EMSB 2013

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

ãAustralia 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 2

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


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


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: © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 3

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]


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.


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)


COURSE PROGRAM

EMSB Course - Outline and Timeline Part One – Lectures 08:00–08:10 08:10–08:20 08:20–08:45 08:45–08:50 08:50–09:05 09:05–09:20 09:20–09:35 09:35–09:40 09:40–09:55 09:55–10:05

Welcome & Introduction Local & General Response to Burn Injury Emergency Examination & Treatment Short Break Airway Management & Inhalation Injury Burn Wound Assessment Shock & Fluids Short Break Burn Wound Management Documentation & Transfer / Review

(10 min) (10 min) (25 min) ( 5 min) (15 min) (15 min) (15 min) ( 5 min) (15 min) (10 min)

10:05–10:20

Morning Tea

(15 min)

10:20–10:40 10:42–11:02 11:04–11:24 11:26–11:46 11:48–12:08 12:10–12:40

ROTATE ROOMS

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

14:10–14:45

(20 min) (20 min) (20 min) (20 min) (20 min)

Lunch

ROTATE ROOMS

Faculty Faculty Faculty Faculty Faculty

Timekeeper:Faculty

Burn Area & Fluid Requirements Documentation & Transfer Escharotomy Wound Assessment &Mx Airway Management

Faculty Faculty Faculty Faculty Faculty

(30 min)

Part Three – Interactive Discussion Groups(20 min + 2 min turnover) 12:40–13:00 13:02–13:22 13:24–13:44 13:46–14:06

Faculty Faculty Faculty

Paediatric Chemical Electrical Multiple Injuries

(20 min) (20 min) (20 min) (20 min)

Demonstration of Simulation + Break

Timekeeper:Faculty Faculty Faculty Faculty Faculty

(20 + 15 min)

Part Four – Multiple Choice Exam & Simulations

Timekeeper: Faculty

14:45–15:50

Group A MCQ Exam Group B Simulations

14:45–15:00 15:02–15:14 15:16–15:26 15:28–15:38 15:40–15:50

– simulation practice 1 – simulation practice 2 – simulation test 1 – simulation test 2 – simulation test 3

15:50–16:00

Break & Turnover

16:00–17:05 16:00–16:15 16:17–16:29 16:31–16:41 16:43–16:53 16:55–17:05

Group B MCQ Exam Group A Simulations – simulation practice 1 – simulation practice 2 – simulation test 1 – simulation test 2 – simulation test 3

17:05–

Re-sits of Simulations if required (with 4 Patient individually as required)

–18:00

Faculty st

(1 Patient as a Group) nd (2 Patient as a Group) rd (3 Patient Individually) (3rd Patient Individually) rd (3 Patient Individually)


Pt A Pt B Pt C Pt D

Faculty / Faculty Faculty /Faculty Faculty / Faculty Faculty / Faculty

(10 min)

st

(1 Patient as a Group) nd (2 Patient as a Group) rd (3 Patient Individually) rd (3 Patient Individually) rd (3 Patient Individually)


th

Summation and Presentations


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. www.anzba.org.au 8

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. www.anzba.org.au 9

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]. © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 10

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.


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]) © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 12

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% © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 13

Scald Contract Chemical Friction Electrical Other

28% 13% 5% 5% 2% 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 ·

Burns requiring medical attention affect 1% of the population per year.

·

Burns are frequently caused by carelessness and inattention, and the influence of intoxicating drugs is common.

·

The majority of burn injuries in all age groups occur in the home.

·

Burning can be a method of assault in adults, and a method of child abuse. The correct diagnosis of these injuries requires vigilance, and accurate reporting can ensure that appropriate help is given to patiens and relatives


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).


Structure of EMSB L O O K

D O

A

B

C

D

E

I R W A Y

R E A T H I N G

I R C U L A T I O N

I S A B I L I T Y

X P O S U R E

AVPU & Pupils

Environmental Control

C spine

O2

Haemorrhage control I.V.

FLUIDS ANALGESIA TESTS TUBES

Primary Survey©EMSB

A.M.P.L.E. History Head to Toe Examina on Tetanus Documenta on and Transfer Support

First Aid

Secondary 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.


B. · · · · · ·

C.

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?

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: AVPU-

· ·

E. · · · ·

Alert Response to Vocal stimuli Responds to Painful stimuli 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].

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


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 © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 18

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 © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 19

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 © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 20

- 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 © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 21

(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 © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 22

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 lifethreatening conditions as required. · Fluid resuscitation, analgesia, tests and tubes represent treating the ‘burn injury’ once lifethreatening 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 reevaluation: 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


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].

Jackson’s Burn Wound Model

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 © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 24

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 capillary wall are summarised by Starling’s Hypothesis[2, 32] (see footnote)1. 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


(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.


(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.

Summary ·

The local effect of thermal injury on the skin and subcutaneous tissues causes three zones of injury. Progression of the intermediate zone to necrosis tends to occur.

·

Normal capillary exchange is disturbed leading to oedema formation and loss of albumin from the circulation.

·

Burn injury also causes widespread general effects on the circulation, the metabolism, temperature control, immune competence, and function of the gut and lungs as well as long-term growth changes.


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 © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 28

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) © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 29

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 lobin (%) 0 –15

Symptoms None - (Smokers, long distance lorry drivers)

15 – 20

Headache, Confusion

20 –40

Nausea, Fatigue, Disorientation, Irritability

40 –60

Hallucination, Ataxia, Syncope, Convulsions, Coma © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 30

> 60

Death

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 © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 31

Sputum containing Soot Croup -like Breathing Flaring of Nostrils Inspiratory Stridor Respiratory Difficulty Productive Cough Tracheal Tug In-drawing of Supraclavicular Fossae Rib Retraction

The symptoms and signs of an inhalation injury change or evolve over time according to the particular site and type of the injury. An indication of this change is given in Table 4.2.

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 Type of Inhalation

Timing

Signs/Symptoms

1. Above the Larynx

4 to 24 hours

Increasing Stridor Hoarseness or Weak Voice Brassy Cough Restlessness Respiratory Difficulty Respiratory Obstruction DEATH

2. Below the Larynx

(i) Immediate

Restlessness Life Threatening Anoxia DEATH Increasing Hypoxia Pulmonary Oedema/ARDS Respiratory Failure

(ii) Gradual Onset 12 hrs to 5 days 3. Intoxication

Death At Scene Worse Initially

Obtundation/Unconsciousness Stupor Confusion Drowsiness Poor Mentation Visual Disturbances Headache

Improves with Time

Diagnosis of Intoxication

Inhalation

Injury

Producing

Systemic

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. © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 32

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 © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 33

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 © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 34

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.


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 © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 36

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


Figure 5.3


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 middermal 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, middermal, 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]. © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 39

Depth of Burn Burn Wound Healing = re-epithelisation

Epidermis

Epidermal

Dermis

Superficial Dermal

- capillaries - nerves - collagen & elastin fibres

Mid Dermal

Sebaceous gland

Deep Dermal

Hair follicle Sweat gland

Full Thickness

Subdermal fat

Figure 5.4

Table 5.1 Diagnosis Of Burn Depth[10]

Depth

Colour

Blisters

Capillary Refill

Sensati on

Heal ing

Epiderma l

Red

No

Present

Present

Yes

Superficia l Dermal

Pale Pink

Small

Present

Painful

Yes

Mid Dermal

Dark Pink

Present

Sluggish

+/-

Usu ally

Deep Dermal

Blotchy Red

+/-

Absent

Absent

No

Full Thickness

White

No

Absent

Absent

No

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 © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 40

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 reepithelialisation 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. © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 41

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 ·

The seriousness of a burn is determined by the area of patient burnt, and the depth of the burn.

·

The mortality from burns is related to the age of the patient and to the extent of the burns.

·

The Adult and the Paediatric Rule of Nines enable a reproducible assessment of burn extent to be calculated.

·

By clinical examination of the burn wound it may be possible to diagnose the depth of the burn.


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) 2) 3)

Central zone of coagulative necrosis. Intermediate zone of injury characterised by stasis of blood flow. 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 © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 43

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.


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… Children (< 30kg)…

0.5ml/kg/hr = 30–50ml/hour 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. © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 45

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.


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 Fluid resuscitation is necessary for survival. ·

Intravenous fluids for:

children >10% TBSA adults >20% TBSA

Two large bore peripheral cannulae ·

Calculation fluids commences at time of injury:

· ·

Child (<30kg)… Adult…

3–4 ml x kg x %TBSA burn plus maintenance 3–4 ml x kg x %TBSA burn

Half in first 8 hours, rest over next 16 hours. · Use crystalloids (e.g. Hartmann's solution) during first 24 hours. · Children need carbohydrate. · Insert a urinary catheter. · Haemochromogens: increase fluid resuscitation to double urine output. · Measure blood glucose, serum electrolytes, blood pressure, pulse, arterial blood gases, chest xray.


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 © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 48

then be removed as quickly as possible. It does not help the patient if observers or assistants have burned hands so it is important that any assistance be rendered in such a way that the helpers are not themselves injured. In a scald burn the clothing soaked with fluid acts as a reservoir of heat and so removal of clothing as rapidly as possible will stop the burning process. In addition to removing the clothing, all jewellery should be removed[2]. If clothing is firmly stuck to the surface of the skin cut around the area leaving the adherent cloth in place. However melted synthetic compounds adhere to the surface of the skin which is non-viable and will come away quite easily. Because it is non-viable this is no disadvantage to the patient.

Cooling the Burn Surface The burn surface should be cooled with cold running water [73-78]. The ideal temperature is 15°C and the range that is useful is between 8°C and 25°C [76, 79]. Cooling the surface reduces the inflammatory reaction and can therefore stop progression of necrosis in the zone of stasis [73, 80]. The technique of application is by allowing cold water to flow over the burn wound, if this is possible. Methods such as spraying or sponging water over the wound, wet towels or hydrogels are not as efficient as running water and should not be used unless there is no water readily available i.e. in transit to medical care[73, 81]. Wet towels are less efficient as they are not in contact with the burn wound in all areas, and quickly heat up due to proximity to the body [73]: if used, they must be changed frequently. The duration of application should be for twenty minutes unless some other factor prevents this from happening [73-76, 80].For example, the patient may have multiple injuries and there may not be personnel available to perform first aid for this length of time. First aid is effective within the first three hours following the burn injury. Small children are at significant risk of becoming hypothermic and if this is detected either by taking the temperature or by clinical assessment of the blue shivering child, application of cold water should cease. To reduce the risk of hypothermia it is desirable to raise the ambient temperature to over 30°C and to keep the rest of the child well wrapped[4]. Ice or iced water should not be used. The extreme cold causes vasoconstriction and experimentally has been shown to deepen the tissue injury. There is also a greater risk of hypothermia. Cooling the surface of the burn is also an extremely effective analgesic [22, 74, 76]. If pain reappears within minutes of ceasing cold-water application, and there is no other factor preventing its continued application, it may be continued for its analgesic effects. Hypothermia should be prevented at all costs.

Early Management © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 49

Once first aid has been completed the burn wound can be covered with plastic wrap or a clean dry non-stick dressing while other aspects of the patient’s care are performed [2, 24]. If the burn wound has not had cold fluid applied and the lapse of time since the accident is greater than three hours, application of cold water does not have a beneficial effect. The wound should therefore be washed and this can be done with saline, soap and water, or chlorhexidine 0.1% solution. Other antiseptics should not be applied. In preparation for transport the patient may need a dressing on the burn wound. Depending upon the time between injury and transport and the expected time taken during the transporting process, it may be necessary to apply something more than simply wrapping the area in a clean cloth. Plastic cling film can be used and is particularly useful in children because it limits evaporation and hence heat loss [22]. Chlorhexidine impregnated Vaseline gauze (e.g. Bactigras) held on with a light bandage is suitable for patients who are going to take some hours during the transport process. The use of topical agents on the burn wound is reserved for those patients in whom there is significant delay or prolonged transport time and should be done in consultation with the receiving burn centre. For these patients the use of an antimicrobial dressing (e.g. Acticoat, Flamazine or Bactigras) is suggested.

Elevation Elevation of an injured limb is useful during initial treatment and transport, as it tends to limit swelling. In the limbs this may make a difference between the need to perform an escharotomy or not. There is also a theoretical possibility that tissue nutrition is impaired by oedema increasing the diffusion distance between the capillaries and the cells.

Special Areas As mentioned in the section on respiratory burns, thermal burns of the upper airway are often associated with rapidly accumulating swelling and early intubation is necessary[2]. Burns of the perineum require early urinary catheterisation in order to prevent contamination. Delay in catheterisation may cause extreme difficulty in insertion of the catheter once swelling has become established. Burns of the head and neck should have elevation of the head to limit upper airway swelling. Children with extensive burns or with burns of the head and neck benefit from the head up position because they have a greater risk of cerebral oedema with fluid resuscitation.

Escharotomy When the burn injury affects the whole of the dermis the skin loses its ability to expand as oedema progresses [82]. It therefore may become necessary to release the burn wound surgically by incising the burned skin down to the subcutaneous fat [7, 82]. This procedure is called escharotomy.

Trunk © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 50

When the trunk is extensively burned rigidity of the chest wall decreases compliance and this may reduce ventilation [2, 82]. In adults this problem is seen with circumferential burns of the chest with or without involvement of the abdomen. In children whose breathing is principally diaphragmatic, the problem can be seen when the anterior aspect of the chest and abdomen are burned without the injury extending to the posterior aspect. The incisions to be made run longitudinally along the anterior axillary lines to the costal margin or to the upper abdomen if this is burnt [82]. In severe cases it may be beneficial to connect these incisions by two cross incisions which may be convex upwards across the upper chest below the clavicles and across the upper part of the abdomen.

Extremities When a limb is burned circumferentially the increase in pressure due to the accumulation of oedema under the rigid burned skin may interfere with circulation and cause death of tissue in the distal part of the extremity [21]. The onset of circulatory embarrassment is slowly progressive and subtle if not sought. The increase in pressure may be detected by the appearance of one or more of the following [82, 83]: · · ·

· ·

Deep pain at rest Pain on passive movement of distal joints Loss of distal circulation Pallor Loss of capillary return (especially in the nail beds) Coolness Decrease in pulse pressure as detected by Doppler ultrasound Loss of palpable pulses Numbness Decreased oxygen saturation as detected by pulse oximetry

The interpretation of these signs may be made difficult by the presence of burned skin (which makes feeling the pulses difficult), by cold (which gives the appearance of decreased capillary return), and by hypovolaemia. The most accurate method of assessment is the use of Doppler ultrasound. The earliest changes will be loss of Doppler signals from the digital vessels. Escharotomies should be performed before pulses are lost when there is evidence of decreasing circulation. The incisions should extend by a few millimetres onto normal skin above and below. The incisions are in the mid-axial lines between flexor and extensor surfaces. Avoid incisions across the flexural creases of joints. They should be carried down to the fat sufficiently to see obvious separation of the wound edges. Running a finger along the incision will detect residual restrictive areas. Sometimes one incision is enough but often incisions on both sides are necessary to restore circulation. The palpable softness of the limb is a useful guide. The danger of escharotomy is to structures under the skin. In particular medially at the elbow the ulnar nerve is vulnerable and laterally at the knee the common peroneal nerve is at risk. Transverse incisions in the limbs should not be made. © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 51

The distal extent of escharotomy is sometimes difficult to assess. In the upper limb the medial incision can pass along the medial border of the hand to the base of the little finger. On the lateral aspect the incision can come down to the proximal phalanx of the thumb. Occasionally further hand incisions may be necessary but before embarking on this the burn referral unit should be contacted. Diagrams of appropriate lines of incision are included in the manual as Appendix 3 and can be rapidly supplied by fax.

Procedure Plan The first step is to define the lines of incision. If the operator is not familiar with the procedure they can be drawn with a pen/marker. For this marking the limb needs to be held in its anatomical position; and then the markings inspected before a final decision is made. When the arm is burnt, the forearm naturally lies in pronation so needs to be supinated before marking and incising. In the upper limb the incision should go in front of the medial epicondyle to avoid damage to the ulnar nerve. In the lower limb the medial incision passes behind the medial malleolus avoiding the long saphenous vein and saphenous nerve. If a second incision is required laterally, care should be taken to avoid the common peroneal nerve where it crosses the neck of the fibula. This incision is in the mid-lateral line. The equipment needed is a scalpel or cutting diathermy and some means of haemostasis. Artery forceps and ties, diathermy or topical haemostatics such as calcium alginate are useful. Blood loss can at times be extreme. Anaesthesia is usually not necessary. Local anaesthetic is necessary at the edge of the burn to extend up into normal tissue adequately. Many of these patients may already be intubated and therefore sedated under which circumstance a little extra sedation can be given. Dressings should be available to dress the area once the incision is performed. The area is prepared as for a surgical procedure and performed in a sterile fashion. Light dressings are applied as firm dressings may interfere with the effectiveness of the procedure. If the patient is conscious the procedure should be explained to them prior to commencement.


Summary ·

Burns interfere with all functions of the skin.

·

First aid consists of stopping the burning process and then cooling the burn wound.

· Immediate treatment of the wound should be kept simple. · Rigid eschar may interfere with body functions so escharotomy may be needed on the chest to allow ventilation, or on the limbs to prevent distal circulatory obstruction.


CHAPTER 8

Indications and Procedures for Referral Introduction The patient with electrical, chemical, or thermal injury requires immediate assessment and stabilisation at the nearest hospital. There is no case for the “occasional” burn surgeon in Australia and New Zealand, as expert multidisciplinary care is readily available at central hospitals. All patients have the right of access to quality burn care. Initial treating personnel should complete a primary and secondary assessment and evaluate the patient for potential referral and transfer. Burn injuries may be a manifestation of multiple traumas, and the patient must be evaluated for associated injuries. All procedures and treatments administered need to be documented to provide the receiving burn unit with a record that includes a flow sheet of observations, medications and treatments.

Influence of Geographic Situation 1.

Urban Areas

In cases of burns that occur in those cities of Australia and New Zealand that have an established burn unit, patients requiring hospital admission should be transported to that unit without unnecessary delay after a primary survey has been conducted, so that resuscitation and definitive care can begin as soon as possible. The only exception to this rule is in those cases that require immediate life-saving intervention, such as endotracheal intubation. When the burn unit is within an hour’s ambulance ride, unnecessary delays to begin IV fluid resuscitation may not be in the patient’s best interests. Nevertheless, significant delays can occur in ‘short transports’, necessitating fluid resuscitation to be

2.

Rural and Isolated Areas

In isolated and rural areas, because of distance and sparse facilities and also because of logistic problems, it may not be possible to transfer the patient immediately. Patients may need to be transferred by road, aeroplane or helicopter. Twenty-four hours of treatment may be required before transport is possible. It may occasionally be necessary to treat patients for longer than 24 hours (see Chapter 12). In these circumstances it is the responsibility of the local treating medical and nursing staff to liaise with the staff at the regional burn unit regarding appropriate emergency management, so that when the transfer occurs the patient is in optimal condition. Only in the most exceptional circumstances are the patient’s best interests served by continuing treatment at a local or district hospital. Sacrificing good physical care for the perceived advantages of “keeping the family together” is detrimental, particularly as the emotional care of the burned patient is as specialised and as important to their long term outcome as the physical care. All specialised burn units © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 54

recognise this need and have facilities for relatives to stay as well as personnel trained to help both patient and family achieve an optimal emotional outcome.

Referral Criteria The Australian and New Zealand Burn Association has identified the following injuries as those requiring referral to a burn unit - see Table 7.1. All patients with these injuries should have early consultation with a burn unit. If there are local resources that are appropriate, some patients may not need transfer, but generally, all patients listed will need transfer.

Table 7.1 · Burns greater than 10% Total Body Surface Area (TBSA) · Burns greater than 5% TBSA in children · Full Thickness burns greater than 5% TBSA · Burns of Special Areas - Face, Hands, Feet, Genitalia, Perineum, Major Joints and circumferential limb or chest burns · Burns with inhalation injury · Electrical burns · Chemical burns · Burns with pre-existing illness · Burns associated with major trauma · Burns at the extremes of age –young children and the elderly · Burn injury in pregnant women · Non-accidental burns If the patient has a pre-existing disorder that could make management more difficult or the risk of injury greater, a specialised team is needed to give maximum chance of an optimal result. Those patients with concurrent trauma should be admitted to a burn unit or a trauma unit depending upon the severity of the associated trauma and the seriousness of the burn. There needs to be a balance based on the clinical findings at the time of emergency assessment and following discussion between the local trauma team and the burn unit personnel. If the associated trauma poses the greater immediate risk the patient may initially be treated in a trauma unit until stable, prior to transfer to the burn unit. Burn care must be provided concurrently and transfer arranged after the patient has recovered from the immediate effects of the multiple trauma. Should the burn injury present the dominant threat to mortality and the greatest risk of morbidity, then primary transfer to the burn unit is correct. The priorities are a matter for medical judgement and should be discussed by the referring doctor, the burns specialist and the trauma or intensive care specialist, bearing in mind that patients at the extremes of age have a higher mortality and morbidity after a burn injury. Their pathophysiological responses are less predictable so they need the benefit of a specialised team. © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 55

The burn team approach, of bringing together doctors, nurses, physiotherapists, occupational therapists, psychiatrists, psychologists, social workers and dietitians in a management team has a significant and beneficial effect on the outcome of major burn injuries [2].

Preparation for Transfer Patients who are physiologically stable are capable of safe transfer over long distances, even after massive injury. It is therefore essential for the patient to be stabilised prior to starting their journey. Stabilisation involves all the aspects of resuscitation and management outlined above.

1.

Respiratory System

· All patients with major injuries should be commenced on high flow oxygen at 15L/min. · Since upper airway obstruction can progress rapidly and its effects peak at a time when the patient is likely to be in the process of transfer, it is essential to consider and decide about the need for endotracheal intubation BEFORE the journey is started. · Infraglottic injury is less likely to be a problem during transport.

2.

Circulatory System

The principles of treatment of the predictable shifts in fluids and electrolytes given above are valid for the stabilisation of the patient prior to transport. · If insertion of 2 cannulae (16 gauge in adults, 20 gauge in children) is not possible, other routes of access should be considered and their feasibility discussed with the referral unit. · The method of vascular access will largely be determined by the experience of the team at the peripheral site or the experience of the retrieval team. · The routes available are percutaneous central venous line (femoral, subclavian, or internal jugular), intra-osseous needle or peripheral cutdown (ankle or elbow usually)[3, 7, 9]. The fluid regime is discussed in Chapter 6. In summary, commence resuscitation with… · 3–4ml crystalloid (e.g. Hartmann’s Solution) x kg x % in 24 hours, 50% of which is given in the first 8 hours post burn · Add maintenance fluid for children [3, 12, 15, 17]. · Adequacy of resuscitation is determined by observation of the patient, particularly the urinary output (via an indwelling catheter), aiming for 30–50 ml/hr in adults, and 1 ml/kg/hr (0.5–2 ml/kg/hr) in children up to 30 kg [3, 11, 14, 20]. · If haemochromogenuria occurs, as is common after electrical injury, the aim is 75–100 ml/hr in adults, or > 2 ml/kg/hr in children.

3.

Burn Wound

The burn wound should be washed with aqueous chlorhexidine solution 0.1% or normal saline and then covered with plastic wrap or a clean dry sheet if evacuation is to occur quickly. Plastic kitchen wrap is useful as a cover for burn wounds as it reduces evaporation thus preserving heat and preventing desiccation [22]. Only if transfer is to be delayed should more formal dressing (such as © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 56

slow-release silver dressings, antibacterial cream or chlorhexidine impregnated Vaseline gauze; and absorbent outer layers) be undertaken. This should only be after liaison with the receiving burn unit.

4.

Pain Relief

A burn injury is extremely painful. Even though skin sensation may be lost locally over a deep burn, the surrounding area is very painful, so all burned patients need adequate pain relief [9]. In all but the most minor burns, it is essential for narcotic analgesia to be given intravenously. Doses are given in small increments allowing 3–5 minutes between each, the final dose being determined by the patient’s response. Any pre-existing disease or associated injury should be taken into account when calculating doses, but a starting dose of morphine is 0.05–0.1 milligrams per kilogram of body weight.

5.

Gastro-Intestinal System

While early enteric feeding is desirable (either oro-gastric or naso-gastric) the transfer process is usually safer if the stomach is empty to minimise the risk of vomiting and aspiration. A naso-gastric tube, regularly aspirated and on free drainage, is needed for adults with burns >20% TBSA, and for children with burns >10% TBSA.

6.

Tetanus

Tetanus prophylaxis should be given at the first point of medical contact. Details are in Appendix 1. In order to ensure that optimal treatment is continuous between the point of first contact and the referral centre, documentation must be complete and should include all the above aspects.

Transfer Mechanism Early telephone contact with a referral unit should be initiated when any patient may need to be transferred. Once the decision to transfer has been made, the receiving burn unit will be responsible for arranging a bed and the referral unit will be responsible for arranging transport. Transfer procedures should be followed in accordance with local protocols. The responsibility of the referring centre is to stabilise the patient and to document the findings of the primary and secondary survey, and the care given. Times of events, tests, fluid balance and treatment, including doses of medications, are important. Transfer the patient and ensure copies of all documentation accompany them. The method of retrieval is determined by the referral centre and the retrieval team, who in turn rely on the advice and assessment of the referring centre.


Summary ·

Patients with electrical, chemical, or thermal injuries which meet the ANZBA Criteria for Burn Unit Referral (Table 7.1) should be assessed and stabilised while referral is initiated.

·

Retrieval and placement are the responsibility of the referral unit. The retrieval team will provide help in the stabilisation of the patient.

·

Documentation is essential for the successful transfer of care from the referring hospital to the burn unit.


CHAPTER 9

Burns in Children Introduction Many of the basic concepts of emergency burn care in adults also apply in children. Children with burns should be assessed and treated in the same way using the Primary and Secondary survey. As in adults, a primary survey should detect and correct immediate life threatening conditions. This should result in the patient having a secure airway, and adequate circulation that will need to be monitored by continual re-assessment of fluid input, based on an adequate urinary output. The significant differences between children and adults are: · · · ·

the size and body proportions of the child[2] fluid dynamics the thickness of the skin the different social and emotional development of children.

Epidemiology There is a higher proportion of the paediatric population which suffer burns compared to adults [3], and causation of paediatric burns differs from adults, as shown in Table 9.1

Table 9.1 Causes of Children’s Burns (%) Scalds Contact Flame Friction Electrical Chemical Other

55% 21% 13% 8% 1% 1% 1%

(ANZBA Bi-NBR Annual Report 2011[8])

Younger children have a higher proportion of scalds while flame burns are more common in older children [84, 85].

History As in all burns an accurate history is essential [21]. This should include a history of the mode of injury and the time of the accident. Particular notice should be taken of any part of a history in which there are inconsistencies with the physical findings or a delay in presentation as these may point to non© ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 59

accidental injury. Occult airway problems such as sleep apnoea or asthma should be identified, and the history is important in forming a basis for the psychological care of the child and family. It is also useful to find out what first aid was given and in the case of scalds how hot the fluid may have been at the time of the incident and what clothes the child was wearing. This will help give an indication of the possible depth and whether any education might be required.

Body Size and Proportions The child differs from the adult in its overall surface area to body weight ratio, and in the relative size of different body parts compared with others [7].The higher surface area to body weight ratio means that for a given body weight there is a [21]: · · ·

higher metabolic rate greater evaporative water loss greater heat loss

All of these are highly relevant to the care of the burned child as fluid replacement formulae for fluid resuscitation are based on weight rather than surface area. Use of formulae based on surface area is complex and therefore too difficult for universal usage, but from a practical standpoint the burned child is more likely to need variations from the calculated volumes than is an adult. In a child the head and neck are comparatively larger than in an adult, and the legs are comparatively smaller (see Figure 5.2) [21]. In a child up to one year of age the head and neck are 18% of the total body surface area whereas each leg is approximately 14%. For every year of life above the first, the head decreases in relative size by approximately 1% and each leg gains 0.5% in comparison with total body surface area [3]. Using this rough modification of the rule of nines it can be seen that for practical purposes the adult proportions are attained at ten years of age. Obviously there is the chance of seriously miscalculating the size of the burn and hence the fluid resuscitation if this factor is not borne in mind.

The Depth of Burn The depth of the burn is proportional to the amount of heat applied and the duration of its application, and inversely proportional to factors that resist tissue damage. The chief of these factors is the thickness of the skin. In children the skin is much thinner than in adults. For this reason a given thermal injury is more likely to result in a deep dermal or full thickness burn in a child than in an adult. An example of this is that in infants water of 60°C will cause · In infants a full thickness burn in less than a second · Older children can tolerate up to five seconds of immersion at this temperature. · An adult will only receive a deep burn after twenty seconds.

Children’s Avoidance Reactions © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 60

Children’s reactions to painful stimuli are not as rapid or as consistent as adults. A toddler standing in hot water or on hot embers may not attempt to move away, thus sustaining a deep burn.

Burn Depth Assessment The assessment of depth of a burn in children is more difficult than in adults. In children scald burns are more common than flame burns, and the depth of the scald burn is more difficult to assess. The child’s thin skin makes the depth of the burn more difficult to assess [7]. The colour changes in burned skin in children are not always the same as those in adults. In particular a dark lobster red with slight mottling in a child is indicative of a deep dermal or full thickness burn, and in a few days will usually become an opaque even yellow colour of an obviously deep burn.

First Aid and Initial Transport The principles of first aid – remove the heat source and apply cold water - are the same in children as in adults. However, hypothermia is a much greater risk in children than in adults. Hypothermia in children is due to a number of factors. The larger body surface area to mass ratio is of particular importance. Children under one year of age do not have a shivering reflex. Older children may have a shivering reflex but their muscle bulk is much smaller. Total body mass and therefore heat content is much smaller. The risk of hypothermia should be born in mind whilst applying first aid during initial emergency transport. Good first aid is as important as in an adult but care must be taken to keep cool water applied only to the burn surface and to keep the rest of the child warmly wrapped. If there is an extensive burn it may be necessary to reduce the period of application of cold water from the optimal twenty minutes in order to prevent hypothermia.

Ice should never be used. During initial stabilisation and transport a space blanket is very useful to reduce heat loss. Parts of the body exposed at the time should be covered, preferably with a moisture-proof sheet such as plastic, to reduce heat loss from evaporation and convection.

Airway Occult upper airway obstruction in children is common. Enlargement of adenoids and tonsils and laryngomalacia may pre-exist the burn injury [3] and are detected historically by evidence of sleep apnoea such as snoring or waking at night, somnolence during the day, or noisy breathing. Narcosis may not only depress respiration but also may relax pharyngeal muscles and thus increase obstruction. Any swelling on top of occult obstruction may cause problems early. The lower airway is narrower in absolute diameters in children than in adults [2, 3]. Therefore swelling of the bronchial mucosa or accumulation of secretions within the bronchi causes a comparatively larger reduction in cross-sectional area and so interferes with gas flow[2]. For these © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 61

reasons an uncuffed tube has commonly been used up to the age of 10 years, although the use of specialised paediatric cuffed tubes is increasing. Bronchial hyper-reactivity (asthma) is extremely common in children and is indicated by a history of nocturnal cough in winter or for weeks following viral respiratory infection. Smoke inhalation will frequently lead to bronchospasm in children prone to this reaction. Endotracheal intubation technique is slightly different in children from in adults. The larynx is more cephalad compared with adults. Because narrow tubes are used, frequent gentle suction is necessary to clear secretions. Stabilising tubes is more difficult particularly when the face is burned, and two woven cotton tapes, one above and one below the ear, which can be lengthened if swelling increases, are useful in this regard. The position of the tip of the tube should be checked by auscultation before fixing the tube in position and subsequently followed by chest x-ray to confirm satisfactory position of the tube tip. Endotracheal intubation should only be attempted by a suitably trained and experienced practitioner. If airway obstruction occurs and endotracheal intubation is not possible, a large bore (14 gauge) needle passed through the cricothyroid membrane should be used instead of cricothyroidotomy. This is only a temporising solution and urgent tracheostomy may be required.

Fluid Management 1.

Differences between Children and Adults

Fluid dynamics and body compartment sizes differ in children and adults. In the child a higher proportion of body water is extra-cellular. Blood volume in children is 80ml/kg compared with 60– 70ml/kg in adults[2]. Renal tubular concentrating capacity in very young children is reduced compared with adults. For all these reasons the proportion of fluid loss which can occur in a child is greater and may be more rapid than in an adult[2, 3], and excessive fluid intake is less easily handled. On the other hand, occult depression of functional cardio-respiratory and renal reserve does not usually occur in children as it does in adults. Therefore, unless there is a known pre-existing disease, the physiology of the child can usually be relied upon to cope with a rapid fluid load although large excesses are less easily dealt with as mentioned above. Cerebral oedema is more likely in children with fluid overload particularly with hyponatraemia. This risk can be reduced by the use of the ‘head up position’ in the first 24 hours. Due to these differences fluid resuscitation is started in children with 10% burns rather than 20% as with adults.

2.

Assessment of Fluid Status

Good compensatory mechanisms in a child mean that circulation is apparently well maintained in the face of fluid deficit. Thus little overt warning of circulatory collapse is given until late in the progression of the pathophysiology of shock. Furthermore, useful signs of shock and hypoxia in the adult, such as agitation and tachycardia, are less useful in children because they can occur for other reasons. The observer may therefore not appreciate their significance. For instance tachycardia may © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 62

be due to distress or the hypermetabolic response of an early burn, and visible agitation may be due to pain or anxiety [7]. Hypotension is a late sign of hypovolaemia and indicates decompensation of homeostasis: by the time it occurs the patient is rapidly accelerating down the slippery slope that leads to irreversible shock. More reliance must be placed therefore on the subtle signs of decreased circulation. The following indicators of compromise are recommended by the Advanced Paediatric Life Support (APLS) course:

·

Tachycardia (age appropriate) Capillary refill >2 seconds (sternum) Mottled or pale cool peripheries Organ dysfunction: tachypnoea, altered mental status

3.

Urine Output

· · ·

The most reliable parameter of adequate resuscitation is the urinary output [3, 7, 11, 14, 18, 20, 35]. However this measurement is more difficult in children as mechanical obstruction of fine urinary catheters occurs more easily, and the collection of a few more millilitres of urine in large bore drainage tubing can cause errors of assessment. It is important to keep output as close to 1ml / kg / hr as possible with the acceptable range being 0.5–2ml / kg / hr [3, 7]. When extra fluid is needed, boluses of 5 to 10ml / kg can safely be given quite rapidly. Additional fluid can also be given by increasing the next hour’s fluid to 150% of the calculated volume. Both methods may be needed if the patient’s fluid status has become seriously depleted. Frequent reassessment at periods of 15 to 30 minutes is needed to decide whether another bolus should be given.

4.

Intravenous Cannulae

As in adults, the first choice of route of administration is percutaneous cannulation of veins through unburned skin[2]. If the expertise is available, percutaneous insertion of larger catheters into major veins such as the femoral is useful. In inexperienced hands in children these techniques are hazardous. Percutaneous cannulation of peripheral veins through burned skin is perfectly acceptable although more difficult to accomplish[2]. Cut-downs on veins require some expertise, is slow, and permanently obliterates the vein, so is no longer a recommended technique. Intra-osseous administration of fluids is relatively safe[2, 3, 7, 9, 72] quick to establish and is now the preferred technique for emergency venous access.

5.

Maintenance Fluids

In children maintenance requirements are significant in relation to the amount of resuscitation fluid [3]. Maintenance requirements can be calculated: 100ml/kg for the first 10 kg of body weight + © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 63

50ml/kg for each kg over 10 kg & less than 20 kg body weight + 20ml/kg for each kg over 20 kg of body weight ·

5% Glucose in 0.45% (½normal) saline [3].

This maintenance fluid should contain glucose which should be added to the volume of resuscitation fluid of all children whose total body weight is up to 30kg. The addition of glucose is necessary because of the decreased glycogen stores in children and the speed with which hypoglycaemia can occur, particularly in association with hypothermia. Regular blood glucose estimations are necessary during initial stabilisation and transport.

Escharotomies Limb escharotomies are needed in children as they are in adults[2]. Trunk escharotomies, however, are necessary more often in children than in adults. The reason is that breathing by diaphragmatic movement is more important in children and this means that abdominal wall rigidity is more likely to restrict tidal volume. For this reason interference with gas movement may occur with trunk burns that are not circumferential. Therefore, if a burn involves the anterior and lateral aspects of the chest and the upper half of the abdomen, trunk escharotomies should be considered. In this situation in addition to the procedures outlined in Chapter 7 under Escharotomy, an incision should also be made across the upper abdomen and parallel with the costal

Gut Children are more prone to gastric dilatation than adults and tend to swallow air when crying. A nasogastric tube on free drainage is therefore necessary in the initial assessment phase and during transport particularly if aerial evacuation is needed. However, children’s high metabolic rate and their nutritional needs for growth mean that they have less tolerance of nutritional deprivation. Very early enteral feeding should be established as soon as they arrive at the definitive treatment centre, as it prevents loss of gut function and maintains nutrition.

Progressive Assessment of Burn Wound Assessment of the depth of the burn wound can remain difficult in children up to seven to ten days after the injury. However, a burn wound that is unhealed in a child at day 10 should be considered as needing skin grafting.

Emotional Aspects Pre-existing psychosocial pathology is common in paediatric burns as well as in adults, but the type of pathology is different. The cycle of deprivation, lack of societal and parental skills causing impoverishment and further deprivation is common because the parents of such families lack satisfactory parenting techniques to protect their child, often themselves indulging in risk-taking behaviour. They are frequently pre-occupied by their own emotional and social problems. Teenage © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 64

children of such families are frequently involved in risk-taking behaviour and are frequently without any parental influence. The emotional and social needs of children are very different from adults. “Play” is an essential part of a child’s normal daily activities and the frivolous connotation that adults give to the word is not appropriate in children. Socialisation in their peer group and minimisation of separation are important aspects of a child’s emotional life. Person-to-person interaction is different and language used should be appropriate for the age of the child. The importance children place on trust in their relationships demands that adults be truthful with their paediatric patients at all times but stark or brittle phraseology should be avoided as it can frighten a child unnecessarily. After a child is burned the whole family suffers from major emotional disturbance of which guilt and blame are prominent features. Siblings are often severely affected. The wider peer group (e.g. the child’s school class) is also often affected. All these aspects of a paediatric burn need to be addressed eventually, and appreciated from the outset. The long-term emotional outcome after a paediatric burn is more dependent on the whole family’s emotional care than in adult burns where the concentration is on the patient. Therefore early and adequate care of the family is essential, and this starts from the moment of burn injury.

Non-Accidental Injury The emotional factors which often contribute to the causation of a child’s burn form a spectrum which varies from momentary lack of supervision through more overt, long-term psychopathology to the other extreme of deliberate abuse [7]. The point on the spectrum at which “Non-accidental Injury” begins is often difficult to define. The decision as to which children may be “at risk” in future is often easier. While medical attendants have legal obligations (which vary from state to state) to report suspicious or deliberate injury, the report can be made by the referral unit [7]. Suspicion of child abuse requires transferring the child to a specialist burn unit, and during this transfer process such suspicions should be passed on and clearly documented. Each hospital should have its own protocol to follow with the key emphasis being placed on good inter-agency communication to protect the child in need. Suspicion of non-accidental injury may be raised by [1, 10]: · delay in presentation · vague or inconsistent history from different observers · history not compatible with pattern of injury · presence of other signs of trauma · certain patterns of injury (e.g. cigarette marks or bilateral “shoes and socks” scalds Remember that false accusation of non-accidental injury is extremely damaging to the family. Unusual and bizarre distribution of burns can be caused by accidental injury and should not automatically be assumed to be deliberate trauma. These children should be transferred to a paediatric burn unit so that experts in child protection and burns can assess the situation and act appropriately.


In practice the distinction between accidental and non-accidental is less important medically than socially because all of these families will need considerable help over a prolonged period so that the patient’s long-term functional result is as good as possible.

Transfer Criteria In children the need to transfer occurs at a lower threshold than in adults. A child with more than 5% deep burns should be considered for transfer. Some children may need to be transferred simply for pain relief if techniques such as continuous narcotic infusion are not available locally. Finally, the possibility of non-accidental injury should prompt early consultation with the Burn Unit regarding the need for transfer. Other criteria applicable to adults, such as burns of special areas (hands, face, feet, perineum), and known or suspected respiratory burn, burns with associated major trauma, or burns in patients with significant pre-existing disease, are also valid criteria for transfer in children.

Summary ·

The principles of burn care are as valid in children as in adults.

· -

Factors that modify the care of children are: different body proportions different fluid dynamics thinner skin different psychosocial needs

· -

Major physical differences in care are: tendency to hypothermia increased depth of burning for a given insult increased fluid needs

· The psychosocial background and emotional needs of the burned child and its family are very different to those of adult burn patients.


CHAPTER 10

Electrical Injuries Introduction Electrical injuries are divided into three groups; low voltage, high voltage and lightning strike. Each group has its own particular features which are worthy of separate consideration. The common feature of each is heat generation resulting in a thermal burn. Table 10.1 Overview of Electrical Injuries Voltage

Skin

Deep tissue

Cardiac arrhythmias

Low voltage (<1000V)

Local entrance and exit wounds

Unlikely

Immediate cardiac arrest possible, otherwise nil

High voltage (>1000V)

Flashover burn, fullthickness entrance and exit wounds

Muscle damage with rhabdomyolysis and compartment syndrome,

Transthoracic current may cause myocardial damage and delayed arrhythmias

Lightning

Superficial or dermal flashover burns. Exit burns on feet

Eardrum perforation and corneal damage

Respiratory arrest – needs prolonged CPR

Low Voltage is considered to be anything below 1000 volts. This includes standard single-phase household electrical supply in Australia and New Zealand which is 240 volts alternating current (AC) at 50 cycles per second. Industrial power supplies are often three phase and commonly 415 volts. Other low voltage electrical accidents can occur with direct current (DC) which is used in the electroplating industry, electrolyte purification and some transport systems. The common car battery is capable of producing a current of sufficient amperage at only 12 volts to cause a significant thermal burn when a short circuit occurs through such articles as metallic watch bands, wedding rings and jewellery. Surgical diathermy is a commonly encountered direct current in operating theatres.


High Voltage includes anything above 1000 volts [10]but is often 11000 or 33000 volts which are the currents most commonly encountered in high tension transmission cables. Even higher voltages occur in power stations and substations. Lightning is an extremely high voltage, high amperage, DC electrical discharge of ultra-short duration which produces its own peculiar injury pattern.

Pathophysiology Tissue damage from electrical injury results from the generation of heat which is a function of · the resistance of the tissue · the duration of the contact · the square of the current [86]. Different tissues exhibit characteristic electrical resistance according to their electrolyte content. In order of decreasing resistance, the various tissues may be listed: · · · · · ·

bone skin fat nerve muscle blood and body fluids.

