscle spasm due to pain may make adequate washing difficult. Careful retraction of the eyelids will
facilitate correct irrigation. An early ophthalmological opinion is necessary in these cases.

Support and Reassure Patient, their Relatives and Staff

Burns are associated with significant emotional overlay in the patient and also their relatives and
friends [25].

Feelings of grief and loss are common and are normal accompaniments of burns. In addition feelings
of guilt, self reproach, fear, depression and often anger in the victim and their relatives need to be
addressed.

Burning is a frequent method of successful and attempted suicide. Patients with mortal injuries
require sympathetic handling and counselling during the brief lucid period before death. Large doses
of narcotics or inappropriate endotracheal intubation prevents this important aspect of terminal
management. It also makes the important final rapport with grieving relatives impossible. Every
effort must be made to facilitate this communication.

Patients with non-fatal injuries will require psychiatric assessment and this may be needed urgently
to prevent immediate further suicide attempts.

Some patients with abnormal personalities or under the influence of intoxicating substances may be
violent during their emergency management and staff need to take care to avoid personal injury.
Assistance

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Definitive Care
Definitive burn care is described elsewhere in this manual. Transfer to a burn unit where other
specialised services are available is indicated in accordance with ANZBA referral criteria. (See
Chapter 8.)

Summary
 The burn injury may only be part of the problem. Other injuries may also be present and
should be dealt with according to the principles of rapid primary assessment, correcting life-
threatening conditions as required.

 Fluid resuscitation, analgesia, tests and tubes represent treating the ‘burn injury’ once life-
threatening conditions have been dealt with.

 Once the patient is stable, an ordered and complete ‘head to toe’ examination of the patient
beginning with a history should then be undertaken. Definitive care and transfer follow.

 In the multiply injured burn patient the following points should be the focus of regular re-
evaluation:
- Adequacy of fluid resuscitation
- Airway or respiratory embarrassment from inhalation injury or constricting eschar
- Peripheral circulatory insufficiency from constricting burn wounds, dressings or oedema
- Neurological deterioration
- Concealed (intra-cavity) bleeding

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 CHAPTER 3

Local and General Response

to Burn Injury

A. Local Response
Based on the experimental work undertaken in the 1950’s by Jackson in Birmingham, a burn wound
model was created which aided the understanding of the pathophysiology of a burn [26-32].

Jack e

Zone of Coagulation

Zone of Stasis
Zone of Hyperaemia

Figure 3.1

Figure 3.1 depicts this wound model. Nearest the heat source (or other injuring agent) where the
heat cannot be conducted away rapidly enough to prevent immediate coagulation of cellular
proteins, there is rapid cell death. This central zone of tissue death is best called the Zone of
Coagulative Necrosis, but is also referred to as the Zone of Coagulation[25, 26, 29, 32, 33].

Surrounding the Zone of Coagulative Necrosis is an area of tissue where the damage is less severe
than that required to produce immediate cell death, but the circulation in this area of skin and
subcutaneous tissue is compromised due to damage to the microcirculation. Because the circulation
to this area is sluggish, it is called the Zone of Stasis [25, 26, 29, 32]. Untreated, this relatively narrow
zone will undergo necrosis as the inflammatory reaction progresses under the influence of
mediators produced by the tissue’s response to injury [29]. Clinically this is seen as progression of

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the depth of burning. This produces the phenomenon of areas of burn that appear viable initially but
subsequently (3–5 days after burning) become necrotic [32].

Surrounding this region of compromised vasculature is a zone where damage to the tissues causes
production of inflammatory mediators which cause widespread dilatation of blood vessels. This zone
is called the Zone of Hyperaemia[25, 26, 29, 32]. Following the resolution of this hyperdynamic
vascular response, the tissues of this area return to normal [27, 34]. In a burn which covers more
than 10% in children or 20% in adults of the total body surface area (TBSA), the Zone of Hyperaemia
may involve virtually the whole of the body.

The contribution of each of these three zones (Necrosis, Stasis and Hyperaemia) to the overall burn
wound depends upon the circumstances of the burn itself. On occasions the Zone of Stasis may
include the mid dermis, but progressive vascular compromise extends the Zone of Necrosis
producing a deep burn. (see Fig 5.4) This is particularly likely to occur in the elderly patient and in
those patients in whom appropriate treatment of post-burn shock and sepsis is not undertaken [14].
Thus timely and effective emergency care of the burned patient can promote wound healing.

B. The General Response

1. Normal Capillary Exchange

(i) Substances pass through the capillary wall in one of three ways: diffusion, filtration, and
large molecular transport.

a) Diffusion is the mechanism of transfer of very small particles such as oxygen, carbon dioxide
or sodium. It implies that these particles cross the capillary wall (membrane) easily and so move in
the direction of concentration (“downhill” from more concentrated to less).

b) Filtration is the mechanism of transfer of water and some other substances. The amount of
water filtered through the capillary depends on the forces pushing water in and out across the
capillary wall, as well as factors in the capillary wall. The forces causing movement across the
1
capillary wall are summarised by Starling’s Hypothesis[2, 32] (see footnote) .

c) Large molecule transport is less well understood. Large molecules probably cross the
capillary wall mostly by passing through spaces between the endothelial cells. Most capillaries are
fairly impervious to large molecules which is why they are called “semi-permeable” (easily
permeable to water and small particles such as Na, Cl, but relatively impermeable to large molecules
such as albumin). Even so, each day 50%–100% of the body’s serum albumin crosses the capillaries
and is returned to the blood via the lymphatic system.

