Académique Documents
Professionnel Documents
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TOXICOLOGY HANDBOOK
Second edition
Churchill Livingstone
is an imprint of Elsevier
CONTENTS
ix
x
xi
xii
Foreword
Preface
Authors
Contributors
CHAPTER 1: APPROACH TO THE POISONED PATIENT
1.1
1.2
1.3
1.4
1.5
1.6
1.7
1.8
1.9
Overview
Resuscitation
Risk assessment
Supportive care and monitoring
Investigations
Gastrointestinal decontamination
Enhanced elimination
Antidotes
Disposition
2
4
10
13
15
17
24
29
30
2.1
2.2
2.3
2.4
2.5
2.6
2.7
2.8
2.9
2.10
2.11
2.12
2.13
2.14
2.15
2.16
2.17
2.18
2.19
2.20
2.21
2.22
2.23
Approach to snakebite
Approach to mushroom poisoning
Approach to plant poisoning
Coma
Hypotension
Approach to seizures
Delirium and agitation
Serotonin syndrome
Anticholinergic syndrome
Cholinergic syndrome
Neuroleptic malignant syndrome
Alcohol abuse, dependence and withdrawal
Amphetamine abuse, dependence and withdrawal
Opioid dependence and withdrawal
Sedative-hypnotic dependence and withdrawal
Solvent abuse, dependence and withdrawal
Body packers and stuffers
Osmolality and the osmolar gap
Acidbase disorders
The 12-lead ECG in toxicology
Poisoning during pregnancy and lactation
Poisoning in children
Poisoning in the elderly
36
44
50
55
59
61
62
66
72
76
80
85
93
94
97
100
104
107
109
113
119
120
126
3.1
3.2
3.3
3.4
3.5
3.6
3.7
Alcohol: Ethanol
Alcohol: Ethylene glycol
Alcohol: Isopropanol (isopropyl alcohol)
Alcohol: Methanol (methyl alcohol)
Alcohol: Other toxic alcohols
Amiodarone
Amisulpride
130
133
136
138
142
144
146
TABLE OF CONTENTS
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TOXICOLOGY HANDBOOK
vi
3.8
3.9
3.10
3.11
3.12
3.13
3.14
3.15
3.16
3.17
3.18
3.19
3.20
3.21
3.22
3.23
3.24
3.25
3.26
3.27
3.28
3.29
3.30
3.31
3.32
3.33
3.34
3.35
3.36
3.37
3.38
3.39
3.40
3.41
3.42
3.43
3.44
3.45
3.46
3.47
3.48
3.49
3.50
3.51
3.52
3.53
3.54
3.55
3.56
3.57
3.58
3.59
3.60
Amphetamines
Angiotensin converting enzyme inhibitors
Anticoagulant rodenticides
Anticonvulsants: Newer agents
Antihistamines (non-sedating)
Antihistamines (sedating)
Arsenic
Beta-blockers
Baclofen
Barbiturates
Benzodiazepines
Benztropine
Bupropion
Button batteries
Calcium channel blockers
Cannabinoids (marijuana)
Carbamazepine
Carbon monoxide
Chloroquine and hydroxychloroquine
Chloral hydrate
Clonidine
Clozapine
Cocaine
Colchicine
Corrosives
Cyanide
Digoxin: Acute overdose
Digoxin: Chronic poisoning
Diphenoxylate-atropine
Gamma-hydroxybutyrate (GHB)
Glyphosate
Hydrocarbons
Hydrofluoric acid
Hydrogen peroxide
Insulin
Iron
Isoniazid
Lead
Lithiumacute overdose
Lithiumchronic poisoning
Local anaesthetic agents
Mercury
Metformin
Methotrexate
Mirtazapine
Monoamine oxidase inhibitors (MAOIs)
Non-steroidal anti-inflammatory drugs
Olanzapine
Opioids
Organochlorines
Organophosphorus agents
Paracetamol: Acute overdose
Paracetamol: Repeated supratherapeutic ingestion
148
152
154
157
159
162
164
168
171
173
177
179
181
184
186
190
193
196
200
202
205
208
210