Skin resistance varies according to whether it is thick and callused like the sole of the foot, or thin skin. It also depends on whether the skin is wet or dry, dry skin having a higher resistance than moist or sweaty skin. The rise in temperature produced by a conductor depends on the heat produced and the rate at which heat can escape from the conductor by conduction, convection and radiation. Electricity conducted through bone therefore may cause a substantial rise in temperature. The increase in bone temperature continues even after the current flow has ceased causing secondary thermal damage. This phenomenon is known as the Joule effect. Due to the depth of the bone, heat escape is slow and considerable periosteal, muscle and nerve damage close to the heated bone may occur. The high concentration of current at the contact points and the high resistance of the skin causes intense heat and charring occurs. Once the skin has been breached increased current is permitted to flow. In high voltage injuries arcing may occur across such joints as the wrist and elbow causing charring and penetration wounds. Similar charring and exit wounds occur on the feet and hands because of the thick skin and resistance to flow resulting in intense heat and blowout type injuries.

Types of Burn Injury Low voltage current will cause significant local contact, entrance and exit, wounds [10, 87] and may cause cardiac arrest but no deep tissue damage. The 50 cycles per second alternating household © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 68

current can cause muscle spasm or tetany and prevent the victim from releasing the source of discharge[2][23]. High voltage current causes injury in two ways; flash burns and current transmission. A cutaneous burn without deep tissue damage results when there is a high-tension discharge or “flash over”, the current not passing through the victim. The arc ignites clothing and causes deep dermal burns without the formation of contact sites or entrance and exit wounds[10]. High voltage current transmission generally results in both cutaneous and deep tissue damage and the entrance, exit and contact areas are always full thickness defects [23]. Less commonly there may be internal organ damage, though this is more likely to occur as a result of an associated injury such as a fall from a pole or tower. Deep muscle damage which occurs under apparently normal skin and subcutaneous tissue may be very extensive and involve whole compartments of the limbs [88]. Swelling within the limbs as a result of the muscle damage may produce a situation similar to the “crush” syndrome where fasciotomy may be required. The limb becomes very swollen and tense to palpation. The symptoms are severe deep pain and tenderness. It eventually causes decrease in peripheral circulation and loss of pulses. If fasciotomy is required it should be done as an open procedure and will probably require a general anaesthetic. The muscle injury and necrosis results in release of myoglobin from the muscle cells into the circulation. This pigment along with haemoglobin from haemolysis of red cells may lead to renal impairment. As both these haemochromogens precipitate in the renal tubules, they can cause rapid onset of acute renal failure[10]. Lightning injuries result from an ultra high tension, high amperage short duration electrical discharge of direct current. This form of injury is not particularly common in Australia or New Zealand. 5 to 10 Australians, 90 in the US, and 10,000 people worldwide die from lightning strikes each year. The pattern of injury is variable[2]. A direct strike is where the discharge occurs directly through the victim and this, as expected, has a very high mortality. More commonly a side flash or splash occurs, when lightning strikes an object of high resistance such as a tree and the current is then deflected through a victim on its way to the ground. Stride potential may occur as the discharge flowing through the ground may pass up one leg and down the other. Typically the current flows over the surface of the victim causing superficial or dermal thickness burns. However, there may be significant exit burns on the feet. The short duration of lightning strike is not commonly associated with significant internal tissue damage but respiratory arrest is common and this is followed by cardiac arrest[2]. The initial respiratory arrest occurs as a result of the discharge affecting the medullary respiratory centre. This is usually reversible so prolonged efforts at resuscitation are justified. Another organ which can be damaged is the ear. The tympanic membrane may be perforated due to the blast and should be checked at the time of the strike[2]. Corneal damage has also been recorded and this may be acute, or a long-term sequel of the injury. © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 69

Lightning may also be responsible for unusual skin damage which has an arborescent or splashed on appearance. These are known as Lichtenberg flowers. These lesions are pathognomonic of lightning strike[2].

Management Initial rescue of the victim of an electrical accident may place the rescuer at risk of succumbing to the same fate [24]. First switch off the power source or remove the live wire from the victim [24]. If this is not possible, remove the victim from the power source with a non-conductor. Remember that high voltage electricity will discharge through air; 1,000 volts will only jump a few millimetres, 5,000 volts will bridge one centimetre, and 40,000 volts, 13 centimetres. Once clear of the power source the primary survey begins as with any burn injury. The airway must be cleared and the cervical spine protected. Breathing may be arrested as a result of the discharge affecting the medulla and cardiac arrest may also have occurred due to the effect of the current on the myocardium. C.P.R. is therefore vital to the resuscitation of victims of electrical injury. Endotracheal intubation may be indicated to maintain airway patency. Protection of the cervical spine is of importance because trauma may be associated with the electrical injury [24]. Violent muscular spasms may occur with alternating household current, which can produce fractures. Electrical workers may suffer from falls from poles, towers or elevated equipment. Cervical spine fracture should be excluded using appropriate methods of examination or imaging before abandoning immobilisation with hard collar, sand bag or simply holding the head immobilised. A spine board or sandbags should be used to protect the thoracic and lumbar spines until fractures of these areas have been excluded.

History of the Event Having completed the primary survey, a full history of the circumstances of the electrical injury should be obtained either from the patient, bystanders, or paramedics. · · · · · ·

How did the accident occur? How long ago did the accident occur? Was there loss of consciousness and for how long? Is there amnesia for the event? Was there any associated trauma? Did cardiac arrest occur or was any dysrhythmia recorded?

Secondary Survey © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 70

· First remove all clothing and in particular any watches and jewellery. · Examine for sites of entry or contact wounds with particular attention to scalp, hands and feet. · Estimate the total area of burn wound and the burn depth. · Undertake neurological examination with particular reference to the peripheral and spinal nerves. · Thoroughly document all clinical findings.

Resuscitation If, on completion of the secondary survey, the extent of the injury is sufficient to require fluid resuscitation, use two large bore intravenous cannulae as for other major burns. Fluid requirements in electrical injuries are likely to be greater in volume than would be anticipated in a pure cutaneous burn. Concealed muscle damage in the limbs will be responsible for fluid loss which is not accounted for by the standard formula. In those patients with deep tissue damage, haemochromogenuria is to be anticipated [2, 23]. A urinary catheter should be inserted both to detect the earliest sign of urine discolouration, and to monitor urine output. If pigments appear in the urine, the infusion rate of fluids must be increased to maintain a urine output of 75–100 ml/hr for adults, 2ml/kg/hr for children. In circumstances where urine output cannot be maintained by appropriate IV infusion, 12.5g of mannitol should be added to each litre of replacement fluid to produce an osmotic diuresis. Alkalisation of the urine [23] by the addition of sodium bicarbonate has traditionally been used to increase the solubility of haemochromogens in the urine, but its efficacy has been brought into doubt by more recent work. If more than simple fluid replacement is required to clear the urine pigment it is suggested that the advice of the receiving burn unit be obtained. On clearing the haemochromogens from the urine the rate of fluid replacement should be reduced to a level which will maintain the urine output of 30–50 ml/hr, or in children < 30kg, an output of 1 ml/kg/hr.

Dysrhythmias Conduction of electrical current through the chest may cause transient cardiac arrhythmias or cardiac arrest, though this is rare in low voltage injuries (<1000V). 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.[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.

Assessment of Peripheral Circulation Hourly assessment of the peripheral circulation must be made: · Skin colour © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 71

· · · ·

Oedema Capillary refill Peripheral pulses Skin sensation

Where there is evidence of an entrance or exit wound on an extremity, the possibility of sub-fascial oedema must be anticipated. This oedema may cause an increase in muscle compartment pressure sufficient to obstruct the circulation[2]. This increase in muscle compartment pressure causes severe deep-seated pain. The limb becomes stony-hard to palpation and there is progressive loss of peripheral sensation and loss of pulses. Under these circumstances fasciotomy is required.

Fasciotomy Unlike escharotomy which is used to release constrictive dermal eschar, a fasciotomy is used to relieve deep compartment pressure and restore muscle perfusion. Fasciotomy is best done under a general anaesthetic and in a sterile environment. Blood loss may be considerable and facilities for diathermy and ligature haemostasis should be available. Again, delayed haemorrhage may be considerable after resuscitation. The fasciotomy incisions should be dressed with Vaseline gauze and a lightly applied gauze dressing. It is important to have the patient well resuscitated prior to fasciotomy so that haemochromogens released from the newly perfused muscle are flushed rapidly through the kidneys. The burn unit should be contacted regarding prophylactic mannitol prior to fasciotomy.

1.

Upper Limb

The forearm muscles are very susceptible to ischaemia and the development of a compartment syndrome. This is relieved by performing a longitudinal incision along the mid-medial and mid-lateral lines of the forearm, extending from just above the elbow down to the wrist. The incision is made through skin and subcutaneous fat to expose the deep fascia which is then incised. Particular care must be taken to protect the ulnar nerve at the elbow. Bleeding may be brisk and require control with diathermy or ligature. If the patient is hypotensive at the time of the procedure then delayed haemorrhage may occur. Carpal tunnel release may be necessary for burns to the hands. Before proceeding with this measure, consultation with the receiving burn unit is advised.

2.

Lower Limb

There are four compartments of the lower limb which may be affected by sub-fascial oedema resulting in a compartment syndrome[2]. Each of these compartments requires incision. The four incisions can be made through two cutaneous incisions. The lateral incision is made over the fibula, extending from the head down three quarters of its length, care being taken not to damage the peroneal nerve which passes around the neck of the fibula. The intermuscular septum separating the anterior and lateral compartments is incised over the full length of the skin incision. The medial incision begins proximally, commencing one fingerbreadth below the subcutaneous border of the tibia, and extends down to the medial malleolus. The incision is made through the skin, subcutaneous fat and the investing fascia with care being taken not to injure the saphenous nerve © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 72

and vein. Carefully retracting this incision the deep posterior compartment can be identified and decompressed over the full length of the incision. As in the forearm, fasciotomy of the leg is best done under a general anaesthetic and in a sterile environment. Blood loss may be considerable and facilities for diathermy and ligature haemostasis should be available. Again, delayed haemorrhage may be considerable after resuscitation. The fasciotomy incisions should be dressed with Vaseline gauze and a lightly applied gauze dressing.

Wound Care The general principles of burn wound care apply to electrical burns and are described elsewhere. The presence of large amounts of dead muscle make meticulous wound management and infection prevention mandatory by use of a topical antimicrobial.

Paediatric Electrical Injury The majority of electrical burn injuries in children are low voltage accidents which occur at home [65, 86]. Discharge from faulty insulation of electrical appliances and cords, or placing metal objects in power points are responsible for most paediatric injuries [65]. The very young who are prone to picking up and sucking electrical cords sustain deep burns around the mouth when the saliva soaks into the faulty or frayed insulation resulting in a discharge [86, 89]. Finger and hand injuries are seen in older children, handymen, and electricians while playing with or working on radio or TV sets or household appliances which are still turned on. Many of these accidents could be avoided by the use of earth leakage circuit breakers. Most of these low voltage discharges will result in small full thickness defects which require excision and closure, skin grafting or even small flap repairs and should be referred to a burn unit for definitive care. Low voltage household accidents do not usually result in deep muscle damage in the limbs, however 24 hours of ECG monitoring may be required if they have suffered a high voltage injury, unconsciousness, or have an abnormal ECG on arrival, as previously stated [23].


Summary ·

Avoid injury to those rendering assistance.

·

Treat cardiac and respiratory arrest.

·

Assess and manage associated trauma.

· 24 hours of ECG monitoring may be required for high voltage injury, loss of consciousness, or abnormal ECG on arrival ·

Patterns of injury are specific to high voltage, low voltage and lightning strike.

·

Standard burns resuscitation formula may be inadequate.

· Haemochromogenuria is common in high voltage injury and requires maintenance of a urine output 75–100ml/hr in adults, 2ml/kg/hr in children, until urine clears. ·

High voltage injury involving limbs may require fasciotomy.

· According to ANZBA referral criteria, all electrical burns should be admitted to a burn unit for definitive treatment.


CHAPTER 11

Chemical Burns Introduction More than 25,000 products capable of producing chemical burns are now marketed for use in industry, agriculture, military science and the home. In the USA more than 3,000 deaths directly related to cutaneous or gastrointestinal chemical injury are documented each year with an estimated 60,000 patients requiring medical care for chemical burns. As an exposed part of the body and the part handling these noxious materials, the hands and upper limbs are the most frequently injured sites and, indeed, suffer chemical burns as often as all other sites combined.

Protection It is vital that all carers and first aid workers are aware of the need to protect themselves from the contaminant e.g. wearing gloves, aprons and protective face mask and overalls. All clothes should be removed as soon as possible if contaminated and stored in a protective container for disposal later.

Aetiology and Classification Laboratory accidents, civilian assaults, industrial mishap and inexpert application of agents used for medical purposes account for most of the chemical burns in the civilian population.

Commonly used chemicals capable of producing burns are:

1.

Industry

Alkalis - sodium, potassium, ammonium, lithium, barium and calcium hydroxide (washing powders, drain cleaners, paint removers). · Acids - picric, sulfasalicylic, tannic, trichloroacetic, cresylic, acetic, formic, hydrochloric and hydrofluoric (etching glass and electronics). ·

2.

Household

· · · · ·

Alkalis (lyes) - drain cleaners, paint removers, urine sugar reagent test tablets. Phenols - deodorants, sanitizers, disinfectants. Sodium hypochlorite - disinfectants, bleaches, deodorants. Sulphuric acid - toilet bowl cleaners Phosphorous - fireworks, insecticides, fertilizers. © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 75

3.

Military

· ·

Phosphorous red or white Vesicants

Pathophysiology Tissue damage as a direct result of exposure to any chemical is dependent upon:

· · · · ·

strength or concentration of agent quantity of agent manner and duration of skin/mucosa contact extent of penetration into tissue mechanism of action

The principal difference between thermal and chemical burns is the length of time during which tissue destruction continues since the chemical agent causes progressive damage until it is inactivated by a neutralizing agent or by dilution with water. The estimation of burn depth by clinical examination following chemical injury may be difficult during the first few days after injury. The above agents all cause cell injury but by means of different types of chemical reactions. Generally speaking: · · · ·

Acids produce a coagulative necrosis[10]. Alkalis produce a liquefactive necrosis. Vesicants cause ischaemic and anoxic necrosis (liberate tissue amines and cause blistering). All produce coagulation of protein by oxidising, corrosive or salt forming effects on protein.

An important feature of some chemicals is their systemic toxicity. · Hypocalcaemia - oxalic, hydrofluoric acid and phosphorous burns. · Liver and/or kidney damage - tannic, formic and picric acid, phosphorous injury and petroleum · Inhalation injuries - strong acids or ammonia. · Methaemoglobinaemia and massive haemolysis - cresol · Perforation nasal septum - chromic acid

First Aid


Remove contaminated clothing and dry chemicals [24]. Constant water flow is the most important treatment of most chemical burns[2] (except elemental sodium, potassium or lithium). For best effect it should be started within 10 minutes of contact.

Specific Agents Some[VAC1] non-specific chemical treatments such as Diphoterine are now available and are useful for most chemical injuries

1. Acid Burns · · · ·

Very painful Appearance varies from erythema (superficial) to black eschar (deep) Irrigate with water Surgical treatment as for thermal burn

Hydrofluoric Acid · ·

Very corrosive, inorganic acid of elemental fluorine: 2% body surface area can prove fatal Mechanisms of injury a) Hydrogen ions cause typical acid skin injury which is minimised by irrigation with water. b) Soluble free fluoride ions penetrate damaged skin and bind calcium ions. This causes necrosis of soft tissue and hypocalcaemia that is so severe that mobilisation of calcium ions from the bones is inadequate to overcome it. Extent of injury depends on concentration of acids and extent and duration of contact [90]. · Arrhythmias may occur secondary to hypocalcaemia and hypomagnesaemia.

Treatment[90] · · ·

Prompt water irrigation[10] Trim fingernails Inactivate toxic free fluoride ions and change to insoluble salt with: a) topical calcium gluconate burn gel [10, 90] (10% with Dimethyl sulfoxide [DMSO]). b) local injection with 10% calcium gluconate (multiple injections 0.1–0.2 ml through 30G needle into burn wound). Number and frequency of injections monitored by pain response. c) intra-arterial infusion of calcium gluconate. d) intravenous ischaemic retrograde infusion (Biers block) of calcium gluconate. e) early excision sometimes required.

2. Alkali Burns · most common around house · less immediate damage than acid but more long-term tissue destruction as they liquefy tissue and so penetrate more deeply[10]. · irrigate for longer than acid (at least 1 hour) © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 77

·

surgical treatment required for deep burns

Cement Burns · · ·

wet cement caustic with a pH up to 12.9 pain and burning occur late (after several hours) prolonged irrigation is important

Phosphorous Burns · · · · · ·

more common in military personnel white phosphorus ignites spontaneously when exposed to air oxidises to phosphorous pentoxide is extinguished by water particles of phosphorous embedded in the skin continue to burn treatment a) copious water irrigation b) debride visible particles c) apply copper sulphate (forms black cupric phosphide and facilitates removal of phosphorous particles) · mortality is related to the systemic effects of hypotension and acute tubular necrosis

Petrol (Gasoline) · complex mixture of alkanes, cycloalkanes and hydrocarbons. · hydrocarbon component is incriminated in endothelial cell damage which is the common pathway of injury to the lungs, liver, spleen and kidneys in immersion or extensive skin contact. · petrol dissolves lipid compounds readily, causing increased membrane permeability and fluid loss. · the two types of petrol burn: a) Ignition - fluid requirements frequently higher than other thermal burns. Burns tend to be larger, require more surgery and have longer hospital stays. b) Immersion or extensive skin contact without ignition results in dermal thickness skin injury, sometimes with systemic and inhalation lung damage.

Bitumen · a product of petroleum refining. · miscible with other petroleum products (kerosene, medicinal paraffin, paraffin wax) and vegetable oil. · transported and used at temperatures up to 190°C (150°C is the norm). · liquid at 150°C, but forms semisolid at atmospheric temperatures. · burns are due to the hot liquid, not the toxic effects of bitumen. · treat by cooling bitumen with copious amounts of water. · remove loose clothing but do not attempt to physically remove bitumen. · remove bitumen with paraffin oil (can add 1/3 kerosene). © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 78

Tar · · · · · oils. ·

by-product of coal gas industry. not common in Australasia. contains complex chemicals including phenols, hydrocarbons etc, thus some toxicity. burns by heat and phenol toxicity. soluble only in highly aromatic liquids (e.g. benzene, toluene, xylene) NOT petrol / vegetable treat by cooling and remove with toluene.

Special Anatomic Complications Gastrointestinal · · injury. · · · · · · ·

accidental ingestion of corrosive agents utilized in household are more common in children. 1/3 of all patients with intra-oral burns eventually prove to have associated oesophageal symptoms are unreliable and definitive diagnosis requires endoscopic evaluation. panendoscopy past the initial site of injury desirable to ascertain the extent of the injury. x-ray chest and abdomen; CT scan of chest/abdomen may show extra-luminal damage. surgical exploration and debridement of necrotic tissue may be necessary. steroids are of no proven benefit. stricture formation of the oesophagus is common. endoscopic and surgical treatment of stricture may be necessary.

Eye · chemical burns of eyes are associated with a high incidence of residual ocular impairment. · physical signs include blepharospasm, tearing, conjunctivitis and uncontrolled forceful rubbing of the eye. · rapid swelling of corneal epithelium, clouding of the anterior layers of stroma and cells floating within the anterior chamber occur. · treat with copious irrigation of water. Diphoterine very useful. · prolonged period of time (48 hours) in hospital. · topical antibiotics prevent secondary infection. · corneal ulceration and perforation, cataract formation, secondary glaucoma, iridocyclytis and symblepharon are possible late complications.

Tracheobronchial Tract · direct injury to trachea and bronchi rare, but occurs occasionally after ingestion of caustic agents or exposure to chemical gases (e.g. ammonia). · respiratory distress or hypoxia call for prompt investigation by fibre-optic bronchoscopy. · Bronchodilators and steroids minimise bronchospasm and inflammation. · temporary mechanical ventilatory support may be necessary. · bronchiectasis as a late complication may occur. · follow up pulmonary function studies and chest x-ray are necessary. © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 79

Summary ·

Agents capable of causing chemical burns are common in the environment.

·

All chemical burns require copious irrigation with water.

·

Hydrofluoric acid burns require neutralisation with calcium gluconate.

·

Systemic toxicity is common after exposure to hydrofluoric acid, petrol, or cresol.

· Bitumen and alkali burns require irrigation with water for an even longer period than other chemical burns. ·

Chemical injuries to the eye also require copious irrigation, and then referral.


CHAPTER 12

Management ofthe Burn Patient afterthe First 24 Hours Introduction In Australia and New Zealand there are times when a burn patient cannot be transferred immediately to a burn unit due to difficulties of transport and access. This chapter is designed to help doctors and nurses who are placed in the situation of having to continue the care of a patient who fits the ANZBA criteria for transfer, but for whom it is impossible to arrange evacuation within 24 hours. It may be necessary to continue care of the patient for longer than 24 hours, but it should be emphasised that failure to transfer a patient to a burn unit early will adversely affect the outcome. It is important to heal the patient’s burn wound as quickly as possible following the injury. In the deep dermal and full thickness burn this is accomplished by early excision and skin grafting. The optimal time to undertake this is between days three and five post burn. Delays in undertaking this surgery may allow infection to supervene and morbidity and mortality rate can rise. Even though it may not be possible to evacuate a patient to a burn unit within 24 hours after injury it is emphasised that every effort must be made to transfer the patient as soon as possible after that time. The principles described in this chapter are not seen as a means of justifying the treatment of severely burned patients in outlying centres. These guidelines are designed to assist you in keeping the severely burned patient in an optimal condition, so that when the transfer is possible, definitive management of the patient can proceed as part of the normal course of events. These guidelines are designed to supplement telephone, email and fax contact with the burn unit. Many of the principles in this chapter are guidelines and are designed to complement the assistance and further advice that may be available to remote centres either locally or from a distance. Personnel with intensive care, anaesthesia or trauma management backgrounds may be more directly available than staff of the regional burn unit and their expertise can be drawn upon in an emergency.

A.

Respiratory Support

It may be beneficial for severely burnt patients to continue to breathe high flow oxygen at 15 litres per minuteuntil their COHb levels are normal and then titrated to maintain a PaO2 sufficient to maximise oxygenation of burned tissues. Repeated reassessment of the patient should be undertaken, particularly when there are burns to the head and neck or a history or suspicion of inhalation injury because, as is highlighted in Chapter © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 81

2, endotracheal intubation may be required at this stage. Clinicians may also be in the position of having to continue care of the patient who has been intubated and whose transfer for logistic reasons was not possible. Access to investigations, including blood gas estimation and chest X-rays is useful to help monitor treatment. During this time it may also be necessary for efforts at non-invasive respiratory support to be undertaken. This includes frequent suctioning and positioning of the patient’s head and neck. If it is not possible to secure the airway by these means then endotracheal intubation will be required and this must be undertaken as soon as it appears to be necessary, before increased swelling of the pharynx makes intubation impossible.

1.

Endotracheal Intubation

A correctly placed endotracheal tube guarantees a patent and protected airway, allows high concentrations of oxygen to be delivered reliably, provides airway access for secretion clearance, may allow large doses of analgesia and sedation to be given safely and enables mechanical ventilation to be carried out. In the presence of an upper airway burn or smoke inhalation, intubation may become progressively more difficult as airway swelling or hypoxia worsens and therefore should be considered early. On the other hand, endotracheal intubation may be technically difficult, especially in an upper airway burn with severe swelling already present or facial injuries. The most important complication is technical failure and this is often lethal for the patient. Other short-term problems include endobronchial tube misplacement, upper airway trauma and tube obstruction by secretions or mechanical kinking. Any burn patient requiring intubation needs definitive care by a specialist intensivist in a major hospital, preferably one which also has a specialised burn unit.

2.

Indications and Techniques

Intubation and ventilation should be considered in patients with clinically apparent respiratory distress, severe or worsening hypoxia or hypercarbia, an obtunded neurological state with impaired airway reflexes or respiratory drive, severe chest injuries, or upper airway obstruction from swelling due to an airway burn. Occasionally mechanical ventilation may be indicated for “logistical” reasons, such as safe transport or to facilitate some therapeutic or diagnostic procedure. The oro-tracheal route is usually the simplest, but naso-tracheal intubation may occasionally be successful where oral intubation is impossible. If neither can be performed quickly in a patient with complete or near complete airway obstruction, surgical cricothyroidotomy is the only alternative. It is usually straightforward and should be performed without hesitation. Anaesthetic induction agents or muscle relaxants may make intubation easier, but should only be used by those with confidence and training. All these agents have significant side effects of their own and there is the potential to convert a patient with impaired but acceptable airway, and adequate ventilation, to one who is apnoeic and unable to be intubated or ventilated. Following intubation the tube position should be checked both clinically and radiologically. © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 82

3.

Physiology

Oxygen transport from inspired gas to alveolar capillary blood occurs predominantly by diffusion and continuous removal of oxygenated blood from the lungs depends on pulmonary blood flow (i.e. cardiac output). By contrast CO2 diffusing into the alveoli from capillary blood is removed from the airways by ventilation, which is necessary to provide a “downhill” gradient for CO2. Thus oxygenation depends mainly on inspired oxygen concentration, diffusing capacity of the lungs and the cardiac output, whereas the main determinant of arterial pCO2 is alveolar ventilation. The alveolar ventilation can be delivered in a variety of patterns. A small tidal volume with a rapid rate would minimise the adverse effects of a high intrathoracic pressure (see below), but a substantial proportion of each breath would be wasted, ventilating dead space (which is increased by endotracheal tube and ventilator circuitry as well as by a number of patient factors), and there would be a greater tendency to atelectasis. Conversely large volumes at a slow rate minimise atelectasis and waste the least possible ventilation on dead space, but problems due to high pressure and volume are maximised. Clinical practice is always a compromise between these extremes.

4.

Benefits and Disadvantages of Mechanical Ventilation

In addition to replacing or supplementing inadequate spontaneous breathing, mechanical ventilation allows control of arterial pO2 and pCO2. It also eliminates the work of breathing and hence saves the oxygen used in this process. However, positive pressure breathing reduces venous return and may result in hypotension, especially in a hypovolaemic patient. Matching ventilation and perfusion is generally less efficient than with spontaneous breathing. Over distension may occur if pathology (including respiratory burns and smoke inhalation) makes the lungs stiff (non-compliant), excessive tidal volumes are used, or the presence of lower airway obstruction (asthma or chronic obstructive lung disease) causes hyperinflation. This can produce lifethreatening complications such as tension pneumothorax. Finally, mechanical ventilation almost always requires sedation and possibly muscle relaxation introducing still further potential for complications and side effects.

5.

Specific Respiratory Problems in Burns

(i) Carbon Monoxide (CO) Poisoning Where hyperbaric facilities are immediately available, most authorities would recommend their use. However, the elimination of CO when the patient breathes 100% oxygen is rapid and the early use of oxygen is mandatory when there is reasonable suspicion of CO poisoning. A decision regarding hyperbaric oxygen can be made electively in consultation with the burn unit. (ii) Respiratory Burns and Smoke Inhalation These injuries affect both the gas exchange function of the lung and its mechanical stiffness (compliance). Presentation is usually with otherwise unexplained worsening respiratory distress and hypoxaemia. A cough productive of soot particles may be present and the chest X-ray may show a diffuse interstitial/alveolar opacity consistent with other forms of acute respiratory distress © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 83

syndrome (ARDS). This situation mandates definitive management by a specialist intensivist in a major hospital with sophisticated facilities. (iii) Chest Injuries Pulmonary contusion may result in significant hypoxia or haemoptysis and a large flail segment will render spontaneous breathing inefficient. The presence of these injuries in a burn patient increases the likelihood that mechanical ventilation will be required. Chest injuries increase the likelihood of lung injury during mechanical ventilation. The possibility of tension pneumothorax, in particular, should be carefully considered. If a severe injury with multiple fractured ribs is present and mechanical ventilation is required prophylactic intercostal drainage may be appropriate. Such cases should be discussed with a specialist intensivist. (iv) Chest Wall Burns The presence of a circumferential deep chest wall burn may markedly affect chest wall compliance. This situation should be distinguished from that of poor lung compliance and the use of higher inspiratory pressures to achieve the required tidal volumes is probably less dangerous. Chest escharotomies may, however, be needed.

6.

Optimal Ventilatory Patterns/Settings

A tidal volume of 5–7ml/kg body weight with a rate of 10 breaths/min and an inspired oxygen concentration of 50% is commonly used initially in adults. This is reasonably safe provided adequate oxygen saturation can be maintained, inspiratory pressures do not rise above 35cmH2O, and there is cardiovascular stability. Rates of 15–20 may be more appropriate in children. Arterial blood gases should be checked as soon as practicable after ventilation is initiated and appropriate adjustments made. These should be repeated frequently until the patient is stable. If lung compliance is poor or cardiovascular instability occurs, the tidal volume should be reduced, even if normocarbia cannot be attained. This will not be harmful in the short term unless severe head injury is present. If there is suspicion of CO poisoning or continuing cardiovascular instability 100% oxygen should be used. Progressive deterioration in lung compliance suggests the development of a tension pneumothorax or some other mechanical problem and a chest X-ray should be obtained as soon as possible. Modern intensive care ventilators allow a wide variety of settings, allowing the patient to breathe spontaneously but with variable degree of assistance from the machine. These modes of ventilation offer substantial benefits for difficult problems, long-term management and ventilator weaning, but they require more expertise and sophisticated equipment. For the occasional practitioner using simple equipment, full control of ventilation assisted by heavy sedation and where necessary, muscle relaxation may be the simplest short-term option. However, extremely close monitoring and one to one nursing is essential to ensure safety under these circumstances.

7.

Sedation/Muscle Relaxation During Ventilation © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 84

Sedation during mechanical ventilation is usually provided by a combination of opioids and benzodiazepines. Morphine and midazolam are most commonly given as a single continuous infusion, titrated to achieve the desired effect (0–10mg/hr of each in adults), with occasional supplementary boluses as required. If adequate control of ventilation cannot be achieved by this means a non-depolarising muscle relaxant may be added. Pancuronium and vecuronium are most commonly used and are usually given by intermittent IV boluses (6-8mg adult dose, followed by 2-4mg prn). It must be stressed that heavy sedation or paralysis renders the patient completely helpless in the event of ventilator malfunction or disconnection and constant vigilance is required.

8.

Simple Monitoring of Ventilation

Pulse oximetry, heart rate, blood pressure, end tidal CO2 and pressure-disconnect alarms should be regarded as an absolute minimum requirement for any such mechanically ventilated patient. Pressure disconnect alarms are built into all but the simplest portable ventilators but are also available as stand-alone units. Some monitoring of tidal/minute volume is also highly desirable and may also be built-in but is most simply provided by a Wright’s respirator. The ability to perform blood gases and serial X-rays is desirable if ventilation is undertaken. The use of monitors is no substitute for the continuous presence of a trained and attentive nurse at the bedside performing frequent clinical observations. This is mandatory for any ventilated patient.

9.

Ventilation during Transport

Transport of a ventilated patient involves a level of risk substantially greater than in a hospital environment. In addition to the increased potential for accidental extubation, dislodgment of lines and equipment malfunction, movement and vibration may contribute to further cardio-respiratory deterioration. Those attending to the patient must often work in cramped, dimly lit, unstable environment and may themselves be affected by problems such as motion sickness. The transport team must be fully self-contained with respect to portable equipment, power, oxygen, supplies and consumables and must be capable of dealing with unforseen problems arising en route. Altitude results in reduced inspired oxygen tension, especially if non pressurised aircraft are used an increase in the volume of any gas collections (such as a pneumothorax, the air in an endotracheal tube cuff or the dead space in an IV flask) and may alter the performance of some ventilators. All these issues must be carefully considered when planning to transport any seriously ill patient. Before such a patient is moved there should be discussion between the transferring and receiving institutions. Reliable vascular access and monitoring should be secured and every effort should be made to stabilise the patient’s condition as far as practicable. If experienced critical care transport teams are available it is almost always preferable to use them even if this further delays definitive care. No ventilated patient should be transported without medical and nursing escorts of appropriate seniority and skill.


B.

Circulatory Support

Patients with major burns continue to remain haemodynamically unstable in the second 24 hours. Fluid requirements often do not follow standard rules and continuing reassessment using the general criteria of clinical appearance, pulse, urine output and blood pressure is necessary to ensure that the correct amount of fluid is given. The following laboratory investigations will help guide the fluid treatment:· · · ·

Haemoglobin and Haematocrit Urea and Electrolytes Arterial blood gases (as appropriate) Blood glucose (in children)

1.

Composition of Fluid

As capillary permeability gradually returns to normal during the end of the first post-burn day, colloid containing fluids can be used to keep the intravascular space expanded. The amount of overall volume is adjusted to keep urine output of 30–50ml/hour in the adult and children (less than 30 kg) 1.0 ml/kg/hour. The fluids given during the second 24 hours should include 0.3–0.5 ml of colloid per kg body weight per percentage body surface area burn. The colloid should be 5% normal serum albumin (50g per litre). In the adult 4% dextrose in 0.18% normal saline is added to maintain an adequate urinary output. In children half normal saline with glucose added as necessary is used to maintain an adequate urine output.

2.

Ora/Nasogastric/Nasojejunal Fluids

Patients who are able to tolerate oral fluids can take small amounts in addition to the intravenous regime, or oral fluids can be substituted for the dextrose/saline component. Patients with severe burns should receive high protein fluid supplements either freely by mouth if tolerated or by nasogastric/nasojejunal tube if there is no evidence of ileus. This will be further discussed in the section on nutrition but care must be taken not to overload the patient.

3.

Fluid Balance

During the second 24 hours the fluid requirements are less than in the first 24 hours and it is important not to overload the patients with fluid, particularly those with pre-existing pulmonary and cardiac abnormalities. A fluid regime that produces an excessive urinary output is not appropriate and it is possible to produce pulmonary oedema during this time by giving the patient too much fluid [16].


Abdominal Compartment Syndrome can develop as serious secondary complication if excessive fluid volumes have been given to maintain or achieve adequate urine output and hemodynamic stability. Bladder pressure monitoring can give valuable information about intra-abdominal pressures. During the second 24 hours a natural diuresis should begin and urinary output may increase above the levels expected from the amount of fluid infused. In addition any haemochromogenuria will begin to settle from 24 to 48 hours post burn. Estimation of the haemoglobin and haematocrit at this stage may demonstrate a falling haemoglobin due to haemolysis and whole blood may need to be introduced at this stage. Consequently the haematocrit becomes an increasingly unreliable guide to fluid requirement.

C.

Wound Care

The wound should be reassessed to obtain a more accurate diagnosis of the extent and depth of burning. Areas of the burn which during the first 24 hours were thought to have been erythema only may progress in depth and in the second 24 hours be diagnosed as a significant dermal thickness burn. Formal reassessment of the area of the burn will enable a recalculation of fluid replacement for the second 24 hours. Burns which were judged to be superficial to mid dermal thickness may well have been treated with a biologically compatible dressing (Biobrane, Opsite, Duoderm or similar) and if these dressings are in a satisfactory condition during the second 24 hours then they do not need to be changed. Any areas of burn judged to be deep dermal or full thickness should be treated with the topical antimicrobial, in all patients for whom evacuation has been abnormally delayed. Contact the appropriate burn unit for advice on the most appropriate dressing. Continuing care of the burn dressed with antimicrobial dressing is best achieved by washing, either in a bowl, bath, or shower. Old dressings and sloughing skin should be removed and loose pieces of skin debrided with sterile forceps and scissors. After drying the patient digital images should be taken for monitoring of the wound. A clean dressing should then be applied to the wound and the patient left comfortable. Care should be taken to ensure that dressings are not too tight and that on completion of the dressing the underlying limbs have appropriate sensation and circulation distally. In the initial 24-48 hours dressings on limb burns should be applied to leave the tips of the fingers and toes exposed so that the colour and circulation can be frequently checked. Upper and lower limbs should be elevated on pillows or foam wedges to encourage resolution of dependant oedema. If available a Doppler may be used to assist in the monitoring of circulation of swollen limbs.

Escharotomy and Haemorrhage


Regular capillary refill and limb observations should indicate the possible need for an escharotomy. Post burn swelling may continue during the second 24 hours post burn, so an escharotomy may be necessary to ensure adequate circulation. As peripheral circulation returns to normal during this stage there will be a gradual opening up of peripheral vessels and so bleeding may occur from previously performed escharotomy sites. Bipolar diathermy or simple application of an artery forcep with ligature may be necessary to control this bleeding. It is not appropriate to attempt to control bleeding by application of firm bandages as this may restore the peripheral constriction released by the escharotomy.

D.

Pain Relief

During the second 24 hours the simplest, safest, way of providing adequate analgesia is with small incremental doses of intravenous narcotics. The dose should be titrated against the patient’s response including the respiratory rate, and no sophisticated facilities are required for administration or monitoring [9]. However, if facilities for morphine infusions are available a 20-30 microgram per kg per hour dose (after the loading dose) may be the most flexible form of pain relief. Higher doses may be needed and it may be necessary to top up this intravenous infusion with small incremental intravenous doses as it takes many hours for the infusion alone to provide a blood level that will give satisfactory analgesia. There are no concerns regarding addiction to narcotics at this stage. When pain is genuinely present appropriate analgesia should be given. Pain will be most severe during dressing changes, episodes of mobilisation, and physiotherapy. Adequate levels of intravenous narcotics should be provided to cover the patient during these painful episodes. Patient controlled analgesia (PCA) is extremely effective in burns and if PCA is available it is the method of choice. PCA can be used in quite small children with care. An acute pain expert or anaesthetist may be necessary to assist with the regime. Nitrous oxide or methoxyfluorane administered by a device which prevents inadequate oxygen delivery is a useful supplement, particularly when procedures are being undertaken but it should be supervised by an anaesthetist or other experienced staff member.

E.

Nutrition

It is important to establish normal gastric feeding as soon as possible after burn injury. The presence of food passing through the intestine protects the small bowel mucosa from damage that occurs following trauma and starvation. This damage to the mucosal cells allows bacteria from the bowel to move into the blood stream and it is this translocation of intestinal bacteria that is responsible for the severe secondary gram-negative sepsis that is often fatal in severe burns. Early introduction of food helps prevent this. Patients with severe burns (>10% in children, >20% in adults) frequently have intestinal ileus, particularly if their intravenous fluid resuscitation is delayed and they suffer significant shock. A © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 88

naso-gastric tube must be passed to empty the stomach to avoid vomiting and aspiration but as soon as bowel sounds are present or if present at the time of admission then feeding should begin. Approximately twice the usual amount of energy is required per day in severely burned patient and this can be given using a number of propriety dietary supplements. If these are not available milk based foods are most useful. Patients may be able to eat a normal diet. This should be rich in eggs and dairy products so that sufficient protein and calories are provided. The addition of skimmed milk powder to ordinary milk (200 gm per litre) significantly increases the protein level. In addition, high protein high calorie milkshakes can be made by adding ice-cream, eggs and glucose based flavouring agents to milk. These are often well tolerated. Patients with large burns are often unable to consume adequate amounts of nutrients. In these patients a naso-gastric feeding tube or naso-jejunal tubeshould be inserted for supplemental feeding. The head of the bed should be elevated 30° whilst the feed is being given. Gradual increase in rate often overcomes the problem of troublesome diarrhoea. The patient should be weighed daily, bowel movements should be recorded to document any change and if the patients are eating spontaneously extra time should be allowed for them to complete their meals. Extra food can be provided as small snacks between meals if patients are not able to eat a full meal at regular times. Patients with hand burns may need assistance with their eating. Because the risk of acute gastric ulceration following severe burn injuries is so high, protection in the form of proton-pump inhibitors, H2 antagonist, and most importantly, enteral feeding should be instigated.

F.

Physiotherapy/Occupational Therapy

Because deep burn wounds contract, it is important to maintain all joints in an appropriate position. Prevention of contractures starts early (first few days). Patients should not be allowed to adopt positions that are those of contracture. The position of comfort is the position of contracture. The precise position depends on the aspect of the joint involved. Usually the correct positions are: · · · · · · · ·

neck - extension axilla - abduction elbows - extension wrists - neutral or extension metacarpophalangeal joints - flexion interphalangeal joints of fingers - extension knees - extension ankles - 90o dorsiflexion

A splinting regime may be required and at least once a day all joints should be put through a range of movement as far as pain will allow. Those patients with respiratory burns who are conscious, or © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 89

who have chest wall burns should have supervised breathing or coughing exercises to ensure adequate pulmonary expansion. As part of the splinting regime it is particularly important to avoid tight bandages and splints that press on nerves surrounding joints. Particularly at risk is the ulnar nerve at the elbow which may be easily damaged from splints or from resting on the edge of a bed or operating table. Also, the common peroneal nerve around the head of the fibula is frequently damaged in elderly people by bandages or incorrectly applied splints and often results in permanent foot drop. During ICU admission the severely burned patient is usually immobile so meticulous care of pressure areas is essential. In the elderly, sacral, occipital and calcaneal pressure sores are very common. Other pressure sores may also occur at less usual sites. Patients should be turned every two hours around the clock utilising pillows for comfort. Pressure relieving beds and mattress should be used but care should be taken to prevent the patient getting into the position of contracture.

G.

Infection Control

· All equipment should be cleaned effectively between use of each patient. Hand washing between patients is the most effective means of preventing cross infection. · A three-minute scrub should be performed prior to the beginning of each shift. · When undertaking direct patient care a different isolation gown should be worn for each patient. · The patient’s mattress and beside area should be wiped down daily with an antiseptic.

Summary ·

Patients should be transferred to a burn unit within 24 hours of burning to maximise survival. If this is not possible intensive care management is required to keep the patient in the best state for transfer.

·

Attention to respiratoryand circulatory support, careful wound care, pain relief, nutrition, physiotherapy, and infection control will present the patient to the burn unit in the optimal condition.

·

Frequent telephone contact with the burn referral unit or receiving ICU is essential.


CHAPTER 13

The Outpatient Management of the Minor Burn Introduction Approximately 1% of all Australians seek treatment after sustaining a burn injury every year.Of these 220,000 peopleburnt each year approximately 10% (22,000) are hospitalised and close to 100 die as a result of their burns (Source: 2001 Australian National Health Survey) Many patients sustaining acute burns will attend the emergency department of a rural or urban hospital. Many patients receive primary care from their General Practitioner.

A.

Burn Assessment

1.