1
Starling’s Hypothesis states that nett fluid movement is the difference between the forces moving fluid out (hydrostatic pressure in the
capillary pushing fluid out plus the colloid osmotic pressure in the interstitial fluid pulling fluid out) and the forces moving fluid in
(hydrostatic pressure in the interstitial space pushing fluid back in and plasma colloid osmotic pressure pulling fluid in.
1
Hipotesis Starling menyatakan bahwa gerakan fluida nett adalah perbedaan antara kekuatan pindah fluida (tekanan hidrostatik dalam
cairan mendorong kapiler keluar ditambah tekanan osmotik koloid dalam cairan interstitial menarik keluar cairan) dan kekuatan bergerak
cairan ke dalam (tekanan hidrostatik dalam interstitial ruang mendorong cairan kembali dan tekanan osmotik koloid plasma menarik
cairan masuk
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(ii) Normal variations in filtration occur because of factors in the capillary wall (e.g. kidney
capillaries let out much more water than muscle capillaries) as well as the factors mentioned in
Starling’s Hypothesis. The capillary hydrostatic pressure depends on the pressure of the blood
flowing in as well as the resistance to blood flowing out (controlled by the pre- and post-capillary
sphincters respectively). Normally most capillaries undergo cycles of active blood flow, interspersed
by long periods of low flow and hence low pressure. The colloid osmotic pressure of the plasma is
almost totally dependent on the serum albumin concentration. The colloid osmotic pressure of the
interstitial fluid is due to the small amount of albumin and the ground substance present between
cells.

2. Abnormal Capillary Exchange

These changes are caused by inflammatory mediators released by damaged endothelial cells, by
platelets, and by leucocytes.

(i) Vasodilatation is one of the major vascular responses to inflammation and causes [32]:

a) Increase in capillary hydrostatic pressure.

b) Opening up of all capillaries instead of only a few.

c) Stretching of the capillary wall which increases the surface area of the capillary
membrane and opens the spaces between endothelial cells.

d) Pooling of blood in small veins.

(ii) There is a marked increase in the permeability of the capillary membrane [7, 18]. This causes
increased transport of substances by all three mechanisms, diffusion, filtration and large molecule
transport. However, large molecule transport is most affected, and there is a dramatic increase in
the movement of albumin across the capillary membrane. This causes mass movement of albumin
out of the circulation and into the interstitial space producing oedema.

(iii) Tissue damage by burning may produce breakdown of intercellular ground substance. This
can contribute to a rapid increase in the colloid osmotic pressure of the interstitial space which has
been observed experimentally. Another effect of burn injury on the intercellular ground substance is
uncoiling of long molecules, which is thought to cause expansion of the space and thereby lower its
hydrostatic pressure.

3. Effects of Burn Injury on the Whole Body

There are changes in virtually every organ system in the body after a burn injury [25]. When the burn
is less than 20% TBSA these effects may not be of great practical significance [20].

The cause of these changes is release of inflammatory mediators and neural stimulation. The result
is that there are major changes in control of body functions as well as direct reactions in some
organs to circulating mediators.

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(i) The most profound and immediate effect is on the circulation. Hypovolaemia is principally
due to loss of protein and fluid into the interstitial space. Loss of albumin alters capillary exchange at
sites remote from the burn. If the burn involves more than 20% TBSA the whole body is affected by
circulating mediators so that capillary permeability is generally increased. Correction of
hypovolaemia is a life saving task in the first hours after major thermal injury [16, 18, 27, 35-40].

(ii) As a result of the injury a hypermetabolic state is caused by the secretion of the stress
hormones cortisol, catecholamines and glucagon. In addition the suppression of (or resistance to)
anabolic hormones (growth hormone, insulin and anabolic steroids) and neural mechanisms cause
profound catabolism resulting in muscle protein breakdown [25]. Clinically these changes are
expressed as tachycardia, hyperthermia and protein wasting.

(iii) Immunosuppression is due to depression of many facets of the immune mechanism, both
cellular and humoral[25]. This is why infection is still the leading cause of mortality in burn patients.

(iv) As part of the reaction to injury and to shock the barrier function of the gut is greatly
impaired leading to an increase in bacterial translocation. This can be minimised by beginning very
early enteral nutrition.

(v) The lungs frequently suffer from the changes of the post-burn systemic inflammatory
response (Acute Respiratory Distress Syndrome [ARDS]) even in the absence of inhalation injury [25,
41].

(vi) Widespread whole body changes in growth also occur and persist for months or years after
healing of the burn wound. There is increased central deposition of fat, decreased muscle growth,
decreased bone mineralisation, and decreased longitudinal growth of the body. Although growth
velocity may return to normal after 1–3 years it does not exceed normal growth so that catch-up
does not occur.

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 CHAPTER 4

Inhalation Injury
Inhalation of hot gases and the products of combustion injure various parts of the respiratory tract
in different ways [2, 42]. In addition, the absorption of the products of combustion may lead to
serious local or systemic toxic effects.

Inhalation injury increases mortality in all burns [41-49]. For example, in a middle-aged man with
cutaneous burns, an inhalation injury may increase the mortality rate by 30% and increase the risk of
pneumonia[46]. If pneumonia supervenes, the mortality rate may rise by up to 60%. In children it
has been reported that a 50% TBSA burn with associated inhalation injury carries the same mortality
as a 73% TBSA without an associated inhalation injury[50].

Inhalation injury, previously known as respiratory tract burns, is most likely to be associated with
burns of the head and neck. Forty-five percent of patients with burns to the face have an inhalation
injury.

Classification of Inhalation Injury

An inhalation injury can be broadly classified according to the site of the injury[2].