214
216
219
222
226
230
232
235
237
240
244
247
250
254
256
260
263
265
269
273
276
279
280
284
287
290
295
298
302
311
315
319
322
325
327
330
333
335
339
342
345
347
351
353
356
360
363
367
CHAPTER 4: ANTIDOTES
4.1
4.2
4.3
4.4
4.5
4.6
4.7
4.8
4.9
4.10
4.11
4.12
4.13
4.14
4.15
4.16
4.17
4.18
4.19
4.20
4.21
4.22
4.23
4.24
4.25
4.26
4.27
4.28
4.29
Atropine
Calcium
Cyproheptadine
Desferrioxamine
Dicobalt edetate
Digoxin immune Fab
Dimercaprol
Ethanol
Flumazenil
Folinic acid
Fomepizole
Glucagon
Glucose
Hydroxocobalamin
Insulin (high dose)
Intravenous lipid emulsion
Methylene blue
N-acetylcysteine
Naloxone
Octreotide
Penicillamine
Physostigmine
Pralidoxime
Pyridoxine
Sodium bicarbonate
Sodium calcium edetate
Sodium thiosulfate
Succimer
Vitamin K
372
373
376
377
379
381
383
385
387
389
391
392
394
396
398
400
401
403
406
408
410
411
413
415
417
420
422
424
426
CHAPTER 5: ENVENOMINGS
5.1
5.2
Black snake
Brown snake
430
433
TABLE OF CONTENTS
Paraquat
Phenothiazines and butyrophenones (antipsychotic agents)
Phenytoin
Potassium chloride
Quetiapine
Quinine
Risperidone
Salicylates
Selective serotonin reuptake inhibitors (SSRIs)
Strychnine
Sulfonylureas
Theophylline
Thyroxine
Tramadol
Tricyclic antidepressants (TCAs)
Valproic acid (sodium valproate)
Venlafaxine and desvenlafaxine
Warfarin
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TOXICOLOGY HANDBOOK
3.61
3.62
3.63
3.64
3.65
3.66
3.67
3.68
3.69
3.70
3.71
3.72
3.73
3.74
3.75
3.76
3.77
3.78
TABLE OF CONTENTS
5.3
5.4
5.5
5.6
5.7
5.8
5.9
5.10
5.11
5.12
5.13
5.14
5.15
5.16
viii
Death adder
Tiger snake
Taipan
Sea snake
Australian scorpions
Bluebottle jellyfish (Physalia)
Stonefish
Box jellyfish (Chironex fleckeri)
Irukandji syndrome
Blue-ringed octopus
Redback spider
Funnel-web (big black) spider
White-tailed spider
Ticks
436
439
442
445
447
449
450
452
454
457
459
461
463
465
CHAPTER 6: ANTIVENOMS
6.1
6.2
6.3
6.4
6.5
6.6
6.7
6.8
6.9
6.10
6.11
470
471
473
475
477
479
481
482
484
486
488
ii
vi
TOXICOLOGY HANDBOOK
APPENDICES
492
493
498
499
500
502
503
FOREWORD
Poisoning is a common emergency department presentation, and the third
major injury cause of hospital admissions after falls and motor vehicle
crashes. Alcohol, benzodiazepines, antidepressants, paracetamol and heroin
are frequently involved, yet there are literally thousands of hazardous
substances that can be ingested, as well as envenomings by terrestrial animals
and sea creatures.
The challenge for the emergency physician is to be able to recognise the
poisoned patient, provide supportive care, administer a specific antidote in a
minority of cases, escalate management up to a full intensive care level when
necessary, and know when a patient is safe to be medically cleared pending
a thorough psychiatric examination (in cases of deliberate self-harm). This
presents a huge challenge to any doctor, who individually may infrequently see
a severe poisoning and or can be confronted with a first case of a particular type.