History

The history of the incident is essential [21]. A history of what the causative agent was, and any first aid received, will give clues as to whether the burn is likely to be superficial, mid, deepdermal or full thickness. Scald burns, receiving recommended first aid, are less likely to be deep than flame burns, but in a child, as in the elderly, scald burns are frequently deeper than first assessed. An idea of how hot the scalding liquid was should be obtained. Flame burns are usually deep, particularly where flammable solvents were involved, or the clothing has caught fire. Suspicion of non-accidental injury in a child or assault in an adult can often be guided by an inconsistency noted between the appearance of the visible injury and the history of occurrence. Any suspicion of non-accidental injury or assault should prompt referral to a burn unit for further investigation.

2.

Examination

The burnshould be carefully examined and the appearance recorded[2]. Note: i. the colour of the burn ii. the presence or absence of blistering iii. the presence or absence of capillary return following digital pressure iv. the level of pain caused by the burn (superficial burns are more painful than deep burns) v. the nature of any exudate on the burn wound (which can indicate possible wound infection in a burn presenting after a delayed period) © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 91

vi.

the presence or absence of surrounding inflammation suggesting invasive sepsis It is usually possible to diagnose the depth of burning with reference to the above findings. This is set out in more detail in Chapter 7 Wound Management. The small burn can be referred to a surgeon with an expertise in excision and skin grafting if it is not appropriate for these patients to be referred to a burn unit (refer to criteria in Chapter 10). If there is any doubt about the depth or treatment required for a burn, contact the burn unit for advice.

3.

Assessment of the Area of Burn

Use of the Wallace “Rule of Nines” as discussed in Chapter 5, should enable accurate assessment of the area of burning [21, 25, 27, 56-58]. Alternatively, the palmar surface of the hand (from fingertips to wrist) is approximately 1% of body surface area and this can be used as a guide to assess the extent of small or patchy burns [21, 56-58]. Superficial to mid-dermal thickness burns less than 10% TBSA for adults, 5% TBSA for children, are ideally suited to outpatient management, and with the advent of the newer biologically compatible dressings it is possible to treat these burns with dressings that protect the wound and facilitate normal healing. However, larger superficial burns approaching 10% consume considerable dressing resources and may be outside the scope of frequent redressing in the General Practitioner or regional hospital setting. For this reason they may be better off treated at an outpatient department and all burn units have associated outpatient clinics where these burns can be readily managed in conjunction with care provided by the General Practitioner.

B.

Pain Relief

Small burns, when appropriately dressed, are well suited to oral administration of paracetamol with codeine in various concentrations.Oral, intranasal or inhaled analgesia may be used in the outpatient setting with appropriate protocols butf this is not sufficient or available to provide appropriate analgesia admission of the patient for interim treatment should be considered, until the pain of the burn wound has decreased. Subsequently, it may be appropriate for outpatient management to recommence. Dressing of burns may be difficult and produce considerable pain, particularly in children. Oral sedatives and analgesics can be given 30–45 mins before dressings are undertaken to enable these burns to be treated as outpatients. Intranasal opioids have a quicker onset and duration of action which are suited to the outpatient environment. Again, if it is not possible to provide adequate analgesia in the outpatient or primary care setting, then hospital admission should be sought.

C.

Wound Management

Following first aid (Chapter 2), management of the burn should be based on the same principles that apply to treatment of any wound. Aseptic technique should be used to minimise the risk of contamination, and care should be taken to prevent further tissue damage. In the acute stage the burn wound should be washed using a dilute antibacterial agent. Dilute aqueous chlorhexidine 0.1 or 0.2% is often used, but if this is not available it is appropriate to wash © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 92

the area with saline or soap and water[10]. During cleansingit is important to have a clean wound bed thus the clinician should remove any loose skin with sterile scissors. Small blisters can be left intact. In cases where there are large areas of blisters which have ruptured and the skin has rolled up, the loose skin should be removed[10]. Once the area has been cleansed and debrided, further examination will help assess the depth of the burn.

Epidermal burns Burns that are bright pink to red, very tender without blistering are likely to be epidermal only[2]. The typical examples are sunburn or a minor flash from a gas explosion. These burns do not need specific treatment, but may be very painful and require pain relief. Moisturising cream may be all that is needed, dressings are not required.

Dermal burns Burns that have blistered are usually dermal burns. The base below the blister skin should have capillary return and sensation if the burn is only superficial dermal, and should heal spontaneously[2]. After the blistered superficial dermis and epidermis have been removed, the papillary dermis will be exposed. If this is allowed to dry out or become infected, the contained epidermal elements that should heal the burn by epithelialisation will die and the burn wound will become deeper. As a consequence it may not heal spontaneously and may require skin grafting. The appropriate treatment for these wounds is a biologically compatible dressing such as one of the silicone dressings a hydro-colloid a silver dressing or a film. For some dressing selection suggestions see table in Appendix 4. Dressings such as Biobrane, pig skin or preserved human cadaver skin are also ideal. However, these are very expensive and generally only applied in a burn unit. The superficial dermal burn will continue to exude serum secondary to the inflammatory reaction. Some dressings may becomesaturated with blister fluid and require more frequent dressing changes.Hydrocolloid dressings will need to be changed approximately every 3–5 days, or more frequently if there is excess exudate or a foul odour. Dressings that adhere to the wound such as Biobrane or various forms of preserved human skin should gradually peel off at the edges as epithelialisation proceeds. In most burn wounds a repeat wound inspection after approximately 3 days is advised to make sure that the initial assessment of burn depth was correct and that complications of the burn (particularly infection) have not occurred. A change in management may be required if repeat assessment suggests that the burn is deep dermal or full thickness or that the burn is infected.

Infected burns Burn wound sepsis may occur in those burns contaminated at the time of injury, or where the wound has been treated with a dressing lacking antibacterial properties. © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 93

Those burns which appear infected at the time of initial presentation, or are judged likely to have been contaminated at the time of injury, should be treated initially with a topical anti-microbial agent. The most appropriate product in Australia and New Zealand is a slow-release silver dressing. After applying the primary dressing it is important to secure the dressing with a bandage or adhesive dressing. Flammazine may be used however this preparation often converts the burn wound into a moist wound witha khaki coloured exudates which makes inspection of the base of the burn difficult. Any evidence of surrounding inflammation or systemic signs of infection is suggestive of invasive burn wound sepsis. At this stage it is appropriate for a referral to occur because invasive burn wound sepsis in a dermal thickness burn usually produces a deep dermal or full thickness injury. Because exposure allows desiccation which produces deepening of the wound, exposure treatment of the minor burn, except for epidermal burns is not appropriate. If at re-examination of the burn, the initial diagnosis of superficial burn appears incorrect, then referral for surgery should occur.

D.

Follow Up

Depending on the primary dressing applied, follow up is usually at 2 to 3 days following initial dressing, then at 3 to 7 day intervals. On these occasions, it is important to determine whether the patient’s home circumstances are satisfactory for continuing outpatient management. In situations where the patient may not be able to cope, hospital admission may be needed, e.g. the elderly, the patient who lives alone, or the child with working parents whose ongoing outpatient care may be compromised by lack of family support. Patient’s co-morbidities can also affect possible outpatient management. Those patients with incontinence or mental impairment may require more frequent dressing changes and wound management. Home nursing services may be useful in extending the role of the primary care outpatient service and can assist in provision of repeated dressings of the minor burn, particularly when it is difficult for the patient to come to the outpatient clinic or surgery.

1.

Physiotherapy/Occupational Therapy

Minor burns to the hands, limbs and around joints that do not fit the criteria for admission to a burn unit may need therapy. In burns that take longer than 2 weeks to heal, or those requiring surgery, hypertrophic scarring may occur. Physiotherapists and occupational therapists might be required for scar management using elasticised garments, contact media or adhesive tape[2]. The General Practitioner can co-ordinate the management, and burn units are able to give advice as to the availability of physiotherapists and occupational therapists to provide this care.

2.

Education Post Healing © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 94

It is important to protect the recently healed burn and to provide appropriate protection from sunburn by use of 30+ sunscreens and appropriate clothing. Recently healed burns may not stand up to the rigours required during work, and some time off may be needed to allow normal thickening of the healed area. Frequent application of moisturising creams to overcome the problem of lack of natural skin moisture due to the damage of sebaceous glands might also be needed for some time after the burn has healed. Itching may be a problem in the recently healed minor burn and is helped by moisturising creams and massage. Pressure also helps. Prescription of antihistamines and application of cold compresses may help relieve itch. Bathing in lukewarm water with solutions such as Pinetarsal, an oatmeal treatment or aloe vera solution can also be helpful, particularly in hot weather.

3.

Post Burn Functional Impairment

Some small burns that take longer than 14 days to heal and produce hypertrophic scar tissue may leave a primary skin shortage or contracture. If this occurs around joints there might be secondary loss of function. Burns with loss of function that do not respond to scar management and physiotherapy may require referral to a burn unit for secondary reconstruction to overcome this functional problem. Many minor degrees of skin shortage and contracture are well treated by therapists and the majority of these patients with good therapy do not need secondary surgical treatment.

4.

Post Burn Cosmetic Disability

Small burns may produce considerable cosmetic disability either due to colour match defects following spontaneous healing of the dermal thickness burn or as a result of post burn hypertrophic scarring. Some patients will not be concerned, but occasionally a patient will be abnormally distressed by the appearance of what is otherwise a minor burn. The secondary body image disturbance that may occur following a minor burn is sometimes quite out of proportion to the size of the burn itself. Counselling at the primary care facility or by a psychologist or psychiatrist skilled in body image problems may assist in the management at this stage. There may be unreasonable requests for cosmetic correction of these minor defects. Revision surgery by excision of scar and skin grafting might leave a blemish that is no better than the original appearance. In these cases, supportive psycho-therapy with repeated counselling sessions is the appropriate management. In addition to the cosmetic defect, many patients and relatives may have unresolved anger or guilt relating to the circumstances of burning and this may need to be dealt with as part of treatment. Make-up preparations can mask many skin colour mismatches.


Summary ·

Many minor burns can be satisfactorily treated at the primary care level. As the great majority of burns in Australia and New Zealand fall into this category, it is appropriate for local practitioners to develop expertise in the management of these minor burns and for burn units to remain available to provide advice or treatment as necessary.

·

Management of the burn patient includes meticulous attention to the burn wound to facilitate normal healing and prevent complications. Many products are not mentioned in this chapter which are just as effective. The list of products mentioned is not all inclusive.

·

Secondary referral of the healed minor burn may be required for reconstructive surgery, scar management, physiotherapy, occupational therapy or psychotherapy.


References 1. Peck, M. Epidemiology of burn injuries globally. www.uptodate.com/contents/epidemiologyof-burn-injuries-globally 2011. 2. Herndon, D.N., ed. Total Burn Care. 3rd ed. 2007, Saunders: London. 3. Holland, A.J., Pediatric burns: the forgotten trauma of childhood. Canadian Journal of Surgery, 2006. 49(4): p. 6. 4. Singer, A.J., et al., The association between hypothermia, prehospital cooling, and mortality in burn victims. Acad Emerg Med, 2010. 17(4): p. 456-9. 5. Gurfinkel, R., et al., Development of a novel animal burn model using radiant heat in rats and swine. Acad Emerg Med, 2010. 17(5): p. 514-20. 6. Taira, B.R., et al., Rates of compliance with first aid recommendations in burn patients. J Burn Care Res, 2010. 31(1): p. 121-4. 7. Williams, C., Assessment and management of paediatric burn injuries. Nurs Stand, 2011. 25(25): p. 60-4, 66, 68. 8. ANZBA, Bi-National Burns Registry: Annual Report 1st July 2009 - 30th June 2010. 2011, Autralian and New Zealand Burn Association: Melbourne. 9. Hettiaratchy, S. and R. Papini, Initial management of a major burn: II--assessment and resuscitation. BMJ, 2004. 329(7457): p. 101-3. 10. Benson, A., W.A. Dickson, and D.E. Boyce, ABC of wound healing: burns. British Medical Journal, 2006. 332: p. 649-652. 11. Blumetti, J., et al., The Parkland formula under fire: is the criticism justified? J Burn Care Res, 2008. 29(1): p. 180-6. 12. Kahn, S.A., M. Schoemann, and C.W. Lentz, Burn resuscitation index: a simple method for calculating fluid resuscitation in the burn patient. J Burn Care Res, 2010. 31(4): p. 616-23. 13. Greenhalgh, D.G., Burn resuscitation. J Burn Care Res, 2007. 28(4): p. 555-65. 14. Jaskille, A.D., et al., Repetitive ischemia-reperfusion injury: a plausible mechanism for documented clinical burn-depth progression after thermal injury. J Burn Care Res, 2007. 28(1): p. 1320. 15. Saffle, J.I., The phenomenon of "fluid creep" in acute burn resuscitation. J Burn Care Res, 2007. 28(3): p. 382-95. 16. Ipaktchi, K. and S. Arbabi, Advances in burn critical care. Crit Care Med, 2006. 34(9 Suppl): p. S239-44. 17. Freiburg, C., et al., Effects of differences in percent total body surface area estimation on fluid resuscitation of transferred burn patients. J Burn Care Res, 2007. 28(1): p. 42-8. 18. Ansermino, J.M., C.A. Vandebeek, and D. Myers, An allometric model to estimate fluid requirements in children following burn injury. Paediatr Anaesth, 2010. 20(4): p. 305-12. 19. Maybauer, D.M., M.O. Maybauer, and D.L. Traber, Resuscitation with hypertonic saline in burn shock and sepsis. Crit Care Med, 2006. 34(6): p. 1849-50. 20. Jeng, J.C., et al., Improved markers for burn wound perfusion in the severely burned patient: the role for tissue and gastric Pco2. J Burn Care Res, 2008. 29(1): p. 49-55. 21. Moss, L.S., Treatment of the burn patient in primary care. Adv Skin Wound Care, 2010. 23(11): p. 517-24; quiz 525-6. 22. Hudspith, J. and S. Rayatt, First aid and treatment of minor burns. BMJ, 2004. 328(7454): p. 1487-9. 23. Maghsoudi, H., Y. Adyani, and N. Ahmadian, Electrical and lightning injuries. J Burn Care Res, 2007. 28(2): p. 255-61. © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 97

24. Laskowski-Jones, L., First aid for burns. Nursing, 2006. 36(1): p. 41-3. 25. Evers, L.H., D. Bhavsar, and P. Mailander, The biology of burn injury. Exp Dermatol, 2010. 19(9): p. 777-83. 26. Jackson, D.M., [The diagnosis of the depth of burning]. Br J Surg, 1953. 40(164): p. 588-96. 27. Kagan, R.J. and S.C. Smith, Evaluation and treatment of thermal injuries. Dermatol Nurs, 2000. 12(5): p. 334-5, 338-44, 347-50. 28. Devgan, L., et al., Modalities for the assessment of burn wound depth. J Burns Wounds, 2006. 5: p. e2. 29. Singh, V., et al., The pathogenesis of burn wound conversion. Ann Plast Surg, 2007. 59(1): p. 109-15. 30. Loos, M.S., B.G. Freeman, and A. Lorenzetti, Zone of injury: a critical review of the literature. Ann Plast Surg, 2010. 65(6): p. 573-7. 31. Demling, R.H., The burn edema process: current concepts. J Burn Care Rehabil, 2005. 26(3): p. 207-27. 32. Shupp, J.W., et al., A review of the local pathophysiologic bases of burn wound progression. J Burn Care Res, 2010. 31(6): p. 849-73. 33. Jackson, D.M., Second thoughts on the burn wound. J Trauma, 1969. 9(10): p. 839-62. 34. Merz, J., et al., Wound care of the pediatric burn patient. AACN Clin Issues, 2003. 14(4): p. 429-41. 35. Bak, Z., et al., Hemodynamic changes during resuscitation after burns using the Parkland formula. J Trauma, 2009. 66(2): p. 329-36. 36. Fodor, L., et al., Controversies in fluid resuscitation for burn management: literature review and our experience. Injury, 2006. 37(5): p. 374-9. 37. Kramer, G., Lund, T. & Beckum, O., Pathophysiology of burn shock and burn edema, in Total Burn Care, D.N. Herndon, Editor. 2007, Saunders: London. p. 93-106. 38. Latenser, B.A., Critical care of the burn patient: the first 48 hours. Crit Care Med, 2009. 37(10): p. 2819-26. 39. Pham, T.N., L.C. Cancio, and N.S. Gibran, American Burn Association practice guidelines burn shock resuscitation. J Burn Care Res, 2008. 29(1): p. 257-66. 40. Sheridan, R.L., Burns. Crit Care Med, 2002. 30(11 Suppl): p. S500-14. 41. Palmieri, T.L., Use of beta-agonists in inhalation injury. J Burn Care Res, 2009. 30(1): p. 156-9. 42. Fidkowski, C.W., et al., Inhalation burn injury in children. Paediatr Anaesth, 2009. 19 Suppl 1: p. 147-54. 43. Shirani, K.Z., B.A. Pruitt, and A.D.J. Mason, The influenece of inhalation injury and pneumonia on burn mortality. Annals of Surgery, 1987. 205(1): p. 82-87. 44. Maybauer, M.O., D.M. Maybauer, and D. Herndon, Incidence and outcomes of acute lung injury. N Engl J Med, 2006. 353(16): p. 1685-93. 45. Kimmel, E.C. and K.R. Still, Acute lung injury, acute respiratory distress syndrome and inhalation injury: an overview. Drug Chem Toxicology, 1999. 22(1): p. 91-128. 46. Smith, D.L., et al., Effect of inhalation injury, burn size, and age on mortality: a study of 1447 consecutive burn patients. J Trauma, 1994. 37(4): p. 655-9. 47. Finnerty, C.C., D.N. Herndon, and M.G. Jeschke, Inhalation injury in severely burned children does not augment the systemic inflammatory response. Crit Care, 2007. 11(1): p. R22. 48. Palmieri, T.L., et al., Inhalation injury in children: a 10 year experience at Shriners Hospitals for Children. J Burn Care Res, 2009. 30(1): p. 206-8. 49. Fraser, J.F. and B. Venkatesh (2005) Recent advances in the management of burns. Australasian Anaesthesia, 23-32. 50. Endorf, F.W. and R. Gamelli, Inhalation injury, pulmonary pertubations, and fluid resuscitation. Journal of Burn Care & Research, 2007. 28(1): p. 80-3. © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 98

51. Mlcak, R.P., O.E. Suman, and D.N. Herndon, Respiratory management of inhalation injury. Burns, 2007. 33(1): p. 2-13. 52. Toon, M.H., M.O. Maybauer, and J.F. Fraser, Management of acute smoke inhalation injury. Crit Care Resusc, 2010. 12: p. 53-61. 53. Bartlett, D., Tricky toxic presentation at triage. HJournal of Emergency Nursing, 2005. 31(4): p. 403-404. 54. Kealey, G.P., D.J. Barillo, and S.M. Wells, Study proposals for inhaled gases. Journal of Burn Care & Research, 2009. 30(1): p. 154-155. 55. Cochran, A., Inhalation injury and endotracheal intubation. J Burn Care Res, 2009. 30(1): p. 190-1. 56. Robb, B.W.K., R.J., Outpatient and emergency department management of thermal injuries. Problems in General Surgery, 2003. 20(1): p. 7-15. 57. Reed, J.L. and W.J. Pomerantz, Emergency management of pediatric burns. Pediatr Emerg Care, 2005. 21(2): p. 118-29. 58. Johnson, R.M. and R. Richard, Partial-thickness burns: identification and management. Adv Skin Wound Care, 2003. 16(4): p. 178-87; quiz 188-9. 59. Harris, P.N., S. & Vardaxis, N., ed. Mosby's Dictionary Of Medicine, Nursing & Health Professionals. 2nd ed. 2010, Elsevier: Sydney. 60. Bensouilah, J.B., P., Aromadermatology: Aromatherapy in the treatment and care of common skin conditions. 2006: Radcliffe Publishing. 61. Brown, D.E., H., Lewis's Medical Surgical Nursing. 2nd ed. 2008, Marrickville: Mosby. 62. Copstead-Kirkhorn, L.C.B.J.L., Pathophysiology. 4th ed. 2009: WB Saunders. 63. MacNeal, R.J. Structure and function: biology of the skin: Merck Manual Home Edition. http://do3.jcsb.org/jde/2011/6th_Grade_Science/5_Organization_Dev_Living_Organisms/resources _organization_organisms/BODY_SYSTEMS/Structure_and_Function_Skin.pdf 2006. 64. Brannon, H., Skin anatomy, in About.com Dermatology. 2007. 65. Chen, L.S., M.; Chen, P.; Liu, W. & Hsu, C., Hypertonic saline enhances host defence and reduces apoptosis in burn mice by increasing toll-like receptors. Shock, 2010. 35(1): p. 59-66. 66. Lawrence, A., et al., Colloid administration normalizes resuscitation ratio and ameliorates "fluid creep". J Burn Care Res, 2010. 31(1): p. 40-7. 67. Mitra, B., et al., Fluid resuscitation in major burns. ANZ J Surg, 2006. 76(1-2): p. 35-8. 68. Foldi, V., et al., Effects of fluid resuscitation methods on burn trauma-induced oxidative stress. J Burn Care Res, 2009. 30(6): p. 957-66. 69. Cartotto, R. and A. Zhou, Fluid creep: the pendulum hasn't swung back yet! J Burn Care Res, 2010. 31(4): p. 551-8. 70. Mosier, M.J., et al., Early acute kidney injury predicts progressive renal dysfunction and higher mortality in severely burned adults. J Burn Care Res, 2010. 31(1): p. 83-92. 71. Kahn, S.A., R.J. Beers, and C.W. Lentz, Resuscitation after severe burn injury using high-dose ascorbic acid: a retrospective review. J Burn Care Res, 2011. 32(1): p. 110-7. 72. Marshall, W.B., Resuscitation of combat casualties. AACN Advanced Critical Care, 2010. 21(3): p. 279-287. 73. Yuan, J., et al., Assessment of cooling on an acute scald burn injury in a porcine model. J Burn Care Res, 2007. 28(3): p. 514-20. 74. Bartlett, N., et al., Optimal duration of cooling for an acute scald contact burn injury in a porcine model. J Burn Care Res, 2008. 29(5): p. 828-34. 75. Rajan, V., et al., Delayed cooling of an acute scald contact burn injury in a porcine model: is it worthwhile? J Burn Care Res, 2009. 30(4): p. 729-34. 76. Cuttle, L., et al., The optimal temperature of first aid treatment for partial thickness burn injuries. Wound Repair Regen, 2008. 16(5): p. 626-34. © ANZBA 2013AUSTRALIAN AND NEW ZEALAND BURN ASSOCIATION Ltd. www.anzba.org.au 99

77. Cuttle, L., et al., The optimal duration and delay of first aid treatment for deep partial thickness burn injuries. Burns, 2010. 36(5): p. 673-9. 78. Cuttle, L., et al., A review of first aid treatments for burn injuries. Burns, 2009. 35(6): p. 76875. 79. Jandera, V., et al., Cooling the burn wound: evaluation of different modalites. Burns, 2000. 26(3): p. 265-70. 80. Cuttle, L., et al., An audit of first-aid treatment of pediatric burns patients and their clinical outcome. J Burn Care Res, 2009. 30(6): p. 1028-34. 81. Cuttle, L., et al., The efficacy of Aloe vera, tea tree oil and saliva as first aid treatment for partial thickness burn injuries. Burns, 2008. 34(8): p. 1176-82. 82. Orgill, D.P. and N. Piccolo, Escharotomy and decompressive therapies in burns. J Burn Care Res, 2009. 30(5): p. 759-68. 83. Feldmann, M.E., J. Evans, and S.J. O, Early management of the burned pediatric hand. J Craniofac Surg, 2008. 19(4): p. 942-50. 84. Spallek, M., et al., Scald prevention campaigns: do they work? J Burn Care Res, 2007. 28(2): p. 328-33. 85. Abeyasundara, S.L., et al., The changing pattern of pediatric burns. J Burn Care Res, 2011. 32(2): p. 178-84. 86. Ogilvie, M.P. and Z.J. Panthaki, Electrical burns of the upper extremity in the pediatric population. J Craniofac Surg, 2008. 19(4): p. 1040-6. 87. Vierhapper, M.F., et al., Electrical injury: a long-term analysis with review of regional differences. Ann Plast Surg, 2011. 66(1): p. 43-6. 88. Li, Y.Y., et al., Successful treatment of a case of severe electrical burns with heart and lung injuries. J Burn Care Res, 2007. 28(5): p. 762-6. 89. Yeroshalmi, F., et al., Oral electrical burns in children-a model of multidisciplinary care. J Burn Care Res, 2011. 32(2): p. e25-30. 90. Roblin, I., et al., Topical treatment of experimental hydrofluoric acid skin burns by 2.5% calcium gluconate. J Burn Care Res, 2006. 27(6): p. 889-94.


APPENDIX 1

Neurological Assessments Glasgow Coma Scoring RESPONSE

SCORE

Eye Opening

Spontaneous To name To pain None

4 3 2 1

Best Verbal Response

Oriented Confused Inappropriate Incomprehensible None

5 4 3 2 1

Best Motor Response

Obeying Localizing Withdrawal Abnormal Flexion Extension None

6 5 4 3 2 1 15

Figure 2.1

Severity of Head Injury Severe

GCS < 9

Moderate

GCS 9 - 12

Minor

GCS 13 - 15

Figure 2.2


APPENDIX 2

Tetanus Protocol Table 3.21.1: Guide to tetanus prophylaxis in wound management History of Time tetanus since last vaccination dose

Type of wound

DTPa, DTPacombinations, dT, dTpa, as appropriate.

Tetanus immunoglobulin* (TIG)

≥3 doses

<5 years

All wounds

NO

NO

≥3 doses

5–10 years

Clean minor NO wounds

NO

≥3 doses

5–10 years

All other wounds

YES

NO

≥3 doses

>10 years All wounds

YES

NO

<3 doses or uncertain †

Clean minor YES wounds

NO

<3 doses or uncertain †

All other wounds

YES

YES

The recommended dose for TIG is 250 IU, given by IM injection using a 21 gauge needle, as soon as practicable after the injury. If more than 24 hours has elapsed, 500 IU should be given. † Individuals who have no documented history of a primary vaccination course (3 doses) with a tetanus toxoid-containing vaccine should receive all missing doses. See Section 1.3.5, Catch-up.

(Source: The Australian Immunisation Handbook (Ninth edition) Page 288)


APPENDIX 3

Recommended Escharotomy Incision Lines


APPENDIX 4 Selecting an Appropriate Dressing Wound Care Product What? Silicone/foam · Hydrophilic polyurethane foam + soft silicone layer + waterproof outer layer Also available with silver Hydrocolloid · Hydrocolloid wafer

Function Why?

Indications When?

Application How?

Note / Precautions

· Nonadherent · Conformable

· Superficial burns

· Apply to clean wound bed · Cover with fixation/retention dressing

· Do not use if any infection

· Aids autolysis of devitalised tissue · Provides moist wound environment · Absorbs exudate

· Superficial to mid dermal burns · Low to moderately exudating wounds

· Allow 2-5cm margin around wound. · Can remain intact 2-3 days · Wafers up to 5 days if no signs infection.

· Do not use if any infection

•

· Dermal thickness burns · Grafts & donor sites

· Soak off if adhered to wound bed

Silver · Sodium carboxymethycellulose (CMC) & 1.2% ionic Ag in fibrous material Also Contreet H

· Broad spectrum antimicrobial · Facilitates debridement · Absorbs exudate

· Mid to deep dermal thickness burns · Moderately exuding wound

Silver · Nanocrystalline Ag coated mesh with inner rayon layer.

· Broad spectrum antimicrobial protection · Decreases exudate formation

· Dermal to full thickness burns · Grafts & donor sites · Infected wounds

Silver · Silver Sulphadiazine 1%

· Reduces infection

· Infected wounds · Dermal to full thickness burns if only available option

· Apply directly to wound · 2-3 layers for acute wounds · Cover with secondary dressing · Change every 1-3 days · Apply to moist wound bed · Allow 2-5 cm overlap · Cover with secondary dressing · Review 7-10 days · Leave intact until healed · Wet with H20; drain and apply blue/silver side down · Moistened secondary dressing · Replace 3-4 days (Acticoat) or 7 days (Acticoat 7) · Apply generous amount to sterile handtowel to ease application · Apply to wound · Cover with secondary dressing

Vaseline Gauze

•

Vaseline petroleum coated gauze

Antiseptic dressing • Conformable


· Exudate level indicates frequency of dressing change

· Temporary skin staining · Avoid if allergy to Silver · Avoid hypothermia

Not recommended for most burns due to changes to wound appearance and frequency of required dressing changes

Bab 1

Introduksi: Epidemiologi dan Etiologi Pendahuluan Luka bakar merupakan suatu tantangan bagi para tenaga kesehatan. Selain perjalanan penyakit suatu bentuk trauma dan ketidaknyamanan yang nyata, gangguan permanen pada penampilan dan fungsi diikuti oleh ketergantungan, kehilangan pekerjaan dan ketidakpastian masa depan. Masalah ini tidak hanya dihadapi oleh pasien, namun juga keluarga mereka dan orang di sekitar. Pepatah menyatakan, pasien trauma yang nyata, ditolong dan dirawat lebih awal oleh personil yang terampil akan sembuh lebih cepat dibandingkan pasien yang perawatannya tertunda. Demikian pula halnya dengan pasien luka bakar maupun trauma lainnya [1]. KArenanya, sangatlah penting untuk melakukan perawatan yang tepat dilakukan secara cepat. Hal ini tidak saja menyelamatkan nyawa seseorang, tapi lebih jauh, demi masa depan mereka. Kursus ini didasari prinsip bahwa penilaian emergensi yang tepat waktu, resusitasi dan rujukan merupakan kunci keberhasilan tatalaksana yang akan diikuti penyembuhan. Dengan mengikuti kursus ini, pasien luka bakar berat akan memperoleh pelayanan yang sesuai dengan prinsip di atas. Kursus in bertujuan menghadirkan informasi akurat mengenai diagnosis dan penanganan awal pada pasien dengan luka bakar berat, yang memungkinkan para praktisi medis dan keperawatan memiliki kompetensi menangani masalah mendesak dan mengancam nyawa. Kursus ini disusun oleh para anggota dari Komite Pendidikan ANZBA dimana tiap bab ditulis berdasarkan pengalaman pribadi para anggota berbagai disiplin ilmu dalam penanganan luka bakar. Kursus ini memuat materi orisinil yang belum pernah dipublikasikan sebelumnya. Kursus ini mengikuti protokol penanganan trauma seperti yang diajarkan oleh Royal Australasian College of Surgeons pada Emergency Management of Severe Trauma course (EMST) dan diterima sebagai suatu sistem pendidikan trauma bagi para praktisi medis di Australia dan Selandia Baru. Kursus Emergency Management of Severe Burns (EMSB) memuat pedoman dan prokol penanganan trauma yang spesifik untuk luka bakar; merupakan tambahan EMST. EMSB dirancang sebagai suatu kursus yang berdiri sendiri, menghadirkan informasi dalam

KOLEGIUM ILMU BEDAH INDONESIA 107

menentukan standar minimal perawatan luka bakar akut (dari ANZBA) dan dapat pada EMST dengan menghadirkan informasi yang lebih spesifik pada penanganan dari luka bakar. EMSB mencakup prinsip–prinsip dari penanganan emergensi luka bakar berat di Australia dan Selandia Baru. Kursus ini sesuai bagi praktisi medis dan keperawatan dimanapun yang melakukan pelayanan luka bakar; baik bagi mereka yang bekerja di unit luka bakar maupun staf medis dan keperawatan yang bekerja di daerah terpencil. Selain menyampaikan materi, kursus ini menekankan keuntungan memiliki pengetahuan yang sama mengenai protokol penanganan luka bakar darurat pada semua petugas pelayanan, karena memfasilitasi penanganan utama serta rujukan yang sesuai; yang merupakan keutamaan pendekatan ini. Informasi mengenai kursus dibagi dalam enam bagian terpisah di tambah bagian komplementer:

1. Pegangan Kursus Buku pegangan berisi silabus lengkap kursus yang dikirim ke semua peserta kursus sebelum kursus. Peserta diharapkan membaca buku ini beberapa kali bila memungkinkan, sebelum menghadiri kursus dimaksud. Gambar 'Struktur EMSB' (halaman 15) disertakan sebagai upaya membantu pengenalan aspek penting dalam kursus.

2. Kuliah Formal Kuliah diselenggarakan di awal kursus. Dijelaskan garis besar kursus dan akan memperjelas hal–hal yang sudah dibaca pada buku pegangan. Kuliah tidak menggantikan buku pegangan, disampaikan secara bervariasi berdasarkan pengalaman klinis para pemberi kuliah.

3. Stasi Keterampilan Di stasi ini diajarkan aspek praktis dari kursus dan memberikan kesempatan pada peserta kursus untuk menerapkan pengetahuan yang telah mereka peroleh dari buku pegangan maupun kuliah.

4. Kelompok Diskusi (Interaktif) Pada bagian ini diajarkan lingkup manajemen luka bakar dalam kelompok–kelompok kecil secara interaktif untuk memberikan kesempatan sebesar mungkin bagi peserta melkukan diskusi topik dan menerapkan pengalaman klinis mereka masing–masing sesuai tingkat kompetensi masing–masing, dalam mengeksplorasi topik.

5. Simulasi Kasus Luka Bakar Pada bagian ini, dilakukan simulasi menggunakan model pasien luka bakar oleh relawan, yang memberikan kesempatan bagi peserta untuk melaksanakan praktik dalam


penanganan luka bakar berat. Bagian ini akan menggabungkan kursus dan membuatnya relevan secara klinis.

6. Ujian Di akhir kursus, peserta menjawab pertanyaan dalam bentuk soal pilihan ganda, kasus klinis, (menggunakan model pasien luka bakar simulasi), dalam menguji tingkat pengetahuan peserta dan efektivitas kursus. Peserta yang berhasil akan menerima sertifikat resmi dari Australian and New Zealand Burn Association (ANZBA).

Konsep Kerja Tim dalam Pentalaksanaan Luka Bakar Sejak Perang Dunia kedua, dicapai kemajuan bermakna dalam penatalaksanaan luka bakar yang diikuti penurunan mortalitas dan morbiditas luka bakar berat secara bertahap [2]. Resusitasi cairan intravena, perbaikan gizi, penggunaan antimikroba topikal, dan penerapan protokol bedah yang menerapkan konsep penutupan luka lebih awal, kesemuanya memberi kontribusi untuk kemajuan yang luar biasa dalam hal ketahanan hidup (survival) [2].

Unit Luka Bakar Dengan adanya perbaikan dalam penanganan luka bakar ini, terealisasi bagi seorang staf terlatih untuk melakukan bekerja secara lebih efektif di suatu fasilitas akut [2]. Pada fasilitas ini, penatalaksanaan berkualitas baik dimungkinkan terselenggara; bahkan untuk luka bakar ringan sekalipun, dibandingkan pelayanan yang tersedia di luar suatu unit luka bakar. Konsentrasi tim spesialis di satu fasilitas memiliki nilai tambah yang efektif dengan biaya yang relatif hemat, berbagi pengetahuan di antara anggota tim yang akan mengembangkan tingkat keahlian tinggi pada masing–masing anggota tim [2]. Hal ini memastikan bahwa pasien mendapatkan pelayanan terbaik. Dukungan yang diberikan anggota tim satu sama lain mengahdapi stres akan memberi kontribusi bagi moral para staf dan memaksimalkan keterpaduan.

Tim Luka Bakar Tim Luka Bakar terdiri dari kelompok multidisiplin di mana keterampilan masing–masing individu saling melengkapi satu sama lain. Anggota tim menyadari keuntungan kerjasama tim interdisipliner dalam penyelenggaraan pelayanan luka bakar berkualitas [2, 3].

Tenaga Pra–rumah sakit KOLEGIUM ILMU BEDAH INDONESIA 109

Petugas ambulans dan layanan rujukan menyediakan pelayananan pra–rumah sakit yang penting bagi pasien luka bakar dengan pengadaan fasiliats resusitasi cairan, stabilisasi jalan napas dan transportasi pasien. Penanganan awal pra–rumah sakit memberi kesempatan pasien luka bakar untuk bertahan hidup dan memperoleh hasil optimal.

Unit Gawat Darurat Pasien luka bakar dinilai dan memperoleh tatalaksana awal di unit gawat darurat; baik di rumah sakit yang memiliki unit luka bakar, atau di rumah sakit tanpa unit luka bakar. Keterkaitan yang baik antara unit luka bakar dan unit gawat darurat sangat penting dalam pelayanan bekualitas.

Ahli Bedah Bedah luka bakar telah berkembang menjadi suatu sub–spesialisasi dari bedah plastik, bedah umum, dan bedah anak. Ahli bedah luka bakar memiliki peminatan khusus dalam pengelolaan pasien luka bakar kritis, dalam penyembuhan luka, rehabilitasi, dan penelitian terkait [2].

Perawat Perawat luka bakar merupakan anggota tim yang sangat penting dalam perawatan berkesinambungan. Perawat luka bakar memiliki keahlian khusus dalam perawatan intensif luka bakar, perawatan luka, perawatan skin graft, perawatan psikiatrik dan perencanaan rawat jalan [2].

Anestesi Bedah luka bakar membutuhkan teknik anestesi khusus yang membantu para ahli bedah dalam menangani pasien kritis, mengelola perdarahan, dan memaksimalkan area operasi luka yang dapat ditangani dalam satu kesempatan [2]. Hal ini memberikan kontribusi dalam penutupan luka bakar dini.

Perawatan Intensif Banyak pasien luka bakar berat memerlukan perawatan intensif. Hubungan kerja berkualitas antara unit perawatan intensif dan unit luka bakar merupakan hal yang sangat penting dalam pelayanan berkualitas.

Fisioterapi, Terapi Okupasi


Terapis sangat berperan dalam perawatan dan rehabilitasi pasien luka bakar [2]. Tindakan ini dimulai sejak masuk ke unit luka bakar dan berlanjut hingga rawat jalan. Terapi rehabilitatif pada luka bakar merupakan suatu sub–disiplin tersendiri yang umumnya tidak tersedia pada fasilitas pelayanan rawat jalan lainnya.

Terapi wicara Para ahli terapi wicara memberikan pelayanan komprehensif dalam manajemen pasien luka bakar berat yang disertai gangguan menelan, gangguan bicara dan gangguan komunikasi akibat luka bakar atau komplikasi sekunder termasuk sepsis, kondisi debil, kontraktur wajah serta pasien–pasien dengan trakeostomi.

Ahli Gizi Nutrisi optimal diperlukan untuk mengatasi respon katabolik yang terjadi pada luka bakar [2]. Untuk tujuan itu, para ahli gizi ada di unit luka bakar.

Psikososial Pekerja Sosial, Psikiater, Psikolog dan rohaniawan merupakan bagian dari tim luka bakar; memberikan dukungan yang diperlukan dan penatalaksanaan berbagai masalah psikososial yang dihadapi pasien luka bakar. Masalah–masalah sulit yang dihadapi tersebut memerlukan penanganan oleh pakar yang memiliki keahlian khusus [2]. Kapasitas pasien menjalankan fungsi di masyarakat jangka panjang sangat bergantung pada penyesuaian psiko–sosial akibat kendala fisik yang dialaminya.

Rehabilitasi Rehabilitasi pasien luka bakar dimulai sejak pasien dirawat [2]; pada luka bakar ringan biasanya dapat dilaksanakan rawat jalan. Pasien luka bakar berat kerap memerlukan rehabilitasi jauh lebih intensif untuk tercapainya fungsi maksimal, sehingga dapat kembali ke aktivitas sehari– hari terutama bekerja. Hubungan yang dekat dengan petugas rehabilitasi dapat memfasilitasi. Tim luka bakar membuat protokol manajemen optimal yang dapat diterapkan dalam perawatan dan memberikan dukungan pada setiap anggota tim, optimalisasi pelayanan yang bersifat profesional, dan memberikan kualitas terbaik perawatan pasien luka bakar [2].

Epidemiologi and Etiologi dari Luka Bakar


A. Epidemiologi Luka bakar adalah bentuk umum dari trauma [2, 4–6]. Sebagian luka bakar terjadi akibat kecelakaan murni, tetapi sebagian besar disebabkan oleh kelalaian atau kurangnya perhatian, kondisi medis yang sudah ada (kondisi yang menyebabkan pasien kolaps), atau penderita penyalahgunaan alkohol dan narkoba. (Lihat Tabel 1) Sekitar 1% dari penduduk Australia dan Selandia Baru (220. 000) menderita luka bakar dan membutuhkan perawatan medis setiap tahunnya. Dari mereka, 10% memerlukan rawat inap, dan 10% dari tergolong luka bakar berat yang mengancam jiwa. 50% pasien mengalami keterbatasan dalam kegiatan kehidupan sehari–hari. (Sumber 2001 Survei Kesehatan Nasional Australia) Luka bakar 70% mungkin menghabiskan biaya 700. 000 dolar untuk perawatan fase akut, belum termasuk biaya rehabilitasi, cuti kerja, dan hilangnya kesempatan mendapatkan penghasilan. Baik pada dewasa maupun anak–anak, umumnya kecelakaan terjadi di rumah [1, 7]. Pada anak–anak, lebih dari 80% terjadi di rumah. Lokasi paling berbahaya adalah dapur dan kamar mandi. Selain itu, larutan pencuci yang mengandung bahan kimia berbahaya, dan garasi atau gudang berisi bahan kimia dan cairan berbahaya yang mudah terbakar. Tabel 1 Lokasi Anak Terbakar (%) Rumah 82% Luar Rumah 12% Jalan 3% Tempat Kerja 1% Lembaga / Sekolah 1% Lainnya 1% (ANZBA Laporan Tahunan Bi–NBR 2011 [8]) Tabel 2 Lokasi Dewasa Terbakar (%) Rumah 56% Tempat Kerja 17% Jalan 11% Luar Rumah 11% Lembaga 3% Lainnya 2% (ANZBA Laporan Tahunan Bi–NBR 2011 [8])


Cedera yang terjadi di tempat kerja kerap terjadi akibat kecerobohan dan tidak memperhatikan faktor keamanan, terutama dalam penggunaan cairan yang mudah terbakar. Perhatian terhadap regulasi kesehatan dan keselamatan kerja sangat penting untuk mencegah terajdinya hal ini.

Luka bakar Militer Lebih kurang dua per tiga luka bakar pada militer tidak berhubungan dengan pertempuran [2]. Kejadiannya sama dengan kecelakaan pada kehidupan sipil. Luka bakar akibat pertempuran mencapai hanya 10%. Luka bakar akibat ledakan memiliki risiko tinggi mengyebabkan cedera inhalasi dan kerusakan kulit. Selain itu, trauma multipel kerap dijumpai. Segala upaya harus dilakukan agar tentara yang cedera memperoleh pelayanan emergensi maupun definitif yang sama dengan masyarakat sipil. Persiapan dan pencegahan saat bertempur, rencana evakuasi dan pemegang kebijakan penanganan korban, bersamaan dengan logistik dan pemasokan, memerlukan penerapan protokol manajemen yang sangat berbeda dibandingkan dengan perawatan yang optimal di masa damai.