1. Airway Injury Above the Larynx (obstruction)

2. Airway Injury Below the Larynx (pulmonary damage)

3. Systemic Intoxication (cell hypoxia)

A patient may have one or a combination of these types of injury.

Management of the airway aims at providing a patent and protected airway first and foremost. The
airway may also need to be secured to improve oxygenation and ventilation in the setting of
respiratory failure.

1. Airway Injury above the Larynx (obstruction)

These are actually thermal burns produced by the inhalation of HOT GASES, and so occur in those
patients who have no alternative but to breathe these gases. This is most likely to occur in an
enclosed space, if trapped in a fire, or with the inhalation of steam.

These burns produce the same pathophysiological changes that are produced by thermal injury to
skin with damage proportional to exposure. Inflammatory mediators cause oedema of the tissues
which leads to obstruction initially, and later loss of the protective functions of the mucosa [42].

Respiratory obstruction often develops as a result of soft tissue swelling and may persist beyond the
time of maximal wound oedema (between 12 and 36 hours). A burn to the skin of the neck may
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aggravate this obstruction by producing neck oedema[2]. The latter is much more likely to occur in
children who have relatively narrow airways and short necks with soft tissues that are readily
distorted by oedema.

It should be remembered that burns involving more than 20% TBSA result in a systemic
inflammatory response, even when there is no direct injury to the tissues. The airway mucosa may
become oedematous, especially if large volumes of fluid are required for resuscitation, and this may
further compromise the airway.

The upper respiratory tract has such an efficient ability to conduct heat away that it is only after
extreme heat exposure that direct heat damage to the lower respiratory tract occurs.

2. Airway Injury below the Larynx (pulmonary damage)

These burns are produced by the inhalation of the products of combustion. Fires cause oxidation and
reduction of compounds containing carbon, sulphur, phosphorus and nitrogen. The list of chemical
compounds produced includes carbon monoxide and dioxide, cyanide, esters and complex organic
compounds, ammonia, phosgene, hydrogen chloride, hydrogen fluoride, hydrogen bromide and the
oxides and aldehydes of sulphur, phosphorus, and nitrogen [42]. Polyvinyl chloride (PVC), for
example, produces at least 75 potentially toxic compounds when burnt [51]. Acids and alkalis are
produced when these compounds dissolve in the water contained in respiratory mucous and tissue
fluids. These compounds produce a chemical burn. In addition, the particles of soot less than 1µm
are aerosolised. They also contain similar irritant chemicals and can produce damage to the alveolus
[42]. These compounds contact the airway mucosa and lung parenchyma initiating the production of
inflammatory mediators and reactive oxygen species. This results in oedema and potentially
shedding of the trachea-bronchial mucosa. The lower airways too are involved with cast formation
and plugging that may result in distal airway obstruction. The lung parenchyma may be affected with
disruption of the alveolar-capillary membrane, the formation of inflammatory exudates and loss of
surfactant. This results in atelectasis, interstitial and pulmonary oedema causing hypoxaemia and
reduced lung compliance [51, 52].

A number of pathophysiological factors contribute to lung injury, leading to impaired gas exchange
[47]:

 Obstruction due to…

- bronchoconstriction
- mucus production
- cast formation
 Alveolar dysfunction and shunting due to…
- emphysematous alveolar destruction
- atelectasis / alveolar collapse
 Alveolar fluids…
- non-cardiac pulmonary oedema / chemical pneumonitis
- secondary bacterial pneumonia

3. Systemic Intoxication (cell hypoxia)

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The two common intoxications occurring in association with inhalational burns are caused by carbon
monoxide and cyanide[42].

Carbon monoxide (CO)

This is produced by incomplete oxidation of carbon. Carbon monoxide (CO) is a colourless odourless
gas which diffuses rapidly into the blood stream. It combines readily with haemoglobin (Hb), having
a greater affinity for haemoglobin than oxygen (240 times greater) and forms carboxyhaemoglobin
(COHb). This binding to form COHb effectively reduces the oxygen carrying capacity of the blood. CO
causes tissue hypoxia by reducing oxygen delivery and utilisation at a cellular level [42]. It also
dissociates from Hb less readily than does oxygen and so occupies an oxygen-binding site for a long
period of time [42].

In addition to binding preferentially with haemoglobin, CO also binds with great affinity to other
haem- containing compounds, most importantly the intracellular cytochrome system. It may also
have a direct toxic effect. This causes abnormal cellular functioning which is a major component of
CO toxicity. [53]. Post intoxication encephalopathy may be a serious sequel of poisoning; the exact
mechanism of how this develops is not fully understood but may be due to cerebral lipid
peroxidation.

The usual indicators of hypoxia may not be present:

 Haemoglobin not carrying O2 causes skin to have a blue colour (cyanosis). COHb gives false
reassurance with a normal pink colour (some say ‘cherry red’)
 A pulse oximeter (O2 saturation probe) cannot distinguish between COHb and O2-Hb
(oxyhaemoglobin) so even in severe poisoning, the oxygen saturation will read as normal
 A standard blood gas machine measures PaO2 as the amount of oxygen dissolved in the
blood. The dissolved oxygen in the plasma remains unaffected so the PaO2may be normal.

Blood gas analysers using co-oximetry are the only reliable way to assess oxyhaemoglobin and
carboxyhaemoglobin levels[54]. Carboxyhaemoglobin dissociates slowly, having a half-life of 250
minutes in room air.

Patients who have CO intoxication are often confused and disorientated, exhibiting symptoms
similar to those of hypoxia, head trauma and acute alcohol intoxication. It is important to consider
CO intoxication in this clinical setting.

Table 4.1
Carbon Monoxide Intoxication[9, 42, 53].