Clinical Toxicology has developed rapidly as a subspecialty of Emergency
Medicine in Australasia, led by a small group of expert clinicians dedicated
to providing information, advice, research and teaching in this important area.
The authors are in the vanguard of this group. All regularly direct and assist
toxicology patient care in emergency departments, intensive care units and
small rural hospitals across the country, locally as well through the national
Poisons Information Centres.
Their risk assessment-based approach is maintained in this new version that
builds on the success of the first edition. This handbook has been updated and
expanded with the addition of many new chapters, yet it retains its award-winning
format recognised for its lucidity and readability. The compact size of the book
belies the true wealth of clear, practical evidence-based information covering a
vast array of poisonings and their management in a logical, consistent format.
This book should live in the pocket or at the bedside, be used daily and
be referred to as a prevailing standard of care not just in Australasia, but
internationally. With the exception of some envenomings, the book will be just
as valuable to clinicians in the UK, Europe and Asia as no doubt it will again
prove to be here in Australasia. It is a truly outstanding text that will improve
the care of poisoned patients to their benefit, and the readers edification.
Professor Anthony FT Brown MB ChB, FRCP, FRCS(Ed), FACEM, FCEM
Senior Staff Specialist, Department of Emergency Medicine, Royal
Brisbane and Womens Hospital
Professor, Discipline of Anaesthesiology and Critical Care, University
of Queensland
Editor-in-Chief, Emergency Medicine Australasia
Senior Court of Examiners, ACEM
August 2010
[AQ1]
ix
PREFACE
Lindsay Murray
Frank Daly
Mark Little
Mike Cadogan
Jason Armstrong
Kerry Hoggett
David McCoubrie
Mark Monaghan
Jessamine Soderstrom
Ovidiu Pascu
A UTHORS
Lindsay Murray MBBS FACEM, Consultant Emergency Physician and
Clinical Toxicologist, Sir Charles Gairdner Hospital, Perth, WA; Clinical
Associate Professor of Emergency Medicine, University of Western
Australia
Frank Daly MBBS FACEM, Consultant Clinical Toxicologist, Emergency
Physician and Director of Clinical Service Redesign, Royal Perth Hospital;
Professor in Emergency Medicine, University of Western Australia;
Consultant Clinical Toxicologist WA and NSW Poisons Information
Centres
Mark Little MBBS DTM&H (Lond) FACEM MPH&TM IDHA, Consultant
Emergency Physician and Clinical Toxicologist, Royal Perth Hospital;
Clinical Senior Lecturer in Emergency Medicine, University of Western
Australia; Consultant Clinical Toxicologist, WA and NSW Poisons
Information Centres
Mike Cadogan MA (Oxon) MBChB FACEM, Consultant Emergency
Physician, Sir Charles Gairdner Hospital, Perth
CONTRIBUTORS
Jason Armstrong MBChB FACEM, Consultant Emergency Physician and
Clinical Toxicologist, Sir Charles Gairdner Hospital, Perth; Clinical
Senior Lecturer in Emergency Medicine, University of Western Australia;
Medical Director, WA Poisons Information Centre; Consultant Clinical
Toxicologist, NSW Poisons Information Centre
Kerry Hoggett MBBS GCertClinTox FACEM, Emergency Physician, Clinical
Toxicology Fellow, Royal Perth Hospital
David McCoubrie MBBS FACEM, Consultant Emergency Physician
and Clinical Toxicologist, Royal Perth Hospital; Consultant Clinical
Toxicologist, WA and NSW Poisons Information Centres
Mark Monaghan MBBS FACEM, Consultant Emergency Physician and
Fellow in Clinical Toxicology 20052007, Fremantle Hospital; Consultant
Clinical Toxicologist, WA and NSW Poisons Information Centres
Jessamine Soderstrom MBBS FACEM Grad Cert Toxicology, Clinical
Toxicologist, Emergency Physician, Royal Perth Hospital, Perth, Clinical
Senior Lecturer, University of Western Australia
Ovidiu Pascu MD FACEM, Consultant Emergency Physician and Clinical
Toxicologist, Sir Charles Gairdner Hospital, WA, WA and NSW Poisons
Information Centres; Clinical Senior Lecturer in Emergency Medicine,
University of Western Australia
xi
REVIEWERS
Belinda Bray PhD, Lecturer, Science Communication, University of Auckland
Philip G. Kerr PhD, Lecturer in Medicinal Chemistry, School of Biomedical