B. Etiologi Pada tabel 3 dan 4 tercantum penyebab luka bakar pada anak–anak dan dewasa yang dirawat di unit luka bakar di Australia atau Selandia Baru 2009–2010. Tabel 3 Penyebab Luka Bakar Anak (%) Air panas 55% Kontak 21% Api 13% Gesekan 8% Listrik 1% Kimia 1% Lainnya 1% (ANZBA Laporan Tahunan Bi–NBR 2011 [8]) Tabel 4 Penyebab Luka Bakar pada Dewasa (%) Api 44% Air panas 28% Kontak 13%


Kimia 5% Gesekan 5% Listrik 2% Lainnya 3% (ANZBA Laporan Tahunan Bi–NBR 2011 [8]) Penyebab luka bakar pada dewasa dan anak–anak berbeda. Penyebab umum pada dewasa adalah api sedangkan pada anak–anak umumnya air panas. Penyebab pada anak–anak yang berusia lebih besar, umumnya sama dengan pola dewasa. Semakin tua, pola cedera mereka juga berubah. Orang tua berisiko mengalami luka bakar karena air panas di rumah atau di rumah jompo (panti wreda). Pada semua kelompok usia kemungkinan cedera terjadi pada kondisi disharmoni sosial atau keretakan. Khususnya pada anak–anak, terutama bayi dan balita, yang tergantung pada dewasa di sekitarnya dalam hal perawatan dan keamanan. Kecelakaan karena kurang perhatian atau kelalaian, asuhan yang buruk dan sangat penyiksaan anak kerap terjadi; dan bila dicurigai, perlu penyidikan.

Ringkasan -

Luka bakar yang membutuhkan perhatian medik, melibatkan 1% dari penduduk per tahun. Luka bakar umumnya disebabkan oleh kecerobohan dan kurangnya perhatian, serta pengaruh keracunan obat. Sebagian besar luka bakar untuk semua kelompok usia terjadi di rumah. Luka bakar dapat merupakan akibat kejahatan pada dewasa dan penyiksaan anak. Diagnosis yang tepat mengenai cedera ini memerlukan kewaspadaan, dan pelaporan yang akurat dapat memastikan bahwa bantuan sesuai diberikan pada pasien maupun keluarga.


Bab 2

Penilaian dan Tatalaksana Emergensi Pendahuluan Pada kesempatan pertama berjumpa korban, tenaga medis melakukan penilaian cepat dan penanganan untuk menyelamatkan jiwa [9]. Sementara pasien luka bakar ringan tidak disertai cedera penyerta, pasien luka bakar berat umumnya disertai cedera lainnya. Berapapun luas luka bakar yang dialami, ada dua kemungkinan yang dihadapi, cedera non–luka bakar yang jelas terlihat maupun tersembunyi. Pasien dengan luka bakar ringan disertai cedera non–luka bakar biasanya dihadapkan pada kemungkinan pertama. Bagaimanapun, umumnya cedera mengancam jiwa sering terliwatkan dari perhatian dokter yang menangani karena terfokus luka yang menarik perhatian [9]. Pada anamnesis, petugas medik harus mendapatkan informasi mengenai kemungkinan adanya cedera lain pada beberapa kondisi di bawah ini [9]: - Kecelakaan lalu lintas, terutama terlontar pada kecepatan tinggi - Letusan atau ledakan - Luka bakar listrik, terutama tegangan tinggi - Lompat dan jatuh saat terjadi kepanikan Pasien yang non–komunikatif, baik dalam keadaan tidak sadar, diintubasi, psikotik, atau berada di bawah pengaruh obat, harus dianggap berpotensi mengalami cedera multipel dan diperlakukan dengan sesuai dengan kondisi pada cedera multipel. Setelah pertolongan pertama diberikan, prinsip–prinsip survei primer dan sekunder dan resusitasi simultan harus diterapkan [2]. Petugas harus mengenakan alat pelindung diri (APD) i seperti sarung tangan, kacamata goggle dan gaun khusus sebelum menangani pasien [2].

Pertolongan Pertama Pertolongan pertama terdiri dari: - Hentikan proses pembakaran - Turunkan suhu luka


Hal ini efektif dalam 3 jam pertama sejak terbakar (Lihat Bab 7).

Survei Primer Segera identifikasi kondisi–kondisi mengancam jiwa dan lakukan manajemen emergensi [9, 10]. Jangan terpengaruh oleh luka bakarnya. A. B. C. D. E.

Penatalaksanan jalan napas dan manajemen tulang servikal Pernapasan dan ventilasi Sirkulasi dengan kontrol perdarahan Disabilitas – Status neurologik Paparan + pengendalian lingkungan

A. Penatalaksanaan jalan napas dan manajemen tulang servikal -

-

Nilai patensi jalan napas, cara termudah adalah berbicara dengan pasien. Jika tidak paten, bersihkan jalan napas dari benda asing dan membuka jalan napas dengan manuver chin lift/jaw thrust. Jaga gerakan tulang servikal seminim mungkin dan jangan melakukan fleksi dan ekstensi kepala dan leher [2, 9]. Manajemen tulang belakang servikal (terbaik dengan rigid collar). Adanya cedera di atas klavikula seperti trauma muka atau tidak sadarkan diri kerap disertai patah tulang belakang servikal.

B. Pernapasan dan Ventilasi -

Paparkan dada dan pastikan bahwa ekspansi rongga toraks adekuat dan simetri [2]. Berikan oksigen 100% (15 L/menit) menggunakan non–rebreather mask [2, 9]. Bila diperlukan, ventilasi menggunakan bag dan sungkup atau, intubasi bila perlu.


-

Keracunan karbon monoksida dapat menyebabkan pasien bewarna merah–buah cherry, dan pasien tidak bernapas. Hati–hati bila frekuensi pernapasan <10 atau> 30 kali per menit. Waspada pada luka bakar melingkar dada dan apakah memerlukan eskarotomi

C. Sirkulasi dan Kontrol Perdarahan -

-

-

Lakukan penekanan pada pusat perdarahan - Pucat menunjukkan kehilangan 30% volume darah. - Perubahan mental terjadi pada kehilangan 50% volume darah. Periksa pulsasi sentral – apakah kuat atau lemah? Periksa tekanan darah Periksa capillary refill (sentral dan perifer) – normal bila ≤2 detik. Bila >2 detik menunjukkan hipovolemia atau kebutuhan untuk eskarotomi pada tungkai bersangkutan, periksa tungkai lainnya. Masukkan 2 buah kateter IV berdiameter besar, sebaiknya daerah yang tidak terbakar (normal) Ambil darah untuk pemeriksaan darah lengkap / ureum kreatinin / fungsi hari / koagulasi / β–hCG / Cross Match / carboxyhaemoglobin [2, 9]. Bila pasien syok lakukan resusitasi cairan bolus dengan metode Hartmann untuk memperbaiki pulsasi radialis. Pertanda klinis–awal syok biasanya ditimbulkan penyebab lain. Carilah dan atasi.

D. Disabilitas: Status Neurologis -

Tetapkan derajat kesadaran: A– dari Alert (Sadar, waspada) V– dari Vocal (Respon terhadap rangsang suara) P– dari Pain (Respon terhadap rangsang nyeri) U– dari Unresponsive (Tidak memberi respon)

-

Lakukan pemriksaan respon pupil terhadap cahaya. Harus cepat dan sama. Tanggap terhadap hipoksemia dan syok yang menyebabkan kegelisahan dan penurunan derajat kesadaran [9].

E. Paparan dan Pengendalian Lingkungan -

Lepaskan semua pakaian dan perhiasan termasuk anting dan jam tangan [2] Miringkan pasien untuk visualisasi sisi posterior


-

Jaga agar pasien tetap hangat [7, 9] Area luka bakar dihitung menggunakan metode Rule of Nines atau palmaris (Rule of One).

Cairan, Analgesia, Penilaian dan Pipa Hubungan 'Fatt' antara survei primer dan sekunder.

Resusitasi Cairan (Lihat Bab 6) -

-

Cairan inisial diberikan menggunakan rumus Parkland yang dimodifikasi [7, 11–19]: 3–4 mL / kg berat badan / % luas luka bakar + tetes maintenance pada anak–anak Kristaloid (misal: larutan Hartmann atau Plasmalyte) adalah cairan yang direkomendasikan. Separuh cairan berdasarkan perhitungan diberikan dalam delapan jam pertama, sisanya diberikan selama enam belas jam berikutnya [3, 12, 15, 19]. Saat terjadinya trauma ditetapkan sebagai awal resusitasi cairan [7]. Bila dijumpai perdarahan atau syok non–bakar, perlakukan sesuai pedoman trauma. Pantau adekuasi resusitasi [3, 7, 11, 14, 18, 20]: - Produksi urin melalui kateter per jam - EKG, denyut nadi, tekanan darah, frekuensi pernapasan, analisis gas darah arterial dan pulse oxymetri Sesuaikan cairan resusitasi sesuai indikasi.

Analgesia [9] -

Nyeri: berikan morfin iv 0. 05–0.1 mg/kg Titrasi untuk memperoleh efek (pemberian dosis lebih kecil secara frekuen akan lebih aman).

Pemeriksaan ·

Radiologi - Tulang belakang servikal - Toraks - Panggul - Pencitraan lain sesuai indikasi klinis

Pipa • Pemasangan NGT


Insersi NGT pada luka bakar luas (> 10% pada anak–anak,> 20% pada dewasa) bila dijumpai cedera penyerta, atau untuk melakukan dekompresi saluran cerna. Gastroparesis merupakan hal yang umum terjadi.

Survei Sekunder Merupakan pemeriksaan menyeluruh mulai dari kepala sampai kaki. Pemeriksaan dilaksanakan setelah kondisi mengancam nyawa diyakini tidak ada atau telah diatasi [2]. Riwayat Penyakit: A – Alergy M – Medicine (obat–obatan yang baru dikonsumsi) P – Past illness (penyakit sebelum terjadi trauma) L – Last meal (makan terakhir) E – Event (peristiwa yang terjadi saat trauma)

Mekanisme trauma Informasi yang harus didapatkan mengenai interaksi antara pasien dengan lingkungan: Luka bakar [9] - Durasi paparan - Jenis pakaian yang dikenakan - Suhu dan kondisi air, jika penyebab luka bakar adalah air panas - Kecukupan tindakan pertolongan pertama. Trauma tajam - Kecepatan proyektil - Jarak - Arah gerakan pasien saat terjadi trauma - Panjang pisau, jarak dimasukkan, arah Trauma tumpul - Kecepatan dan arah benturan - Penggunaan sabuk pengaman - Jumlah kerusakan kompartemen penumpang - Ejeksi (terlontar)? - Jatuh dari ketinggian - Jenis letupan atau ledakan dan jarak terhempas


Pemeriksaan Kepala - Mata . . . luka tembus kerap terlewatkan – Cek ketajaman penglihatan - Kulit kepala . . . luka tidak beraturan, benda asing Wajah - Stabilitas tulang – tulang wajah 1/3 tengah - Periksa adanya gigi yang hilang /maloklusi - Kebocoran cairan serebrospinal melalui hidung, telinga atau mulut - Jelaga, lepuh, edema lidah atau faring Leher - Inspeksi, palpasi, pemeriksaan radiologi. Selalu curigai adanya fraktur servikal - Luka menembusmuskulus platisma – ruang operasi atau pemeriksaan angiografi Dada - Periksa seluruh dada–depan dan belakang - Tulang iga, klavikula dan tulang dada - Periksa bising napas dan suara jantung - Luka bakar melingkar mungkin perlu eskarotomibila menyebabkan restriksi ventilasi - Batuk yang produktif - Perubahan suara, parau Abdomen - Memperlukan evaluasi berulang untuk menilai nyeri dan distensi abdomen - Bila dijumpai memar terutama jejas sabuk pengaman, curiga adanya kelainan intra– abdomen seperti ruptur viskus - Bila penilaian abdomen tidak dapat jelas, samar atau tidak praktis, misalnya pada luka bakar di daerah abdomen yang luas, maka investigasi lebih lanjut menggunakann CT scan, atau Focused Assessment with Sonography for Trauma (FAST) merupakan pemeriksaan mandatorik. Perineum - Jejas, hematoma, darah keluar melalui meatus uretra eksterna Rektum - Darah, laserasi, tonus sfingter, prostat mengambang Vagina - Benda asing, laserasi


Tungkai - Kontusio, deformitas, nyeri, krepitus - Lakukan penilaian pulsasi ekstremitas secara reguler. Pada luka bakar melingkar diikuti perkembangan edema, awalnya eskar mengnyebabkan terhambatnya aliran balik vena diikuti terhambatnya aliran arteri yang mengakibatkan iskemia jaringan. Hal ini mengakibatkan penurunan perfusi ekstremitas diikuti nyeri, parestesia, tidak ada denyut dan paralisis. Eskarotomi merupakan indikasi saat aliran balik vena ekstremitas terhambat oleh edema; untuk mengembalikan kecukupan sirkulasi (Lihat Bab 7) Pelvis - Diperlukan akses cepat pemeriksaan radiologi di unit gawat darurat untuk menilai stabilitas tulang pelvis. Bila pemeriksaan raadiologi tidak dimungkinkan, pemeriksaan stabilitas dengan menekan simfisis dan ilium anterior harus dilakukan. Manuver ini hanya dapat dilakukan satu kali saja oleh seorang senior. Pemeriksaan Neurologik - Pemeriksaan Glasgow Coma Scale (lihat lampiran) - Penilaian sensorik dan motorik semua tungkai - Paralisis atau paresis menunjukkan adanya cedera berat, segera lakukan imobilisasi menggunakan papan spinal dan semi–rigid collars. Catatan: 1) Pada pasien luka bakar, paresis tungkai mungkin disebabkan oleh insufisiensi vaskular akibat eskar yang kaku. Pada kondisi ini, eskarotomi merupakan indikasi. 2) Penurunan tingkat kesadaran bisa disebabkan: - Hipovolemia akibat pendarahan tak terdiagnosis atau resusitasi yang inadekuat. - Hipoksemia - Lesi yang menyebabkan pendesakan ruang intrakranial.

Dokumentasi -

Buatcatatan Mintakan persetujuan untuk dokumentasi fotografi dan persetujuan prosedur Berikan profilaksis tetanus jika diperlukan (lihat lampiran) [21]

Re–evaluasi Re–evaluasi Survei Primer – khususnya untuk: - Gangguan pernapasan - Insufisiensi sirkulasi perifer - Gangguan neurologis - Kecukupan resusitasi cairan - Penilaian radiologi: foto radiologi toraks


-

-

Warna urine untuk deteksi haemochromogens Pemeriksaan laboratorium: - Hemoglobin / hematokrit - Urea / kreatinin - Elektrolit - Urine mikroskopik - Analisis gas darah - Karboksihaemoglobin (jika tersedia) - Kadar gula darah - Skrining obat (mungkin diperlukan oleh Polisi) Elektrokardiogram

Perawatan Emergensi Luka (Lihat Bab 7) Umumnya, luka bakar steril saat luka bakar terjadi. Perawatan luka bakar berlebihan menggunakan balutan modern tidak diperlukan bahkan hal ini menyebabkan penanganan yang memerlukan prioritas tertunda. Tindakan yang tepat untuk penatalaksanaan luka adalah menutupinya dengan penutup plastik atau kain bersih dan mengatur prosedur evakuasi [22]. Bila rujukan pasien tertunda lebih dari 8 jam, atau pada luka telah terkontaminasi air tercemar atau limbah industri, maka antimikroba topikal harus digunakan. Bersihkan luka dan konsultasi ke unit luka bakar rujukan untuk balutan yang dianjurkan. Umumnya direkomendasikan pembalut antimikroba antimikroba yang mengandung silver atau krim silver sulfadiazin. Jangan menggunakan balut tekan yang memperberat gangguan sirkulasi pada tungkai yang sebelumnya memang sudah terganggu. Balutan harus sesering mungkin dibuka untuk menghilangkan konstriksi.

Luka Bakar Listrik (Lihat Bab 10) Konduksi arus listrik melalui dada menyebabkan aritmia jantung sepintas atau henti jantung; meski hal ini jarang terjadi pada tegangan rendah (<1000 V). Pasien sengatan listrik tegangan tinggi, penurunan kesadaran atau memiliki EKG abnormal saat masuk rumah sakit mungkin memerlukan pemantauan EKG 24 jam [23]. Gangguan ritmik jantung lebih mungkin terjadi pada pasien yang memiliki gangguan jantung sebelumnya. Selalu ingat bahwa luka masuk atau luka keluar yang lebih kecil dapat disertai kerusakan jaringan yang berat.


Luka Bakar Kimia (Lihat Bab 11) Bila dijumpai residu bahan kimia di kulit, proses pembakaran akan terus berlanjut. Karenanya, pakaian yang terkontaminasi harus dibuka dan luka dicuci menggunakan sejumlah besar air dalam waktu cukup lama [24]. Informasi khusus untuk keracunan zat kimia dapat menghubungi Poisons Information Australia (13 11 26) danNew Zealand National Poisons Centre (0800 764 766). Luka bakar kimia pada mata memerlukan pembilasan secara kontinu menggunakan air. Adanya pembengkakan kelopak mata dan spasme otot disertai nyeri akan menghalangi pencucian adekuat. Untuk irigasi kadang diperlukan prosedur retraksi kelopak mata yang baik, konsultasi dengan oftalmologi pada kasus ini sangat diperlukan.

Dukungan pada pasien, dan keluarga Luka bakar kerap diikuti gangguan emosional baik pada pasien maupun keluarga dan kerabatnya [25]. Kesedihan dan kehilangan merupakan hal yang lazim, kadang disertai rasa bersalah atau menyalahkan diri, ketakutan, depresi atau amarah. Kesemuanya ini perlu diatasi. Bakar diri merupakan suatu cara tersering yang diambil dalam upaya bunuh diri. Pasien ini dalam masa kritisnya memerlukan penanganan yang simpatik dan konseling. Penggunaan narkotik dosis tinggi dan intubasi yang tidak tepat akan menghalangi aspek terpenting pada manajemen di fase terminal. Hal ini juga menjadikan hubungan harmonik di akhir hayat dengan keluarga tidak dimungkinkan. Untuk itu, komunikasi yang baik perlu diupayakan. Sedangkan untuk kasus–kasus yang bersifat non–fatal diperlukan bantuan psikiatrik dalam mencegah upaya bunuh diri terulang kembali. Beberapa kasus dengan kelainan kepribadian atau di bawah pengaruh zat toksik sering menunjukkan sikap kasar saat manajemen emergensi, hal ini memerlukan perhatian khusus untuk tidak mencelakai diri sendiri maupun orang lain. Bantuan tenaga dari disiplin ilmu lainnya (dalam hal ini konsultasi psikiatri) mungkin diperlukan untuk dapat menagani pasien– pasien ini dengan aman. Lain halnya pada kasus anak, uraian mengenai mekanisme trauma sulit diperoleh dan kemungkinan penyebabk non–aksidental harus dipikirkan. Dokumentasi akurat merupakan hal yang sangat penting dan melaporkan pada yang berwajib merupakan proses yang harus dijalankan untuk penyidikan lebih lanjut [7].

Perawatan definitif


Perawatan definitif luka bakar dijelaskan lebih lanjut pada buku pegangan ini. Rujukan ke unit luka bakar dengan perawatan spesialistik multidisipliner mengacu pada kriteria rujukan dari ANZBA (Lihat Bab 8)

Ringkasan Luka bakar sendiri mungkin hanya sebagian dari masalah yang dihadapi; trauma lain sangat mungkin dijumpai dan ditatalaksanai sesuai survei primer dan sekunder – ABC traumatologi. Demikian pula mengenai perawatan definitif dan kriteria rujukan. Pada luka bakar terutama dengan trauma penyerta lainnya, beberapa hal di bawah ini perlu dilakukan evaluasi secara teratur: - Gangguan jalan napas dan proses pengembangan rongga dada dalam mekanisme bernapas, terutama karena adanya eskar - Kecukupan resusitasi cairan - Insufisiensi sirkulasi perifer karena adanya luka bakar melingkar, edema dan balutan - Gangguan neurologik - Perdarahan di dalam rongga


Bab 3

Respon Lokal dan Sistemik pada Luka Bakar A. Respon Lokal Jackson di Birmingham pada tahun 1950 melakukan studi eksperimental dengan menciptakan model luka bakar yang selanjutnya memperkaya pemahaman mengenai patofisiologi luka bakar[26–32].

Gambar 3. 1 Luka Bakar model Jackson Gambar 3. 1 Menunjukkan model luka bakar. Pada daerah yang paling dekat dekat sumber termal (atau penyebab lainnya), panas tidak dapat dikonduksi secara cepat dan baik, sehingga terjadi koagulasi protein sel; selanjutnya terjadi kematian sel yang berlangsung sangat cepat. Daerah ini disebut zona koagulasi atau zona nekrosis (atau zona nekrosis koagulatif) [25, 26, 29, 32, 33]. Di sekitar zona koagulasi adalah daerah dengan kerusakan tidak seberat zona pertama, namun sirkulasi di daerah tersebut mengalami kerusakan diikuti gangguan mikrosirkulasi. Dengan terhambatnya mikrosirkulasi, daerah ini disebut zona statis [25, 26, 29, 32]. Bila tidak ditatalaksanai dengan baik, maka daerah yang cukup luas ini akan mengalami nekrosis saat dilepaskannya mediator–mediator inflamasi sebagai respon terhadap jaringan yang rusak [29]. Secara klinis, hal ini disebut sebagai degradasi luka (bertambah dalamnya luka bakar). Dalam 3–5 hari pasca luka bakar, luka yang awalnya terlihat vital akan tampak nekrotik. [32].


Di sekitar zona stasis adalah suatu daerah dimana jaringan melepaskan mediator–mediator inflamasi yang menyebabkan dilatasi pembuluh darah. Daerah ini terlihat kemerahan dan disebut zona hiperemia [25, 26, 29, 32]. Dengan kembalinya respon vaskular yang bersifat hiperdinamik, daerah ini akan kembalii normal [27, 34]. Pada luka bakar yang mencakup luas melebihi 10% pada anak atau 20% pada dewasa, zona hiperemia sangat mungkin terjadi di seluruh tubuh. Kondisi ketiga zona ini berbeda pada setiap luka itu bakar. Kadang zona statis mencapai kedalaman dermis namun disertai gangguan vaskular yang progresif pada zona nekrosis sehingga hal ini menyebabkan luka bakar dalam. (lihatgambar 5. 4) Hal ini umumnya dijumpai pada orang tua dan pasien–pasien luka bakar (maupun sudah mengalami sepsis) dengan perawatan luka yang tidak tepat. [14]. Dengan demikian, waktu dan penatalaksanaan tindakan emergensi yang efektif sangat berperan pada proses penyembuhan luka.

B. Responsistemik 1. Permeabilitas kapiler dalam keadaan normal 1) Suatu zat dapat melintas dinding pembuluh kapiler melalui tiga cara: difusi, filtrasi dan transport molekul. a) Difusi. Partikel berukuran sangat kecil misalnya oksigen, karbondioksida dan natrium akan melintasi dinding pembuluh kapiler (membran) dengan mudah dan berhubungan dengan konsentrasi zat bersangkutan (dari arah konsentrasi tinggi ke konsentrasi rendah). b) Filtrasi adalah suatu mekanisme perpindahan air dan zat lainnya. Sejumlah air terfiltrasi melalui kapiler tergantung pada daya dorong menembus dinding kapiler. Daya yang menyebabkan pergerakan air tersebut dijelaskan pada hukum Starling [2, 32] (lihat footnote)1. c) Transpor molekul besar sangat minim dimengerti. Transpor mungkin berlangsung melalui ruang yang terbentuk di antara sel–sel endotel. Umumnya pembuluh kapiler memiliki karakteristik ini (mudah ditembus oleh suatu molekul) sehingga disebut semipermeabel (permeabelterhadap air dan partikel kecil seperti Na dan Cl, namun relatif impermeabel terhadap molekul besar misalnya albumin). Namun, faktanya 50%––100% serum albumin melintas kapiler dan kembali ke sirkulasi melalui sistem limfatik dalam sehari.

1

Hukum Starlingmenyatakan bahwa pergerakan cairan netoadalah perbedaan antara gaya yang mendorong cairan keluar (tekanan hidrostatik dalam kapiler mendorong cairan keluar intravaskular disertai tekanan osmotik cairan interstisium yang menarik cairan keluar ruang intravaskular) dengan gaya yang mendorong cairan masuk ke ruang intravaskular (tekanan hidrostatikdi ruang interstisium mendorong cairan masuk kembali ke ruang intravaskular disertai tekanan osmotik cairan plasma menarik cairan interstisium masuk ke ruang intravaskular).


2) Variasi normal filtrasi dimungkinkan terjadi karena peran beberapa faktor dinding kapiler (misalnya, pembuluh kapiler di ginjal lebih banyak dapat dilintasi air, dibandingkan pembuluh kapiler pada otot) sebagai faktor yang dijelaskan pada hukum Starling. Tekanan hidrostatik pada pembuluh kapiler tergantung pada tekanan darah yang mengalir dan tekanan yang menahan (resistance) darah untuk keluar (masing–masing dikendalikan oleh sfingter pre– dan post–kapiler). Pada keadaan normal, pembuluh kapiler dilalui oleh sirkulasi darah secara aktif, dengan interval periode panjang aliran yang rendah diikuti tekanan yang rendah. Tekanan osmotik koloid plasma yang terutama dipengaruhi konsentrasi albumin sedangkan tekanan osmotik koloid cairan interstisium dipengaruhi albumin dan substansi dasar yang terdapat di antara sel–sel.

2. Peningkatan permeabilitas kapiler Perubahan ini terjadi karena dilepaskannya mediator–mediator inflamasi oleh sel–sel endotel yang rusak, trombosit dan leukosit. 1)

Vasodilatasi merupakan suatu respon vaskular utama pada proses inflamasi dan menyebabkan[32]: a) Peningkatan tekanan hidrostatik di kapiler b) Terbukanya semua pembuluh kapiler; tidak hanya sebagian. c) Meregangnya dinding kapiler yang meningkatkan area permukaan membran kapiler dan terbentuknya celah di antara sel–sel endotel. d) Berkumpulnya darah di pembuluh vena kecil.

2) Terjadi peningkatan permeabilitas membran kapiler yang nyata [7, 18]. Hal ini menyebabkan peningkatan transpor zat melalui ketiga mekanisme, yaitu difusi, filtrasti dan transpor molekul. Namun, mekanisme ketiga yang tampaknya paling dipengaruhi, kemudian diikuti oleh meningkatnya perpindahan albumin melintas membran kapiler (kebocoran). Perpindahan cairan disertai albumin ke ruang interstisium mengalami akumulasi menyebabkan edema. 3) Kerusakan jaringan akibat paparan terhadap sumber termal menyebabkan terurainya substansi dasar intersel. Hal ini mempercepat peningkatan tekanan osmotik koloid di ruang interstisium; yang dapat diamati secara eksperimental. Efek lainnya dari luka bakar substansi dasar intersel adalah terurainya molekul yang diduga berperan menyebabkan ekspansi ruang diikuti penurunan tekanan hidrostatik.

3. Efek Sistemik Pada luka bakar dijumpai perubahan pada semua organ sistem yang nyata [25]. Bagaimanapun, pada luka bakar dengan luas <20% efek dimaksud tidak terlalu bermakna [20].


Perubahan ini terjadi karena dilepaskannya mediator inflamasi dan rangsang neural, yang menyebabkan perubahan dalam pengendalian fungsi tubuh akibat reaksi langsung terhadap mediator di sirkulasi. 1) Efek langsung yang nyata pada sirkulasi. Hipovolemia terjadi karena kebocoran cairan dan protein ke jaringan interstisium. Albumin menngalami kebocoran akibat peningkatan permeabilitas kapiler di daerah luka bakar. Pada luka bakar dengn luas >20%, seluruh sirkulasi sistemik dipengaruhi dengan akibat peningkatan permeabilitas kapiler sistemik. Koreksi hipovolemia merupakan tindakan life saving pada jam pertama pada luka bakar berat [16, 18, 27, 35–40]. 2) Pada luka bakar berlangsung kondisi hipermetabolik yang disebabkan sekresi hormon stres seperti kortisol, katekolamin danglukagon disertai supresi (atau resistensi) hormon anabolik (growth hormone, insulin dansteroid) dan mekanisme sarafi yang menyebabkan katabolisme dan mengakibatkan penguraian protein otot [25]. Perubahan–perubahan, ini dapat diamati secara klinis dengan adanya takikardia, hipertermia dan balans protein negatif. 3) Imunosupresi akibat depresi berbagai mekanisme imun, baik seluler maupun humoral [25]. Hal ini menjelaskan, mengapa infeksi merupakan faktor penyebab tingginya mortalitas pada luka bakar 4) Sebagai bagian dari respon terhdap trauma dan syok, fungsi barier usus terganggu demikian nyata, diikuti translokasi bakteri. Kejadian ini dapat dihindari dan dicegah dengan penerapan pemberian nutrisi enteral dini. 5) Paru kerap mengalami perubahan inflamatorik yaitu Acute Respiratory Distress Syndrome (ARDS) meski tanpa cedera inhalasi [25, 41]. 6) Perubahan sistemik yang melibatkan gangguan pertumbuhan terjadi dan dapat dijumpai selama beberapa bulan hingga beberapa tahun pasca luka bakar setelah penyembuhan luka. Respons yang dijumpai berupa deposisi lemak, gangguan pertumbuhan massa otot, berkurangnya mineralisasi tulang dan terhambatnya pertumbuhan longitudinal tubuh. Meski kecepatan pertumbuhan kembali normal dalam waktu 1–3 tahun, namun pertumbuhan normal secara keseluruhan tidak pernah tercapai.

Ringkasan -

-

Efek lokal terhadap cedera termal pada kulit dan jaringan subkutan terlihat sebagai tiga zona kerusakan. Progresivitas zona nekrosis merupakan hal yang lazim dan berkaitan dengan tatalaksana awal. Peningkatan permeabilitas kapiler diikuti edema dan penurunan kadar albumin dari darah sirkulasi. Luka bakar menyebabkan gangguan sirkulasi sistemik, gangguan metabolisme, pengendalian suhu, status imun, fungsi usus, gangguan paru dan gangguan pertumbuhan jangka panjang.


Bab 4

Cedera Inhalasi Terhirupnya uap panas dan atau produk pembakaran menyebabkan kerusakan traktus respiratorius dalam berbagai cara [2, 42]. Lebih lanjut, absorpsi produk pembakaran menimbulkan efek toksik yang serius, baik lokal maupun sistemik. Cedera inhalasi diikuti tingginya mortalitas pada luka bakar [41–49]. Dengan adanya cedera inhalasi, angka mortalitas luka bakar meningkat 30% diikuti risiko timbulnya pneumonia [46]. Bila dijumpai pneumonia, angka mortalitas meningkat hingga 60%. Pada anak–anak, luka bakar dengan luas 50% disertai cedera inhalasi memiliki mortalitas yang sama dengan luas 73% tanpa cedera inhalasi [50]. Cedera inhalasi yang sebelumnya disebut luka bakar traktus respiratorius, kerap menyertai luka bakar di daerah kepala dan leher. Lebih kurang 45% luka bakar pada muka, disertai cedera inhalasi.

Klasifikasi cedera inhalasi Cedera inhalasi dibagi menurut lokasi cedera [2]. 1. Kerusakan jalan napas di atas laring (obstruksi) 2. Kerusakan jalan napas di bawah laring (kerusakan pulmoner) 3. Intoksikasi sistemik (hipoksia sel) Seorang pasien dapat menderita satu atau kombinasi ketiga jenis kelainan yang disebutkan di atas. Manajemen jalan napas bertujuan untuk mempertahankan patensi dan melindungi jalan napas. Pada gagal napas, jalan napas harus diamankan untuk memperbaiki oksigenasi dan ventilasi.

1. Cedera jalan napas di atas laring (obstruksi) Cedera jalan napas di daerah ini umumnya disebabkan oleh terhirupnya uap panas, terutama pada mereka yang terpaksa menghirupnya tanpa ada pilihan lain. Hal ini dimungkinkan terjadi saat seorang terperangkap di ruang tertutup pada ruang yang terpenuhi oleh api maupun uap panas.


Perubahan patologik yang terjadi adalah sama dengan yang terjadi di kulit; dengan kerusakan sesuai proporsinya. Dilepaskannya mediator inflamasi pasca paparan ini menyebabkan edema yang awalnya mengakibatkan obstruksi, selanjutnya menyebabkan hilangnya fungsi proteksi mukosa. [42]. Obstruksi jalan napas akibat edema ini dapat menetap, melampaui batas waktu edema pada luka (umumnya antara 12–36 jam). Edema di kulit leher kerap memperberat obstruksi [2]. Hal ini lebih sering dijumpai pada anak–anak yang memiliki jalan napas lebih sempit disamping leher yang pendek, sehingga edema sangat cepat menimbulkan abnormalitas. Harus selalu diingat, bahwa luka bakar yang mencakup luas lebih dari 20% permukaan tubuh, kerap dijumpai respon inflamasi sistemik. Meski tidak ada cedera langsung pada jalan napas, mukosa mengalami edema, terutama kasus–kasus yang memerlukan cairan dalam jumlah besar untuk tujuan resusitasi; hal ini akan memperburuk kondisi jalan napas. Jalan napas bagian atas memiliki kemampuan lebih efektif untuk menyalurkan panas pada paparan termal dibandingkan saluran napas bagian bawah.

2. Cedera jalan napas di bawah laring (kerusakan pulmonar) Perubahan patologik terjadi akibat terhirupnya produk pembakaran. Api menyebabkan oksidasi dan reduksi dari komponen yang mengandung karbon, sulfur, fosfor dan nitrogen. Komponen kimiawi yang terbentuk antara lain adalah karbon mono–oksida,karbon dioksida, sianida, ester dan komponen organik kompleks seperti amonia, fosgen, hidrogen klorida [42]. Polyvinyl chloride (PVC), misalnya, saat terbakar menghasilkan sekurangnya 75 macam zat toksik potensial yang berbahaya untuk jalan napas [51]. Asam dan basa dihasilkan saat komponen ini terlarut di dalam cairan yang ada di saluran napas (mukus, dsb). Zat–zat ini selanjutnya menyebabkan luka bakar kimia. Disamping itu, partikel berukuran kurang dari 1µm yang terhirup mengandung zat kimia yang bersifat iritan dan menyebabkan kerusakan alveolus [42]. Zat–zat kimia ini, saat kontak dengan mukosa dan parenkim paru menginisiasi produksi mediator inflamasi dan reactive oxygen species. Kondisi ini memicu edema dan memiliki potensi melapisimukosa trakea–bronkus. Jalan napas bagian bawah juga terpapar pada kemungkinan terbentuknya cast dan sumbatan yang mengakibatkan obstruksi. Selanjutnya, parenkim paru mengalami kerusakan. Terjadi disrupsi membran alveolar–kapilar, terbentuknya eksudat inflamasidan hilangnya surfaktan. Kondisi ini menyebabkan atelektasis, edema interstisium dan edema paru yang mengakibatkan hipoksemia dan menurunnya compliance paru [51, 52]. Faktor–faktor berepran pada kerusakan paru yang mengakibatkan gangguan pertukaran gas antara lain[47]:


3. Intoksikasi sistemik Terdapat dua penyebab intoksikasi pada cedera inhalasi, yaitu karbon mono–oksida dan sianida [42]. Keduanya menyebabkan oksidasi karbon inkomplit. Carbon monoxide (CO) Merupakan gas tidak bewarna dan tidak berbau yang sangat cepat masuk ke aliran darah dan mengalami difusi dengan hemoglobin (Hb), karena memiliki afinitas terhadap hemoglobin 240 kali lebih besar dibandingkan dengan oksigen; selanjutnya membentuk carboxyhaemoglobin (COHb). Ikatan ini menurunkan efektivitas kemampuan darah mengikat oksigen karena menempati oxygen–binding site untuk duatu kurun waktu yang panjang. CO menyebabkan hipoksia jaringan dengan cara mengurangi oxygen delivery dan utilisasi di tingkat sel [42]. Selain mengikat hemoglobin, CO juga memiliki afinitas kuat untuk berikatan dengan komponen selain haem–, diantaranya yang sangat penting adalah sistem cytochrome intrasel. Ikatan ini memiliki dampak toksik langsung diikuti abnormalitas fungsi sel sebagai komponen utama toksisitas CO. [53]. Pada intoksikasi CO ini, ensefalopati merupakan gejala sisa (sequelae) yang serius; meski mekanismenya belum diketahui secara pasti, namun diduga kuat terjadi akibat proses peroksidasi lipid serebral. Kadar oksigen terlarut dalam plasma tidak terpengaruhi, sehingga kerap dijumpai nilai PaO2dalam batas normal. Indikator hipoksia umumnya tidak menghadirkan informasi adanya hipoksia. Hemoglobin yang tidak berikatan dengan O2 menyebabkan perubahan warna kulit menjadi kebiruan (sianosis). COHb menunjukkan perubahan warna merah muda (cherry red) Pemeriksaan oksimetri standar tidak dapat membedakan oxyhaemoglobin dengan carboxyhaemoglobin sehingga jarang digunakan pada metode asesmen pada keracunan CO. Analisis gas darah dengan co–oximetry merupakan satu–satunya metode yang dapat diandalkan untuk menilai kadar oxyhaemoglobin dan carboxyhaemoglobin [54]. Carboxyhaemoglobin mengalami disosiasi lambat, dengan waktu paruh 250 menit pada suhu kamar. Penderita dengan intoksikasi CO kerap mengalami confusion dan disorientasi, menunjukkan gejala serupa dengan hipoksia, cedera kepala dan keracunan alkohol.


Tabel 4. 1 Intoksikasi karbon monoksida[9, 42, 53] Carboxyhaemoglobin (%) 0 ––15 15 –– 20 20 ––40 40 ––60 > 60

Gejala Tidak ada – (Perokok, pekerja tambang) Nyeri kepala, Confusion Nausea, Fatigue, Disorientasi, Iritabel Halusinasi, Ataksia, Sinkop, konvulsi, koma Meninggal

Pasien luka bakar dengan perubahan status kesadaran harus dianggap mengalami intoksikasi CO hinggaterbukti tidak. Keracunan sianida (HCN) Terjadi karena produksi hidrogen sianida akibat terbakarnya plastik [2] atau lem yang digunakan untuk furnitur. Zat ini diabsorbsi melalui paru dan berikatan dengan sistem cytochrome. Fungsi cytochrome terhambat mengakibatkan berlangsungnya metabolisme anaerob. Secara bertahap dimetabolisme oleh enzim hati (rhodenase). Kadar sianida dalam darah hampir tidak dapat dideteksi dan maknanya masih diperdebatkan. Pada perokok kadarnya mencapai 0. 1mg/L, dan diketahui bahwa kadar letal mencapai 1. 0 mg/L. Gejala yang ditimbulkannya antara lain hilangnya kesadaran, neurotoksitas dan konvulsi. Pada praktek sehari–hari, keracunan sianida termasuk jarang terjadi, kerap dijumpai bersama intoksikasi CO.

Diagnosis cedera inhalasi Semua kasus luka bakar harus menjalani pemeriksaan untuk menyingkirkan adanya cedera inhalasi. Karena gejala dan tanda mungkin baru dijumpai setelah suatu kurun waktu tertentu, sebagaimana pada semua trauma, harus dilakukan evaluasi ulang setiap saat karena memiliki potensi berakhir fatal [41, 42, 47, 48]. Pasien dengan cedera inhalasi mungkin mengalami distres pernapasan berat pada fase awal di tempat kejadian. Kematian awal dapat terjadi dan dalam kondisi seperti ini resusitasi jalan napas sangat diperlukan sebagai prosedur penyelamatan jiwa [42]. Distres pernapasan di tempat kejadian dapat terjadi karena anoksia, hal ini disebabkan karena oksigen terpakai pada proses pembakaran. Intoksikasi harus dicurigai kaerna merupakan penyebab utama kematian di tempat kejadian; dengan skenario terselubung oleh sisa pembakaran (toxic fumes). Gambaran umum pada cedera inhalasi adalah obstruksi jalan napas yang semakin hebat dan terjadi dalam beberapa jam. Untuk itu, dibutuhkan kewaspadaan penuh dalam deteksi. Hal ini umumnya dijumpai pada obstruksi di atas laring. Sedangkan kecurigaan adanya obstruksi di bawah laring timbul bila dijumpai pasien gelisah dan confusion.


Anamnesis Riwayat terbakar di ruang tertutup atau adanya ledakan bahan bakar (bensin, gas), ledakan bom harus dicurigai adanya cedera inhalasi. [42].

Pemeriksaan fisik Pemeriksaan berikut menunjukkan adanya kecurigaan cedera inhalasi[2, 24, 42, 55]: Hal yang diobservasi Luka bakar di rongga mulut, hidung dan faring, Bulu hidung terbakar Sputum mengandung sisa karbon Nostril datar Kesulitan bernapas Tracheal Tug Fosa supraklavikula mendatar Retraksi iga

Yang didengar Perubahan suara Suara parau berdahak Napas pendek Stridor Inspirasi Batuk produktif

dengan

batuk

Gejala dan tanda dapat berubah dengan berjalannya waktu tergantung letak cedera. Indikasi adanya perubahan dimaksud terlihat pada tabel 4. 2 berikut.

Tabel 4. 2 Perubahan gambaran klinik cedera inhalasi sesuai perubahan waktu Jenis inhalasi 1. Di atas laring

2. Di laring

Periode waktu 4 –24 jam

bawah i.

ii.

Segera

Timbul bertahap 12 jam – 5 hari

Gejala dan tanda Bertambahnya stridor Suara parau atau melemah Batuk basah Gelisah Kesulitan bernapas Obstruksi jalan napas Kematian Gelisah Anoksia yang mengancam jiwa Kematian Bertambahnya hipoksia Edema paru /ARDS Gagal pernapasan


3. Intoksikasi

Meninggal di tempat Perburukan awal Perbaikan dengan berjalannya waktu

Penurunan kesadaran Stupor Confusion Drowsiness Poor Mentation Gangguan visual Nyeri kepala

Cedera inhalasi dan intoksikasi sistemik Intoksikasi sistemik dicurigai secara klinis sejak awal [48]. Setiap penderita dengan confusionatau penurunan kesadaran pasca trauma termal atau inhalasi produk pembakaran dianggap mengalami intoksikasi CO sampai terbukti tidak. Diagnosis dikonfirmasi oleh adanya COHb di dalam darah [48]. Kadar CO yang diestimasi saat datang mungkin tidak memiliki korelasi dengan gejala pada susunan saraf pusat akibat intoksikasi CO. Mungkin dijumpai kadarnya demikian rendah karena terjadi pembersihan CO dari darah saat masuk rumah sakit. Meski demikian pemeriksaan dapat menunjukkan bahwa intoksikasitelah terjadi.