Carboxyhaemog Symptoms
lobin (%)
0 –15 None - (Smokers, long distance lorry drivers)

15 – 20 Headache, Confusion
20 –40 Nausea, Fatigue, Disorientation, Irritability
40 –60 Hallucination, Ataxia, Syncope, Convulsions, Coma

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Patients with an altered state of consciousness after burns have CO intoxication unless proven
otherwise.

Cyanide Poisoning (HCN)

This may occur because of the production of hydrogen cyanide from burning plastics[2] or glue used
in furniture. It is absorbed through the lungs, and binds readily to the cytochrome system, inhibiting
its function resulting in anaerobic metabolism. It causes loss of consciousness, neurotoxicity and
convulsions. It is gradually metabolised by the liver enzyme rhodenase. Blood cyanide levels are not
readily available and their usefulness is debated. Smokers will often have levels of 0.1mg/L, while
lethal levels are 1.0 mg/L. In practice, pure HCN poisoning is rare, most patients suffering mixed HCN
and CO poisoning.

Diagnosis of Inhalation Injury

All cases of burns should be examined with a view to excluding the diagnosisof inhalation injury.
As the clinical signs and symptoms may evolve over a period of time, as with all traumas, the patient
must be repeatedly re-evaluated. This is a potentially fatal injury[41, 42, 47, 48].

Patients with severe inhalation injury may present early with severe respiratory distress or
obtundation at the scene of the fire. Early death may occur and emergency resuscitation at the
scene may be required to save life [42]. The respiratory distress seen at the scene of the fire may be
due to anoxia, as oxygen is consumed by the fire itself. CO intoxication is however thought to be
responsible for the majority of
deaths occurring at the scene of the fire, the scenario of “being overcome by the fumes”.

A common presentation of inhalation injury is one of increasing respiratory obstruction, occurring

over several hours. This requires ongoing vigilance to detect and is due to thermal injury above the
larynx. Increasing abnormalities in oxygenation as shown by increasing restlessness and confusion
suggest injury below the larynx.

History
A history of burns in an enclosed space, such as a house, a motor vehicle, an aeroplane or an
armoured vehicle, or burns with an associated explosion resulting from a petrol or gas fire, from
shells or bombs, should alert medical personnel to the likelihood of an associated inhalation injury
[42].

Examination

The following clinical findings are the signs suggestive of inhalation injury [2, 24, 42, 55]:

Observe for… Listen for…

Burns to Mouth, Nose and Change of Voice,
Pharynx,
Singed Nasal Hairs Hoarse Brassy Cough
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Sputum containing Soot Croup -like Breathing
Flaring of Nostrils Inspiratory Stridor The symptoms and signs of an inhalation
Respiratory Difficulty Productive Cough injury change or evolve over time
Tracheal Tug according to the particular site and type of
In-drawing of Supraclavicular the injury. An indication of this change is
Fossae given in Table 4.2.
Rib Retraction
After the initial assessment the
subsequent clinical course can be altered by the onset of the known complications of inhalation
injury.

Table 4.2
Change in Clinical Presentation of Inhalational Injury Over Time
Signs/Symptoms

Respiratory Difficulty
Respiratory Obstruction

Pulmonary Oedema/ARDS

Visual Disturbances

Diagnosis of Inhalation Injury Producing Systemic

Intoxication
Diagnosis of systemic intoxication is made initially by clinical suspicion [48]. Any patient, who is
confused or has an altered state of consciousness after being burned, or inhaling products of
combustion, is deemed to have carbon monoxide intoxication until proven otherwise.

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The diagnosis is confirmed by the presence of COHb in the blood [48]. CO levels estimated on arrival
in hospital may not correlate well with the severity of the CNS symptoms of CO intoxication. They
may appear to be too low. This is due to the washout of CO from the blood between exposure and
arrival in hospital, and although the COHb level may appear to be low, the value of the test is that it
confirms that this type of inhalation injury has occurred.

Treatment of Inhalation Injury

The management of inhalational injury is focussed on the following priorities:
 Ensure a patent airway
 High flow oxygen
 Frequent monitoring for respiratory deterioration
 Discuss suspected systemic intoxication (CO, HCN) with a toxicologist by calling Poisons
Information (Australia – 13 11 26, New Zealand – 0800 764 766)

During initial assessment (The Primary Survey), it is important that all patients with burns be given
high flow oxygen by non re-breathing mask at 15 litres per minute [9]. This will facilitate maximum
tissue oxygenation while emergency assessment and management continues. Remember a patent
airway is required to deliver oxygen to the lungs.

1. Treatment of Inhalation Injury above the Larynx

All patients with suspected inhalation injury should be under close observation. Because early and
rapidly progressive respiratory obstruction is likely (particularly in children who have relatively small
airways), the equipment for emergency intubation should be readily available [55]. Frequent
reassessment of the patient’s clinical condition is vital. As soon as increasing airway obstruction is
detected the airway must be secured by endotracheal intubation.

Cervical spine protection is mandatory.

The endotracheal intubation should be performed as soon as possible. Delay may allow further
airway oedema to occur and make subsequent intubation impossible. Stridor and respiratory
distress are definite indications for intubation.

The indications for intubation include:

 Need to maintain a patent / protect airway

- impending airway obstruction
- impaired level of consciousness
- to facilitate safe transport

 Need for ventilation

- deteriorating oxygenation

If in doubt, intubate.

2. Treatment of Inhalation Injury below the Larynx

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Treatment in this category is primarilythat of Respiratory Support:

(i) High Flow Oxygen

All burn patients should receive high flow oxygen at 15 litres per minute via a non-re-breathing
mask. This is made even more necessary in the face of parenchymal lung injury.