Sciences, Charles Sturt University; Australasian Regional Representative
for International Council for Medicinal and Aromatic Plants (ICMAP)
Ian Spence BSc PhD, Associate Dean (International), Faculty of Science
and Honorary Associate Professor, Discipline of Pharmacology, Sydney
Medical School, The University of Sydney
Scott Twaddell BMedSc(Hons) BMed GCClinTox FRACP, Clinical
Pharmacologist and Toxicologist, Respiratory and General Physician, Staff
Specialist Physician, John Hunter Hospital and Calvary Mater Newcastle
Hospital; Conjoint Lecturer in Medicine, University of Newcastle
xii
i
xi
CHAPTER 1
Overview
Resuscitation
Risk assessment
Supportive care and monitoring
Investigations
Gastrointestinal decontamination
Enhanced elimination
Antidotes
Disposition
2
4
10
13
15
17
24
29
30
2
2
TOXICOLOGY HANDBOOK
1.1 OVERVIEW
Acute poisoning is a common emergency medicine presentation. Between
150 and 400 acute poisoning presentations annually can be expected
for each 100 000 population served by an emergency department.
Acute poisoning is a dynamic medical illness that frequently represents
a potentially life-threatening exacerbation of a chronic psychosocial
disorder. However, this is a highly heterogeneous patient population:
deliberate self-poisoning, recreational drug abuse, occupational poisoning
and envenoming challenge with myriad potential presentations. The
clinician needs a robust and simple clinical approach that can address
this heterogeneity, but which allows the development of a management
plan tailored to the individual patient at that particular presentation at that
particular medical facility.
Risk assessment is pivotal to that robust approach. It is a distinct
cognitive process through which the clinician attempts to predict the
likely clinical course and potential complications for the individual at
that particular presentation. Risk assessment should wherever possible be
quantitative and take into account the agent, dose and time of ingestion,
clinical features and progress, and individual patient factors (e.g. weight
and co-morbidities).
Toxicology management guidelines frequently focus on the agent
involved. This makes adaptation of treatment recommendations to an
individual patient in a particular location difficult. A risk-assessmentbased approach ensures the clinician addresses potentially time-critical
management priorities in an appropriate order, but avoids unnecessary
investigations or interventions.
Risk assessment is secondary only to resuscitation in the management
of acute poisoning. It allows subsequent management decisions regarding
supportive care and monitoring, investigations, decontamination, use of
enhanced elimination techniques, antidotes and disposition to be made in
a sensible structured manner.
Ideally, this risk-assessment-based approach is supported by a
healthcare system designed to address both the medical and psychological
needs of the poisoned patient. Where the medical needs of a patient
exceed local resources, a risk-assessment-based management approach
ensures that this is identified early and disposition planning and
communication occur in a proactive manner within that organised system.
In this handbook, the authors offer a systematic risk-assessmentbased approach to the management of acute poisoning as it presents to
the emergency department. Separate chapters cover the pharmaceutical,
chemical and natural toxins of most importance to the practitioner in
emergency departments in Australia and New Zealand. It will also be of
Resuscitation
Airway
Breathing
Circulation
Detect and correct
hypoglycaemia
seizures
hyper-/hypothermia
Emergency antidote administration
Risk assessment
Agent
Dose
Time since ingestion
Clinical features and course
Patient factors
Supportive care and monitoring
Investigations
Screening12-lead ECG, paracetamol
Specific
Decontamination
Enhanced elimination
Antidotes
Disposition
3
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4
4
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1.2 RESUSCITATION
INTRODUCTION
Poisoning is a leading cause of death in patients under the age of 40 years
and is a leading differential diagnosis when cardiac arrest occurs in a
young adult.