Tatalaksana Tatalaksana cedera inhalasi terfokus pada prioritas sebagai berikut: - Patensi jalan napas - Oksigen tinggi - Pemantauan gangguan respirasi secara frekuen - Diskusikan kecurigaan adanya intoksikasi sistemik (CO, HCN) dengan ahli toksikologidi Poisons Information (Australia – 13 11 26, New Zealand – 0800 764 766) Pada asesmen awal (survei primer), berikan oksigen dosis tinggi (15L/menit) menggunakan non re–breathing mask [9]. Hal ini akan memfasilitasi oksigenasi jaringan selama asesmen dan tatalaksana berikutnya. Patensi jalan napas mutlak diperlukan untuk sampainya oksigen ke paru.

1. Tatalaksana cedera inhalasi di atas laring Proteksi tulang belakang servikal bersifat mandatorik. Semua penderita dengan kecurigaan cedera inhalasi harus diobservasi secara ketat. Karena obstruksi yang berlangsung progresif


dan cepat sangat mungkin terjadi (terutama pada anak–anak dimana jalan napas relatif pendek dan kecil), maka peralatan emergensi untuk prosedur intubasi harus disiapkan [55]. Asesmen mengenai kondidi klinik penderita secara frekuen menjadi sangat penting karenanya. Bila dijumpai obstruksi, segera amankan jalan napas dengan intubasi endotrakea. Intubasi harus dikerjakan segera. Keterlambatan akan diikuti edema jalan napas semakin berat yang menyebabkan kesulitan dalam prosedur intubasi. Stridor dan distres pernapasan merupakan indikasi intubasi. Indikasi intubasi: - Kebutuhan mempertahankan patensi jalan napas / proteksi jalan napas - Obstruksi mengancam - Penurunan tingkat kesadaran - Fasilitasi transpor penderita - Kebutuhan untuk penggunaan ventilator - Oksigenasi terganggu Bila dijumpai keraguan, intubasi.

2.

Tatalaksana cedera inhalasi di bawah laring

Tatalaksana ditujukan sebagai penopang respirasi: a. Oksgen dosis tinggi Pada semua penderita luka bakar harus diberikan oksigen dosis tinggi (15 L/menit) menggunakannon–re–breathing mask. Hal ini terutama diperlukan pada kecurigaan mengenai parenkim paru. b. Intubasi[9, 55] Intubasi endotrakea diperlukan untuk memfasilitasi pencucian brokus (bronchialtoilet) untuk mengatasi hipersekresi, sehingga pemberian oksigen efektif c. Intermittent Positive Pressure Ventilation (IPPV) Hal ini menjadi penting bila oksigenasi pada penderita tidak menunjukkan respon pada pemberian oksigen melalui prosedur sederhana sebagaimana diuraikan sebelumnya. Karena itu diperlukan ventilasi manual menggunakan bag yang terpasang pada pipa endotrakea dan pasokan oksigen, atau menggunakan ventilator mekanik.

3. Tatalaksana pada cedera inhalasi dengan intoksikasi sistemik a.

b.

Topangan respirasi Penting untuk meyakinkan bahwa jaringan mendapatkan perfusi oksigen sebayak mungkin. Untuk itu dilakukan pemberian oksigen dosis tinggi (15 L/menit) menggunakan non–re–breathing mask. [9]. Proteksi pada penderita tidak sadar


c.

d.

e.

f.

g.

Penurunan kesadaran terjadi akibat respon intoksikasi sistemik. Tatalaksana emergensi termasuk mengupayakan posisi penderita miring ke sisi kiri diikuti pemberian oksigen. Proteksi tulang belakang servikal jangan pernah dilupakan. Jalan napas diamankan, mulanya dengan prosedur chin lift, dilanjutkan dengan pemasangan oropharyngeal airway, namun yang terpenting adalah pemasangan intubasi endotrakea. Efek pencucianalamidengan berjalannya waktu CO dieliminasi bertahap dari darah melalui difusi di alveoli. Waktu yang diperlukan adalah saat bernapas lambat pada suhu ruangan dengan tekanan atmosfir, namun akan berkurang dengan meningkatkan konsentrasi oksigen. Bila tersedia, berikan oksigen dengan tekanan hiperbarik untuk tujuan pencucian CO [2] meski masih dijumpai keraguan evidencedalam perbaikan neurologik. Oksigen Tatalaksana emergensi standar adalah menghembuskan oksigen 100% menggunakan sungkup (mask) [2, 9]. Proedur ini dilanjutkan hingga kadar COHb kembali normal. Prosedur pencucian COsekunderpada ikatannya dengancytochrome hanya akan menyebabkan peningkatan kecil kadar COHb dalam 24 jam berikutnya, dan pemberian oksigen dalam hal ini harus dilanjutkan Oksigen + IPPV Modalitas ini diperlukan pada penderita tidak sadar, atau cedera inhalasi dengan respon intoksikasi sistemik. Intoksikasi sianida Intoksikasi sianida kerap bersifat fatal. Prosedur eliminasi sianida di hepar berlangsung sangat lambat. Meski pemberian hydroxycobolamindosis tinggi dalam bentuk injeksi dianjurkan, namun pada umumnya tidak tersedia di instalasi gawat darurat. Intoksikasi Hidrogen Fluorida (HF) Bila HF diabsorbsi sistemik, akan memengaruhi efisiensi kalsium serum. Hal ini akan mengakibatkan hipokalsaemia. Pemberian cairan yang ditambahkan kalsium akan melawan efek negatif HF.

HubungiPoisons Information Australia (13 11 26) atau New Zealand National Poisons Centre (0800 764 766) untuk informasi mengenai intoksikasi sianida, hydrofluoric acid, dan lainnya.


Ringkasan -

Cedera inhalasi dan respon intoksikasi sistemik merupakan suatu keadaan berpotensi fatal. Diagnosis tergantung adanya kecurigaan klinik yang diperoleh dari anamnesis dan deteksi gejala serta tanda pada pemeriksaan. Tatalaksana emergensi terdiri dari upaya menopang respirasi dengan pemberian oksigen dan pengamanan jalan napas, disertai insersi pipa endotrakea bila diperlukan. Penderita dengan cedera inhalasi atai dengan kecurigaan cedera inhalasi harus dirujuk ke unit luka bakar untuk memperoleh tindakan sesuai setelah stabilisasi.


Bab 5

Asesmen Luka Introduksi Apapun penyebabnya (termal, kimiawi atau listrik), kerusakan jaringan khususnya kedalaman luka berhubungan dengan suhu dan kekuatan agen penyebab dan lamanya kontak [2, 10][21, 56] Suhu di atas 50°C menyebabkan nekrosis jaringan, terutama pada anak–anak dan usia lanjut.

1. Estimasi luas luka bakar Terdapat dua faktor yang menentukan beratnya luka bakar, luas dan kedalaman luka [32]. Mortalitas dihubungkan dengan kedua faktor tersebut, yaitu: · Usia penderita · Luas luka bakar Semakin luas luka bakar, semakin tinggi angka mortalitas Asesmen yang tepat dalam estimasi luas luka bakar diperoleh dengan melakukan perhitungan berdsarkan Rule Of Nines (gambar 5. 1) [21, 25]. Rule of Ninesmembagi permukaan tubuh ke area seluas 9 atau kelipatan 9%, dengan pengecualian perineum yang diestimasikan seluas 1% [21, 25, 27, 56–58]. Dengan menerapkan perhitungan berdasrkan metode ini, diperoleh estimasi luas dengan akurasi yang dapat dipertanggungjawabkan. Namun, selain melakukan perhitungan luas luka bakar, perlu pula diperhitungkan area yang tidak mengalami luka bakar; kemudian menggabungkan keduanya hingga mencapai 100% [7, 21, 56–58]. Cara ini bermanfaat pada luka bakar yang tidak luas, luka tersebar, atau mereka yang tidak berkenan menggunakan metode estimasi menurut Rule of Nines (gambar 5. 2) Perhitungan menggunakan Rule of Nines relatif akurat pada dewasa, namun tidak demikian halnya pada anak–anak [21]. Hal ini disebabkan karena perbedaan proporsi luas permukaan tubuh dibandingkan dewasa. Anak–anak secara proporsional memiliki panggul dan tungkai lebih kecil, namun memiliki kepala dan bahu lebih besar dibandingkan dewasa. Penerapan Rule of Nines dewasa pada anak–anak akan menyebabkan kekurangan atau kelebihan estimasi ukuran, dan diikuti konsekuensi ketidaktepatan dalam perhitungan kebutuhan cairan resusitasi.


Atas dasar hal ini, digunakan Rule of Nines pediatrik (gambar 5. 3) Pada metode ini, perhitungan dimodifiaksi pada berbagai kelompok usia untuk memperoleh akurasi perhitungan (lihat bab 9) [2, 21].

Struktur dan fungsi kulit Kulit terdiri dari dua lapis, yaitu epidermis dan dermis[2, 57, 59–62]. Epidermis merupakan lapisan tipissuperfisial yang ebrperan mengendalikan evaporasi cairan tubuh, dan secara teratur diproduksi oleh proses divisi lamina basalis epidermis [63, 64]. (gambar 5. 3).

Dibawah epidermis, terdapat lapis dermis yang membatasi kulit dengan lapis lemak subkutis [63] dan fasia yang memisahkan kulit dari lapisan muskular dan struktur tulang. Lapis ini memberi bantalan dan pelindung terhadap trauma. Pada luka bakar, kerusakan lapis ini menyebabkan kerusakan jaringan yang lebih dalam.


Anatomi kulit hidung dan telinga memiliki perbedaan dengan kulit di bagian tubuh lainnya, karena kulit melekat dengan kartilago dan hanya dibatasi oleh lapisan lemak subkutis yang tipis. Suplai darah pada kulit maupun kartilago berjalan di antara kedua lapisan tersebut. Luka bakar yang mengenai hidung dan telinga menyebabkan kerusakan pembuluh darah sehingga menimbulkan deformitas yang nyata; terutama saat terdapat infeksi bakterial.

Kedalaman luka bakar Tergantung kedalamannya, dibedakan luka bakar superfisial, sedang dan dalam. Ketiganya masing–masing disebut luka bakar epidermal, mid–dermal dan deep dermal atau seluruh ketebalan kulit (gambar 5. 4 dantabel 5. 1). Pada praktek dilapangan, umumnya dijumpai dalam bentuk gabungan [7, 9, 21].

A. Luka bakar superfisial Disebut juga luka bakar dangkal. Merupakan bentuk luka bakar yang memiliki potensi mengalami proses epitelialisasi spontan. Termasuk ke dalam kategori ini adalah luka bakar epidermal dan dermal bagian superfisial. 1. Luka bakar epidermal Luka bakar ini hanya melibatkan lapis epidermis. Penyebab tersering adalah paparan sinar matahari atau flash injury minor (percikan api). Lapis permukaan mengalami kerusakan dan proses penyembuhan berlangsung melalui regenerasi epidermis yang berasal dari lamina basalis. Dengan adanya produksi mediator inflamasi, didapatkan hiperemia yang menyebabkan luka yang kemerahan dan nyeri (tabel 5. 1)[10]. Adanya eritema, kerap sulitan dinilai pada seorang yang bewarna kulit gelap. Luka bakar jenis ini mengalami


epitelialisai dalam waktu singkat (dalam 7 hari) tanpa parut maupun perubahan warna. [59]. Kadang diperlukan perawatan di rumah askit untuk manajemen nyeri [21]. Eritema (luka bakar epidermal) tidak diperhitungkan pada kalkulasi luas luka bakar [10]. Memang untuk membedakan eritema (luka bakar epidermal) dengan luka bakar superfisial (dermal) adalah sulit dalam beberapa jam pertama pasca luka bakar. Tabel 5. 1 Diagnosis kedalaman luka bakar [10]

Kedalaman Epidermal Dermal–superfisial (dangkal) Mid–dermal Dermal dalam Seluruh ketebalan

Warna Merah Merah muda Pucat Merah mudagelap Merah Bernoda Putih

Bula

Pengisian Kapiler

Sensasi

Penyembu han

Tidak

Cepat

Nyeri

Ya

Kecil

Cepat

Nyeri

Ya

Awal

Lambat

+/–

Biasanya

+/–

Tidak ada

Tidak ada

Tidak

Tidak

Tidak ada

Tidak ada

Tidak

2. Luka bakar dermal–superfisial Luka bakar dermal–superfisial mengenai epidermis dan lapis dermis bagian superfisial, yaitu dermal papilae. Ciri khas luka bakar jenis ini yaitu lepuh (blister, bula) [2]. Lapis kulit di atas bula (non–vital) terlepas dari lapis dermis (vital) karena edema. Edema menyebabkan terlepasnya epidermis dari lapisan dermis dan proses eksudasi menyebabkan akumulasi cairan dan mendorong epidermis; lapis epidermis mengalami kematian. Cairan tersebut selnjutnya menyebabkan kerusakan dermis berlanjut sehingga luka bertambah dalam. Terpaparnya dermal pailae memberikan warna merah muda dan karena ujung–ujung saraf sensorik terpapar, maka hal ini diikuti nyeri yang ekstrim[21]. Dengan suasana kondusif, epitel akan menyebar dari struktur adneksa kulit (folikel rambut, kelenjar sebasea dan kelenjar keringat) dan menutupi dermis (proses epitelialisasi). Proses tersebut berlangsung dalam waktu maksimal 14 hari dengan bekas luka yang menunjukkan perbedaan warna. Tidak ada skar yang dibentuk pada luka bakar dermal–superfisial ini. Bila proses epitelialisasi mengalami keterlambatan, hal ini menunjukkan bahwa kedalaman luka lebih dalam dibandingkan saat diagnosis ditegakkan.


B.

Luka bakar mid–dermal

Luka bakar mid–dermal sebagaimana namanya, melibatkan kedalaman di antara luka bakar superfisial dan luka bakar dalam. Lebih cepat mengalami epitelialisasi dibandingkan luka bakar dalam. Secara klinis, terlihat adanya variasi derajat kerusakan pleksus dermal. Trombosis kapiler dan keterlambatan pengisian kapiler disertai edema dan pembentukan bula dapat diamati. Jaringan bewarna merah muda lebih gelap dibandingkan luka bakar superfisial.

C.

Luka bakar dalam

Luka bakar dalam lebih berat dibandingkan dua jenis luka bakar yang dijelaskan sebelumnya. Proses epitelialisasi spontan tidak terjadi, atau terjadi dalam waktu relatif panjang dengan skar yang nyata. Luka bakar ini terdiri dari dermal–dalam dan seluruh ketebalan kulit. 1.

Luka bakardermal–dalam Pada luka bakar dermal–dalam mungkin dapat dijumpai bula, namun di dasar bula ditunjukkan karakteristik luka bakar dalam, retikulum dermis menunjukkan warna merah berbercak [2, 10]. Hal ini disebabkan karena ekstrapasasi hemoglobin dari sel–sel darah merah yang rusak dan keluar dari pembuluh darah. Pertanda khas pada luka bakar ini adalah suatu tampilan yang disebut fenomena hilangnya capillary blush. Ini menunjukkan kerusakan pleksus dermal. Ujung–ujung saraf di lapis dermis juga mengalami nasib yang sama, karenanya akan diikuti hilang sensasi terutama saat dilakukan uji pinprick.

2.

Seluruh ketebalan kulit (Full Thickness Burns) Full thickness burns menyebabkan kerusakan lapis epidermis dan dermis dan dapat menyebabkan kerusakan struktur jaringan yang lebih dalam [2]. Pada penampilan klinik dijumpai kulit bewarna putih (dense white, waxy, dancharredappearance). Ujung saraf sensorik di dermis rusak sehingga hilang sensasi. [2, 10]. Kulit yang mengalami koagulasi menunjukkan konsistensi seperti kulit ini disebut eskar.


Ringkasan – – – –

Masalah pada luka bakar dikaitkan pada beratnya luka bakar. Mortalitas pada luka bakar berhubungan dengan usia dan beratnya luka bakar. Rule of Ninespada dewasa dan anak–anak dapat diterapkan untuk memperhitungkan luas luka bakar. Pemeriksaan klinik luka sangat penting dalam menentukan kedalaman luka.


Bab 6

Syok Luka Bakar dan Resusitasi Cairan Pada luka bakar, terjadi sekuestrasi cairan ke daerah cedera dan saat mencapai atau melebihi 20–30%, akan bersifat masif (sistemik) [32, 35]. Edema dalam jumlah besar ditambah adanya evaporative loss pada luka akan menyebabkan defisit volume plasma. Hal ini akan menyebabkan hipovolemia yang manakala tidak dikoreksi, akan memicu terjadinya gagal organ yang bersifat sistemik, khususnya acute kidney injury [16]. Dalam bab ini akan dijelaskan patogenesis edema dan syok hipovolemia pasca luka bakar, resusitasi dan pemantauannya. Cedera termal menyebabkan perubahan nyata pada mikrosirkulasi baik di daerah luka bakar maupun di daerah non–luka bakar (sistemik). Tiga zona terbentuk pada suatu cedera termal (gambar 3. 1 Model Jackson): 1) Zone sentral,nekrosis koagulatif. 2) Zona intermediate atau zonastasis, tidak ada aliran darah. 3) Zona perifer, menunjukkan vasodilatasi, peningkatan aliran darah dan hiperemia. Mediator inflamasi yang dilepaskan dari daerah cedera menyebabkan perubahan integritas dinding vaskular diikuti peningkatan permeabilitas [2]. Mediator–mediator ini diantaranya adalah histamin, serotonin, prostaglandin, bradikinin dan vasokonstriktor poten seperti tromboksan dan angiotensin. Pada luka bakar luas (>20––30% luas permukaan tubuh), jumlah mediator yang diproduksi demikian banyak diikuti peningkatan permeabilitas yang berlangsung luas hingga dijumpai pembentukan edema yang masif dan sistemik [18]. Hal ini menyebabkan terjadinya syok hipovolemia dalam waktu singkat. Hal ini ditunjang adanya kerusakan anatomik endothelial lining sistem mikrovaskulatur yang terdeteksi pada pemeriksaan mikroskop elektron. Dijumpai berbagai metode resusitasi cairan yang masing–masing menunjukkan hasil berbeda. [19, 65]. Secara praktis, bagaimanapun, larutan kristaloid misalnya larutan Hartmann (Lactated Ringers) atau Plasmalyte diakui secara luas untuk digunakan sebagai inisiasi prosedur resusitasi [2, 66]. Pada kasus anak, dijumpai keterbatasan sistem cadangan fisiologik dan besarnya rasio luas permukaan tubuh terhadap massa tubuh dibandingkan dengan dewasa. Dengan demikian, ambang cairan resusitasi yang perlu diberikan pada anak lebih rendah dibandingkan dewasa


(kurang lebih 10%) dan cenderung memerlukan volume yang lebih tinggi untuk tiap kilogram [3, 18]. Karenanya, diperlukan cairan lebih banyak untuk menyeimbangkan kebutuhan cairan yang diperoleh melalui perhitungan formula resusitasi. Pada cedera inhalasi dibutuhkan lebih banyak cairan. Pembentukan edema semakin berkurang dalam 18–30 jam pasca luka bakar. Dengan demikian, durasi resusitasi merupakan suatu variabel dan jumlah cairan yang dibutuhkan untuk maintenance dapat diketahui dari mengetahui jumlah cairan yang diperlukan untuk mempertahankan jumlah produksi urin adekuat.

Estimasi kebutuhan cairan Luas luka bakar dihitung menggunakan rule of nines atau burn body chart bila tersedia. Timbang berat badan pasien bila mungkin, atau peroleh informasi data tersebut pada anamnesis. Data ini diperlukan dalam memperhitungkan formula resusitasi [3, 12, 13, 15, 17, 18, 35, 67, 68]: Dewasa

:

Anak–anak

:

3–4 mL kristaloid (larutan Hartman atau Plasmalyte) / berat badan / luas luka bakar (%) 3–4 mL kristaloid (larutan Hartman atau Plasmalyte) / berat badan / luas luka bakar (%) di tambah maintenance glukosa 5% + 20 mmol Kcl dalam larutan salin 0. 45% – Untuk 10 kg pertama 100 mL/kg – 10–20 kg 50 mL/kg

Catatan: Kalkulasi kebutuhan cairan dimulai sejak saat terjadi cedera, bukan terhitung sejak masuk rumah sakit. Cairan diberikan melalui dua buah kanul berdiameter besar (pada dewasa 16G) sedapat mungkin di daerah non–luka bakar. Pertimbangkan akses intra–osseous (IO) bila diperlukan. Larutan salin normal umumnya dikemas bersama dekstrosa 2.5%: untuk kemasan ini, tambahkan 25mL dekstrosa 50% ke dalam kantong berisi 500 mL cairan. Bila larutan tersedia merupakan larutan salin hipotonik tanpa glukosa, tambahkan 50 mL dekstrosa 50% ke dalam kantong berisi 500mL cairan) Kalkulasi volume yang diestimasi dalam 24 jam pertama [12] saat edema terbentuk beberapa saat pasca luka bakar: – Separuh kebutuhan berdasarkan kalkulasi volume diberikan dalam 8 hours [3] dan separuh sisanya diberikan dalam16 jam berikutnya [12, 15, 19, 67]. – Cairan maintenance bagi anak–anak dibagi dalam 24 jam secara merata. Pengurangan cairan tidak sebanding dengan berkurangnya pembentukan edema; formula ini hanya merupakan petunjuk (panduan, guidelines) yang harus disesuaikan sesuai kebutuhan individu [15].


Bila produksi urine tidak mencukupi, berikan cairan ekstra: – Bolus cairan 5–10 mL/kg dan / atau tingkatkan jumlah cairan berikutnya sejumlah 150% volume sebelumnya. Dalam 24 jam kedua pasca luka bakar, larutan koloid dapat diberikan untuk restorasi volume sirkulasi menggunakan formula [66, 69]: – 0. 5mL albumin 5% x kg berat badan x % luas luka bakar. Disamping itu, larutan elektrolit harus diberikan untuk kebutuhan evaporative lossdan kebutuhan maintenance normal. Untuk tujuan ini, larutan yang umum digunakan adalah larutan salin normal Kcl (+ dekstrosa untuk anak–anak)

Pemantauan kecukupan resusitasi cairan Metode terbaik dan termudah adalah melakukan pemantauan jumlah produksi urine [3, 7, 11, 14, 18, 20, 35]: – Dewasa : 0. 5mL/kg/jam = 30–50mL/jam – Anak (< 30kg): 1. 0mL/kg/jam (rentang 0. 5–2mL/kg/jam) [66, 68–71] Bila jumlah produksi urine berkisar pada nilai ini, maka kecukupan perfusi ke organ akan terpelihara [20]. Produksi urine yang berlebih menunjukkan pemberian cairan berlebihan dan akan menyebabkan terbentuknya edema masif; produksi urine yang rendah menunjukkan perfusi ke jaringan yang buruk yang diikuti kerusakan sel Terlihat bahwa pemasangan kateter urine menjadi sangat penting pada pemantauan dan menjadi suatu keharusan dilakukan pada: • Luka bakar >10% pada anak–anak dan • Luka bakar >20% pada dewasa. Pemantauan hemodinamik invasif sentral diperlukan pada luka bakar dengan kondisi pre– morbid seperti adanya penyakit jantung atau cedera penyerta yang disertai kehilangan darah seperti adanya fraktur multipel. Asidosis yang nyata (pH<7. 35) pada analisis gas darahu menunjukkan perfusi jaringan yang tidak tercukupi dan menyebabkan asidosis laktat. Pada konsisi demikian, penambahan cairan resusitasi merupakan indikasi. Bila tindakan koreksi mengalami kegagalan dan dijumpai adanya hemochromogen di urine, pertimbangkan pemberian bikarbonat setelah melakukan diskusi dengan intensivis. Asidosis juga menunjukkan kebutuhan, atau ketidakcukupan (inadekuasi) prosedur eskarotomi.


Pada luka bakar luas, tekanan darah yang diukur menggunakan sphygmomanometer kerap tidak akurat karena edema; pengukuran akurat hanya didapatkan pada pemeriksaan melalui jalur arterial. Laju jantung kerap mengalami peningkatan karena nyeri dan faktor emosional; merupakan indikator yang buruk untuk digunakan pada pemantauan kecukupan resusitasi cairan. Elektrolit serum harus diukur pada kesempatan awal dan selanjutnya secara regular dalam interval waktu tertentu. Adanya hiponatremia ringan merupakan hal yang umum akibat dilusi karena pemberian cairan infus dan sangat tergantung pada konsentrasi natrium pada larutan kristaloid yang diberikan (larutan NaCl Hartmann hanya mengandung natrium 130 mEq/L). Hiperkalemia merupakan hal umum dijumpai; terjadi karena kerusakan jaringan pada luka bakar. Bikarbonat dan glukosa ditambah insulin mungkin diperlukan untuk melakukan koreksi. Gelisah, perubahan mental dan ansietas sering dijumpai dan merupakan indikator hipovolemia; dan harus diamati sebagai respon pertama dalam menilai kecukupan resusitasi cairan.

Hemoglobinuria Kerusakan jaringan khususnya jaringan otot akibat cedera termal, trauma tumpul atau iskemia (eskarotomi!) menyebabkan dilepaskannya mioglobin dan hemoglobin. Pertimbangan kuat untuk melakukan fasiotomi (eskarotomi tidak membebaskan fasia otot). Urine yang mengandung hemochromogen ini menunjukkan warna merah gelap. Gagal gnjal akut (GGA, Acute kidney injury, AKI) merupakan suatu kondisi yang sangat mungkin dijumpai karena penimbunan deposit haemochromogen di tubulus proksimal dan memerlukan terapi yang sesuai [23]: -

-

Pemberian cairan hingga produksi urine mencapai 2 mL / kg / jam Pertimbangkan pemberian Mannitol 12.5g dosis tunggal selama 1 jam / L dalam pola resusitasi cairan dan Observasi respon yang terjadi

Masalah yang dijumpai pada resusitasi cairan Formula yang ada hanya merupakan estimasi kebutuhan, sementara kebutuhan tiap individu harus dipantau secara ketat.

Oliguria Rendahnya jumlah produksi urinmenunjukkan ketidakcukupan cairan resusitasi. Dalam hal ini, tindakan pertama yang dilakukan adalah meningkatkan jumlah tetesan cairan. Diuretikum


sangat jarang diperlukan dan jangan pernah dipertimbangkan untuk diberikan sebelum penderita sampai di unit luka bakar. Diuretikum diberikan hanya pada penderita dengan haemochromogen di urine dan kadang pada penderita luka bakar luas. Penderita–penderita di bawah ini termasuk kelompok yang kerap memerlukan ekstra cairan resusitasi [15]: - Anak–anak - Penderita dengan cedera inhalasi [19] - Luka bakar listrik - Keterlambatan - Dehidrasi – petugas pemadam kebakaran, penderita intoksikasi Neonatus dan usia lanjut dengan kelainan jantung harus dipantau ketat karena kelebihan cairan sangat mudah terjadi. Untungnya, edema paru merupakan hal yang jarang dijumpai karena peningkatan resistensi vakcular di pulmoner jauh lebih tinggi secara disproporsional dibandingkan resistensi sistemik. Hal ini terjadi karena terjadinya hipokinesia miokardial dan kerap memerlukan pemantauan invasif, topangan inotropik, ventilasi dan manajemen cairan secara khusus.

Anak–anak Anak–anak sangat rentan terhadap hipoglikemia, kelebihan cairan dan hiponatremia karena keterbatasan simpanan glikogen, rasio luas permukaan tubuh yang lebih besar dibandingkan berat badan dan volume cairan intravaskular. Kadar glukosa darah dan elektrolit harus dipantau secara reguler. Pemberian air harus dibatasi dan pemberian glukosa dilakukan sejak awal. Hal ini dapat dilakukan melalui pemberian enteral maupun penambahan dekstrosa ke dalam larutan elektrolit. Sindroma kompertemen abdominal (Abdominal Compartment Syndrome, ACS) Keadaan ini jarang dijumpai namun merupakan suatu kondisi serius; merupakan komplikasi yang timbul pada luka bakar luas baik pada kasus dewasa maupun anak–anak, terutama bila kebutuhan cairan demikian besar untuk mencapai produksi urine yang cukup [15, 16, 72]. Adanya ACS dapat diketahui dengan melakukan pengukuran tekanan intra vesika (urinaria).


Ringkasan -

-

Resusitasi cairan diperlukan agar penderita luka bakar dapat bertahan hidup Cairan intravena untuk anak–anak dengan luas luka bakar>10% dan dewasa dengan luka bakar >20% Dua buah kanula perifer berdiameter besar Kalkulasi cairan dihitung berdasarkan saat terjadinya trauma: - Anak–anak (<30kg) : 3–4 mL /kg /% luas luka bakar ditambah maintenance - Dewasa : 3–4 ml /kg /% luas luka bakar - Separuh jumlah dari perhitungan tersebut diberikan dalam 8 jam, sisanya diberikan dalam 16 jam berikutnya Berikan kristaloid (misal, larutan Hartmann atau Plasmalyte) dalam 24 jam pertama. Anak–anak memerlukankarbohidrat. Pasang kateter urine Haemochromogens: tambahkan cairan untuk meningkatkan produksi urine. Lakukan pemeriksaankadar glukosa darah, elektrolit serum, tekanan darah, frekuensi nadi, analisis gas darah dan foto toraks.


Bab 7

Tatalaksana Luka Introduksi Dalam penatalaksanaan luka, hal penting yang perlu dipahami yaitu mekanisme trauma dan penilaian luas–beratnya trauma. Hal ini merupakan titik awal tatalaksana, yang akan menentukan hasil yaitu fungsi dan penampilan. Luka adalah disrupsi arsitektur jaringan dan proses–proses seluler. Pada luka bakar, denaturasi protein dan disrupsi struktur sel terjadi akibat kontak dengan sumber termal (baik suhu tinggi maupun suhu rendah), listrik, kimiawi atau radiasi. Luka bakar demikian merusak karena menyebabkan terganggunya ketujuh fungsi utama kulit. - Regulasi suhu - Pengaturan sensorik - Respon imun - Proteksi dari invasi bakteri - Pengendalian kehilangan (penguapan) cairan - Fungsi metabolik - Fungsi estetik dan psikologi Tujuan tatalaksana adalah untuk memperkecil terganggunya fungsi baik di tingkat lokal maupun sistemik. Pemahaman luka sebagai suatu hal yang bersifat dinamik dan heterogen adalah sangat penting. Jangan sampai diduga bahwa luka di berbagai area adalah sama.

Pertolongan pertama Prinsip penanganan pertama adalah - Menghentikan proses pembakaran - Menurunkan suhu luka [22]. Menghentikan proses pembakaran akan mengurangi kerusakan jaringan. Menurunkan suhu permukaan akan mengurangi produksi mediator inflamasi (cytokines) dan promosi maintenance viabilitas di zona stasis. Oleh karenanya, hal ini sangat membantu pencegahan progres kerusakan yang terjadi pada luka bakar dalam 24 jam pertama[25].

Hentikan proses pembakaran Pada luka bakar api, penderita berguling di tanah secara aktif maupun pasif menerapkan Stop, Drop, Cover (face) & Roll technique [10, 24]. Pakaian yang terbakar harus segera dilepaskan


secepat mungkin. Perhatikan jangan sampai penolong mengalami cedera akibat pertolongan ini. Pada luka bakar karena air panas, pakaian yang dibasahi air panas berperan sebagai reservoir, karenanya segera lepaskan sesegera mungkin. Selain melepaskan pakaian, setiap jenis perhiasan juga harus dilepaskan[2]. Bila pakaian melekat pada permukaan kulit, potong dan biarkan melekat di tempatnya. Namun, pakaian terbuat dari bahan sintetik yang meleleh melekat pada kulit yang tidak vital akan mudah dilepaskan.

Menurunkan suhu luka Permukaan luka harus diturunkan suhunya menggunakan air mengalir[73–78]. Suhu ideal adalah 15°C atau berkisar antara 8°C sampai 25°C [76, 79]. Dengan menurunkan suhu permukaan luka, reaksi inflamasi diredam dan menghentikan progress pengrusakan zona stasis [73, 80]. Berbagai cara dapat diterapkan untuk tujuan ini. Menyemprotkan air atau melekatkan busa basah di atas luka, handuk basah atau hidrogel dapat dilakukan, namun tidak seefektif air mengalir dan hanya dianjurkan saat air mengalir tidak ada (misalnya saat meminta pertolongan ke pusat pelayanan medik) [73, 81]. Handuk basah tidak efektif karena tidak seluruhnya melekat dengan permukaan luka dan cepat menjadi panas akibat proksimitas terhadap tubuh[73]: karenanya, bila digunakan, harus sering diganti. Lamanya aplikasi minimal adalah dua puluh menit, kecuali tidak dimungkinkan [73–76, 80]. Misalnya pada penderita multi trauma dan tidak ada petugas yang memberi pertolongan pertama untuk menerapkan metode tersebut. Lebih lanjut, diperoleh data bahwa pertolongan pertama efektif bila dilakukan dalam tiga jam pertama pasca luka bakar. Anak–anak terpapar pada risiko hipotermia dan hal ini terdeteksi pada pengukuran suhu saat asesmen klinik dimana dijumpai anak kebiruan dan mengigil. Aplikasi penurunan suhu luka harus dihentikan. Pada keadaan seperti ini, dianjurkan mengupayakan suhu si atas 30°C dan membungkus anak bersangkutan [4]. Es atau air es jangan pernah digunakan untuk menurunkan suhu. Suhu yang ekstrim dingin ini akan menyebabkan vasokonstriksi dan secara eksperimen menunjukkan luka yang semakin dalam; disamping risiko hipotermia. Penurunan suhu permukaan sekaligus merupakan analgetik yang efektif [22, 74, 76]. Saat nyeri timbul kembali dalam beberapa menit setelah aplikasi penurunan suhu dihentikan, dan bila tidak ada kontra indikasi, maka lanjutkan penurunan suhu hingga dicapai efek analgetik. Hipotermia harus dicegah

Manajemen awal KOLEGIUM ILMU BEDAH INDONESIA 151

Setelah pertolongan pertama, luka ditutup menggunakan bungkus plastik atau bahan keringyang tidak melekat selama prioritas manajemen lainnya dilakukan [2, 24]. Bila luka sebelumnya tidak diturunkan suhunya, lanjutkan metode penurunan suhu sebagaimana dianjurkan dalam waktu tersisa hingga mencapai tiga jam. Setelah tiga jam, tidak ada efek benefit. Karenanya, luka kemudian dicuci menggunakan air atau salin, dengan sabun atau larutan klorheksidin 0. 1% Antiseptik lain jangan digunakan. Pada penyiapan prosedur transpor, luka dibalut. Tergantung waktu terjadinya trauma, saat transportasi dan waktu tempuh, diperlukan lebih dari sekedar pembalutan luka menggunakan kain kering. Lembar plastik dapat dipakai terutama pada anak–anak untuk membatasi penguapan dan kehilangan panas tubuh [22]. Klorheksidin pada tulle (misal: Bactigras®) dibalut dengan kasa akan sangat bermanfaat pada penderita yang memerlukan perjalanan beberapa jam ke pusat rujukan. Aplikasi krim topikal seyogyanya dihindari karena akan memperpanjang waktu dan menyebabkan keterlambatan transportasi ke pusat rujukan.

Elevasi Elevasi ekstremitas yang mengalami cedera sangat bermanfaat selama tatalaksana awal dan selama prosedur transpor karena akan mengurangi edema. Pada tungkai, dijumpai perbedaan bermakna dengan kasus–kasus yang tidak dilakukan elevasi dalam hal perlunya dilakukan eskarotomi.

Area khusus Pada luka bakar dengan cedera inhalasi kerap diikuti berkembangnya edema jalan napas sehingga diperlukan intubasi [2]. Luka bakar perineum memerlukan pemasangan kateter lebih awal untuk mencegah kontaminasi. Bila pemasangan kateter terlambat, prosedur insersi pada saat edema akan mengalami kesulitan. Luka bakar pada kepala dan leher. Kepala harus dilakukan elevasi untuk menghambat edema jalan napas bagian atas. Pada anak–anak dengan luka bakar luas, prosedur elevasi kepala ini sangat bermanfaat karena risiko besar terjadinya edema serebral pada resusitasi cairan.

Eskarotomi Bila luka bakar melibatkan seluruh ketebalan dermis dan kulit mengalami kehilangan elastisitas saat edema berkembang,[82] maka diperlukan tindakan melakukan sayatan pada kulit hingga kedalaman subkutis [7, 82]. Prosedur ini disebut eskarotomi.


Trunkus Bila trunkus mengalami luka bakar ekstensif, elastisitas dinding dada menurun diikuti penurunan compliance yang menyebabkan berkurangnya ventilasi [2, 82]. Pada dewasa, kerap terlihat luka bakar melingkar (sirkumferensial) di dada dengan atau tanpa melibatkan abdomen. Pada anak–anak yang bernapas terutama dengan diafragma, terlihat eskar di dinding anterior dan abdomen tanpa luka bakar di sisi posterior. Insisi dilakukan longitudinal sepanjang linea aksilaris anterior ketepi kosta atau ke abdomen bagian atas [82]. Pada kasus berat, mungkin diperlukan insisi yang menghubungkan kedua insisi sebelumnya (kanan dan kiri) berbentuk konvekspada sisi atas (kranial) dinding dada, di bawahklavikuladan melintang di abdomen.

Ekstremitas Bila pada ekstremitas dijumpai luka bakar melingkar (sirkumferensial), dengan adanya edema di bawah kulit yang tidak elastik tersebut maka aliran sirkulasi akan terganggu dan menyebabkan gangguan perfusi diikuti kematian jaringan bagian distal [21]. Gangguan ini bersifat progresif lambat dan tidak terduga. Adanya peningkatan tekanan kompartemen dapat diamati dengan adanya gejala dan tanda sebagaimana diuraikan berikut [82, 83]: - Pain (nyeri)

:

- Pallor (pucat)

:

- Pulseless teraba)

- Parestesia

(nadi

tak :

Nyeri saat istirahat Nyeri saat menggerakkan sendi–sendi distal Sirkulasi ke distal terganggu Pengisian kapiler terhambat (terutama di kuku) Saturasi oksigen tidak terdeteksi pada pemeriksaan pulse oximetry Dingin Tidak teraba denyut nadi

:

Tidak ada denyut, terutama pada pemeriksaan USG Doppler Kesemutan hingga hilang rasa (numbness)

Interpretasitanda–tanda ini mungkin sulit karena terbakarnya kulit (yang menyebabkan palpasi denyut nadi sulit teraba), suhu dingin (gambaran aliran darah terganggu), dan adanya hipovolemia. Pemeriksaan akurat didapatkan dengan melakukan USG Doppler. Perubahan paling awal ditandai hilangnya sinyal Doppler pada pembuluh di jari–jari. Eskarotomi harus segera dilakukan sebelum pulsasinadi hilang dan saat menurunnya sirkulasi. Sayatan dilakukan hingga kulit sehat beberapa milimeter di proksimal dan distal; di garis mid– aksial antara permukaan fleksor dan ekstensor. Hindari melakukan sayatan melintas lengkung


fleksura pada sendi–sendi. Sayatan harus dilakukan hingga ke lemak subkutis dan kulit terpisah secara nyata. Perabaan menggunakan jari akan dapat meraba adanya sisa tahanan. Kadang satu insisi cukup namun kadang diperlukan sayatan di kedua sisi untuk restorasi sirkulasi. Perabaan mengenai ketegangan ekstremitas bersangkutan merupakan petunjuk yang sangat berharga. Penyulit eskarotomi adalah tercederainya struktur di bawah kulit. Disisi medial siku, saraf ulnaris berjalan dan di sisi lateral lutut berjalan saraf peroneal komunis. Jangan melakukan sayatan transversal di ekstremitas. Batas distal dari suatu eskarotomikadang sulit ditentukan. Di ekstremitas atas, sayatan lateral dapat dilakukan sepanjang batas lateral tangan hingga pangkal jari kelima. Di sisi medial, sayatan dapat dilakukan hingga proksimal ibu jari. Kadang–kadang beberapa sayatan tambahan di tangan diperlukan, dan sebelum memberangkatkan penderita, hubungi unit luka bakar yang menjadi rujukan. Diagram lokasi sayatan terdapat di lampiran 3 dalam buku pegangan.

Prosedur Pertama, tentukan lokasi sayatan. Bila operator belum terbiasa, maka tandai dengan tinta sementara ekstremitas bersangkutan berada pada posisi anatomik. Perhatikan kembali garis sayatan. Lengan dalam posisi supinasi sebelum member tanda dan sayatan berjalan di depan epikondilus medialis untuk menghindari cedera saraf ulnaris. Pada tungkai, insisi medial berjalan di belakang maleolus medialis untuk menghindari cedera pembuluh darah dan saraf safena. Bila diperlukan sayatan lateral, hindari tercederainya saraf peroneus komunis yang melintas leher fibula; karenanya lokasi sayatan terletak pada garis mid–lateral. Instrumen yang diperlukan yaitu pisau atau elektrokauter dan sarana haemostasis seperti klem arteridan benang, diatermi atau hemostatiktopikal misalnyacalcium alginate. Perdarahan akan terjadi dalam jumlah ekstrim. Anestesia umumnya tidak diperlukan. Anestesi lokal diperlukan hanya diperlukan di tepi luka ke daerah normal. Selain itu, penderita umumnya sudah terintubasi, sehingga sedasi ringan dapat diberikan. Prosedur ini dikerjakan dalam kondisi steril. Kasa disiapkan untuk membalut luka sayatan dan balutan ini seyogyanya tidak menekan agar efektivitas prosedur tercapai. Pada penderita yang sadar, penjelasan mengenai prosedur harus diberikan sebelum melakukan tindakan (informed consent)


Ringkasan -

Luka bakar merusak seluruh fungsi kulit Pertolongan pertama adalah hentikan prose pembakaran dan menurunkan suhu luka. Tatalaksana luka dilakukan sesederhana mungkin. Eskar yang kaku memengaruhi fungsi dan memerlukan eskarotomi; di dada untuk memperbaiki ventilasi, di ekstremitas untuk memperbaiki sirkulasi ke distal.


Bab 8

Indikasi dan Prosedur Rujukan Introduksi Penderita luka bakar listrik, kimia, atau cedera termal memerlukan asesmen dan stabilisasi di rumah sakit terdekat. Tidak ada istilah ahli bedah musiman Australia dan New Zealand, karena tatalaksana multidisiplin tersedia di rumah sakit pusat. Semua penderita memiliki hal untuk memperoleh pelayanan luka bakar yang berkualitas. Petugas kesehatan yang mengawali pertolongan harus melakukan asesmen (survei) primer dan sekunder dan melakukan evaluasi untuk menilai penderita yang harus dirujuk. Luka bakar kerap dijumpai sebagai suatu trauma multipel, dan setiap penderita harus dilakukan evaluasi untuk trauma lain atau penyerta. Semua prosedur dan terapi yang diberikan dicatat dan di informasikan ke unit luka bakar rujukan, termasuklembar pemantauan, obat–obatan dan tindakan yang dilakukan.