(ii) Intubation[9, 55]

Endotracheal intubation may be necessary to perform bronchial toilet to clear secretions, or to allow
higher oxygen concentrations to be given

(iii) Intermittent Positive Pressure Ventilation (IPPV)

This may become necessary if a patient’s oxygenation is not responding to the administration of
oxygen and simple securing of the airway. This can be achieved by manual ventilation with a bag
attached to the endotracheal tube and the oxygen supply, or by a mechanical ventilator.

3. Treatment of Inhalation Injury Producing Systemic Intoxication

(i) Respiratory Support

As above, it is important to ensure that burnt tissue is perfused with as much oxygen as possible.
High flow oxygen by mask should be administered [9].

(ii) Protection of the Unconscious Patient

As a result of systemic intoxication patients may be unconscious. Emergency treatment consists of
rolling the patient into the left lateral coma position and administration of oxygen. Cervical spine
protection should occur at all times. The airway should be secured, firstly by chin lift,then an
oropharyngeal airway, but in most instances endotracheal intubation will be necessary.

(iii) Natural Washout Effect with Time

Carbon monoxide (CO) is gradually removed from the blood by diffusion in the alveoli. The time
taken for this to occur is slowest breathing room air at atmospheric pressure but can be reduced by
increasing the concentration of the oxygen administered. When available, hyperbaric administration
of high oxygen concentrations will also increase the speed of washout of carbon monoxide[2]
although the evidence is conflicting as to whether their results in improved neurological outcomes.
Logistics may be complicated in a critically ill patient with major burns.

(iv) Oxygen
The standard emergency treatment is breathing 100% oxygen by mask [2, 9]. This should be
continued until COHb levels return to normal. The secondary washout of CO that occurs from the
cytochrome binding may cause a smaller secondary rise of COHb 24 hours later, and oxygen should
be continued.

(v) Oxygen + IPPV

May be necessary in the unconscious patient, or in the patient who has other types of inhalation
injury apart from systemic intoxication.

(vi) Cyanide Intoxication

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Cyanide intoxication is often fatal.Washout of cyanide from the blood by metabolism in the liver is
slow. Whilst formulations containing hydroxycobolamin for injection have been advocated, this
treatment requires large doses and is not readily available in most emergency departments.

(vii) Hydrogen Fluoride Intoxication

HF when absorbed systemically in significant amounts efficiently binds serum calcium.
Hypocalcaemia is likely to develop. Infusion fluids should contain added calcium to counteract this.

Seek advice for inhaled substances such as cyanide, hydrofluoric acid, etc from Poisons
Information Australia (13 11 26) or New Zealand National Poisons Centre (0800 764 766).

Summary
 Inhalation Injury and the related Systemic Intoxication are potentially fatal injuries.

 Their diagnosis depends upon the clinical suspicion of their occurrence, and the recognition
of their signs from the history and examination.

 Emergency treatment consists of providing respiratory support with oxygen and securing of
the airway, undertaking endotracheal intubation if necessary.

 Patients with an inhalation injury or suspected inhalation injury should be referred to a burn
unit for ongoing care after initial emergency stabilisation.

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 CHAPTER 5

Burn Wound Assessment

Introduction
Whatever the cause of burns, whether they be thermal, chemical or electrical, the amount of tissue
damage and particularly the depth of burning, is related to the temperature or strength of the
injuring agent, and the length of time that the agent has been in contact with the skin[2, 10][21, 56]

Temperature above 50C will produce tissue necrosis, particularly when the skin is thin as in children
and the elderly.

1. Estimation of the Area of the Burn

The two important determinants of the seriousness of the burn injury are the area and depth of the
burn [32]. The likelihood of mortality following burns is a function of the
 Age of the Patient
 Percentage of the Total Body Surface Area Burnt (% TBSA)

The greater the surface area of the body injured, the greater the mortality rate.

Accurate assessment of the area of the burn requires a method that allows easy estimation of the
size of the burn as a percentage of the body surface area. This is readily accomplished using the
“Rule Of Nines” (See Figure 5.1)[21, 25].

The “Rule of Nines” divides the body surface into areas of nine percent or multiples of nine percent,
with the exception that the perineum is estimated at one percent[21, 25, 27, 56-58]. This allows the
extent of the burn to be estimated with reproducible accuracy. In addition to calculating the area
burnt, it is useful to calculate the area not burnt, and to check whether both calculations add up to
100%.

A method of estimating small burns is to use the area of the palmar surface (fingers and palm) of the
patient’s hand, which approximates to 1% TBSA [7, 21, 56-58]. This method is useful in smaller,
scattered burns that do not lend themselves to a “Rule of Nines” method. (see Fig 5.2)

The Rule of Nines is relatively accurate in adults, but may be inaccurate in small children [21]. This
is because the child has different body surface area proportions than the adult. Children have
proportionately smaller hips and legs and larger shoulders and heads than adults. Using the “Adult
Rule of Nines” may seriously under or over estimate the size of the burn wound of a child, and lead
to inaccurate intravenous fluid resuscitation.