Unlike cardiac arrest in the older population, resuscitation following
acute poisoning may be associated with good neurological outcomes even
after prolonged periods (hours) of cardiopulmonary resuscitation (CPR).
Therefore, while poisoning is considered part of the differential diagnosis
in a patient with cardiac arrest, resuscitation should continue until
expert advice can be obtained. Cardiopulmonary bypass has been used
successfully in a number of poisonings.
Attempts at decontamination of the skin or gastrointestinal tract
never take priority over resuscitation and institution of supportive care
measures.
5
TOXICOLOGY HANDBOOK
Various
Opioid mu receptor
stimulation
Cholinergic crisis
Hypoventilation
Respiratory failure
Corrosive injury to
oropharynx
Mechanism
Acidosis
Acidaemia
BREATHING
Airway compromise
AIRWAY
Life-threat
l
l
l
l
l
l
l
l
l
l
Carbamates
Nerve agents
Organophosphates
Opioids
Ethylene glycol
Methanol
Salicylates
Alkalis
Acids
Glyphosate
Paraquat
Agent(s)
l
l
Comments
TABLE 1.2.2 Specific resuscitation situations in toxicology where conventional algorithms or approaches may not apply
TOXICOLOGY HANDBOOK
Hypocalcaemia
Halogen-induced
myocardial
sensitisation to
catecholamines
Ventricular
tachycardia
Ventricular ectopy/
Ventricular
tachycardia
Oxygen-free
radical mediated
cellular injury,
particularly type II
pneumocytes
Ventricular
fibrillation
CIRCULATION
Acidosis;
Hypoxaemia;
Multiple organ
failure (MOF)
l
l
l
l
l
l
l
l
l
l
l
l
l
l
l
l
Continued
TOXICOLOGY HANDBOOK
Chloral hydrate
Organochlorines
Chloroquine
Cocaine
Flecainide
Local anaesthetic
agents
Procainamide
Propranolol
Quinine
Tricyclic
antidepressants
Hydrofluoric acid
ingestion or massive
cutaneous burn
Paraquat
Mechanism
Various
Central and
peripheral
sympathomimetic
response
Adenosine
antagonism
Central and
peripheral
sympathomimetic
response
Na+/K+ ATPase
pump inhibition
Life-threat
Refractory
hypotension
Tachycardia
Supraventricular
tachycardia
Hypertension
Asystole
Bradycardia
Tachycardia
l
l
l
l
l
l
l
Digoxin
Amphetamines
Cocaine
Theophylline
Amphetamines
Cocaine
Beta-blockers
Calcium channel
blockers
Local anaesthetic
agents
Agent(s)
l
l
l
l
l
l
Beta-blockers contraindicated
Administer IV benzodiazepines, titrated to gentle
sedation and heart rate control
If further therapy necessary use agents that can be
given by titratable intravenous infusion
Glycerol trinitrate (GTN)
Phentolamine
Nitroprusside
Beta-blockers contraindicated
Administer IV benzodiazepines, titrated to gentle
sedation and heart rate control
Comments
TABLE 1.2.2 Specific resuscitation situations in toxicology where conventional algorithms or approaches may not applycontd
TOXICOLOGY HANDBOOK
Central and
peripheral
sympathomimetic
response
Acute coronary
syndrome
Na+/K+ ATPase
pump inhibition
Hyperinsulinaemia
Inhibition of GABA
production
Adenosine
antagonism
Hyperkalaemia
Hypoglycaemia
Refractory seizures
Seizures
OTHER
Calcium channel
blockade
Bradycardia
Hypotension
Cardiac conduction
defects
l
l
l
l
l
l
l
l
l
l
Beta-blockers contraindicated
Benzodiazepines
GTN
Antiplatelet and anticoagulation therapy if no
neurological deficits (otherwise cranial CT first)
Reperfusion therapy along conventional lines
TOXICOLOGY HANDBOOK
Theophylline
Isoniazid
Sulfonylureas
Digoxin
Amphetamines
Cocaine
Calcium channel
blockers
10
10
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1
2
3
4
5
6
7
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14
The needs of the vast majority of patients can be met in the emergency
department, emergency observation unit or intensive care unit. The
emergency observation unit is appropriate for the ongoing management
of most acute poisonings, where the general supportive measures outlined
below can be provided.