Peran faktor geografik 1. Daerah perkotaan Luka bakar yang terjadi di daerah perkotaan di Australia dan New Zealand yang telah memiliki unit luka bakar, penderita yang memerlukan perawatan langsung dirujuk setelah survei primer dikerjakan. Resusitasi dan tatalaksana definitif dengan demikian dapat dilaksanakan sesegera mungkin tanpa keterlambatan, dengan pengecualian mereka yang memerlukan tindakan intervensi sebagai tatalaksana penyelamatan hidup seperti prosedur intubasi. Bila diperkirakan perjalanan ambulans memakan waktu 1 jam atau lebih, maka prosedur resusitasi cairan dimulai baik di ambulans menuju ke rumah sakit, menghindari syok luka bakar. Hal ini akan sangat bermakna pada anak–anak dan usia lanjut, karena keterlambatan akan mempengaruhi hasil akhir.

2. Daerah perifer dan terisolasi Di daerah perifer dan terisolasi, karena keterbatasan fasilitas dan masalah logistik, prosedur rujukan segera tidak dimungkinkan; penderita memerlukan sarana transportasi darat, udara atau laut. Dalam keadaan seperti ini, tatalaksana dalam 24 jam pertama dilakukan sebelum penderita dirujuk; kadang diperlukan tatalaksana lebih dari 24 jam (lihat bab 12). Konsultasi dengan personel di unit luka bakar regional untuk tatalaksana yang tepat, sehingga penderita berada pada kondisi optimal saat dirujuk.


Hanya ada beberapa kondisi penderita yang mengharuskannya tetap dirawat di rumah sakit lokal atau distrik. Mengorbankan pelayanan yang baik dengan mempertahankan konsep perawatan ‘agar dekat dengan keluarga’ merupakan suatu konsep yang kurang baik, terutama menyangkut penanganan masalah gangguan emosi yang penting dalam tatalaksana.

Kriteria rujukan Australian and New Zealand Burn Association menetapkan kasus–kasus berikut memerlukan rujukan ke unit luka bakar (lihat tabel 7. 1). Tabel 7. 1 - Luka bakar > 10% luas permukaan tubuh pada dewasa dan >5% pada anak–anak - Luka bakar seluruh ketebalan kulit (luka bakar dalam, full thickness burns)> 5% - Luka bakar mengenai area khusus, termasuk wajah, tangan, kaki, genitalia dan perineum, persendian serta luka bakar melingkar pada dada dan tungkai - Luka bakar dengan cedera inhalasi - Luka bakar listrik - Luka bakar kimia - Luka bakar dengan penyakit pre–morbid - Luka bakar dengan trauma berat lainnya - Luka bakar pada usia tertentu: anak–anak dan usia lanjut - Luka bakar pada wanita hamil - Luka bakar bukan karena kecelakaan Bila penderita memiliki kelainan yang menyebabkan tatalaksana menjadi sulit dengan risiko yang semakin besar, diperlukan penatalaksanaan oleh tenaga dalam tim spesialis yang akan memberi kesempatan sebesar mungkin untuk mendapatkan hasil optimal. Penderita–penderita dengan trauma penyerta harus dibawa ke unit trauma atau unit luka bakar sesuai dengan beratnya trauma. Harus ada pertimbangan antara temuan klinik saat asesmen emergensi dan diskusikan dengan pengelola petugas di unit luka bakar rujukan. Pada trauma berat yang memiliki risiko besar, maka perlu prioritas penaganan dan stabilisasi sebelum dirujuk. Perawatan luka bakar dilaksanakan dan prosedur rujukan direncanakan segera setelah penderita berhasil menjalani prosedur emergensi yang diperlukan. Bila luka bakar merupakan kondisi yang dominan dalam hal mortalitas dan morbiditas, maka prosedur rujukan ke unit luka bakar merupakan tindakan yang tepat. Prioritas merupakan suatu pertimbangan klinik yang didiskusikan oleh dokter yang merujuk, ahli luka bakar dan tim trauma serta ahli intensivis; dengan mempertimbangkan usiapenderita yang memiliki mortalitas tinggi. Hal ini disebabkan respon pada kelompok usia tertentu yang tidak dapat diprediksi sehingga mereka memerlukan penanganan spesialistik oleh tim multidisipliner.


Pendekatan tim menunjukkan banyak kelebihan dalam penatalaksanaan luka bakar [2].

Persiapan rujukan Dalam keadaan stabil secara fisiologik, penderita luka bakar masif dapat dan aman ditransfer meski dalam waktu yang relatif lama. Namun untuk dapat ditransfer, penderita harus stabil. Stabilisasi mencakup semua aspek yang diuraikan sebelumnya.

1. Sistem respirasi -

-

Semua penderita cedera berat diberi oksigen 15L/menit. Karena obstruksi jalan napas bagian atas dapat mengalami progres dengan cepat dan mencapai puncaknya saat penderita ditransfer, maka pentiing untuk mempertimbangkan intubasi endotrakea sebelum penderita di rujuk. Cedera inhalasi dengan kerusakan infraglotik kerap menimbulkan masalah saat transportasi berlangsung.

2. Sistem sirkulasi Prinsip tatalaksana gangguan sirkulasi akibat perpindahan cairan dan elektrolit sebagaimana diuraikan sebelumnya diberikan untuk stabilisasi penderita sebelum proses transfer. - Bila insersi 2 kanul (16G pada dewasa, 20G pada anak–anak) tidak dimungkinkan, ambil rute lain untuk pemberian cairan, dan diskusikan sebelumnya dengan unit luka bakar rujukan. - Metode akses vaskular umumnya tergantung pengalaman tim baik di perifer maupun di unit luka bakar rujukan. - Rute yang dapat digunakan antaralain adalah jalur vena sentral perkutan (femoral, subklavia, atau jugularinterna), intra–osseous atauvena seksi (ankleatausiku) [3, 7, 9]. - Regimen pemberian cairan dibahas pada diskusi di bab 6. Ringkasnya, mulai resusitasi cairan - 3–4mLkrstaloid (misal, larutan Hartmann atau Plasmalyte) /kg / % luas luka bakar dalam 24 jam, 50% diberikan dalam 8 jam pertama - Tambahkan cairan maintenancepada anak–anak [3, 12, 15, 17]. - Kecukupan resusitasi ditentukan berdasarkan observasi penderita, dalam hal ini terutama jumlah produksi urine (yang dipantau melalui kateter) bertujuan mencapai 30–50 mL/jampada dewasa, dan 1 mL/kg/jam (0. 5–2 mL/kg/jam) pada anak sampaidengan 30 kg [3, 11, 14, 20].


-

Bila dijumpai haemochromogenuria sebagaimana kerap dijumpai pada luka bakar listrik, kebutuhan cairan ditujukan untuk menghasilkan urine 75–100 mL/jam pada dewasa, dan> 2 mL/kg/jam pada anak–anak.

3. Luka Luka dicuci dengan air mengandung larutan klorheksidin 0. 1% atausalin normal dan dibungkus dengan plastik atau kain kering bila prosedur transfer harus disegerakan. Plasticwrapyang kerap digunakan untuk membungkus makanan sangat bermanfaat digunakan untuk mencegah evaporasi, mempertahankan panas dan mencegah desikasi (luka mengering) [22]. Hanya bila prosedur transfer tertunda, gunakan balutan atau pembalut formal (misalnya, slow–release silver dressings, krim antibakteri atau chlorhexidine impregnated vaseline gauze; dan bahan penutup absorben). Hal ini dikerjakan setelah melakukan konsultasi dengan unit luka bakar.

4. Manajemen nyeri Luka bakar diikuti nyeri yang ekstrim. Meski sensasi kulit hilang pada luka bakar dalam, area sekitar luka dirasakan sangat nyeri; karenanya pemberian analgetika sangat diperlukan [9]. Pada semua kasus, kecuali luka bakar ringan, pemberisan analgetika diberikan secara intra vena. Dosis awal diberikan relatif kecil selang waktu tiap 3–5 menit, dan dosis akhir sangat tergantung respon penderita. Trauma penyerta maupun kelainan yang ada sebelumnya harus diperhitungkan dalam menetapkan dosis, umumnya diberikan morfin dengan dosis awal 0. 05– 0. 1 miligram per kilogram berat badan.

5. Sistem gastrointestinal Bila dimungkinkan, segera memulai pemberian nutrisi enteral dini melalui akses pipa oro– atau naso–gastrik. Selama proses transfer, umumnya lebih aman lambung dalam keadaan kosong untuk memperkecil risiko aspirasi saat terjadi muntah. Untuk tujuan ini, pipa oro– atau naso– gastrik secara reguler diaspirasi dan dilakukan drenase terbuka. Hal ini diterapkan pada kasus dewasa dengan luka bakar>20% atau anak–anak dengan luka bakar >10%.

6. Tetanus Profilaksis tetanus diberikan pada kesempatan pertama. Detilnya dapat dilihat dalam lampiran 1. Untuk mendapatkan hasil optimal, lakukan kontak secara berkesinambungan dengan unit luka bakar rujukan, lengkapi semua dokumentasi termasuk hal–hal yang diuraikan di atas.


Mekanisme Transfer Hubungan telefon dengan unit luka bakar rujukan saat penderita memerlukan prosedur rujukan. Bila keputusan untuk rujukan telah ditetapkan, unit luka bakar rujukan berkewajiban menyiapkan tempat dan unit luka bakar rujukan bertanggungjawab mengatur prosedur transportasi. Prosedur transpor mengikuti protokol yang ada. Pusat pelayanan yang melakukan rujukan bertanggungjawab pada stabilisasi penderita dan membuat dokumentasi asesmen awal (survei primer dan sekunder) serta tatalaksana yang sudah dilakukan; termasuk saat melakukan pemeriksaan, balans cairan, terapi termasuk dosis obat yang diberikan. Pada saat transfer, sertakan dokumentasi ini. Metode pengiriman ditentukan oleh pusat pelayanan yang melakukan rujukan beserta tim dan petugas yang selanjutnya mengambil alih tugas dalam asesmen dan tindakan selama pengiriman.

Ringkasan -

-

Penderita luka bakar listrik, kimia, cedera termal yang memenuhi kriteria rujukan yang ditetapkan dalam ANZBA Criteria for Burn Unit Referral (Tabel 7. 1) harus memperoleh asesmen dan dilakukan stabilisasi saat dirujuk ke unit luka bakar rujukan. Prosedur pengiriman merupakan tanggungjawab unit rujukan. Tim yang ikut dalam proses rujukan bertugas melakukan stabilisasi penderita selama proses transfer. Dokumentasi merupakan hal yang sangat penting untuk suatu mekanisme transfer pelayanan dari unit pelayanan pertama ke unit luka bakar.


Bab 9

Luka Bakar pada Anak Introduksi Demikian banyak konsep emergensi penatalaksanaan luka bakar pada dewasa berlaku pula pada anak–anak. Kasus anak dengan luka bakar harus dinilai dengan pola yang sama sebagaimana asesmen pada kasus dewasa. Pada survei primer, harus terdeteksi adanya kondisi mengancam jiwa. Prosedur tersebut dilanjutkan dengan melakukan pengamanan jalan napas dan kecukupan sirkulasi yang perlu dipantau secara berkesinambungan berdasarkan produksi urine. Perbedaan bermakna antara anak–anak dengan dewasa adalah sebagaimana diuraikan berikut: - Ukuran dan proporsi tubuh pada anak [2] - Dinamika cairan - Ketebalan kulit - Perbedaan sosial dan perkembangan emosional.

Epidemiologi Insiden luka bakar pada populasi anak jauh lebih tinggi dibandingkan dewasa [3], dengan penyebab yang berbeda sebagaimana terlihat pada tabel 9. 1 Tabel 9. 1 Penyebab luka bakar pada anak (%) Air panas 55% Kontak 21% Api 13% Friksi 8% Listrik l 1% Kimia 1% Lainnya 1% (ANZBA Bi-NBR Annual Report 2011[8])


PAda anak yang usianya lebih kecil, insiden luka bakar karena air panas menempati urutan pertama, sementara luka bakar akrena api lebih umum dijumpai pada anak yang usianya lebih besar [84, 85].

Riwayat Sebagai pada luka bakar pada umumnya, anamnesis merupakan hal yang sangat penting [21]. Pada anamnesis harus diperoleh informasi mengenai modus dan waktu terjadinya cedera. Catatan khusus harus diperoleh dari anamnesis tersebut adalah adanya inkonsistensi dari riwayat dengan dengan temuan pada pemeriksaan fisik atau keterlambatan karena ada kemungkinan berhubungan dengan luka bakar yang bukan terjadi karena kecelakaan. Masalah jalan napas yang tidak nyata tampak seperti sleep apnoea atau asma harus teridentifikasi, demikian pula halnya dengan hubungan psikologik anak dengan keluarganya. Informasi penting lainnya yang perlu diperoleh adalah pertolongan yang sudah diberikan. Pada kasus air panas, berapa suhu air, termasuk jenis pakaian yang dikenakan saat terjadi cedera. Hal ini akan membantu memperkirakan kedalaman luka bakar dan perlunya diberikan edukasi lebih lanjut.

Ukuran dan proporsi tubuh Anak berbeda dengan dewasa dalam hal rasio luas permukaan tubuh terhadap berat badan dan dalam hal ukuran relatif bagian tubuh tertentu dengan bagian tubuh lainya [7]. Dengan besarnya rasio luas permukaan tubuh terhadap berat badan maka [21]: - Rasio metabolisme besar - Proses evaporasi tinggi - Proses kehilangan panas lebih besar Kesemuanya memiliki relevansi dengan penatalaksanaan luka bakar pada anak, karena pemebrian cairan resusitasi didasarkan pada berat badan ketimbang luas permukaan. Penerapan formula karenanya menjadi kompleks, sehingga sulit untuk diterapkan secara universal. Namun, pada prakteknya, kasus luka bakar pada anak memerlukan lebih banyak variasi kalkulasi volume cairan dibandingkan pada dewasa. Pada anak, kepala dan leher merupakan bagian yang secara komparatif lebih besar dibandingkan dewasa; demikian pula ukuran tungkai yang secara komparatif lebih kecil dibandingkan dewasa (gambar 5. 2) [21]. Bayi berusia sampai satu tahun, luas permukaan kepala dan leher berkisar 18% luas permukaan tubuh dan tungkai berkisar 14%. Dalam masa pertumbuhannya, setiap tahun di atas usia satu tahun, maka ukuran kepala berkurang sekitar 1% dan ukuran tungkai bertambah 0. 5% dibandingkan luas permukaan tubuh [3]. Dengan modifikasi kasar dari rule of nines terlihat untuk kepentingan klinik bahwa proporsi dewasa tercapai saat seorang anak mencapai usia sepuluh tahun. Karenanya, dapat terjadi kesalahan kalkulasi perhitungan laus luka bakar dan perhitungan kebutuhan cairanresusitasi.


Kedalaman Luka Bakar Kedalaman luka bakar sebanding dengan suhu, durasi penggunaan dan berbanding terbalik dengan faktor–faktor yang merusak jaringan. Salah satu faktor adalah ketebalan kulit. Pada anak–anak, kulit lebih tipis dibanding dewasa. Atas dasar ini, cedera termal menyebabkan kerusakan deep–dermal atau bahkan seluruh ketebalan kulit; dibandingkan suhu dan durasi yang sama pada dewasa. Pada bayi, air dengan 60°C akan menyebabkan - Luka bakar seluruh ketebalan kulit dalam waktu kurang dari satu detik - Anak yang sudah besar mampu bertahan sampai lima detik pada suhu ini. - Dewasa hanya mendapat luka bakar yang dalam setelah 20 detik.

Refleks menghindar pada anak–anak Adanya rangsang menyakitkan tidak menimbulkan respon dalam waktu cepat dan konsisten sebagaimana pada dewasa. Seorang balita yang berdiri di air panas atau api tidak akan berusaha menjauh, hal ini menyebabkan luka bakar dalam.

Asesmen kedalaman luka bakar Pemeriksaan kedalaman luka bakar pada anak–anak lebih sulit dibanding pada dewasa. Pada anak–anak, luka bakar superfisial (dengan lepuh) lebih umum dibandingkan luka bakar api dan kedalamannya sangat sulit dinilai. Kulit tipis pada anak–anak menyebabkan kesulitan dalam asesmen kedalaman luka bakar[7]. Perubahan warna kulit yang terbakar pada anak tidak selalu sama dengan dewasa. Warna merah tua dengan sedikit bintik pada anak merupakan indikasi dari deep–dermal atau seluruh ketebalan kulitdan beberapa hari berikutnya akan berubah suram bahkan kekuningan yang menunjukkan kerusakan seluruh ketebalan kulit.

Pertolongan pertama dan transpor Prinsip dari pertolongan pertama hentikan kontak dengan sumber panas, hentikan proses pembakaran dan gunakan air dingin adalah sama sebagaimana pada dewasa. Namun, harus diingat bahwa risiko hipotermia lebih besar pada anak dibandingkan dengan dewasa. Hipotermia pada anak dikarenakan beberapa faktor. Besar rasio luas permukaan tubuh terhadap massa tubuh merupakan hal yang sangat penting. Anak di bawah usia 1 tahun tidak memiliki refleks mengigil. Anak yang lebih besar mungkin memiliki refleks mengigil, namun


massa otot mereka jauh lebih kecil; dengan demikian, rasio total massa tubuh dan konten suhu jauh lebih kecil. Risiko hipotermia harus diperhatikan saat melakukan pertolongan pertama dan selama transportasi. Pertolongan pertama yang baik dan beanr harus diterapkan sebagaimana pada dewasa namun harus benar–benar diaplikasikan pada daerah luka dan menjaga agar tubuh anak tetap hangat. Pada luka bakar ekstensif, waktu penggunaan air dingin optimal dibatasi hanya selama 20 menit guna menghindari hipotermia. Jangan menggunakan es Selama stabilisasi dan selama transportasi, selimut sangat sangat berguna mencegah kehilangan panas tubuhmelalui evaporasi dan konveksi.Bagian tubuh yang terpapar harus ditutup, sebaiknya gunakan lembaran yang menjaga kelembabansemacam plastik.

Jalan napas Obstruksi jalannapas atas pada anak–anak merupakan hal umum. Pembesaran kelenjar gondok, amandel dan laryngomalacia mungkin ada sebelum cedera termal (3) dan menurut anamnesis terdeteksi adanya sleep apnoea seperti mendengkur atau melindur, mengantuk di siang hari atau pernapasan bising. Narkosis mungkin tidak hanya akan menyebabkan depresi respirasi namun juga menyebabkan relaksasi otot–otot faring dan meningkatkan kemungkinan obstruksi. Adanya pembengkakan pada obstruksi dapat menimbulkan masalah. Diameter saluran napas bagian bawah memiliki ukuran absolut lebih kecil pada anak dibandingkan dewasa (2,3). Karenanya, adanya pembengkakan di mukosa bronkus atau akumulasi sekret di bronkus menyebabkan jauh berkurangnya penampang dearah permukaan mukosa sehingga menganggu aliran udara (2). Atas dasar ini, pipa tanpa cuff digunakan pada anak dengan usia di bawah 10 tahun. Reaksi hiperaktivitas bronkus (asma) merupakan kondisi umum dijumpai pada anak–anak yang ditandai adanya riwayat batuk malam hari terutama dimusim dingin atau setelah suatu infeksi pada sistem respirasi. Inhalasi asap sering menyebabkan bronkopasme pada anak–anak yang rentan terhadap reaksi ini. Teknik intubasi endotrakea sedikit berbeda pada anak dibandingkan dewasa. Laring lebih tinggi ke arah sefalad dibanding dengan dewasa. Dengan pipayang berdiameter lebih kecil, maka frekuensi suction harus ditingkatkan untuk pembersihan sekret. Stabilisasi pipa lebih sulit khususnya bila wajah terbakar; pengunaan 2 buah pengikat, satu di atas telinga dan satu dibawahnya (dandapat dipanjangkan saat edema bertambah) akan sangat berguna. Posisi ujung pipa harus diperiksa melalui auskultasi sebelum memperbaiki posisi pipa diikuti pemeriksaan foto toraksuntuk konfirmasi posisi pipa. Intubasi endotrakea pada anak hanya dilakukan oleh praktisi yang terlatih dan berpengalaman.


Jika terjadi obstruksi jalan napas dan intubasi endotrakea tidak dimungkinkan, lakukan krikotiroidotomi. Jarum berdiameter besar (14G) melalui membran krikotiroid ditembuskan dan berperan sebagai cricothyroidotomy. Ini merupakan solusi sementara dan mungkin diperlukan trakeostomi emergensi.

Manajemen Cairan 1. Perbedaan antara anak dan dewasa Dinamika cairan dan ukuran tubuh berbeda antara anak dan dewasa. Pada anak, proporsi terbesar cairan tubuh adalah pada ekstra sel. Pada anak volume darah 80mL/kg, sedangkan pada dewasa 60–70mL/kg [2]. Kapasitas konsentrasi tubulus renalis pada anak lebih kecil dibanding dewasa. Berdasarkan hal ini, kehilangan cairan pada anak lebih besar dan mungkin lebih cepat dibandingkan dewasa [2, 3] dan asupan cairan berlebihan sulit ditangani. Disisi lain, depresi fungsi kardio–respirasi dan cadangan renal yang dijumpai pada dewasa tidak terjadi pada anak–anak. Oleh karenanya, kecuali ada penyakit pre–morbid, fisiologi anak dapat diandalkan untuk mengatasi beban cairan dengan cepat, meskipun ekses cairan dalam jumlah besar kurang mudah ditangani seperti yang disebutkan di atas. Edema serebri lebih mungkin dijumpai pada anak dengan kelebihan cairan terutama disertai hiponatremia. Risiko ini dapat dikurangi dengan meninggikan posisi kepala dalam 24 jam pertama. Atas dasar perbedaan ini, resusitasi cairan dimulai pada anak dengan luka bakar 10% bukan 20% seperti dewasa.

2. Asesmen status cairan Mekanisme kompensasi yang baik pada anak menunjukkan sirkulasi yang terpelihara baik pada kondisi dijumpai kekurangan cairan. Dengan demikian, sangat minim informasi yang dapat menunjukkan gagal sirkulasi hingga dijumpainya tanda syok yang nyata. Pertanda syok dan hipoksia yang umum dijumpai pada dewasa seperti agitasi dan takikardia kurang bermakna karena kondisi ini dipengaruhi faktor lain. Misalnya, takikardia dapat disebabkan stres atau respon hipermetabolik pada luka bakar dan agitasi akibat nyeri atau ansietas [7]. Hipotensi merupakan tanda lanjut dari suatu hipovolemia dan menunjukkan adanya dekompensasi homeostasis: dan bila hal ini terjadi, penderita dengan sangat cepat jatuh ke syok ireversibel. Pertanda yang memberikan informasi ketidakcukupan sirkulasi merupakan indikator yang direkomendasikan pada kursus Advanced Paediatric Life Support (APLS):


-

Takikardia(sesuai usia) Waktu pengisian ulangkapiler >2 detik Suhu perifer (akral)dingin, pucat atau berbintik Disfungsi organ,takipnu, perubahan status mental

3. Produksi urin Parameter yang dapat diandalkan untuk mengukur kecukupan resusitasi adalah produksi urin[3, 7, 11, 14, 18, 20, 35]. Namun, pengukuran ini sangat sulit pada anak karena obstruksi mekanik pada kateter urin yang berdiameter kecil sangat mudah terjadi; dan terkumpulnya beberapa mililiter urin dalam pipa berdiameter besar dapat menyebabkan kekeliruan dalam penilaian. Upayakan produksi urin 1mL / kg / jam sedapat mungkin dalam rentang 0. 5–2mL / kg / jam [3, 7]. Saat penambahan cairan diperlukan, berikan 5 sampai 10 mL/kg dengan cepat. Penambahan cairan juga dapat dilakukan dengan meningkatkan kebutuhan cairan berikutnya hingga 150% dari volume kalkulasi. Kedua metode ini mungkin diperlukan saat status cairan mengalami deplesi. Penilaian berulang tiap 15–30 menit diperlukan untuk menentukan apakah perlu diberikan bolus cairan kembali.

4. Kanula intravena Sebagaimana pada dewasa, pilihan utama pada pemberian cairan adalah kanulasi vena perkutan; di daerah yang tidak terbakar [2]. Di tangan yang ahli, insersi perkutan dengan kateter berdiameter besar pada vena utama seeprti femoralis akan sangat bermanfaat. Bagi yang belum berpengalaman, teknik ini sangat berbahaya dilakukan pada anak–anak. Kanulasi vena perifer perkutan pada daerah terbakar dapat dibenarkan meski lebih sulit [2]. Prosedur vena sksi memerlukan keahlian, lebih lamban dan memisahkan vena secara permanen hingga tidak direkomendasikan lagi. Pemberian cairan intra–osseousrelatif lebih aman [2, 3, 7, 9, 72]dan cepat; kini merupakan teknik pilihan untuk akses vena darurat.

5. Maintenance cairan Pada anak–anak, kebutuhan cairan maintenance berhubungan dengan jumlah cairan resusitasi [3]. Perhitungan kebutuhan cairan maintenance: - 100mL/kg untuk 10kg pertama - 50mL/kg untuk berat badan 10 kg–20kg - 20mL/kg untuk berat badan di atas 20kg


-

5% glukosa dalam0. 45% salin (½normal) [3].

Cairan harus mengandung glukosa yang dapat ditambahkan ke dalam volume cairan resusitasi pada anak–anak dengan berat badannya sampai dengan 30 kg. Tambahan glukosa ini sangat diperlukan karena terjadi penurunan glikogen pada anak dan hipoglikemia terjadi dengan cepat dan khususnya berkaitan dengan hipotermia. Estimasi kadar glukosa darah secara reguler sangat diperlukan selama stabilisasi dan transportasi.

Eskarotomi Eskarotomi ekstremitas pada anak sangat diperlukan sebagaimana pada dewasa [2]. Eskarotomi pada trunkus lebih sering diperlukan pada anak dibandingkan dewasa, karena anak bernapas secara diafragmatik; adanya kekakuan dinding abdomen lebih mungkin menyebabkan keterbatasan volume tidal. Untuk alasan ini, gangguan gerakan gas dapat terjadi pada trunkus yang terbakar tanpa harus melingkar. Karenanya, pada luka bakar di sekitar dada anterior, lateral dan bagian atas abdomen, eskarotomi harus dipertimbangkan. Pada situasi ini, prosedur tambahan disamping prosedur yang dijelaskan pada bab 7 eskarotomi; diperlukan sayatan melintas bagian atas abdomen sejajar tepi iga untuk memungkinkan gerakan dinding abdomen terpisah dari gerakan dinding dada.

Saluran cerna Anak–anak lebih rentan terhadap dilatasi lambung dibandingkan dewasa dan cenderung menelan udara saat menangis. Diperlukan insersi pipa nasogastrik pada fase awal pemeriksaan dan selama transportasi khususnya jika diperlukan evakuasi udara. Namun, tingkat metabolisme anak–anak yang tinggi dan kebutuhan gizi mereka untuk pertumbuhan berarti bahwa mereka memiliki toleransi yang sedikit atas kekurangan gizi. Makanan utama yang dini harus diberikan secepat mungkin saat mereka tiba di rumah sakit karena ini dapat mengurangi hilangnya fungsi usus dan menjaga nutrisi mereka.

Penilaian Progresivitas Luka Penilaiankedalaman luka pada anak sulit dalam 7–10 hari pertama. Bagaimanapun, luka bakar pada anak yang tidak mengalami epitelialisasi dalam 10 hari harus dilakukan skin grafting.

Aspek Emosional Patologi psikososial sebelum traumamerupakan hal umum dijumpai pada luka bakar anak sebagaimana dijumpai padadewasa, namun dengan patologi berbeda. Kekurangan dalam berbagai hal, kurangnya bimbingan sosial dan asuhan menyebabkan kekurangan berlanjut


dalam hal perlindungan anak. Orang tua kerap bermuatan dan terlibat dalam kesibukan masing–masing (masalah sosial dan emosional mereka) dan tak jarang membuat keputusan yang berisiko bagi anaknya. Anak–anak remaja dari keluarga dengan orang tua seperti ini sering melakukan pengambilan keputusan berisiko tanpa peran orang tua. Perubahan emosional dan sosial pada anak sangat berbeda dengan dewasa. Bermain merupakan bagian terpenting pada aktivas normal anak sehari–hari. Sosialisasi dalam kelompok sebaya dan pemisahan merupakan aspek yang sangat penting dalam kehidupan emosional seorang anak. Interaksi antar individu berbeda dan bahasa yang digunakan harus sesuai dengan usia anak bersangkutan. Pentingnya menempatkan kepercayaan dalam hubungan anak, menuntut seorang dewasa jujur terhadap anak mereka setiap saat. Pernyataan tegas dan menakutkan harus dihindari. Bila seorang anak mengalami luka bakar, maka seluruh keluarga mengalami gangguan emosional; merasa bersalah dan saling menyalahkan adalah suatu keadaan yang paling menonjol. Saudara sering sangat terpengaruh. Teman bermain, kelompok sebaya (misalnya sekolah) juga terlibat. Semua aspek pada anak ini harus ditangani dan mendapat perhatian sejak awal. Perubahan emosional jangka panjang seorang anak pasca luka bakar tergantung peran / bantuan emosional seluruh anggota keluarga;berbeda dengan dewasa yang terkonsentrasi pada pasien itu sendiri. Oleh karena itu, dukungan keluarga sangat penting dan dimulai sejak awal.

Cedera bukan kecelakaan Faktor emosional yang sering memberi kontribusi pada penyebab luka bakar pada anak terdiri darisuatu spektrum yang bervariasi dari kurang–pengawasan sesaat, hingga suatu kondisi psikopatologik jangka panjang berupa tindak kekerasan pda anak [7]. Untuk menetapkan cedera bukan kecelakaan ini berada di titik mana pada spektrum adalah sulit. Namun, menentukan bahwa seorang anak “memiliki risiko” di masa depan akan lebih mudah. Di sisi lain, petugas medik memiliki kewajiban hukum (yang bervariasi antar di setiap negara) untuk melaporkan cedera yang dicurigai disengaja. Laporan mengenai hal ini dilakukan oleh unit rujukan[7]. Bila terdapat kecurigaan adanya tindak kekerasan anak, maka rujukan ke unit luka bakar diperlukan. Selama proses transfer ini, hal–hal yang menimbulkan kecurigaan didokumentasikan dengan jelas dan dilaporkan. Tiap rumah sakit harus memiliki protokol dalam penanganan hal ini dengan penekanan komunikasi antar–lembaga untuk memberikan perlindungan anak. Dugaan cedera bukan kecelakaan dapat dikemukakan bila [1, 10]:


-

Penderita tidak segera dibawa ke rumah sakit Informasi pada anamnesis tidak konsisten dengan pemeriksaan fisik Informasi pada anamnesistidak sesuai dengan pola cedera Adanya tanda–tanda trauma lainnya Pola cedera tertentu (misalnya tanda rokok atau luka bakar melepuh pada “sepatu dan kaos kaki”

Harus diingat bahwa tuduhan yang tidak benar atas cedera bukan kecelakaan sangat merusak reputasi keluarga.Tampilan luka bakar yang tidak lazim dapat saja disebabkan oleh kecelakaan dan jangan secara otomatis diasumsikan sebagai sesuatu yang disengaja. Anak–anak ini harus ditransfer ke unit luka bakar anakdan mendapatkan penilaian dengan teknik sebagaimana mestinya. Dalam prakteknya, perbedaan antara ‘kecelakaan’ dan ‘bukan karena kecelakaan’ kurang penting secara medis dibanding sosial. Semua anggota keluarga memerlukan bantuan selama jangka waktu panjang dan yang terpenting adalah hasil akhir jangka panjang yang terbaik secara fungsional.

Kriteria transfer Pada anak–anak, batas kebutuhan untuk prosedur transfer lebih kecil dibandingkan dewasa. Anak dengan luka bakar > 5%, prosedur transfer harus dipertimbangkan. Pada beberapa kasus, alasan prosedur transfer mungkin demikian sederhana, misanya untuk manajemen nyeri, karena pemberian opioid perkontinum tidak tersedia. Pada beberapa kasus lain, prosedur transfer timbul pada kasus bukan kecelakaan yang memerlukan konsultasi dini dengan unit luka bakar dan transfer secepat mungkin. Kriteria lainnya yang berlaku pada dewasa, seperti luka bakar di area khusus (tangan, wajah, kaki dan perineum), dan diketahui atau diduga cedera inhalasi, luka bakar disertai trauma berat lain, luka bakar pada pasien dengan kondisi pre–morbid, juga berlaku pada kasus anak.


Ringkasan Semua prinsip pelayanan luka bakar yang berlaku pada dewasajuga berlaku pada kasus anak. Faktor–faktor yang membedakan fokus pelayanan pada anak adalah: - Perbedaan proporsi tubuh - Perbedaan dinamika cairan - Kulit yang tipis - Perbedaan keperluan psikososial Perbedaan fisikpada anak: - Tendensi hipotermia - Kedalaman luka bakar - Tingginya kebutuhan cairan Latar belakang psikososial dan kebutuhan emosional pada anak yang menderita luka bakar beserta keluarganya berbeda dengan pasien dewasa.


Bab 10

Luka Bakar Listrik Introduksi Luka bakar listrik terdiri dari tiga bagian, yaitu listrik tegangan rendah, tegangan tinggi dan sengatan petir. Setiap kelompok memiliki gambaran tersendiri yang patut dipertimbangkan. Gamabaran umum dari masing–masing adalah panas yang dihasilkan dapat berakibat pada luka bakar. Tabel 10. 1 Luka bakar listrik Tegangan

Kulit

Kedalaman jaringan

Gangguan irama jantung

Tegangan Rendah (<1000V)

Luka masuk dan luka keluar

Jarang mencapai kedalaman

Henti jantung dini atau tidak ada sama sekali

Tegangan Tinggi (>1000V)

Luka bakar percikan apidengan luka masuk dan keluar mencapai seluruh ketebalan kulit (full thickness)

Kerusakan otot dan rabdomiolisisdan sindroma kompartemen,

Aliran melalui toraks dapat menyebabkan kerusakanmiokardial dan gangguan ritmik yang timbul lambat

Sambaran Petir

Luka bakar percikan apisuperfisial atau sedalam dermal. Luka bakar keluar di kaki

Perforasi gendang telinga dan kerusakan kornea

Henti napasdan resusitasiberkepanjangan

Tegangan listrik masuk ke dalam kategori rendah bila berada di bawah 1000 volt. Termasuk suplai listrik satu–fase sebesar 240 volt alternating current (AC) dengan 50 siklus (50Hz) per detik yang digunakan untuk perumahan di Australia dan Selandia Baru. Pasokan listrik pada industri umumnya tiga fase dengan tegangan 415 volt. Kecelakaan listrik tegangan rendah dapat terjadi pula pada arus satu arah (direct current, DC) yang digunakan pada industri pelapisan logam, purifikasi elektrolit dan beberapa sistem transportasi. Aki mobil umumnya menghasilkan arus dengan tegangan 12 volt yang menyebabkan luka bakar ketika terjadi sirkuit / hubungan pendek dengan logam (misal, cincin


dan perhiasan). Prosedur hemostasis menggunakan diatermi merupakan penerapan efek kauter direct current (DC). Tegangan listrik masuk ke dalam kategori tinggi bila berada di atas 1000 volt.[10] Arus sebesar 11000 atau 33000 volt dalam kabel transmisi tegangan tinggi merupakan arus yang paling umum digunakan. Tegangan lebih tinggi dijumpai pada pembangkit tenaga listrik maupun gardu listrik. Sambaran petir merupakan tegangan tinggi yang ekstrim, amplitude (amper) yang tinggi, aliran listrik DC yang menghasilkan durasi sangat pendek dan dapat menyebabkan pola cedera yang tidak lazim.

Patofisiologi Kerusakan jaringan pada luka bakar listrik terjadi karena dihasilkannya panas akibat adanya: - Resistensi jaringan - Durasi kontak - Besar arus listrik [86]. Setiap jaringan menunjukkan perbedaan karakteristik resistensi listrik sesuai dengan isi elektrolitnya. Dalam rangka penurunan resistensi, berbagai jaringan terdaftar dibawah ini -

Tulang Kulit Lemak Saraf Otot Darah dan cairan tubuh.

Resistensi kulit bervariasi berdasarkan ketebalan, serta basah atau keringnya kulit. Kulit tebal dan kering memiliki resistensi yang tinggi dibandingkan kulit yang tipis dan lembab (misal berkeringat). Tingginya suhu yang dihasilkan konduktor tergantung pada panas yang melampaui konduktor melalui proses konduksi, konveksi dan radiasi. Listrik melampaui tulang sebagai suatu konduktor buruk menyebabkan kenaikan suhu bermakna karena panas diserap. Kenaikan suhu tulang berkelanjutan bahkan setelah arus listrik berhenti, menyebabkan kerusakan sekunder. Fenomena ini dikenal sebagai the joule effect. Karena kedalaman tulang, panas dilepas perlahan dan menyebabkan kerusakan pada periosteum, otot dan saraf di sekitarnya. Tingginya arus pada titik kontak dan resistensi kulit yang tinggi menyebabkan panas tinggi yang menyebabkan kulit hangus. Pada cedera tegangan tinggi, terjadi proses arcing (locatan arus listrik, red.) pada sendi seperti pergelangan tangan dan siku, menyebabkan gosongnya kulit


dan luka dalam. Kulit hangus dengan luka serupa merupakan luka keluar yang terdapat di kaki atau telapak tangan karena resistensi tinggi dan ketebalan kulit yang menghasilkan panas tinggi.

Jenis luka Pada listrik dengan arus tegangan rendah, terjadi kerusakan lokal yang signifikan di tempat kontak, luka masuk dan luka keluar [10, 87] mungkin dijumpai kelainan jantung tetapi tidak terjadi kerusakan jaringan dalam. Pada arus listrik di perumahan (50 Hz) terjadi kejang otot atau tetani dan menyebabkan penderita tidak dapat lepas dari kontak dengan benda beraliran listrik [2][23]. Pada arus tegangan tinggi ada dua kemungkinan mekanisme cedera. Pertama, luka akibat letupan listrik yang menimbulkan bunga api. Pada luka jenis ini, dijumpai luka bakar di kulit tanpa kerusakan jaringan dalam karena arus tidak melalui tubuh penderita. Adanya letupan menyebabkan pakaian terbakar dan mengakibatkan luka bakar kulit tanpa luka kontak, luka masuk dan luka keluar[10]. Transmisi arus tegangan tinggi umumnya menghasilkan kerusakan jaringan di titik kontak berupa kerusakan seluruh ketebalan kulit (full thickness) dan kerusakan jaringan dalam [23]. Kerusakan organ tubuh adalah hal yang tidak umum, lebih mungkin disenbabkan karena jatuh dari ketunggian (tiang atau menara listrik). Kerusakan otot terjadi dibawah kulit yang kadang terlihat normal mungkin terjadi sangat hebat melibatkan keseluruhan kompartemen di ekstremitas [88]. Pembengkakan ekstremitas akibat kerusakan otot menyebabkan kondisi menyerupai crushed syndrome. Ekstremitas tegang pada perabaan, disertai gejalanyeri hebat, dan kondisi ini menyebabkan penurunan sirkulasi ke distal, hilangnya pulsasi. Kondisi ini memerlukan fasiotomi dan mungkin diperlukan anestesi umum. Kerusakan dan nekrosis otot diikuti pelepasan mioglobin dari sel otot ke sirkulasi. Pigmen ini bersama hemoglobin yang berasal dari hemolisis sel darah merah menyebabkan gangguan ginjal karena kedua jenis haemochromogens tersebut mengendap di tubulus ginjal diikuti gagal ginjal akut [10]. Sambaran petir diakibatkan tegangan yang sangat tinggi, dengan amplitudo (ampere) tinggi dan sirkuit / hubungan pendek arus satu arah (direct current, DC). Bentuk cedera ini kurang populer di Australia dan Selandia Baru. Tiap tahun 5 sampai 10 orang Australia, 90 di Amerika Serikat, 10,000 orang di dunia mengalami kematian yang disebabkan oleh sambaran petir. Pola cederanya sangat bervariasi [2]. Sengatan / sambaran langsung mengenai korban memiliki risiko kematian tinggi. Yang umum terjadi adalah sambaran dalam bentuk kilatan atau


percikan, ketika petir menyambar sebuah obyek dengan resistensi tinggi seperti pohon. Sengatan listrik selanjutnya mengenai tungkai penderita setelah sampai di tanah. Kekhasannya adalah arus mengalir di permukaan tubuh penderita menyebabkan luka bakar superfisial hingga ketebalan dermis. Juga dijumpai luka bakar keluar di tungkai atau kaki. Durasi singkat sambaran petir umumnya tidak diikuti kerusakan jaringan dalam yang nyatanamun kerap terjadi hentinapas henti jantung [2]. Gangguan napas terjadi awal akibat dari dampak arus pada pada pusat napas di medula. Kondisi ini biasanya bersifat reversibel dan memerlukan tindakan resusitasi yang panjang. Organ lain yang dapat mengalami kerusakan adalah telinga. Perforasi membran timpani mungkin dijumpai akibat ledakan dan harus diperiksa [2]. Kerusakan kornea juga dapat terjadi dan ini mungkin dalam bentuk akut atau sekuel jangka panjang. Sambaran petir juga dapat mengakibatkan kerusakan kulit yang tidak biasa, penampilan arborescent atausplashedyang disebut Lichtenberg flowers dan patognomonik suatu sambaran petir [2].

Manajemen Prosedur penyelamatan korban kecelakaan listrik menghadapkan penyelamat pada risiko nasib yang sama[24]. Hal yang harus diperhatikan adalah, pertama putuskan hubungan dengan sumber arus listrik atau singkirkan kabel beraliran dari korban [24]. Jika hal ini tidak dimungkinkan, pindahkan korban dari sumber arus listrik menggunakan sebuah non– konduktor. Harus diingat bahwa listrik bahwa tegangan tinggi akan dialirkan melalui udara; tegangan listrik 1.000 volt hanya akan menimbulkan loncatan beberapa milimeter saja, 5.000 volt akan menyeberang sampai satu sentimeter, dan 40.000 volt hingga 13 sentimeter. Setelah terbebas dari arus listrik, survei primer dapat dilakukan pada tiap cedera luka bakar. Jalan napas harus bebas dan tulang belakang servikal terlindungi. Henti napas dapat terjadi dampak arus listrik pada medula, dan henti jantung akibat efek arus listrik pada miokardium. Sehingga resusitasi jantung–paru sangat penting pada tatalaksana korban luka bakar listrik. Intubasi endotrakea mungkin diindikasikan untuk mempertahankan patensi jalan napas. Proteksi tulang belakang servikal sangat penting karena trauma daerah ini sangat mungkin terjadi bersamaan dengan luka bakar listrik [24]. Kejang otot hebat dapat terjadi pada arus listrik di rumah tangga dan menyebabkan fraktur tulang. Petugas listrik mungkin jatuh dari ketinggian seperti tiang, menara atau peralatan tinggi lainnya). Kemungkinan fraktur pada tulang belakang servikal harus disingkirkan melalui pemeriksaan pencitraan dengan metode khusus (penggunaan meja khusus untuk foto tulang belakang). Sebelum menanggalkan imobilisan (hard collar) saat pemeriksaan radiologik, gunakan kantong


pasir atau fiksasi kepala dengan cara memegangnya. Gunakan papan tulang belakang atau kantong pasir untuk melindungi tulang belakang torasik dan lumbal sampai kemungkinan fraktur di daerah ini tersingkirkan.

