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TOXICOLOGY�HANDBOOK

�RD EDITION

Lindsay Murray Mark Li� le

Ovidiu Pascu Kerry Hogge�

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CONTENTS

Foreword ix

Preface x

Editors xi

Contributors xii

Reviewers xiii

CHAPTER 1 APPROACH TO THE POISONED PATIENT

1.1 Overview 21.2 Resuscitation 41.3 Risk assessment 121.4 Supportive care and monitoring 141.5 Investigations 161.6 Gastrointestinal decontamination 191.7 Enhanced elimination 261.8 Antidotes 321.9 Disposition 32

CHAPTER 2 SPECIFIC CONSIDERATIONS

2.1 Approach to snakebite 382.2 Approach to mushroom poisoning 452.3 Approach to plant poisoning 522.4 Coma 582.5 Hypotension 622.6 Seizures 642.7 Delirium and agitation 652.8 Serotonin syndrome 702.9 Anticholinergic syndrome 762.10 Cholinergic syndrome 802.11 Neuroleptic malignant syndrome 832.12 Alcohol use disorder 892.13 Amphetamine use disorder 982.14 Opioid use disorder 992.15 Sedative-hypnotic use disorder 1032.16 Solvent abuse 1062.17 Body packers and stuffers 1102.18 Osmolar gap 1132.19 Acid–base disorders 1162.20 The 12-lead ECG in toxicology 1212.21 Poisoning during pregnancy and lactation 1272.22 Poisoning in children 1282.23 Poisoning in the elderly 134

CHAPTER 3 SPECIFIC TOXINS

3.1 Alcohol: Ethanol 1403.2 Alcohol: Ethylene glycol 1433.3 Alcohol: Isopropanol (isopropyl alcohol) 1463.4 Alcohol: Methanol (methyl alcohol) 1493.5 Alcohol: Other toxic alcohols 1523.6 Amiodarone 1553.7 Amisulpride 1573.8 Amphetamines and other sympathomimetics 1593.9 Angiotensin-converting enzyme inhibitors 164

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3.10 Anticoagulant rodenticides 1663.11 Anticonvulsants: Newer agents 1693.12 Antihistamines (non-sedating) 1723.13 Antihistamines (sedating) 1743.14 Arsenic 1773.15 Baclofen 1803.16 Barbiturates 1833.17 Benzodiazepines 1873.18 Benztropine 1903.19 Beta-blockers 1913.20 Bupropion 1943.21 Button batteries 1973.22 Calcium channel blockers 2003.23 Cannabinoids (marijuana) 2053.24 Carbamazepine 2083.25 Carbon monoxide 2113.26 Chloroquine and hydroxychloroquine 2153.27 Chloral hydrate 2173.28 Clonidine 2203.29 Clozapine 2233.30 Cocaine 2253.31 Colchicine 2293.32 Corrosives 2323.33 Cyanide 2363.34 Digoxin: Acute overdose 2393.35 Digoxin: Chronic poisoning 2433.36 Diphenoxylate–atropine 2473.37 Gamma-hydroxybutyrate (GHB) 2493.38 Glyphosate 2523.39 Hydrocarbons 2553.40 Hydrofl uoric acid 2583.41 Hydrogen peroxide 2623.42 Insulin 2653.43 Iron 2693.44 Isoniazid 2733.45 Lead 2753.46 Lithium: Acute overdose 2793.47 Lithium: Chronic poisoning 2823.48 Local anaesthetic agents 2843.49 Mercury 2883.50 Metformin 2923.51 Methotrexate 2953.52 Mirtazapine 2983.53 Monoamine oxidase inhibitors (MAOIs) 3003.54 New oral anticoagulants 3043.55 Non-steroidal anti-infl ammatory drugs (NSAIDs) 3083.56 Olanzapine 3113.57 Opioids 3143.58 Organochlorines 3193.59 Organophosphorus agents (organophosphates and carbamates) 3223.60 Paracetamol: Acute overdose 3273.61 Paracetamol: Modifi ed-release formulations 3363.62 Paracetamol: Repeated supratherapeutic ingestion 3403.63 Paraquat 3433.64 Phenothiazines and butyrophenones (antipsychotic agents) 3493.65 Phenytoin 3513.66 Potassium chloride 3543.67 Quetiapine 3573.68 Quinine 3603.69 Risperidone 363