Criteria for admission to an emergency observation unit following
acute poisoning include:
1 Ongoing cardiac monitoring not required
2 Adequate sedation achieved
3 Clinical deterioration not anticipated.
Criteria for admission to an intensive care unit following acute
poisoning include requirements for:
1 Airway control
2 Ventilation
3 Prolonged or invasive haemodynamic monitoring or support
4 Haemodialysis.
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1.5 INVESTIGATIONS
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16
Lithium
Methanol
Methotrexate
Paracetamol
Phenobarbitone
Salicylate
Theophylline
Valproic acid
DECONTAMINATION
Carbamazepine
Digoxin
Ethanol
Ethylene glycol
Iron
17
TOXICOLOGY HANDBOOK
TABLE 1.5.3 Useful drug levels that may assist risk assessment or
management in specific settings
18
TOXICOLOGY HANDBOOK
18
expectation that by reducing the dose absorbed they will also reduce
the subsequent severity and duration of clinical toxicity. Unfortunately,
the tendency has been to overestimate the potential benefits while
underestimating the potential hazards of gastrointestinal decontamination
procedures. These procedures do not provide significant benefit when
applied to unselected deliberate self-poisoned patients and are no longer
considered routine.
The theoretical benefits of gastrointestinal decontamination in selected
poisonings have not been evaluated. The decision to decontaminate is one
of clinical judgment in which the potential benefits are weighed against
the potential risks and the resources required to perform the procedure
(see Figure 1.6.1 and Table 1.6.2).
Employing this rationale, gastrointestinal decontamination is reserved
for cases where the risk assessment predicts severe or life-threatening
toxicity and where supportive care or antidote treatment alone is
insufficient to ensure a satisfactory outcome. There should be reasonable
grounds to believe that a significant amount of agent remains unabsorbed
and is amenable to removal by the selected procedure. This requires some
knowledge of the absorption kinetics of the agent(s) involved. For most
ingested agents, absorption is virtually complete within 1 hour.
Gastrointestinal decontamination is never performed to the detriment
of basic resuscitation or supportive care. To avoid pulmonary aspiration,
the procedure is not performed without first securing the airway in a
patient with a depressed level of consciousness or in whom the risk
TABLE 1.6.1 Methods of gastrointestinal decontamination
l
l
l
l
Potential risks
l
Pulmonary aspiration
l
Gastrointestinal complications
bowel obstruction
perforation
l
Distraction of staff from
resuscitation and supportive
care priorities
l
Diversion of departmental
resources for performance of
procedure
Contraindications
l
l
l
l
l
l
l
l
Non-toxic ingestion
Dose ingested known to be sub-toxic
Seizures or decreased level of consciousness
Risk assessment indicates potential for seizures or decreased level of
consciousness within the next few hours
Activated charcoal available within 1 hour and known to bind agent
Infants <12 months of age
Corrosive ingestion
Hydrocarbon ingestion.
Potential complications
l
l
l
19
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20
20
TOXICOLOGY HANDBOOK
l
l
GASTRIC LAVAGE
This technique attempts to empty the stomach of toxic substances by the
sequential administration and aspiration of small volumes of fluid from
the stomach via an orogastric tube. This previously widely favoured
method of gastrointestinal decontamination has now been all but
abandoned and few emergency departments remain experienced in its use.
The amount of toxin removed by gastric lavage is unreliable and
negligible if performed after the first hour. It does not confer any clinical
benefit when performed routinely on unselected patients presenting to the
emergency department following deliberate self-poisoning. There are few
situations where the expected benefits of this procedure might be judged
to exceed the risks involved and where administration of charcoal would
not be expected to provide equal or greater efficacy of decontamination.