For these reasons the Paediatric Rule of Nines should be used. (see Fig 5.3) This can be modified for
different ages to enable accurate surface area calculations. (see Chapter 9) [2, 21].As the child ages
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the percentages are adjusted. For every year of life after 12 months 1% is taken from the head and
0.5% is added to each leg. Once the child reaches 10 years old their body is proportional to an adult

Figure 5.1

Figure 5.2

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 Figure 5.3

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2. Estimation of the Depth of the Burn
The Structure and Function of the Skin

The skin consists of two parts, the epidermis and the dermis[2, 57, 59-62]. The epidermis is the
superficial thinner layer that is responsible for limiting the evaporation of water from the body, and
is constantly being reproduced by division of the basal layers of the epidermis [63, 64].
(See Figure 5.3).
Figure 5.3 – Cross-section of normal skin

The dermis is the deeper, thicker layer that provides

the strength and durability of the skin [63]. The
dermis contains the blood supply and the sensory
nerves of the skin. The dermis also contains the
epidermal adnexal structures: hair follicles and their
epidermal lining, sebaceous glands, and sweat glands
with their ducts [63][32, 64]. These reservoirs of
epithelial cells under the control of growth factors will
undergo mitosis and can produce an epithelial
covering that will heal a superficial-dermal to mid-
dermal thickness wound [26]. This process is called
epithelialisation.

Underneath the dermis lie the padding layers of subcutaneous fat [63] and fascia that separate the
skin from the deeper muscular and bony structures. These layers provide important cushioning from
trauma and their damage in burns means inevitable tethering of skin to deeper structures.

The anatomy of the skin of the nose and external ears is different from elsewhere in the body, as
here the skin is very closely applied to the underlying cartilage with little subcutaneous fat. The
blood supply for both the skin and cartilage runs between the two. Burns to the nose and pinna may
therefore produce damage to the blood supply of the skin and cartilage. Skin and cartilage loss may
cause significant deformity, particularly if bacterial chondritis supervenes.

Depth of Burn Injury

Depending upon the depth of tissue damage, burns may be grouped in 3 main classifications as
superficial, mid and deep burns. They are then further defined as epidermal, superficial dermal, mid-
dermal, deep dermal or full thickness (see Figure 5.4 and Table 5.1). In practise all burns are a
mixture of areas of different depth [7, 9, 21].
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 Depth of Burn
Burn Wound Healing Epidermal
Epidermis
= re-epithelisation
Superficial
Dermis Dermal

- capillaries
- nerves Mid
- collagen
& elastin fibres
Dermal

Sebaceous
gland Deep
Dermal
Hair follicle
Sweat
gland
Full
Subdermal Thickness
fat

Figure 5.4

Table 5.1
Diagnosis Of Burn Depth[10]

Capillary Sensati Heal

Depth Colour Blisters
Refill on ing
Epiderma
Red No Present Present Yes
l
Superficia Pale
Small Present Painful Yes
l Dermal Pink
Mid Dark Usu
Present Sluggish +/-
Dermal Pink ally
Deep Blotchy
+/- Absent Absent No
Dermal Red
Full
White No Absent Absent No
Thickness

A. Superficial Burns

Superficial burns are those that have the ability to heal themselves spontaneously by
epithelialisation. These superficial burns may either be epidermal or superficial dermal in depth.

1. Epidermal Burns

Epidermal burns include only the epidermis. Common causes of this type of burn are the sun
and minor flash injuries from explosions. The stratified layers of the epidermis are burnt
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 away and healing occurs by regeneration of the epidermis from the basal layer. Due to the
production of inflammatory mediators, hyperaemia is produced so these burns are red in
colour and may be quite painful (see Table 5.1)[10]. This could be difficult to assess in dark
skin individuals as erythema is often masked by the dark pigment of the skin. They heal
quickly (within seven days), leaving no cosmetic blemish [59]. Hospital admission may be
required for pain relief [21].

Pure erythema (epidermal burn) is not included in estimations of the total body surface area
burnt[10]. Differentiation between pure erythema and superficial dermal burn may be
difficult in the first few hours after injury.

2. Superficial Dermal Burns

Superficial dermal burns include the epidermis and the superficial part of the dermis - the
papillary dermis. The hallmark of this type of burn is the blister[2]. The skin covering the
blister is dead and is separated from the viable base by the outpouring of inflammatory
oedema. This oedema tents up the necrotic roof forming a blister. This blister may burst
exposing the dermis which, following exposure, may desiccate and die. This causes increased
depth of tissue loss. The exposed papillary dermis is pink. Because sensory nerves are
exposed, the burn is usually extremely painful [21]. Under suitable conditions epithelium will
spread outwards from the adnexal structures (hair follicles, sebaceous glands and the ducts
of sweat glands) and join neighbouring islands of epithelium to cover the dermis
(epithelialisation).

Superficial dermal burns should heal spontaneously by epithelialisation within 14 days

leaving only a colour match defect. No scarring should be produced in this type of burn.

If healing is delayed it means that the burn is deeper than originally diagnosed.

B. Mid-dermal Burns
A mid-dermal burn, as its name suggests, is a burn injury that lies between a superficial dermal burn
(described above) which will heal relatively rapidly, and a deep dermal burn (described below) which
will not. At the mid-dermal level, the number of surviving epithelial cells capable of re-
epithelialisation is less due to the deeper burn wound and so rapid spontaneous burn wound healing
does not always occur.

Clinically, the appearance is determined by damage to the dermal vascular plexus of varying
degrees. Capillary refill may be sluggish, and tissue oedema and blistering will be present. The
burned area is usually a darker pink than that of a superficial dermal burn’s
light pink, but not as dark as a deep dermal burn’s blotchy red[10]. Sensation to light touch may be
decreased, but pain persists, reflecting the damage to the dermal plexus of cutaneous nerves.

C. Deep Burns
Deep burns are more severe. They will either not heal spontaneously by epithelialisation, or only
heal after a prolonged period with subsequent significant scarring. They may be either deep dermal
or full thickness.