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3.70 Salicylates 3653.71 Selective serotonin reuptake inhibitors (SSRIs) 3693.72 Strychnine 3733.73 Sulfonylureas 3753.74 Theophylline 3783.75 Thyroxine 3833.76 Tramadol 3853.77 Tricyclic antidepressants (TCAs) 3873.78 Valproic acid (sodium valproate) 3913.79 Venlafaxine and desvenlafaxine 3953.80 Warfarin 399

CHAPTER 4 ANTIDOTES

4.1 Atropine 4044.2 Calcium 4054.3 Cyproheptadine 4084.4 Desferrioxamine 4094.5 Dicobalt edetate 4114.6 Digoxin immune Fab 4134.7 Dimercaprol 4164.8 Ethanol 4184.9 Flumazenil 4204.10 Folinic Acid 4224.11 Fomepizole 4244.12 Glucose 4254.13 Hydroxocobalamin 4274.14 Insulin (high-dose) 4304.15 Intravenous lipid emulsion 4324.16 Methylene blue 4334.17 N-acetylcysteine 4354.18 Naloxone 4384.19 Octreotide 4414.20 Penicillamine 4424.21 Physostigmine 4444.22 Pralidoxime 4464.23 Pyridoxine 4484.24 Sodium bicarbonate 4504.25 Sodium calcium edetate 4534.26 Sodium thiosulfate 4554.27 Succimer 4574.28 Vitamin K 459

CHAPTER 5 ENVENOMINGS

5.1 Black snake 4645.2 Brown snake 4685.3 Death adder 4715.4 Tiger snake group 4745.5 Taipan 4785.6 Sea snake 4815.7 Australian scorpions 4835.8 Bluebottle jellyfi sh (Physalia species) 4855.9 Stonefi sh 4865.10 Box jellyfi sh 4885.11 Irukandji syndrome 4915.12 Blue-ringed octopus 4945.13 Redback spider 4965.14 Funnel-web (big black) spider 4985.15 White-tailed spider 5015.16 Ticks 502

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CHAPTER 6 ANTIVENOMS

6.1 CSL Black Snake Antivenom 5066.2 CSL Brown Snake Antivenom 5076.3 CSL Death Adder Antivenom 5096.4 CSL Tiger Snake Antivenom 5116.5 CSL Taipan Antivenom 5136.6 CSL Sea Snake Antivenom 5156.7 CSL Polyvalent Snake Antivenom 5176.8 CSL Stonefi sh Antivenom 5196.9 CSL Box Jellyfi sh Antivenom 5206.10 CSL Redback Spider Antivenom 5226.11 CSL Funnel-web Spider Antivenom 524

APPENDICES

Appendix 1: Poisons information telephone numbers 528Appendix 2: Example ECGs 529Appendix 3: Conversion factors and therapeutic ranges for important toxins 533Appendix 4: Alcohol pathways 534Appendix 5: Therapeutic over-warfarinisation 535Appendix 6: Management of allergic reactions to antivenoms 538

Index 539

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FOREWORD

This is the third edition of the Toxicology Handbook and confi rms clinical toxicology as a sub-specialty in Australasia.

Less than 20 years ago a small cohort of emergency doctors independently sought overseas sub-specialty training in toxicology so that they could bring a higher level of expertise to the management of this heterogeneous and vulnerable group of patients in Australasian emergency departments. They joined a small and informal collection of clinical pharmacologists, intensivists and paediatricians to provide telephone advice across the country through the National Poisons Centre system.