Riwayat trauma Selesai melakukansurvei primer, dapatkan riwayat trauma baik dengan melakukan anamnesis pada pasien, saksi atau paramedis. - Bagaimana terjadinya kecelakaan? - Kapan terjadinya? - Apakah pasien pinsan, bila ya, berapa lama? - Apakah terjadi amnesia pada saat itu? - Apakah terdapat trauma yang terkait? - Apakah terjadi serangan jantung atau apakah terdapat gangguan aritmia?

Survei Sekunder -

Pertama, lepaskan semua pakaian dan barang–barang seperti jam tangan dan perhiasan. Lakukan pemeriksaan luka masuk atau kontak luka dengan perhatian khusus pada kulit kepala, tangan dan kaki. Memperkirakan total area luka bakar dan kedalaman luka bakar tersebut. Lakukan pemeriksaan neurologik dengan fokus khusus pada susunan saraf pusat dan perifer. Dokumentasikan semua temuan klinis.

Resusitasi Jika pada saat penyelesaian survei sekunder, cedera yang ada memerlukan resusitasi cairan, gunakan dua jalur intravena kanula besar seperti pada luka bakar luas lainnya. Kebutuhan cairan pada luka bakar listrik cenderung volumenya lebih besar dibandingkan jumlah yang diantisipasi pada luka bakar kulit saja. Kerusakan otot yang tidak tampak pada ekstremitas mengakibatkan kehilangan cairan yang tidak diperhitungkan menggunakan rumus standar. Pada pasien dengan kerusakan jaringan yang dalam, haemochromogenuria harus diantisipasi [2, 23]. Kateter urin harus dimasukkan untuk deteksi gejala dini perubahan warna urin dan untuk memantau produksi urin. Jika terlihat pigmen pada urin, laju infus cairan harus ditingkatkan guna mempertahankan produksi urin 75–100 mL/jam bagi dewasa dan 2 mL/kg/jam pada anak–anak.


Bila produksi urin tidak tercapai dengan pemberian cairan yang sesuai, tambahkan 12.5 g mannitol ke setiap liter cairan untuk tujuan dieresis osmotik. Alkalisasi urin [23] dengan penambahan natrium bikarbonat secara tradisional telah digunakan untuk meningkatkan larutan haemochromogens pada urin. Namun rasionalnya kini dipertanyakan. Jika diperlukan penggantian cairan yang lebih dari sederhana untuk membersihkan pigmen urin, diusulkan untuk meminta saran ke unit luka bakar. Bila haemochromogens tidak dijumpai lagi di urine, jumlah cairan harus dikurangi hingga produksi urine dapat dipertahankan 30–50 mL/jam pada dewasa, atau pada anak–anak < 30kg 1 mL/kg/jam.

Gangguan aritimia Konduksi arus listrik melalui dada dapat menyebabkan gangguan ritmik jantung mulai dari aritmia yang bersifat temporer hingga henti jantung; meskipun hal ini jarang terjadi pada cedera tegangan listrik rendah (<1000V). Penderita dengan sengatan listrik mungkin memerlukan pemantauan EKG selama 24 jam; jika mereka terpapar pada tegangan tinggi, pingsan atau menunjukkan EKG abnormal saat datang di instalasi gawat darurat (23). Aritmia mungkin terjadi jika pasien memiliki gangguan miokardium yang sudah ada sebelumnya dan diperburuk oleh adanya aliran listrik.

Penilaian Sirkulasi Perifer Penilaian sirkulasi perifer harus dilakukan setiap jam: - Warna kulit - Edema - Pengisian ulang kapiler - Pulsasi perifer - Sensasi kulit Jika terdapat luka masuk atau keluar yang ekstrim, kemungkinan edema di bawah fasia harus diantisipasi. Edema ini sangat mungkin menyebabkan peningkatan tekanan kompartemen pada yang menyebabkan gangguan sirkulasi [2]. Peningkatan tekanan kompartemen pada otot menyebabkan nyeri hebat. Ekstremitas tegang pada palpasi dan hilangnya pulsasi perifer. Dalam keadaan ini, diperlukan tindakan fasiotomi. Fasiotomi


Berbeda dengan eskarotomi yang dilakukan untuk melepaskan jeratan eskar, fasiotomi dilakukan untuk melepas tekanan di suatu kompartemen untuk memperbaiki perfusi ke otot. Cara terbaik dalam melakukan fasiotomi adalah dalam anestesia umum dan dilakukan di ruang steril. Kehilangan darah mungkin dapat diperkirakan, dan fasilitas hemostasis seperti diatermi dan ligasi harus tersedia. Pendarahan yang timbulnya perlahan dan lambat dapat terajdi setelah penderita teresusitasi. Sayatan fasiotomi harus dibalut dengan perban atau kasa pembalut yangn tidak menekan. Sangat penting untuk memberikan resusitasi yang baik kepada pasien sebelum fasiotomi dilaksanakan sehingga haemochromogens terlepas dari otot i yang baru mengalami perbaikan perfus dengan cepat terbilas dan dibuang melalui ginjal. Perlu melakukan konsultasi dengan unit luka bakar untuk pemberian mannitol sebelum fasiotomi sebagai prosedur profilaksis.

1. Ekstremitas atas Otot–otot lengan bawah sangat rentan terhadap iskemia dan sindroma kompartemen. Tekanan ini dibebaskan dengan melakukan sayatan panjang melintang garis mid–medial dan mid–lateral pada lengan, melintas di atas siku dan pergelangan tangan. Sayatan dibuat pada kulit dan lemak subkutis selanjutnya membuka fasia dalam; lakukan sayatan pada fasia. Perhatian khusus untuk melindungi saraf ulnaris di daerah siku. Pendarahan mungkin terjadi dengan cepat dan memerlukan pengendalian hemostasis menggunakan diatermi atau ligasi. Jika pasien mengalami hipotensi saat prosedur dilakukan, maka pendarahan biasanya tertunda. Pembebasan carpal tunnel mungkin diperlukan pada luka bakar di tangan. Sebelum melanjutkan prosedur ini, lakukan konsultasi dengan unit luka bakar.

2. Ekstremitas bawah Ada empat kompartemen ekstremitas bawah yang dipengaruhi adanya edema subfasia yang menyebabkan sindroma kompartemen [2]. Masing–masing kompartemen ini memerlukan sayatan tersendiri. Empat buah sayatan dapat dilakukan melalui dua sayatan di kulit. Sayatan lateral dilakukan di atas fibula, memanjang dari kaput hingga tiga perempat panjangn fibula. Hati–hati jangan sampai mencederai saraf peroneal yang meliwati kolum fibula. Septum intermuskular memisahkan kompartemen anterior dan lateral disayat sepanjang sayatan kulit. Sayatan medial dimulai dari proksimal, berjarak satu jari di bawah margo subkutan tibia dan dilanjutkan hingga maleolus medialis. Sayatan pada kulit, lemak subkutis dan fasia dengan hati–hati agar tidak mencederai vena dan saraf safena. Fasia diretraksi, selanjutnya kompartemen posterior dapat diidentifikasi dan lakukan sayatan dekompresi sepanjang sayatan kulit.


Sebagaimana halnya dengan lengan, fasiotomi ekstremitas bawah terbaik dilakukan dalam anestesia umum dan dilakukan di ruang steril. Pendarahan mungkin terjadi dengan cepat dan memerlukan pengendalian hemostasis menggunakan diatermi atau ligasi. Sekali lagi, Pendarahan yang timbulnya perlahan dan lambat dapat terajdi setelah penderita teresusitasi. Sayatan fasiotomi harus dibalut dengan perban atau kasa pembalut yangn tidak menekan.

Manajemen luka Prinsip–prinsip umum luka bakar berlaku untuk luka bakar listrik dan telah dijelaskan sebelumnya. Banyaknya otot non vital mengharuskan manajemen luka bakar yang baik dan pemberian antibiotika topikal menjadi keharusan untuk pencegahan infeksi.

Luka bakar listrik pada anak Mayoritas luka bakar listrik pada anak disebabkan tegangan rendah yang terjadi di rumah tangga [65, 86]. Isolasi peralatan listrik dan kabel yang rusak atau menempatkan benda logan di titik sumber listrik merupakan penyebab utama luka bakar listrik pada anak–anak [65]. Anak kecil cenderung mengambil dan mengisap kabel listrik dan menyebabkan luka bakar dalam di sekitar mulut; difasilitasi air liur yang membasahi kabel listrik [86, 89]. Luka bakar pada jari dan tangan umumnya terjadi pada anak yang sudah lebih besar, teknisi yang bekerja memperbaiki peralatan rumah tangga dalam keadaan menyala. Pada kebanyakan kejadian, hal ini dapat dicegah menggunakan pemutus sirkuit pengaman. Sebagian besar listrik tegangan rendah menyebabkan luka seluruh ketebalan berukuran kecil yang memerlukan eksisi dan penutupan, skin grafting atau perbaikan lain dan harus dirujuk ke unit pelayanan luka bakar untuk mendapat pelayanan yang memadai. Kejadian pada tegangan rendah rumah tangga biasanya tidak menyebabkan kerusakan jaringan otot yang besar pada ekstremitas. Bagaimanapun, pengawasan EKG selama 24 jam mungkin diperlukan jika mereka menderita luka bakar yang disebabkan oleh listrik tegangan tinggi, pingsan atau menunjukkan EKG abnormal saat masuk rumah sakit sebagaimana dijelaskan sebelumnya (23).


Ringkasan -

-

Hindari cedera bagi mereka yang akan memberikan bantuan Atasi serangan jantung dan pernapassan Periksa dan kelola trauma yang terkait. Pola cedera terbagi dalam tiga bagian: tegangan tinggi, tegangan rendah dan sambaran petir atau halilintar. Rumus standar resusitasi luka bakar mungkin tidak sama. Haemochromogenuria merupakan hal yang umum pada cedera tegangan tinggi dan memerlukan tindakan khusus untuk mengupayakan produksi urine 75–100 mL/jam bagi dewasa, 2 mL/kg/jam pada anak–anak, setelah urine dijernihkan. Cedera tegangan tinggi pada ekstremitas mungkin memerlukan fasiotomi. Berdasarkan kriteria rujukan dari ANZBA, semua luka bakar listrik harus dibawa ke rumah sakit untuk mendapat pelayanan kesehatan yang memadai.


Bab11

Luka Bakar Kimia Introduksi Lebih dari 25,000 produk yang dapat menyebabkan luka bakar kimia saat ini dipasarkan untuk digunakan dalam bidang industri, agrikultur, kepentingan militer dan rumah tangga. Di Amerika Serikat, lebih dari 3,000 kematian terkait langsung dengan cedera kulit kimia atau saluran cerna tercatat setiap tahunnya dengan estimasi penderita 60,000 memerlukan pelayanan medis untuk luka bakar kimia. Sebagai bagian tubuh yang rentan cedera dan bagian tubuh yang berhubungan langsung dengan bahan–bahan berbahaya, tangan dan bagian atas tubuh merupakanarea yang paling sering mengalami cedera.

Proteksi Sangat penting bahwa semua petugas yang memberi pertolongan pertama menyadari kepentingan menjaga diri dari kontaminasi, misalnya menggunakan sarung tangan, masker pelindung wajah. Semua pakaian terkontaminasi harus dilepas secepat mungkin dan ditempatkan dalam wadah pelindung untuk pembuangan selanjutnya.

Etiologi dan Klasifikasi Kecelakaan di laboratorium, penggunaan zat kimiawi dalam industri, penggunaan untuk tujuan medis dan tindak kekerasan menyebabkan sebagian besar luka bakar kimia pada populasi sipil. Bahan kimia yang biasa digunakan dan menyebabkan luka bakar antara lain:

1. Keperluan industri Alkali: Natrium, kalium, amonium, lithium, barium dan kalsium hidroksida (sabun deterjen, pembersih dren, dan penghilang cat). Asam: pikrat, sulfasalisilat, tannic, trichloroacetic, cresylic, asetat, format, klorida dan flourida (kaca dan elektronik).

2. Keperluan Rumah Tangga


Alkali: pembersih dren, penghilang cat, reagen tablet tes glukosa urin. Fenol: deodoran, pembersih, disinfektan. Natrium hipoklorat: disinfektan, pemutih, deodoran. Asam sulfat: pembersih toilet Fosfor: kembang api, insektida, pupuk

3.

Keperluan Militer

Fosfor merah atau putih Vesicants

Patofisiologi Kerusakan jaringan merupakan dampak langsung paparan bahan kimia apapun tergantung pada: - Kekuatan atau konsentrasi agen - Kuantitas agen - Cara dan lamanya kontak dengan kulit /kontak mukosa - Daya penetrasi ke dalam jaringan - Mekanisme kerja Perbedaan utama antara luka bakar kimia dan termal adalah lamanya waktu dimana kerusakan jaringan berlanjut sejak agen kimia menyebabkan kerusakan yang progresif hingga dinonaktifkan menggunakan bahan penetral atau pengeceran menggunakan air. Estimasi kedalaman luka bakar dengan penilaian klinis setelah luka bakar mungkin sulit dalam beberapa hari pertama pasca cedera. Semua agen di atas menyebabkan cedera sel melalui berbagai jenis reaksi kimia. Secara umum dapat dikatakan sebagai berikut: - Asam menghasilkan nekrosis koagulasi. - Alkali menghasilkan nekrosis likuifaktif. - Vesicants menyebabkan nekrosis iskemia dan anoksia (dilepaskannya amin dari jaringan yang menyebabkan terbentuknya bula). - Kesemuanya menyebabkan koagulasi protein melalui proses oksidasi, korosif atau penggaraman protein. Gambaran penting akibat toksisitas sistemik beberapa zat kimia. - Hipokalsemia: oksalat, asam flourida dan fosfor yang terbakar.


-

Gangguan / kerusakan sel hati dan ginjal: tannic, formic dan asam pikrat, fosfor dan minyak bumi Cedera Inhalasi: asam kuat atau amonia. Methemoglobinemia dan hemolisis masif: kresol Perforasi septum nasi: asam kromat

Pertolongan Pertama Tanggalkan semua pakaian yang terkontaminasi bahan kimia yang kering [24]. Alirkan air dengan konstan adalah pertolongan utama pada luka bakar kimia [2] (kecuali unsur natrium, kalium dan lithium). Untuk mendapatkan efek terbaik, tindakan ini dimulai dalam waktu 10 menit setelah terjadinya kontak.

Agen yang Aspesifik Beberapa zat kimia non–espesifik semacam diphoterine saat ini tersedia dan bermanfaat pada kebanyakan luka bakar kimia

1. Luka Bakar karena asam -

Nyeri hebat Penampilannya bervariasi mulai dari eritema (dangkal) hingga eskar hitam (dalam) Irigasi menggunakan air Diatasi dengan tindakan pembedahan seperti pada luka bakar termal

Asam Flourida -

Sangat korosif, asam non–organik dari unsur fluorine: luas permukaan tubuh 2% dapat berakibat fatal

Mekanisme kerusakan a) Ion hidrogen menyebabkan luka bakar asam pada kulit yang khas, yang dapat diminimalisasi dengan air. b) Ion flourida yang bebas masuk melalui kulit rusak akan mengikat ion kalsium. Hal ini menyebabkan nekrosis jaringan yang lunak dan hipokalsemia berat sehingga mobilisasi ion kalsium dari tulang tidak memadai untuk mengatasinya. Derajat kerusakan tergantung pada konsentrasi asam, tingkat dan durasi kontak [90]. c) Aritmia mungkin terjadi akibat hipokalsemia dan hipomagnesemia.


Tatalaksana [90] -

Aliran air [10] Potong kuku Inaktivasi ion fluoride bebas racun dan mengubah garam tidak larut dengan: a) Jel untuk luka bakar mengandung kalsium glukonat [10, 90] (dengan dimetil sulfoksid 10% [DMSO]). b) Injeksi kalsium glukonat 10% topical (injeksi multipel 0.1–0.2 mL menggunakan jarum 30G di jaringan luka bakar). Jumlah dan frekuensi injeksi dipantau dengan menilai respon nyeri. c) Infus kalsium glukonat intra–arterial. d) Infus kalsium glukonat intravena ischaemic retrograde (Biers block). e) Kadang diperlukan eksisi dini.

2. Luka Bakar Alkali -

-

Paling umum terjadi di rumah Kerusakan jaringan tidak secepat zat asam, namun kerusakan jaringan terjadi dalam kurun waktu panjang karena terjadi likuifaksi (pencairan) yang menyebabkan kerusakan lebih dalam [10]. Irigasi lebih lama dibanding dengan asam (kurang lebih 1 jam) Untuk luka bakar dalam diperlukan operasi

Luka Bakar Semen -

Semen basah mengandung zat kaustik dengan pH 12. 9 Nyeri dan luka bakar timbul lambat (dalam beberapa jam) Irigasi dalam waktu lama diperlukan

Luka Bakar Fosfor -

Umumnya terjadi pada tentara Fosfor putih terbakar spontan saat terpapar pada udara Teroksidasi menjadi fosfor pentoksida Diredam dengan air Partikel fosfor yang tertanam di kulit akan terus membakar Pengobatan a) Pemberian air dalam jumlah yang banyak b) Singkirkan partikel yang tampak c) Berikan tembaga sulfat (akan terbentuk tembaga fosfid hitam yang memfasilitasi terlepasnya partikel fosfor) d) Kematian berhubungan dengan efek sistemik dari hipotensi dan tubular nekrosis akut


Bensin -

Campuran alkana, sikloalkana dan hidrokarbon yang kompleks. Komponen hidrokarbon merusak sel endotel yang menyebabkan kerusakan paru–paru, hati, limpa dan ginjal setelah kontak dengan kulit mencakup area luas. Bensin melarutkan senyawa lipid dengan cepat dan menyebabkan peningkatan permeabilitas membran diikuti kehilangan cairan. Ada dua macam luka bakar bensin: a) Terbakar. Kebutuhan cairan sering lebih tinggi dari luka bakar lainnya. Luka bakar cenderung menjadi lebih luas, memerlukan operasi dan perawatan di rumah sakit lebih lama. b) Terendam atau kontak kulit yang luas berdampak pada luka bakar dengan seluruh ketebalan kulit, kadang disertai kerusakan sistemik termasuk paru–paru.

Aspal -

Produk penyulingan minyak bumi. Dilarutkan dengan produk minyak lainnya (minyak tanah, parafin medis, parafin lilin) dan minyak sayuran. Untuk tujuan transportasi dan penggunaan, suhu mencapai 190°C (normal 150°C). Cair pada suhu 150°C, dan semisolid pada suhu atmosfir. Luka bakar disebabkan bentuk cair yang panas, bukan efek racun dari aspal. Diobati dengan mendinginkan aspal menggunakan air dalam jumlah besar. Lepaskan pakaian namun jangan mencoba untuk melepaskan aspal melekat. Lepaskan aspal menggunakan minyak parafin (dapat ditambahkan minyak tanah 1/3 nya).

Ter -

Produk sisa industri gas batubara. Tidak umum di Australasia. Mengandung bahan kimia kompleks termasuk fenol, hidrokarbon dll menyebabkan toksisitas berganda. Luka bakar disebabkan panas dan toksisitas fenol. Hanya larut dalam cairan aromatik (misalnya benzene, toluene, xylene) bukan bensin atau minyak sayuran. Diatasi dengan pendingin dan lepaskan menggunakan toluene.


Komplikasi Anatomik Khusus Gastrointestinal ·

Kecelakaan menelan zat korosif yang digunakan untuk keperluan rumah tangga biasanya terjadi pada anak–anak. 1/3 dari penderita dengan luka bakar intra–oral terbukti diikuti kerusakans esofagus. Gejala yang tidak khas dan untuk diagnosis pasti memerlukan pemeriksaan endoskopik. Panendoskopi yang melalui area cedera diperlukan untuk memastikan luas kerusakan. Foto toraks dan abdomen; CT scan toraks–abdomen menunjukkan kerusakan ekstra– lumen. Eksplorasi bedah dan debriment jaringan nekrotik mungkin diperlukan. Steroid tidak terbukti manfaatnya. Terjadinya striktur esofagus merupakan hal yang umum. Diperlukan tindakan endoskopik dan operasi untuk mengatasi striktur.

Mata -

Luka bakar kimia pada mata diikuti tingginya insiden kerusakan mata residual. Tanda–tanda fisik termasuk blefarospasme, keluarnya air mata berlebihan dan konjungtivitis Pembengkakan cepat epitel kornea, kekeruhan lapis anterior stroma dan terlepasnya sel di kambra anterior. Atasi dengan pemberian air dalam jumlah besar. Diphoterine sangat berguna. Perawatan di rumah sakit lama (48jam). Antibiotika topikal untuk pencegahan infeksi sekunder. Perforasi dan ulserasi kornea, terbentuknya katarak, glaukoma sekunder, iridosiklitis dan simblefaron adalah beberapa komplikasi lanjut.

Saluran Trakeobronkus -

Luka bakar langsung pada trakea dan bronkus jarang, terjadi setelah menghirup agen kaustik atau terpapar gas kimia (misalnya amonia). Gangguan pernapassan atau hipoksia membutuhkan pemeriksaan bronkoskopi fibre–optic Bronkodilator dan steroid mengurangi bronkopasme serta peradangan. Mungkin diperlukan dukungan ventilator mekanik temporer. Dapat terjadi bronkiektasis sebagai komplikasi akhir. Diperlukan pemeriksaan lanjutan untuk fungsi paru–paru dan foto toraks.


Ringkasan -

-

Zat penyebab menyebabkan luka bakar kimia umum di jumpai di lingkungan. Semua luka bakar kimia memerlukan pemberian air dalam jumlah besar. Luka bakar asam hidrofluorat memerlukan netralisasi menggunakan kalsium glukonat. Toksisitas sistemik emrupakan hal umum pasca paparan terhadap asam hidroflourat, bensin atau cresol. Luka bakar aspal dan alkali memerlukan pemberian air dengan waktu yang lama dibanding luka bakar kimia lainnya. Luka bakar kimia pada mata juga memerlukan pemberian air dan selanjutnya rujukan ke pusat pelayanan luka bakar.


Bab 12

Manajemen Penderita Luka Bakar setelah 24 Jam Pertama Introduksi Di Australia dan Selandia Baru, ada kalanya seorang penderita luka bakar tidak dapat segera dirujuk ke unit luka bakar karena kesulitan transportasi dan akses. Bab ini dirancang untuk membantu dokter dan perawat yang ditempatkan dalam situasi yang mengharuskan perawatan berkelanjutan bagi penderita yang memenuhi kriteria ANZBA untuk transfer, namun tidak mungkin dievakuasi dalam waktu 24 jam. Perawatan penderita lebih dari 24 jam diperlukan, namun harus disadari bahwa kegagalan melakukan transfer penderita ke unit luka bakar sedini mungkin akan berdampak buruk pada hasil akhir. Adalah penting menyembuhkan luka bakar penderita secepat mungkin pasca cedera. Pada luka bakar yang tebal dan dalam, perlu dilakukan eksisi dini dan pencangkokan kulit. Waktu yang optimal untuk prosedur ini adalah antara tiga dan lima hari pasca cedera. Keterlambatan dalam melakukan operasi ini memungkinkan timbulnya infeksi yang diikuti tingginya morbiditas dan mortalitas. Meski tidak dimungkinkan untuk melakukan evakuasi penderita ke unit luka bakar dalam waktu 24 jam pasca cedera, perlu ditekankan bahwa setiap upaya harus tetap dilakukan untuk mentransfer penderita sesegera mungkin. Prinsip–prinsip yang diuraikan dalam bab ini tidak dilihat sebagai sebuah pembenaran penanganan penderita luka bakar kritis di pusat pelayanan terpencil. Pedoman ini dirancang untuk membantu untuk menjaga penderita luka bakar kritis berada pada kondisi optimal, sehingga bila transfer dimungkinkan, maka tatalaksana definitif dapat dilanjutkan sebagai bagian dari kasus biasa. Pedoman ini dirancang sebagai suplemen dari kontak telepon, email dan fax dengan unit luka bakar. Prinsip–prinsip berikut adalah petunjuk yang dirancang untuk melengkapi bantuan dan saran lebih lanjut yang mungkin dapat dilakukan di pusat pelayanan terpencil. Personil dengan perawatan intensif dengan latar belakang anestesi atau trauma mungkin ada ketimbang staf unit luka bakar, dan keahlian mereka dapat dimanfaatkan dalam keadaan darurat.

a. Topangan respirasi


Bermanfaat bagi penderita luka bakar kritis untuk terus bernapas dengan aliran oksigen 15 liter per menit sampai kadar COHb normal, kemudian titrasi untuk mempertahankan PaO2 yang cukup untuk oksigenasi jaringan yang terbakar. Penilaian berulang harus dilakukan, terutama pada luka bakar di kepala dan leher, riwayat atau adanya kecurigaan cedera inhalasi, seperti yang diuraikan pada Bab 2, intubasi endotrakea mungkin diperlukan pada fase ini. Tenaga medis berperan melanjutkan perawatan penderita yang terintubasi yang tidak mungkin ditransfer karena alasan logistik. Beberapa pemeriksaan, termasuk analisis gas darah dan foto toraks bermanfaat dalam membantu proses pemantauan. Selama fasse ini, mungkin diperlukan topangan respirasi non–invasif, termasuk penghisapan sekret berkala dan pengaturan posisi kepala dan leher penderita. Perasat chin lift dan pengamanan jalan napas menggunakan oro-pharyngeal airway atau naso-pharyngeal airway direkomendasikan. Bila dengan metode ini pengamanan jalan napas tidak berhasil, mungkin diperlukan intubasi endotrakea dan harus dilakukan secepatnya, sebelum pembengkakan faring semakin berat yang akan menyulitkan prosedur intubasi.

1.

Intubasi endotrakea

Pemasangan pipa endotrakea yang benar menjamin patensi dan terlindunginya jalan napas, memungkinkan pemberian oksigen efektif, mempermudah pembersihan sekret, memungkinkan pemberian analgesia dosis besar, pemberian sedasi yang aman dan memungkinkan diterapkannya ventilasi mekanis. Pada kasus luka bakar dengan cedera inhalasi, prosedur intubasi semakin sulit karena pembengkakan mukosa jalan napas membengkak dan hipoksia semakin berat. Karenanya prosedur intubasi dipertimbangkan lebih awal. Prosedur intubasi endotrakea secara teknis sulit pada luka bakar jalan napas bagian atas disertai edema dan cedera di daerah wajah. Komplikasi ter penting adalah kegagalan teknis yang dalam hal ini sering berakhir fatal. Masalah jangka pendek lainnya termasuk penempatan pipa endobronkea yang salah, trauma pada jalan napas bagian atas dan obstruksi pipa oleh sekret serta tertekuknya pipa. Setiap penderita luka bakar yang memerlukan intubasi membutuhkan perawatan definitif oleh spesialis di rumah sakit besar, sebaiknya sebuah rumah sakit yang memiliki unit luka bakar khusus.

2.

Indikasi dan Teknik

Intubasi dan ventilasi harus dipertimbangkan pada penderita dengan distres pernapasan yang jelas secara klinis, hipoksia berat atau hiperkarbia, defek neurologik disertai gangguan refleks pernapasan atau upaya bernapas, luka dada yang parah, atau obstruksi jalan napas bagian atas akibat pembengkakan karenakan cedera inhalasi. Kadang indikasi ventilasi mekanik didasari


suatu alasan logis, seperti keamanan transportasi atau memfasilitasi beberapa prosedur terapeutik maupun diagnostik. Rute oro–trakea merupakan yang paling sederhana, namun intubasi naso–trakeal terkadang berhasil pada situasi dimana intubasi oral tidak dimungkinkan. Bila tidak dapat dilakukan dengan cepat atau dijumpai obstruksi jalan napas, prosedur kricotiroidotomi merupakan satu– satunya alternatif. Hal ini relatif mudah dan harus dilakukan tanpa keraguan. Zat induksi anestesi atau relaksan otot akan mempermudah prosedur intubasi, namun hanya dapat digunakan oleh mereka yang memiliki kepercayaan diri tinggi dan terlatih. Semua zat ini memiliki efek samping yang signifikandan memiliki potensi terjadinya penurunan status, penderita yang mulanya dihadapkan pada gangguan respirasi namun jalan napas baik dengan ventilasi mencukupi, menjadi penderita yang tidak dapat diintubasi atau diventilasi. Setelah prosedur intubasi, dilakukan penilaian posisi pipa dilakukan secara klinis dan radiologis.

3.

Fisiologi

Transportasi oksigen dari udara ke darah kapiler alveoli berlangsung terutama melalui difusi dan aliran darah di arteri pulmoner (yaitu cardiac output). Sebaliknya, CO2 mengalami difusi dari pembuluh kapiler ke alveoli dan dihembuskan pada proses ventilasi, yang yang akan menurunkan kadar CO2. Dengan demikian, oksigenasi tergantung pada konsentrasi oksigen inspirasi, kapasitas difusi paru dan cardiac output, sedangkan kadar pCO2 arteri ditentukan oleh ventilasi alveolar. Ventilasi alveolar mengalami delivery dalam berbagai pola. Volume tidal yang kecil dengan frekuensi cepat memperkecil efek samping tekanan intratorakal yang tinggi (lihat di bawah), dan sebagian besar udara yang dihirup pada pernapasan terbuang sia–sia, ventilasi ruang mati (yang meningkat pada penggunaan pipa endotrakea, sirkuit ventilator dan faktor penderita lainnya), dan meningkatkan kecenderungan terjadinya atelektasis. Sebaliknya volume besar dengan frekuensi lambat memperkecil kemungkinan atelektasis dan memperkecil terbuangnya ventilasi di ruang mati, namun masalah yang ditimbulkan tekanan tinggi dan volume diperbesar. Pada praktek klinik, hal–hal seperti ini harus dijadikan orientasi dalam tatalaksana.

4.

Kelebihan (keuntungan) dan kekurangan (kerugian) Ventilasi Mekanik

Sebagai upaya memperbaiki pernapasan spontan yang tidak tercukupi, ventilasi mekanik memungkinkan pengendalian pO2 dan pCO2 arteri. Ventilasi mekanik juga meniadakan kerja pernapasan hingga menghemat oksigen yang digunakan dalam proses. Namun, tekanan positif akan mengurangi aliran vena ke jantung (venous return) yang menyebabkan hipotensi,


terutama pada penderita hipovolemik. Kesesuaian ventilasi–perfusi (ventilation–perfusion match) biasanya tidak seefektif pernapasan spontan. Distensi berlebihan dapat terjadi saat dijumpai kondisi patologik (termasuk luka bakar jalan napas dan cedera inhalasi) menyebabkan paru–paru kaku (non–compliant), menggunakan volume tidal berlebihan, atau adanya obstruksi jalan napas letak rendah (asma atau penyakit paru obstruktif kronis) menyebabkan hiperinflasi. Kondisi ini mennimbulkan komplikasi mengancam jiwa seperti tension pneumothorax. Karenanya, ventilasi mekanik hampir selalu membutuhkan sedasi dan pemberian relaksan otot masih tetap dihadapkan pada potensi timbulnya komplikasi dan efek samping.

5. 1.

Masalah Respirasi khusus pada Luka Bakar Intoksikasi Karbon Monoksida (CO)

Bila fasilitas hiperbarik tersedia dan mudah diperoleh, banyak pihak merekomendasikan penggunaannya. Namun, eliminasi CO berlangsung cepat bila penderita segera menghirup oksigen 100% secara cepat. Atas dasar itu, pemberian awal oksigen bersifat mandatorik bila ada kecurigaan keracunan CO. Penggunaan oksigen hiperbarik dapat dilakukan secara elektif setelah konsultasi dengan unit luka bakar. 2.

Cedera inhalasi dan Luka Bakar pada dinding dada

Kedua bentuk cedera ini mempengaruhi pertukaran udara di paru (gas exchange) dan kekakuan mekanik (complaince). Gejala yang ditimbulkannya adalah distres pernapasan dan hipoksemia. Mungkin dijumpai batuk produktif dan partikel jelaga di jalan napas, dan pada foto toraks dijumpai peningkatan densitas jaringan interstisium alveolar difus yang konsisten dengan bentuk sindroma distress pernapasan akut lainnya. Kondisi ini memerlukan penatalaksanaan definitif yang melibatkan spesialis yang intensif di rumah sakit yang besar dengan fasilitas canggih. 3.

Trauma toraks

Kontusio paru dapat menyebabkan hipoksia yang nyata atau hemoptisis dan flail chest yang menimbulkan inefisiensi pernapasan spontan. Dikumpainya cedera ini pada penderita luka bakar meningkatkan kebutuhan penggunaan ventilasi mekanis. Trauma toraks meningkatkan kemungkinan kerusakan paru selama ventilasi mekanik. Kemungkinan timbulnya tension pneumothorax harus dipertimbangkan. Bila terdapat fraktur tulang iga dan ventilasi mekanik diperlukan, maka drenase interkostal (pipa intratorakal) sebagai profilaksis, mungkin merupakan tindakan yang tepat.


Kasus–kasus seperti ini harus didiskusikan dengan spesialis intensif. 4.

Luka bakar pada dinding dada

Adanya eskar melingkar dinding dada memengaruhi compliance dinding dada. Kondisi ini harus dibedakan dengan penurunan compliance paru pada penggunaan tekanan inspiratorik tinggi yang digunakan untuk mencapai volume tidal yang dibutuhkan yang mungkin tidak terlalu membahayakan. Bagaimanapun, pada kondisi ini diperlukan eskarotomi dinding dada.

6. Pola / setting Ventilator optimal Pada umumnya, untuk dewasa dimulai dengan volume tidal 5–7 mL/kg berat badan dengan frekuensi napas 10 kali/menit dan 50% oksigen. Hal ini cukup aman untuk mempertahankan saturasi oksigen adekuat. Tekanan inspiratorik pada dewasa tidak lebih dari 35 cmH2O (pada anak, 15–20 cmH2O), dan sistem kardiovaskular stabil. Analisis gas darah arteri harus diperiksa segera setelah dimulainya ventilasi, dan selanjutnya dilakukan penyesuaiannya. Pemeriksaan diulang secara frekuen hingga penderita dalam kondisi stabil. Bila compliance paru buruk dan atau dijumpai instabilitas sistem kardiovaskular, volume tidal harus diturunkan, juga bila normokarbia tidak tercapai. Dalam jangka pendek, hal ini tidak akan membahayakan kecuali dijumpai cedera kepala berat. Bila ada kecurigaan intoksikasi CO atau instabilitas kardiovaskular berkelanjutan, maka harus diberikan oksigen 100%. Gangguan compliance paru progresif menunjukkan adanya tension pneumothorax maupun beberapa masalah mekanik lainnya, dalam hal ini, pemeriksaan foto toraks harus diperoleh sesegera mungkin. Ventilator perawatan intensif modern memiliki berbagai setting, yang memungkinkan penderita bernapas spontan dengan sejumlah variabel bantuan mesin ventilator yang bervariasi. Tipe ventilator ini bermanfaat pada kasus–kasus sulit dan tatalaksana jangka panjang dan penyapihan (weaning) ventilator, namun memerlukan keahlian dan peralatan canggih. Bagi praktisi umum, penggunaan ventilator sederhana, kontrol–penuh bantuan ventilasi dengan sedasi dalam dan penggunaan relaksan otot merupakan pilihan jangka pendek yang relatif mudah. Namun, pengawasan dan perawatan one to one sangat penting untuk menjamin keamanan penderita pada situasi seperti ini.

7. Sedasi / Relaksan otot selama ventilasi Sedasi selama ventilasi mekanik biasanya menggunakan kombinasi opioid dan benzodiazepin. Morfin dan midazolam paling sering diberikan perinfus secara kontinu, titrasi untuk


mendapatkan efek yang diinginkan (masing–masing 0–10 mg/jam pada dewasa), sesekali dengan bolus tambahan bila diperlukan. Bila pengendalian ventilasi adekuat tidak tercapai, dengan cara ini, maka relaksan non– depolarisasi otot dapat ditambahkan. Pankuronium dan vekuronium paling sering digunakan dan biasanya diberikan bergantian bolus iv (6–8 mg dosis dewasa, diikuti oleh 2–4mg prn). Harus ditekankan bahwa sedasi dalam dan atau kelumpuhan otot menjadikan penderita benar–benar tak berdaya saat terjadi kerusakan ventilator atau terjadi gangguan koneksi; maka dalam hal ini mutlak diperlukan pengawasan yang konstan.

8. Pementauan sederhana pada penggunaan ventilator Pulse oxymetry, denyut jantung, tekanan darah, end tidal CO2 dan alarm pemutus–tekanan merupakan syarat minimal yang mutlak pada semua penderita dengan ventilasi mekanik. Alarm pemutus–tekanan bukan hanya merupakan satu kesatuan dalam unit ventilator, namun juga tersedia dalam bentuk portable tetapi juga tersedia sebagai suatu unit tersendiri; terlepas dari ventilator. Beberapa alat pemantauan volume tidal/menit juga sangat diperlukan, beberapa ventilator memiliki sarana ini dalam kesatuan (built in) namun bentuk yang sederhana tersedia pada ventilator Wright. Pada penggunaan ventilator, sangat dibutuhkan pemantauan analisis gas darah dan foto toraks. Hal yang perlu menjadi perhatian adalah, penggunaan alat pemantau (monitor) bukan sebagai penganti perawat terlatih dalam pemantauan klinis. Pemantauan merupakan suatu yang bersifat mandatorik pada penderita dengan ventilator.

9. Ventilasi selama prosedur transportasi Transportasi penderita terventilasi memiliki risiko jauh lebih tinggi dibandingkan penggunaannya di rumah sakit. Selain dihadapkan potensi terjadinya ekstubasi yang tidak disengaja, perubahan posisi pipa, kerusakan peralatan, pergerakan dan getaran berkontribusi pada gangguan kardio–respirasi. Petugas yang mendampingi harus bekerja di tempat sempit, pencahayaan kurang, lingkungan tidak stabil dan sangat mungkin dihadapkan pada masalah transportasi seperti mabuk perjalanan. Tim petugas yang terlibat dalam transportasi harus dilengkapi peralatan portabel, sumber listrik, oksigen, obat–obatan, dan harus mampu menangani masalah–masalah tak terduga yang muncul di perjalanan. Di ketinggian terjadi penurunan tekanan oksigen inspirasi, terutama pada pesawat tanpa sarana pengatur tekanan, peningkatan volume udara (seperti pada pneumothorax, udara pada balon pipa endotrakea atau ruang mati di iv flask) dapat mengubah kinerja ventilator.


Hal–hal yang diuraikan di atas harus dijadikan pertimbangan saat merencanakan untuk merujuk penderita kritis. Sebelum dipindahkan, harus ada diskusi antara pihak yang merujuk dan pihak yang menerima. Akses vaskular yang handal dan pemantauan harus terjamin, dan setiap upaya harus dilakukan untuk stabilisasi kondisi penderita sejauh mungkin. Bila ada tim transportasi perawatan kritis yang berpengalaman, akan lebih baik memanfaatkan tenaga mereka bahkan bila penundaan terjadi. Tidak ada satupun penderita terventilasi yang harus dirujuk tidak dikawal oleh petugas medis senior yang terampil.

B. Topangan sirkulasi Kondisi hemodinamik penderita luka bakar berat tetap berada pada kondisi tidak stabil dalam 24 jam kedua. Kebutuhan cairan seringkali tidak mengikuti aturan standar dan penilaian berulang berkelanjutan menggunakan kriteria klinis umum, nadi, urine dan tekanan darah diperlukan untuk memastikan bahwa jumlah cairan yang diberikan adalah tepat. Pemeriksaan laboratorium berikut ini akan membantu memandu pengobatan dengan cairan: -

Hemoglobin dan hematokrit Urea dan Elektrolit Analisis gas darah arteri (yang sesuai) Kadar glukosa darah (pada anak)

1. Komposisi Cairan Seiring dengan kembali permeabilitas kapiler secara bertahap di akhir hari pertama pasca luka bakar, cairan koloid dapat diberikan untuk menjaga ruang intravaskular terekspansi. Jumlah keseluruhan volume disesuaikan untuk untuk mempertahankan produksi urin 30–50 mL/jam pada dewasa dan pada anak–anak (kurang dari 30 kg) 1,0 mL / kg /jam. Cairan yang diberikan selama 24 jam kedua harus mencakup 0.3–0.5 mL koloid per kg berat badan per persentase luas luka bakar. Cairan koloid yang diberikan adalah albumin serum normal 5% (50g per liter). Pada dewasa, dekstrosa 4% dengan larutan salin normal 0,18% ditambahkan untuk mempertahankan produksi urin cukup. Pada anak–anak, perlu ditambahkan glukosa dengan larutan salin ½ normaluntuk tujuan yang sama.

2. Cairan per oral / nasogastrik / nasojejunal


Penderita yang tolerir terhadap cairan per oral dapat menerima porsi kecil cairan disamping cairan intravena, atau cairan per oral dapat menggantikan komponen dekstrosa / salin. Penderita luka bakar berat tanpa ileus harus menerima suplementasi cairan tinggi protein baik secara bebas melalui oral bila ditoleransi atau melalui pipa naso–gastric / nasojejunal. Hal ini memerlukan diskusi dengan ahli gizi namun harus diperhatikan jangan sampai menyebabkan kelebihan cairan.

3. Keseimbangan Cairan Selama 24 jam kedua kebutuhan cairan lebih kecil dibandingkan dengan 24 jam pertama, hal terpenting adalah jangan sampai terjadi kelebihan cairan, terutama pada mereka yang disertai kelainan jantung dan paru. Pola cairan yang menghasilkan urin berlebihan tidak tepat dan diikuti kemungkinan terjadinya edema paru karena pemberian cairan terlalu banyak [16]. Sindroma kompartemen abdominal dapat terjadi sebagai komplikasi sekunder serius bila volume cairan berlebihan diberikan untuk mempertahankan produksi urin yang cukup dan mempertahankan stabilitas hemodinamik. Pemantauan tekanan kandung kemih sangat bermanfaat untuk memperoleh informasi penting mengenai tekanan intra–abdomen. Selama 24 jam kedua, diuresis alami harus sudah mulai dan produksi urin mungkin mengalami peningkatan, melebihi jumlah cairan yang diberikan. Sedangkan pada kondisi dimana dijumpai haemochromogenuria, dieresis alami akan dimulai 24–48 jam pasca luka bakar. Pemantauan hemoglobin dan hematokrit pada tahap ini mungkin menunjukkan penurunan hemoglobin yang terjadi akibat hemolisis, sehingga pemberian whole blood mungkin diperlukan pada tahap ini. Dengan demikian, hematokrit tidak dapat digunakan sebagai panduan.