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 1. Deep Dermal Burns

Deep dermal burns may have some blistering, but the base of the blister demonstrates the
character of the deeper, reticular dermis often showing an appearance of a blotchy red
colouration[2, 10]. This red blotchy colouration is due to the extravasation of haemoglobin
from destroyed red cells leaking from ruptured blood vessels. The important hallmark of
these burns is the loss of the capillary blush phenomenon. This demonstrates that the burn
has destroyed the dermal vascular plexus. The dermal nerve endings are also situated at this
level and so in these burns sensation to pinprick will be lost.

2. Full Thickness Burns

Full thickness burns destroy both layers of skin (epidermis and dermis), and may penetrate
more deeply into underlying structures[2]. These burns have a dense white, waxy, or even a
charred appearance. The sensory nerves in the dermis are destroyed in a full thickness burn,
and so sensation to pinprick is lost[2, 10]. The coagulated dead skin of a full thickness burn,
which has a leathery appearance, is called eschar.

Summary

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 CHAPTER 6

Burns Shock and Fluid Resuscitation

Burn injury precipitates a large amount of fluid sequestration into the area of injury and when the
size of greater than 20% TBSA this process becomes generalised [32, 35]. Oedema is formed in great
quantity and when combined with ongoing evaporative loss from the moist burn surface results in
significantly decreased plasma volume. This in turn leads to intravascular hypovolaemia which, if not
corrected, precipitates organ system failure, especially renal failure [16].

This chapter will expand on the pathogenesis of oedema formation and post-burn hypovolaemic
shock, fluid resuscitation and its monitoring.

Thermal injury causes marked changes in the microcirculation both locally at the site of injury and
elsewhere [16]. A burn develops three zones of decreasing injury (see Figure 3.1 Jackson’s Burn
Wound Model p23):

1) Central zone of coagulative necrosis.

2) Intermediate zone of injury characterised by stasis of blood flow.
3) An outer, peripheral zone showing vasodilatation, increased blood flow and hyperaemia.

Mediators are produced and released at the burned site that alter vascular membrane integrity and
so increase permeability[2]. These mediators include histamine, serotonin, prostaglandins,
bradykinin and potent vasoconstrictors such as thromboxanes and angiotensin.

In large burns (20–30% TBSA), the quantity of these mediators produced at the burn site is so great
that they induce widespread increased vascular permeability which leads to generalised oedema
formation [18]. Hypovolaemic shock soon follows. In addition to this, an anatomical derangement of
the endothelial lining of the microvasculature can be detected on electron microscopy.

Evidence in favour of one resuscitation fluid in comparison with another is conflicting [19, 65]. From
a practical point of view, however, the ready availability of crystalloid solutions such as Hartmann’s
Solution (Lactated Ringers) have made them the internationally accepted choice for initiation of
resuscitation [2, 66].

Children have limited physiological reserve and greater surface area to mass ratio compared to
adults. The threshold at which fluid resuscitation is required in children is lower than for adults
(approximately 10%) and they tend to need a higher volume per kilogram [3, 18]. In fact, this
increased need for fluids equates with the volume of normal maintenance requirements over that
calculated by fluid resuscitation formulae. Inhalation injury further increases fluid requirements.
Oedema formation ceases between 18–30 hours post-burn. Therefore, the duration of resuscitation
is variable but can be recognised when the volume needed to maintain adequate urine output is
equal to maintenance requirements.

Estimation of Fluid Needs

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The extent of the burn is calculated using the ‘rule of nines’ or a burn body chart if available. If
possible the patient is weighed or weight obtained during history taking. These data are then used in
a fluid resuscitation formula [3, 12, 13, 15, 17, 18, 35, 67, 68]:

Adults: 3–4ml crystalloid x kg body weight x percent (%) burn

Children:3–4ml crystalloid x kg body weight x percent (%) burn plus maintenance with 5% Glucosein
0.45% (½ normal) saline2

100 ml/kg up to 10 kg
+
50 ml/kg from 10–20 kg
+
20 ml/kg for each kg over 20 kg

NOTE: The calculation of fluid requirements commences at the time of burn, not from the time of
presentation.

Fluid Should Be Administered Via Two Large Cannulae (at least 16g in adults), preferably inserted
through unburned skin. Consider intra-osseous (IO) access if needed.

The calculated volume is that estimated for the first 24 hours [12]. As oedema formation is greatest
soon after injury:

 Half the calculated volume is given in the first 8 hours [3] and the remaining half given
over the subsequent 16 hours [12, 15, 19, 67].

 Maintenance fluid for children is given at a constant rate over 24 hours.

This step-down does not match the gradual decrease in oedema formation and emphasises that
these formulae are only guidelines that may need to be altered to match individual requirements
[15].

If urine output is not adequate, give extra fluid:

 Boluses of 5–10 ml/kg or increase the next hour’s fluids to 150% of planned volume.

In the second 24 hours post burn, colloid fluids can be used to help restore circulating volume using
the formula [66, 69]:

 0.5ml of 5% albumin x kg body weight x % burn.

2
Some half-normal saline is packaged with 2.5% dextrose: to this add a further 25ml of 50% dextrose to each 500ml bag. If
the solution in the pack is half-normal saline without any glucose, add 50 ml of 50% dextrose to each 500ml bag.Whenever
possible use pre-prepared 5% glucose in 0.45% saline.