Technique
l
l
l
l
Absolute contraindications
l
l
l
l
l
Potential complications
l
l
l
l
l
l
l
Pulmonary aspiration
Hypoxia
Laryngospasm
Mechanical injury to the gastrointestinal tract
Water intoxication (especially in children)
Hypothermia
Distraction of staff from resuscitation and supportive care priorities.
21
l
l
TOXICOLOGY HANDBOOK
Corrosives
Acids
Alkalis
Contraindications
l
l
l
l
22
22
TOXICOLOGY HANDBOOK
Metals
Lithium
Iron
Potassium
Lead
Arsenic
Mercury
l
l
Technique
Contraindications
l
l
l
l
l
l
l
Technique
l
l
l
l
l
l
Assign a single nurse to carry out procedure (this is a full-time job for
up to 6 hours)
Obtain sufficient supplies of PEG-ELS and make up solution as directed
Place nasogastric tube
Give activated charcoal 50 g (children 1 g/kg) via the nasogastric tube
in non-metallic ingestions
Administer PEG solution via the nasogastric tube at 2 L/hour (children
25 mL/kg/hour)
Administer metoclopramide to minimise vomiting and enhance gastric
emptying
Position patient on a commode if possible to accommodate explosive
diarrhoea
Continue irrigation until the effluent is clear. This may take up to 6 hours
Cease whole bowel irrigation if abdominal distension or loss of bowel
sounds are noted
l
l
l
l
l
l
23
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24
TOXICOLOGY HANDBOOK
References
American Academy of Clinical Toxicology and the European Association of Poison
Centres and Clinical Toxicologists. Position Paper: Whole bowel irrigation. Clinical
Toxicology 2004; 42:843854.
American Academy of Clinical Toxicology and the European Association of Poison
Centres and Clinical Toxicologists. Position Paper: Single-dose activated charcoal.
Clinical Toxicology 2004; 43:6187.
American Academy of Clinical Toxicology and the European Association of Poison
Centres and Clinical Toxicologists. Position Paper: Ipecac syrup. Clinical
Toxicology 2004; 42:133143.
American Academy of Clinical Toxicology and the European Association of Poison
Centres and Clinical Toxicologists. Position Paper: Gastric lavage. Clinical
Toxicology 2004; 42:933943.
Bailey B. Gastrointestinal decontamination triangle. Clinical Toxicology 2005; 1:5960.
Haemodialysis and
haemofiltration
Lithium
Metformin lactic acidosis
Potassium
Salicylate
Theophylline
Toxic alcohols
Valproic acid
Charcoal haemoperfusion
Theophylline
25
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Phenobarbitone coma
Rare
Used in the in the expectation that enhanced elimination will
reduce duration of ventilation and length of stay in intensive care
Dapsone overdose with methaemoglobinaemia
Very rare
MDAC may enhance elimination of dapsone and reduce the
duration of severe prolonged methaemoglobinaemia
Quinine overdose
Although MDAC might enhance drug elimination, good outcome
can be expected with aggressive supportive care
Theophylline overdose
Attempts at enhanced elimination with MDAC should never delay
more effective elimination with haemodialysis following lifethreatening overdose.
Absolute contraindications
l
Complications
l
l
l
l
l
Fluid overload.
Complications
l
l
l
Technique
l
l
l
Rationale
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URINARY ALKALINISATION
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l
l
l
References
Anonymous. Position Statement and Practice Guidelines on the use of multi-dose
activated charcoal in the treatment of acute poisoning. Clinical Toxicology 1999;
37(6):731751.
Dorrington CL, Johnson DW, Brant R. The frequency of complications associated with
the use of multiple-dose activated charcoal. Annals of Emergency Medicine 2003;
41(3):370377.