C. Perawatan Luka Luka harus diperiksa ulang untuk memperoleh informasi akurat mengenai luas dan kedalaman luka bakar. Luka bakar yang dalam 24 jam pertama hanya berujud eritema mungkin kedalamannya berkembang menjadi luka bakar seluruh ketebalan kulit (full thickness) dalam 24 jam kedua. Penilaian ulang formal luka bakar mengharuskan dilakukannya kalkulasi ulang kebutuhan cairan untuk 24 jam kedua. Luka bakar dangkal hingga mid dermal dirawat dengan pembalut biologik yang sesuai (Biobrane, Opsite, Duoderm atau sejenisnya) dan bila pembalut ini pada 24 jam kedua masih dalam kondisi baik, maka tidak perlu ditukar.


Setiap luka bakar dalam atau tebal harus diberi antimikroba topikal, demikian pula pada semua penderita yang evakuasinya tertunda. Hubungi unit luka bakar untuk mendapat saran tentang pembalut yang tepat. Sebagai kelanjutan perawatan luka bakar menggunakan pembalut antimikroba, yang terbaik adalah melakukan pencucian luka, baik dalam bath tube, di kamar mandi, atau menggunakan shower. Pembalut lama dan kulit yang terkelupas harus dibuang. Setelah pengeringan, ambil foto klinik untuk tujuan pemantauan luka. Aplikasi balutan bersih pada luka agar penderita merasa nyaman. Perhatian ditujukan untuk memastikan balutan tidak terlalu ketat, sensasi dan sirkulasi distal baik. Dalam 24–48 jam pertama, dalam melakukan pembalutan, ujung jari tangan dan kaki harus dubiiarkan terbuka sehingga adanya perubahan warna dan penilaian sirkulasi dapat dilakukan secara reguler. Ekstremitas atas dan bawah harus ditinggikan denegan bantal atau bantalan busa untuk memfasilitasi resolusi edema. Bila tersedia, USG Doppler dapat digunakan untuk membantu pemantauan sirkulasi pada ekstremitas yang mengalami edema.

Eskarotomi dan Pendarahan Pengisian ulang kapiler secara reguler dan observasi ekstrremitas harus memberi informasi kemungkinan dilakukannya eskarotomi. Edema pada luka bakar dapat berlanjut selama 24 jam kedua pasca luka bakar, sehingga mungkin diperlukan eskarotomi untuk memastikan sirkulasi darah yang baik ke distal. Dengan kembali normalnya sirkulasi perifer pada tahap ini, terbukanya pembuluh perifer yang bertahap dari memungkinkan terjadi pendarahan pasca eskarotomi yang dilakukan sebelumnya. Mungkin diperlukan diatermi bipolar atau klem arteri dan ligasi untuk mengendalikan pendarahan. Penerapan balut tekan untuk mengatasi pendarahan adalah tidak tepat karena menghalagi sirkulasi perifer yang telah diperbaiki melalui eskarotomi.

D. Manajemen nyeri Pada 24 jam kedua, cara sederhana dan aman dalam manajemen nyeri adalah pemberian analgesia cukup dengan narkotika intravena dosis rendah. Dosis tersebut harus dititrasi terhadap respon penderita termasuk frekuensit pernapasan. Tidak ada fasilitas canggih diperlukan untuk pemberian dan pemantauannya [9].


Namun, bila fasilitas (pompa infus) tersedia, dosis 20–30 mikrogram per kg per jam (setelah pemberian dosis awal) merupakan bentuk yang paling fleksibel dalam manajemen nyeri. Dosis yang lebih tinggi kadang diperlukan, dan untuk tujuan tersebut dilakukan penambahan kecepatan pemberian infus intravena ini; dibutuhkan waktu cukup panjang agar dicapai kadarnya di dalam darah untuk memberi efek analgesia yang baik. Tidak akan ada efek adiksi narkotika pada tahap ini. Saat nyeri dirasakan, pemberian analgetik yang tepat harus diberikan. Nyeri akan terasa lebih selama penggantian balutan, episode mobilisasi, dan fisioterapi. Analgetik narkotik intravena harus diberikan untuk mengatasi nyeri selama episode nyeri ini. Pemberian analgesia yang dikendalikan penderita (patient controlled analgesia, PCA) sangat efektif pada luka bakar dan bila peralatan ini tersedia, maka menjadi metode pilihan. Peralatan ini dapat digunakan pada anak kecil dengan hati–hati. Diperlukan keahlian bidang anestesi untuk prosedur ini. Oksida nitrit atau methoxyfluorane yang diberikan mencegah distribusi oksigen tidak tercukupi merupakan suplemen bermanfaat, terutama saat melakukan prosedur, namun pemberiannya harus dilakukan oleh seorang ahli anestesi atau staf yang berpengalaman.

E. Nutrisi Pemberian nutrisi melalui rute gastrik seawal mungkin pasca luka bakar adalah penting. Kehadiran nutrien melalui usus akan melindungi mukosa usus halus dari kerusakan yang terjadi pada trauma dan starvasi. Kerusakan sel mukosa memungkinkan terjadinya translokasi bakteri usus ke aliran darah menyebabkan sepsis berat oleh gram negatif yang kerap berakibat fatal pada luka bakar kritis. Pemberian nutrisi dini membantu mencegah hal ini. Pada penderita dengan luka bakar berat (>10% pada anak–anak,>20% pada dewasa) kerap dijumpai ileus, terutama pada keterlambatan resusitasi cairan dan syok yang nyata. Pipa naso– gastrik harus dimasukkan untuk mengosongkan lambung, menghindari aspirasi bila muntah. Nutrisi segera diberikan bila terdengar bising usus atau memang bising usus terdengar sejak penderita masuk rumah sakit. Kurang lebih dua kali jumlah energi yang dibutuhkan per hari pada keadaan normal (biasa). Pada penderita luka bakar kritis, nutrisi diberikan dalam bentuk suplemen diet yang tersedia. Bila ini tidak, produk susu akan sangat bermanfaat. Penderita dapat mengonsumsi diet normal. Komposisi diet harus kaya akan protein dan kalori yang mencukupi. Penambahan susu bubuk skim ke dalam susu biasa (200 gram per liter) secara signifikan meningkatkan kadar protein. Pemberian protein tinggi dengan penambahan telur sering kali dapat ditolerir.


Penderita luka bakar berat sering tidak dapat mengonsumsi cukup nutrisi. Pada kondisi ini, pipa naso–gastrik atau naso–jejunal dimasukkan untuk pemberian nutrisi. Kepala ditinggikan 30° saat pemberian. Pemberian dimulai dengan jumlah kecil dan ditingkatkan secara bertahap. Dengan cara ini masalah diare dapat dicegah. Penderita harus ditimbang setiap hari, peristaltik usus didokumentasikan, demikian pula setiap perubahan dan bila penderita makan secara spontan, berikan waktu ekstra untuk menghabiskan makanan. Makanan ekstra dapat diberikan berupa makanan kecil diantara waktu makan biasa bila penderita tidak mampu menghabiskan makanannya. Penderita luka bakar pada tangan mungkin memerlukan bantuan. Karena risiko ulserasi lambung akut pasca luka bakar kritis demikian tinggi, perlindungan dengan pemberian inhibitor pompa proton, H2 antagonis, dan yang paling penting, pemberian nutrisi enteral.

F. Fisioterapi dan Terapi Okupasional Karena luka bakar dalam cenderung diikuti kontraktur, maka sangat penting menjaga semua sendi berada pada posisi yang tepat. Pencegahan kontraktur dimulai sejak awal (pada hari–hari pertama). Penderita tidak diperbolehkan mengikuti posisi kontraktur karena posisi yang nyaman adalah posisi kontraktur. Posisi yang tepat tergantung pada aspek sendi yang terlibat. Biasanya posisi yang benar adalah: - leher – ekstensi - ketiak – abduksi - siku – ekstensi - pergelangan tangan – netral atau ekstensi - sendi metakarpofalangeal – fleksi - sendi jari interfalangeal – ekstensi - lutut – ekstensi - pergelangan kaki – 90o dorsofleksi Bidai diperlukan dan setidaknya sekali dalam sehari semua sendi harus digerakkan dalam rentang gerak (range of movement, ROM) sejauh nyeri dapat ditolerir. Penderita dengan cedera inhalasi dan dalam keadaan sadar atau yang eskar dinding dada harus menjalani latihan bernapas dan batuk untuk memastikan ekspansi paru. Pada penggunaan bidai, hindari balutan yang ketat dan menekan saraf di sekitar sendi. Saraf ulnaris di siku dihadapkan risiko mengalami cedera pada penggunaan bidai atau tekanan tepi tempat tidur dan meja operasi. Demikian pula saraf peroneal komunis di sekitar kaput fibula dihadapkan pada risiko drop foot.


Selama perawatan di ICU, imobilisasi penderita luka bakar berat dihadapkan risiko ulkus dekubitus sehingga perawatan area tekanan sangat penting, terutama di daerah sakrum, oksipital dan kalkaneus. Penekanan di daerah lain juga mungkin terjadi. Posisi penderita harus diatur setiap dua jam. Penggunaan kasur anti dekubitus menjadi suatu kebutuhan.

G. Pengendalian Infeksi ·

· · ·

Semua peralatan harus dibersihkan secara efektif, terutama alat yang digunakan untuk beberapa penderita. Pencucian tangan sebelum dan sesudah menangani penderita adalah cara yang paling efektif untuk mencegah penularan infeksi. Pembersihan selama tiga menit harus dilakukan sebelum mengawali setiap prosedur. Ketika melakukan perawatan penderita secara langsung, gaun isolasi berbeda harus dipakai untuk setiap penderita. Kasur penderita dan daerah disampingnya harus dibersihkan tiap hari menggunakan antiseptik.

Ringkasan -

-

Penderita harus dirujuk ke unit luka bakar dalam waktu 24 jam untuk memaksimalkan pertolongan penderita. Bila hal ini tidak mungkin, manajemen perawatan intensif diperlukan untuk menjaga penderita dalam keadaan terbaik untuk dirujuk. Perhatian untuk alat penopang respirasi dan sirkulasi, perawatan luka, manajemen nyeri, nutrisi, fisioterapi, dan pengendalian infeksi. Hubungi unit luka bakar atau ICU diperlukan.


Bab 13

Manajemen Rawat Jalan pada Luka Bakar Ringan Introduksi Sekitar 1% warga Australia memerlukan pengobatan setelah mengalami luka bakar setiap tahun. Dari 220.000 penderita setiap tahun, sekitar 10% (22.000) memerlukan perawatan rumah sakit dan 100 orang meninggal akibat luka bakar (Sumber: Survei Kesehatan Nasional Australia 2001 2001) Cukup banyak penderita luka bakar akut pergi ke unit gawat darurat rumah sakit di perifer atau perkotaan dan cukup banyak penderita mendapat perawatan pertama dari dokter umum.

A. Penilaian 1. Riwayat penyakit dan anamnesis Riwayat/ terjadinya kecelakaan sangat penting [21]. Penyebab dan pertolongan yang sudah dilakukan memberi petunjuk dalam menentukan kedalaman luka. Luka bakar akibat air panas yang mendapat pertolongan sesuai dengan rekomendasi cenderung tidak terlalu dalam seperti luka bakar api. Namun pada anak dan orang tua, luka bakar akibat air panas seringkali dijumpai lebih dalam dibandingkan pemeriksaan awal. Informasi mengenai seberapa panas air yang menyebabkan cedera harus diperoleh. Luka bakar api biasanya dalam, terutama bila menggunakan bahan bakar, atau bahan pakaian yang terbakar. Kecurigaan mengenai cedera bukan karena kecelakaan pada anak maupun dewasa seringkali terpandu oleh adanya inkonsistensi antara pemeriksaan fisik dengan anamnesis yang diperoleh. Adanya kecurigaan ini menimbulkan keharusan segera merujuk ke unit luka bakar untuk penyelidikan lebih lanjut.

2. Pemeriksaan fisik Lakukan pemeriksaan dan lakukan pencatatan dengan teliti [2] hal–hal sebagai berikut. 1) Warna 2) Adanya bula


3) 4) 5) 6)

Waktu pengisian kapiler Neyri (luka bakar dangkal lebih nyeri dibandingkan luka bakar dalam) Kondisi eksudat (yang dapat mengindikasikan risiko infeksi bila terjadi penundaan) Adanya inflamasi sekitar yang menunjukkan sepsis.

Umumnya kedalaman luka dapat ditentukan berdasarkan temuan butir–butir di atas; lihat lebih rinci pada Bab 7 Manajemen Luka. Untuk luka bakar tidak luas, dan bila dijumpai kendala rujukan (lihat kriteria di Bab 10), maka kasus ini dapat dikelola oleh ahli bedah untuk prosedur eksisi dan prosedur skin graft. Bila ada keraguan mengenai kedalaman atau tatalaksana, hubungi unit luka bakar.

3. Penilaian luas Luka Bakar Terapkan rule of nines dari Wallace sebagaimana dibahas pada Bab 5 dan dapatkan informasi akurat luas luka bakar [21, 25, 27, 56–58]. Sebagai alternatif, gunakan permukaan telapak tangan (1% dari luas permukaan tubuh) sebagai panduan menilai luas luka bakar [21, 56–58]. Pada penderita dengan luka bakar superfisial dan mid–dengan luas kurang dari 10% pada dewasa atau kurang dari 5% pada anak dapat menjalani rawat jalan. Dengan tersedianya balutan biologis modern yang sesuai, diungkinkan untuk melindungi, mengobati dan memfasilitasi proses penyembuhan alami. Namun, pada luka mendekati 10% dan perawatan yang memerlukan pergantian balutan secara frekuen dengan metode di luar kompetensi dokter umum atau rumah sakit daerah, pertimbangkan untuk merujuk ke rumah sakit yang telah menjalin kerjasama dengan unit luka bakar untuk pelaksanaan rawat jalan.

B. Manajemen Nyeri Pada luka bakar tidak luas, dengan pembalutan yang baik dapat diberikan parasetamol digabung dengan kodein peroral, intranasal atau inhalasi untuk penderita rawat jalan. Pada prosedur pembalutan, kerap dijumpai kesulitan dan nyeri, terutama pada anak–anak. Untuk tujuan ini, pemebrian sedatif dan analgesik oral dapat diberikan 30–45 menit sebelum pembalutan. Opioid intranasal memiliki onset yang lebih cepat dan masa kerja yang cocok untuk lingkungan rawat jalan. Sekali lagi, bila tidak mungkin untuk memberikan analgesia yang memadai dalam kondisi rawat jalan atau perawatan primer, maka perlu untuk dilakukannya rawat inap.

C. Manajemen Luka Setelah pertolongan pertama (Bab 2), manajemen luka harus mengacu pada prinsip yang berlaku untuk penanganan luka apapun. Teknik aseptik harus diterapkan dalam memperkecil


risiko kontaminasi, dan setiap upaya perawatan harus ditujukan mencegah kerusakan jaringan lebih lanjut. Pada tahap akut, luka dicuci menggunakan antibakteri. Cairan mengandung klorheksidin 0,1 atau 0,2% umum digunakan, tetapi bila ini tidak tersedia, gunakan sabun dan air [10]. Selama prosedur pembersihan, harus diperoleh dasar luka yang bersih, sehingga kulit yang terkelupas harus dibuang menggunakan gunting steril. Bula kecil dapat dibiarkan, sedangkan bula berukuran besar maupun pecah dan kulit melipat, maka kulit terkelupas harus dibuang [10]. Setelah luka bersih, pemeriksaan lebih lanjut diperlukan untuk menilai kedalaman luka bakar.

Luka bakar Epidermal Luka bakar bewarna merah muda cerah ke merahan, sangat nyeri tanpa bula menunjukkan kedalaman hanya mencapai epidermis [2]. Contoh yang khas adalah sengatan matahari atau percikan api. Luka kedalaman initidak memerlukan pengobatan spesifik, tapi mungkin sangat nyeri dan membutuhkan analgetik. Krim pelembab mungkin diperlukan tanpa balutan.

Luka bakar Dermal Luka bakar dengan bula biasanya mencapai kedalaman dermis. Dasar luka dengan pengembalian kapiler dengan sensasi menunjukkan luka bakar dangkal dan akan mengalami penyembuhan spontan [2]. Setelah dibersihkan, luka dengan kedalaman dermis dan epidermis superfisial dihadapkan terpaparnya papilae dermis. Bila dibiarkan mengering atau terinfeksi, unsur–unsur epidermis yang berepran untuk proses epitelialisasi akan mati dan luka akan bertambah dalam. Akibatnya penyembuhan spontan tidak dimungkinkan dan memerlukan skin graft. Pengobatan yang tepat untuk luka jenis ini adalah pembalut biologis atau balutan silikon hidro–koloid balutan perak atau film. Beberapa balutan dapat di lihat dalam tabel pada Lampiran 4. Pembalut seperti Biobrane, kulit babi atau kulit kadaver yang diawetkan juga ideal. Namun, sangat mahal dan umumnya hanya dipakai di unit luka bakar. Luka bakar dangkal terus mengeluarkan eksudat sebagai reaksi inflamasi. Balutan mengalami kejenuhan akibat produksi cairan dan harus lebih sering diganti. Balutan hidrokoloid memerlukan penggantian setiap 3–5 hari, atau lebih sering bila eksudat berlebihan atau bau yang menusuk. Balutan yang melekat pada luka seperti Biobrane atau kulit manusia yang diawetkan harus dikelupas secara bertahap (mulai di tepi) setelah epitelialisasi berlangsung. Pada luka bakar, inspeksi luka berulang direkomendasikan setiap 3 hari untuk memastikan bahwa penilaian awal kedalaman luka bakar benar dan komplikasi dari luka (terutama infeksi)


tidak terjadi. Perubahan manajemen mungkin diperlukan bila pada penilaian ulang menunjukkan luka bakar dalam atau terinfeksi.

Luka terinfeksi Sepsis luka mungkin terjadi pada luka yang terkontaminasi saat cedera, atau luka yang dirawat dengan balutan yang tidak mengandung antibakteri. Luka yang terinfeksi di saat awal, atau diduga terkontaminasi saat cedera, harus ditatalaksanai lebih dini menggunakan antimikroba topikal. Produk yang paling tepat di Australia dan Selandia Baru adalah balutan silver slow–release. Setelah menerapkan balutan utama, penting untuk mengamankan balutan dengan perban atau perekat. Silver sulfadiazin dapat digunakan, namun preparat ini sering menyebabkan perubahan luka menjadi luka lembab bewarna kuning kecoklatan yang menyebabkan penilaian dasar luka lebih sulit. Tanda peradangan di sekitar atau tanda–tanda infeksi sistemik menunjukkan sepsis. Bila hal ini dijumpai, maka prosedur rujukan disegerakan karena luka bakar dermal sejenis ini berubah menjadi luka lebih dalam. Dengan perawatan terbuka, luka mengering dan berubah menjadi luka bakar dalam, karenanya perawatan terbuka kecuali untuk luka bakar epidermal sangat tidak tepat. Bila pada penilaian ulang, atau diagnosis awal tidak benar, maka rujukan untuk prosedur operasi harus dilaksanakan.

D. Tindak Lanjut / Follow Up Tergantung pembalut yang digunakan, umumnya penilaian dilakukan dalam 2–3 hari setelah balutan pertama untuk kemudian dilakukan dalam interval 3–7 hari. Pada setiap kesempatan, penting diperoleh informasi apakah lingkungan rumah penderita memenuhi syarat dalam penerapaan manajemen rawat jalan. Dalam situasi dimana penderita tidak mampu mengatasi, maka rawat inap diperlukan. Misalnya orang tua, penderita yang tinggal sendiri, atau anak dengan orang tua yang bekerja, yang kelanjutan rawat jalannya sulit dilanjutkan karena kurang dukungan dari keluarga. Komorbiditas penderita juga memengaruhi manajemen rawat jalan. Penderita dengan inkontinensia atau gangguan mental mungkin memerlukan pergantian balutan lebih sering dan manajemen luka.


Pelayanan keperawatan rawat jalan di rumah bermanfaat dalam esktensi pelayanan rawat jalan primer dan membantu dalam pelaksanaan penggantian balutan luka, terutama pada penderita yang sulit datang ke klinik rawat jalan atau operasi.

1. Fisioterapi / Terapi Okupasi Luka bakar ringan pada tangan, ekstremitas dan di sekitar sendi yang tidak sesuai kriteria rawat unit luka bakar membutuhkan terapi. Pada luka bakar yang memerlukan waktu penyembuhan lebih lama dari 2 minggu atau mereka yang membutuhkan operasi, kerap terjadi parut hipertrofik. Fisioterapi dan terapi okupasi mungkin diperlukan dalam manajemen parut menggunakan garmen elastis, media kontak atau plester [2]. Dokter umum dapat melakukan koordinasi manajemen, dan unit luka bakar dapat memberikan saran fisioterapi dan terapi okupasi untuk perawatan ini.

2. Edukasi pada proses penyembuhan Luka yang baru mengalami penyembuhan (epitelialisasi) memerlukan perlindungan dari sengatan matahari menggunakan pelindung sinar matahari 30+ dan pakaian yang sesuai. Luka yang baru mengalami penyembuhan jangan terlalu banyak dibebani untuk bekerja, dan diperlukan istirahat untuk memungkinkan penebalan normal. Pemakaian krim pelembab yang berkelanjutan untuk mengatasi kurangnya kelembaban alami kulit akibat kerusakan kelenjar sebasea selama beberapa waktu pasca luka bakar. Gatal merupakan masalah pada luka bakar yang baru mengalami penyembuhan. Aplikasi krim pelembab, pijatan dan tekanan sangat membantu mengatasi hal ini. Antihistamin dan kompres dingin dapat meringankan. Mandi air hangat mengandung solusi seperti Pinetarsal, gandum atau aloe vera dapat membantu, terutama pada luka bakar akibat air panas.

3. Penurunan fungsi pasca Luka Bakar Beberapa luka bakar yang memerlukan waktu penyembuhanlebih lama dari 14 hari akan diikuti terbentuknya jaringan parut hipertrofik dan kontraktur. Bila terjadi di sekitar sendi maka akan diikuti gangguan fungsi sekunder. Kehilangan fungsi dan tidak respon terhadap manajemen parut disertai fisioterapi memerlukan rujukan ke unit luka bakar untuk rekonstruksi dalam mengatasi masalah fungsi ini. Pada luka bakar minor dengan kontraktur ringan dapat dirawat oleh terapis dan umumnya dengan terapi yang baik tidak memerlukan operasi.

4. Masalah estetik pasca Luka Bakar


Luka bakar menyebabkan kecacadan yang nyata, baik masalah warna defek pada penyembuhan spontan maupun masalah parut hipertrofik. Beberapa penderita tidak mempedulikan, namun sebagian lainnya mengalami depresi menghadapi hal ini. Ganguan body image pasca luka bakar kadang melebihi proporsi ukuran luka bakar itu sendiri. Konseling pada awal perawatan yang difasilitasi oleh psikolog atau psikiater dapat membantu manajemen. Mungkin ada permintaan tidak masuk akal untuk perbaikan estetik pada cacat ini. Operasi revisi dengan eksisi parut dan skin graft selalu meninggalkan bekas yang tidak lebih baik dibandingkan bentuk awal. Dalam kasus ini, dukungan psikoterapi dengan konseling berulang merupakan manajemen yang tepat. Selain masalah estetik, banyak penderita dan keluarga mungkin dihadapkan pada amarah yang tak kunjung reda atau rasa bersalah terkait dan mungkin memerlukan penanganan yang merupakan bagian dari pengobatan.

Ringkasan -

-

-

Banyak luka bakar ringan dapat ditangani secara memuaskan di tingkat perawatan primer. Karena sebagian besar luka bakar di Australia dan Selandia Baru masuk ke dalam kategori ini, tepat bagi praktisi lokal untuk mengembangkan keahlian dalam manajemen luka bakar ringan dan unit luka bakar tersedia untuk memberi nasihat atau pengobatan yang diperlukan. Pengelolaan penderita luka bakar meliputi perhatian yang cermat pada luka bakar untuk memfasilitasi penyembuhan normal dan mencegah komplikasi. Banyak produk yang tidak disebutkan dalam bab ini yang sama efektifnya. Daftar produk yang dicantumkan pada tabel tidak semuanya termasuk. Rujukan sekunder dari luka bakar ringan yang telah sembuh mungkin diperlukan untuk operasi rekonstruktif, manajemen luka, fisioterapi, terapi okupasi atau psikoterapi.


Referensi 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14.

15. 16. 17. 18. 19. 20.

Peck M. Epidemiology of burn injuries globally. www. uptodate. com/contents/epidemiology–of–burn–injuries–globally 2011. Herndon DN.ed. Total Burn Care. 3rd ed. 2007, Saunders: London. Holland AJ. Pediatric burns: the forgotten trauma of childhood. Canadian J Surg, 2006. 49(4):6. Singer AJ, et al. The association between hypothermia, prehospital cooling, and mortality in burn victims. Acad Emerg Med. 2010. 17(4):456–9. Gurfinkel R, et al. Development of a novel animal burn model using radiant heat in rats and swine. Acad Emerg Med. 2010. 17(5):514–20. Taira BR, et al. Rates of compliance with first aid recommendations in burn patients. J Burn Care Res. 2010.31(1):121–4. Williams C. Assessment and management of paediatric burn injuries. Nurs Stand. 2011. 25(25):60–4,66,68. ANZBA, Bi–National Burns Registry: Annual Report 1st July 2009 – 30th June 2010. 2011, Autralian and New Zealand Burn Association: Melbourne. Hettiaratchy S, Papini R. Initial management of a major burn: II––assessment and resuscitation. BMJ. 2004. 329(7457):101–3. Benson A, Dickson WA, Boyce DE. ABC of wound healing: burns. Bri Med J, 2006. 332:649– 652. Blumetti J, et al. The Parkland formula under fire: is the criticism justified? J Burn Care Res, 2008. 29(1):180–6. Kahn SA, Schoemann M, Lentz CW. Burn resuscitation index: a simple method for calculating fluid resuscitation in the burn patient. J Burn Care Res, 2010. 31(4):616–23. Greenhalgh DG. Burn resuscitation. J Burn Care Res, 2007. 28(4):555–65. Jaskille AD, et al. Repetitive ischemia–reperfusion injury: a plausible mechanism for documented clinical burn–depth progression after thermal injury. J Burn Care Res, 2007. 28(1):13–20. Saffle JI. The phenomenon of "fluid creep" in acute burn resuscitation. J Burn Care Res, 2007. 28(3): 382–95. Ipaktchi K, Arbabi S. Advances in burn critical care. Crit Care Med, 2006. 34(9 Suppl):S239– 44. Freiburg C et al. Effects of differences in percent total body surface area estimation on fluid resuscitation of transferred burn patients. J Burn Care Res, 2007. 28(1):42–8. Ansermino JM, Vandebeek CA, Myers D. An allometric model to estimate fluid requirements in children following burn injury. Paediatr Anaesth. 2010. 20(4):305–12. Maybauer,DM, Maybauer MO, and Traber DL. Resuscitation with hypertonic saline in burn shock and sepsis. Crit Care Med. 2006. 34(6):1849–50. Jeng JC, et al. Improved markers for burn wound perfusion in the severely burned patient: the role for tissue and gastric PCO2. J Burn Care Res. 2008. 29(1):49–55.


21. Moss LS. Treatment of the burn patient in primary care. Adv Skin Wound Care, 2010. 23(11): 517–24;quiz 525–6. 22. Hudspith J, Rayatt S. First aid and treatment of minor burns. BMJ, 2004. 328(7454):1487– 9. 23. Maghsoudi H, Adyani Y, Ahmadian N. Electrical and lightning injuries. J Burn Care Res, 2007. 28(2):255–61. 24. Laskowski–Jones L. First aid for burns. Nursing. 2006. 36(1):41–3. 25. Evers LH, Bhavsar D, Mailander P. The biology of burn injury. Exp Dermatol. 2010. 19(9):777–83. 26. Jackson DM. The diagnosis of the depth of burning. Br J Surg. 1953. 40(164):588–96. 27. KaganRJ,. Smith SC. Evaluation and treatment of thermal injuries. Dermatol Nurs. 2000. 12(5): 334–5,338–44,347–50. 28. Devgan L, et al. Modalities for the assessment of burn wound depth. J Burns Wounds. 2006. 5:e2. 29. Singh V, et al. The pathogenesis of burn wound conversion. Ann Plast Surg. 2007. 59(1):109–15. 30. Loos MS, Freeman BG, Lorenzetti A. Zone of injury: a critical review of the literature. Ann Plast Surg. 2010. 65(6):573–7. 31. Demling RH. The burn edema process: current concepts. J Burn Care Rehabil. 2005. 26(3): 207–27. 32. Shupp JW, et al. A review of the local pathophysiologic bases of burn wound progression. J Burn Care Res. 2010. 31(6):849–73. 33. Jackson DM. Second thoughts on the burn wound. J Trauma. 1969. 9(10):839–62. 34. Merz J, et al. Wound care of the pediatric burn patient. AACN Clin Issues. 2003. 14(4):429–41. 35. Bak Z, et al. Hemodynamic changes during resuscitation after burns using the Parkland formula. J Trauma. 2009. 66(2):329–36. 36. Fodor, L. , et al. , Controversies in fluid resuscitation for burn management: literature review and our experience. Injury, 2006. 37(5): p. 374–9. 37. Kramer G, Lund T, Beckum O. Pathophysiology of burn shock and burn edema, in Total Burn Care, Herndon DN, Editor. 2007, Saunders: London. p. 93–106. 38. Latenser BA. Critical care of the burn patient: the first 48 hours. Crit Care Med. 2009. 37(10): 2819–26. 39. Pham TN, Cancio LC,. Gibran NS. American Burn Association practice guidelines burn shock resuscitation. J Burn Care Res. 2008. 29(1): 257–66. 40. Sheridan RL. Burns. Crit Care Med, 2002. 30(11 Suppl):S500–14. 41. Palmieri TL. Use of beta–agonists in inhalation injury. J Burn Care Res. 2009. 30(1): 156–9. 42. Fidkowski CW, et al. Inhalation burn injury in children. Paediatr Anaesth. 2009. 19 Suppl 1: 147–54. 43. Shirani KZ. , B. A. Pruitt, and A. D. J. Mason, The influenece of inhalation injury and pneumonia on burn mortality. Ann Surg. 1987. 205(1):82–87.


44. Maybauer MO,. Maybauer DM, Herndon D. Incidence and outcomes of acute lung injury. N Engl J Med. 2006. 353(16):1685–93. 45. Kimmel EC, Still KR. Acute lung injury, acute respiratory distress syndrome and inhalation injury: an overview. Drug Chem Toxicol. 1999. 22(1):91–128. 46. Smith DL, et al. Effect of inhalation injury, burn size, and age on mortality: a study of 1447 consecutive burn patients. J Trauma, 1994. 37(4):655–9. 47. Finnerty CC,. Herndon DN,. Jeschke MG. Inhalation injury in severely burned children does not augment the systemic inflammatory response. Crit Care. 2007. 11(1):R22. 48. Palmieri TL, et al. Inhalation injury in children: a 10 year experience at Shriners Hospitals for Children. J Burn Care Res. 2009. 30(1):206–8. 49. Fraser JF, Venkatesh B. (2005) Recent advances in the management of burns. Australasian Anaesthesia. 23–32. 50. Endorf FW, Gamelli R. Inhalation injury, pulmonary pertubations, and fluid resuscitation. J Burn Care Res. 2007. 28(1):80–3. 51. Mlcak RP, Suman OE, Herndon DN. Respiratory management of inhalation injury. Burns. 2007. 33(1):2–13. 52. Toon MH, Maybauer MO, Fraser JF. Management of acute smoke inhalation injury. Crit Care Resusc. 2010. 12:53–61. 53. Bartlett D. Tricky toxic presentation at triage. H J Emerg Nurs. 2005. 31(4):403–404. 54. Kealey GP, Barillo DJ, Wells SM. Study proposals for inhaled gases. J Burn Care Res. 2009. 30(1): 154–155. 55. Cochran A. Inhalation injury and endotracheal intubation. J Burn Care Res. 2009. 30(1): 190–1. 56. Robb BWK, et al. Outpatient and emergency department management of thermal injuries. Problems in General Surgery. 2003. 20(1):7–15. 57. Reed JL, Pomerantz, WJ. Emergency management of pediatric burns. Pediatr Emerg Care. 2005. 21(2):118–29. 58. Johnson RM, Richard R. Partial–thickness burns: identification and management. Adv Skin Wound Care. 2003. 16(4):178–87; quiz 188–9. 59. Harris PNS, Vardaxis N, ed. Mosby's Dictionary Of Medicine, Nursing & Health Professionals. 2nd ed. 2010, Elsevier: Sydney. 60. Bensouilah JBP. Aromadermatology: Aromatherapy in the treatment and care of common skin conditions. 2006: Radcliffe Publishing. 61. Brown DEH. Lewis's Medical Surgical Nursing. 2nd ed. 2008, Marrickville: Mosby. 62. Copstead–Kirkhorn LCBJL. Pathophysiology. 4th ed. 2009: WB Saunders. 63. MacNeal RJ. Structure and function: biology of the skin: Merck Manual Home Edition. http://do3. jcsb. org/jde/2011/6th_Grade_Science/5_Organization_Dev_Living_Organisms/resources_orga nization_organisms/BODY_SYSTEMS/Structure_and_Function_Skin. pdf 2006. 64. Brannon H. Skin anatomy. In About.com Dermatology. 2007. 65. Chen LSM, Chen P, Liu W, Hsu C. Hypertonic saline enhances host defence and reduces apoptosis in burn mice by increasing toll–like receptors. Shock. 2010. 35(1):59–66.


66. Lawrence A, et al. Colloid administration normalizes resuscitation ratio and ameliorates "fluid creep". J Burn Care Res. 2010. 31(1): 40–7. 67. Mitra B, et al. Fluid resuscitation in major burns. ANZ J Surg. 2006. 76(1–2):35–8. 68. Foldi V, et al. Effects of fluid resuscitation methods on burn trauma–induced oxidative stress. J Burn Care Res. 2009. 30(6):957–66. 69. Cartotto R, Zhou A. Fluid creep: the pendulum hasn't swung back yet! J Burn Care Res. 2010. 31(4):551–8. 70. Mosier, M. J. , et al. , Early acute kidney injury predicts progressive renal dysfunction and higher mortality in severely burned adults. J Burn Care Res, 2010. 31(1): p. 83–92. 71. Kahn SA, Beers RJ, Lentz CW. Resuscitation after severe burn injury using high–dose ascorbic acid: a retrospective review. J Burn Care Res. 2011. 32(1):110–7. 72. Marshall WB. Resuscitation of combat casualties. AACN Advanced Critical Care. 2010. 21(3):279–287. 73. Yuan J, et al. Assessment of cooling on an acute scald burn injury in a porcine model. J Burn Care Res. 2007. 28(3):514–20. 74. Bartlett N, et al. Optimal duration of cooling for an acute scald contact burn injury in a porcine model. J Burn Care Res. 2008. 29(5):828–34. 75. Rajan V, et al. Delayed cooling of an acute scald contact burn injury in a porcine model: is it worthwhile? J Burn Care Res. 2009. 30(4):729–34. 76. Cuttle L, et al. The optimal temperature of first aid treatment for partial thickness burn injuries. Wound Repair Regen. 2008. 16(5):626–34. 77. Cuttle L, et al. The optimal duration and delay of first aid treatment for deep partial thickness burn injuries. Burns. 2010. 36(5):673–9. 78. Cuttle, L. , et al. , A review of first aid treatments for burn injuries. Burns. 2009. 35(6): p. 768–75. 79. Jandera V, et al. Cooling the burn wound: evaluation of different modalites. Burns. 2000. 26(3):265–70. 80. Cuttle L, et al. An audit of first–aid treatment of pediatric burns patients and their clinical outcome. J Burn Care Res. 2009. 30(6):1028–34. 81. Cuttle, L. , et al. , The efficacy of Aloe vera, tea tree oil and saliva as first aid treatment for partial thickness burn injuries. Burns, 2008. 34(8): p. 1176–82. 82. Orgill DP, Piccolo N. Escharotomy and decompressive therapies in burns. J Burn Care Res. 2009. 30(5):59–68. 83. Feldmann ME, Evans J. Early management of the burned pediatric hand. J Craniofac Surg. 2008. 19(4):942–50. 84. Spallek M, et al. Scald prevention campaigns: do they work? J Burn Care Res. 2007. 28(2):328–33. 85. Abeyasundara SL, et al. The changing pattern of pediatric burns. J Burn Care Res. 2011. 32(2): 178–84. 86. Ogilvie MP, Panthaki ZJ. Electrical burns of the upper extremity in the pediatric population. J Craniofac Surg 2008. 19(4):1040–6.


87. Vierhapper MF, et al. Electrical injury: a long–term analysis with review of regional differences. Ann Plast Surg. 2011. 66(1):43–6. 88. Li YY, et al. Successful treatment of a case of severe electrical burns with heart and lung injuries. J Burn Care Res. 2007. 28(5): p. 762–6. 89. Yeroshalmi F, et al. Oral electrical burns in children–a model of multidisciplinary care. J Burn Care Res. 2011. 32(2):e25–30. 90. Roblin I, et al. Topical treatment of experimental hydrofluoric acid skin burns by 2.5% calcium gluconate. J Burn Care Res. 2006. 27(6):889–94.


LAMPIRAN 1

Penilaian Neurologik Skoring Coma dari Glasgow Pembukaan mata

Tanggapan verbal terbaik

Tanggapan motor yang terbaik

Respon Spontan Untuk Nama Untuk nyeri Tidak ada Berorientasi Bingung Tidak tepat Tidak dimengerti Tidak ada Mematuhi Melokalisir Penarikan Abnormal Fleksi Perpanjangan Tidak ada

Skor 4 3 2 1 5 4 3 2 1 6 5 4 3 2 1 15

Gambar 2. 1

Cedera Kepala Kategori Berat Sedang Ringan Gambar 2. 2

GCS < 9 9 – 12 13 – 15


LAMPIRAN 2

Protokol Tetanus TabeL 3. 21. 1: Panduan untuk tetanus profilaksis dalam manajemen luka Riwayat vaksinasi tetanus

Waktu sejak Jenis luka dosis terakhir

DTPa, DTPa– Tetanus kombinasi, dT, DTPA, immunoglobulin* yang sesuai (TIG)

≥3 dosis

<5 tahun

Semua luka

Tidak

Tidak

≥3 dosis

5–10 tahun

Luka ringan

Tidak

Tidak

≥3 dosis

5–10 tahun

Semua yang lain

≥3 dosis

>10 tahun

luka Ya

Tidak

Semua luka

Ya

Tidak

<3 dosis atau dak pas †

Luka ringan

Ya

Tidak

<3 dosis atau dak pas †

Semua yang lain

luka Ya

Ya

Dosis yang dianjurkan untuk TIG adalah 250 IU, diberikan melalui suntikan im menggunakan jarum berukuran 21, sesegera mungkin setelah cedera. Bila lebih dari 24 jam telah berlalu, 500 IU harus diberikan. † penderita yang dak memiliki riwayat yang tercatat dari vaksinasi pertama (3 dosis) dengan tetanus toksoid yang mengandung vaksin harus menerima semua dosis yang dilewati. Lihat Bagian 1. 3. 5, diikuti.

(Sumber: Buku Panduan Immunisasi Australia (Edisi Sembilan) Halaman 288)


LAMPIRAN 3

Rekomendasi untuk Sayatan Eskarotomi


LAMPIRAN 4

Balutan Produk Perawatan Luka Apa? - Silikon / busa - busa hidrofilik poliuretan - + Lapisan silikon lembut - +lapisan luar tahan air - Juga tersedia dengan perak - Hydrocolloid - Hydrocolloid wafer

-

Kasa Vaseline dilapisi minyak

-

Perak Sodium carboxymethyc ellulose (CMC) & 1. 2% ion Ag pada bahan berserat Juga Contreet H

-

yang kasa

Fungsi Mengapa? - Tidak patuh - Mematuhi

Indikasi Kapan? - Luka bakar superfisial

Aplikasi Bagaimana? - Dipakai untuk membersihkan luka - Tutup dengan balutan fiksasi

Catatan / Pencegahan - Tidak boleh digunakan bila ada infeksi

- Bantuan autolisis jaringan - Menyediakan lingkungan lembab - Menyerap eksudat - Balutan antiseptik - Mematuhi

- Luka bakar yang superficial hingga mid – dermal - mengeluarkan eksudat rendah sampai sedang

- Tidak boleh digunakan bila ada infeksi

- Spektrum antimikroba yang besar - fasilitas Debridement - Menyerap eksudat

- Luka bakar superficial hingga dalam - Cukup membersihkan luka

- Batas 2–5cm sekitar luka. - Dapat tetap utuk 2–3 hari - Wafer sampai 5 hari bila tidak ada tanda– tanda infeksi. - Digunakan langsung pada luka - 2–3 lapis untuk emergensi - Tutup dengan balutan sekunder - Ganti setiap 1– 3 hari - Digunakan untuk luka yang lembab. - Memunkinkan 2–5 cm bersamaan waktu - Tutup dengan balutan kedua. - Ulas 7–10 hari

- Luka bakar kulit yang tebal - Bagian pengcangkokan dan donor


- Rendam bila digunakan pada dasar luka.

- Kejenuhan eksudat menunjukkan indikasi penggantian balutan

- Biarkan utuh sampai sembuh

- Perak - Nanokristalin Ag yang dilapisi dengan jala

- Proteksi Spektrum antimikroba luas Mengurangi fpembentukane ksudat

- Luka bakar dalam - Bagian pengcangkokan dan donor - Luka terinfeksi

- Perak - Silver Sulfadiazin 1%

- Mengurangi infeksi

- Luka yang terinfeksi - Luka bakar kulit yang besar bila tersedia

- Basahi dengan H2O; alirkan dan terapkan sisi biru / perak menghadap ke bawah. - Lembabkan balutan kedua - Ganti 3–4 hari or 7 hari - Pakailah jumlah yang benar - Gunakan sarung tangan - Terapkan balutan sekunder.


- Hiperpigmentas i temporer - Hindari bila alergi terhadap perak - Hindari hipotermia

- Tidak direkomendasik an untuk semua jenis luka bakar karena perubahan pada penampilan luka dan frekuensi penggantian balutan

EMSB 2013

Recommend Documents