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In addition, electrolyte solution should be provided to account for evaporative loss and normal
maintenance requirements. Vomiting is commonplace and such losses should also be replaced. A
commonly used solution is:

 Normal Saline + Potassium (+ Dextrose for children)

Monitoring adequacy of fluid resuscitation

The best, easiest and most reliable method of monitoring fluid resuscitation is by following urine
output [3, 7, 11, 14, 18, 20, 35]:

Adults… 0.5ml/kg/hr = 30–50ml/hour

Children (< 30kg)… 1.0ml/kg/hr (range 0.5–2ml/kg/hr) [66, 68-71]

If urine output is kept near these levels then adequate organ perfusion is being maintained [20].
Large urine output indicates excessive fluid resuscitation with unnecessary oedema formation; low
urine output indicates poor tissue perfusion and likely cellular injury.

Clearly, a urinary catheter is vital for accurate monitoring and should be inserted for burns
 >10% TBSA in children
 >20% TBSA in adults

Central invasive haemodynamic monitoring is only occasionally indicated and is used for those with
pre-morbid cardiac disease or coexistent injuries causing blood loss such as multiple fractures.

Significant acidaemia (pH 7.35) detected on arterial blood gas analysis commonly indicates
inadequate tissue perfusion and is usually due to lactic acidosis. Increased fluid resuscitation is
indicated. If unsuccessful in restoring pH or if haemochromogens are present in the urine, consider
bicarbonate after discussion with the intensive care unit. Acidosis may also indicate the need for, or
inadequacy of, escharotomy.

Blood pressure readings with a sphygmomanometer are notoriously inaccurate due to oedema
formation and accurate measurements can only be obtained via an arterial line. These are
recommended in large burns.

The heart rate is usually raised in burn patients due to pain and emotion and so is a poor indicator of
adequacy of fluid resuscitation.

Serum electrolytes should be measured initially and at regular intervals. Mild hyponatraemia is
common due to dilution by the infusion depending on the sodium concentrate of the crystalloid
solution used (Hartmann’s solution NaCl is only 130 meq/l.). Hyperkalaemia commonly occurs with
tissue injury in electrocution. Bicarbonate and glucose plus insulin may be required to correct this
problem.

Restlessness, mental obtundation, and anxiety are often indicators of hypovolaemia and the first
response should be to look to the adequacy of fluid resuscitation.
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Haemoglobinuria
Tissue injury, particularly muscle tissue, from electrocution, blunt trauma or ischaemia causes
release of myoglobin and haemoglobin. Strongly consider performing a fasciotomy (as opposed to an
escharotomy which doesn’t release deep muscle fascia). These haemochromogens colour the urine a
dirty red. Acute renal failure will soon ensue as a result of deposition of these haemochromogens in
the proximal tubules, and prompt treatment is required [23]:

 Increase urine output to 2 ml / kg / hr

 Consider a single dose of Mannitol 12.5g over 1 hour and observe response

Problems with Resuscitation

Formulae only estimate requirements and the individual patient must be closely monitored.

Oliguria

Low urine output indicates inadequate fluid resuscitation. The appropriate first response is to
increase the rate of infusion. Diuretics are rarely necessary and should not be considered until after
consultation with a burn unit. They are used in patients with haemochromogens in the urine and
occasionally in patients with very large burns.

The following patient groups routinely require extra fluid resuscitation [15]:
 Children
 Inhalation Injury [19]
 Electrical Injury
 Delayed Resuscitation
 Dehydration - firefighters, intoxicated patients

Infants, elderly and those with cardiac disease should be monitored closely as fluid overload may be
precipitated. Fortunately, pulmonary oedema is uncommon due to disproportionately greater
increase in pulmonary vascular resistance than systemic vascular resistance. It occurs in those with
myocardial hypokinesia and often requires invasive monitoring, inotropic support, ventilation and
difficult alterations in fluid management.

Children

Children are prone to hypoglycaemia, fluid overload and dilutional hyponatraemia due to limited
glycogen stores, higher surface area to weight and intravascular volume ratios. Blood glucose and
electrolyte levels should be measured regularly. Free water should be limited and a source of
carbohydrate instituted early. This could be enteral feeding or addition of dextrose to the electrolyte
solution.

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Abdominal Compartment Syndrome

This rare but serious secondary complication can occur in large burns in adults as well as children
especially when the calculated fluid requirements have been exceeded to achieve adequate urine
output [15, 16, 72]. It is suggested that if the presence or development of Abdominal Compartment
Syndrome is being considered that bladder pressure monitoring can give valuable information.

Summary

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 CHAPTER 7

Management of the Burn Wound

Introduction
In order to manage a burn wound it is essential to understand the mechanism of injury and to be
able to assess the extent of that injury. This establishes a starting point for treatment, the object of
which is the best possible functional and cosmetic outcome.

A wound is a disruption of tissue architecture and cellular processes. In a burn the denaturing of
proteins and disruption of cellular structures is due to thermal insult (either heat or cold), electricity,
chemical action or radiation. The burn wound is significant because it interferes with all seven major
functions of the skin

 Aesthetic and psychological interface

 Temperature regulation
 Sensory interface
 Immune response
 Protection from bacterial invasion
 Control of fluid loss
 Metabolic function

The aim of treatment is to minimise the interference with function both locally and systemically.

It is important to understand that the wound is dynamic and often heterogeneous [7, 9, 21]. DO NOT
assume that all areas of the burn are equally deep.

First Aid
The principles of first aid are to
 stop the burning process
 cool the burn wound [22].

Stopping the burning process reduces tissue damage. Cooling the surface of the burn wound reduces
the production of inflammatory mediators (cytokines) and promotes maintenance of viability in the
zone of stasis. It therefore helps to prevent progression of damage that occurs in an untreated burn
in the first 24 hours after the injury [25].

Stop the Burning Process

In flame burns the flame should be extinguished by the patient rolling on the ground either actively
or passively using the Stop, Drop, Cover (face) & Roll technique [10, 24]. Hot charred clothing should
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