Pond SM, Olson KR, Osterloh JD et al. Randomised study of the treatment of
phenobarbital overdose with repeated doses of activated charcoal. Journal of the
American Medical Association 1984; 251:31043108.
Proudfoot AT, Krenzelok EP, Vale JA. Position paper on urine alkalinization. Journal of
Toxicology Clinical Toxicology 2004; 42:126.
Winchester JF. Dialysis and haemoperfusion in poisoning. Advances in Renal
Replacement Therapy 2002; 9(1):2630.
1.8 ANTIDOTES
Antidotes are drugs that correct the effects of poisoning. Only a few
antidotes exist for a limited number of poisonings and many are used only
extremely rarely. Specific antidotes likely to be used in clinical practice
are discussed in Chapter 4 of this book.
Like all pharmaceuticals, antidotes have specific indications,
contraindications, optimal administration methods, monitoring
requirements, appropriate therapeutic end points and adverse effect
profiles.
The decision to administer an antidote to an individual patient is
based upon a riskbenefit analysis. An antidote is administered when the
potential therapeutic benefit is judged to exceed the potential adverse
effects, cost and resource requirements. An accurate risk assessment
combined with pharmaceutical knowledge of the antidote is essential to
clinical decision making.
Many antidotes are rarely prescribed, expensive and not widely
stocked. Planning of stocking, storage, access, monitoring, training and
protocol development are essential components of rational antidote use.
It is often appropriate for stocking to be coordinated on a regional basis
in association with regional policies concerning the treatment of poisoned
patients. It is frequently cheaper and safer to transport an antidote to a
patient rather than vice versa.
References
Dart RC, Borrow SW, Caravati EM et al. Expert consensus guidelines for stocking of
antidotes in hospitals that provide emergency care. Annals of Emergency Medicine
2009: 54:386394.
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1.9 DISPOSITION
A medical disposition is required for all patients who present with
poisoning or potential exposure to a toxic substance. Those who have
deliberately self-poisoned also require psychiatric and social review.
A risk-assessment-based approach to the management of acute poisoning
allows early planning for appropriate medical and psychosocial disposition.
Patients must be admitted to an environment capable of providing an
adequate level of monitoring and supportive care and, if appropriate,
where staff and resources are available to undertake decontamination,
administration of antidotes or enhanced elimination techniques.
Early risk assessment in the pre-hospital setting, usually by poisons
information centre staff, often allows non-intentional exposures to be
observed outside of the hospital environment. For those that present to
hospital, it minimises the duration and intensity of monitoring. Frequently
patients can be cleared for medical discharge directly from the
emergency department immediately following assessment or following a
few hours of monitoring. No arrangements for admission to hospital need
be made unless unexpected signs or symptoms of toxicity develop.
At other times the risk assessment will indicate the need for ongoing
observation, supportive care or the need for specific enhanced elimination
techniques or antidote administration. Under these circumstances, the
patient must be admitted to an environment capable of providing a level of
care appropriate for the anticipated clinical course. In many hospitals, this is
now the emergency observation unit rather than the general medical ward.
Where ongoing airway control, ventilation or advanced haemodynamic
support is required then admission to an intensive care unit is appropriate.
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The need to retrieve a patient to another centre should not distract attending
staff from resuscitation and supportive care priorities. Attention to airway,
breathing and circulation ensure an optimum outcome in the majority of
cases. Whenever possible, the patient should be stabilised before retrieval
begins. Interventions such as intubation, ventilation, initial resuscitation
of hypotension, cessation of seizures, assessment of blood glucose and
management of hyperthermia are completed before a patient is placed in
the transport vehicle, where further assessment and detailed management
are often impossible. If the referring team does not possess the necessary
skills or resources to complete these resuscitation and stabilisation tasks
adequately, this should be communicated to the receiving and retrieval
teams, so that these resources can be brought to the patient.
Transport
As transport usually occurs during the most severe phase of the poisoning,
the patient should never be subjected to an interval of a lower level of care
during the transfer. Consideration of the mode and staffing of transport
takes this into account.
Planning
Communication
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