Within a few years the collaboration fl ourished and they started local training programs, implemented innovative patient-centred models of care and coordinated research. Wider networks involving rural and remote clinicians, psychiatry, drug and alcohol services and occupational medicine were also formed.

It is now axiomatic that we should endeavour to deliver clinical care that is evidence based. There is also clear evidence that patient experience and outcomes are superior in organisations that have a clear and inspirational vision, unambiguous objectives aligned to that vision and clinicians who work in teams with a philosophy of continuous improvement. This handbook is written by clinicians who have worked in such a way. They have designed the content and format of this book to allow the easy dissemination of their expertise and experience for the benefi t of patients beyond their own hospitals. It is an authentic clinical handbook and not just a text for the shelf or study. It continues the clear and consistent format of previous editions. The clinical approach is based on risk assessment and enables evidence-based and pragmatic management tailored to the individual needs of patients. This is a key element in progressing the ideal of optimal care for the poisoned patient irrespective of location.

The vision has always been to deliver patient care that is safe, effective, personal, timely and effi cient. I believe this handbook represents a practical step to deliver on this vision at an individual patient level and as part of a wider system of care.

Professor Frank FS Daly MBBS FACEM LWA A/Chief Executive, South Metropolitan Health Service University of Western Australia and the Centre for Clinical Research in Emergency Medicine, Western Australian Institute for Medical Research

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PREFACE

The Toxicology Handbook was originally conceived as a distillation of the collective experience of the clinical toxicologists of the West Australian Toxicology Service. It was written with the aim of producing a useful but concise bedside text to assist the clinician in treating the acutely poisoned patient in whatever setting they might be practising within Australasia or elsewhere. With this in mind the authors made every effort not only to provide the necessary factual information but to train the user to adopt a rigorous and structured risk assessment-based approach to decision making in the context of clinical toxicology. The second edition provided an opportunity to expand the coverage of toxins and incorporate changes in management informed by new research.

Feedback from users of the fi rst two editions of the handbook has validated the practical utility of the structured risk assessment-based approach to the management of poisoning and encouraged us to retain this approach for the third edition. This latest edition necessarily incorporates important information regarding poisoning from recently marketed pharmaceuticals. It also incorporates important modifi cations in management advice, particularly in the area of envenoming, informed by recently published clinical research.

Two of the original authors of the Toxicology Handbook were not available to produce the third edition as their careers have since evolved in other exciting directions. However, the contributions of Frank Daly and Mike Cadogan live on in the third edition in a very real way. The unique qualities of these two exceptional doctors provided the conceptual framework and clinical expertise on which the Toxicology Handbook still rests. We dedicate the third edition to Frank Daly and Mike Cadogan together with our patients, who continue to instruct on a daily basis and remind us just how much we have yet to learn.

Lindsay Murray Mark Little Ovidiu Pascu Kerry Hoggett Jason Armstrong

Alan Gault David McCoubrie Kirsty Skinner Jessamine Soderstorm Ioana Vlad Sam

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EDITORS

Lindsay Murray MBBS FACEM , Consultant Emergency Physician, Lismore Base Hospital, Lismore, NSW, Australia

Mark Little MBBS DTM&H (Lond) FACEM MPH&TM IDHA , Consultant Emergency Physician and Clinical Toxicologist, Cairns Hospital, Cairns, Qld; Associate Professor, School of Public Health and Tropical Medicine, Queensland Tropical Health Alliance; Consultant Clinical Toxicologist, NSW Poisons Information Centre, Australia

Ovidiu Pascu MD FACEM , Consultant Emergency Physician and Clinical Toxicologist, Sir Charles Gairdner Hospital, Perth, WA; Clinical Toxicologist, WA Poisons Information Centre; Clinical Senior Lecturer in Emergency Medicine, University of Western Australia, Australia

Kerry Hoggett MBBS GCertClinTox FACEM , Consultant Emergency Physician and Clinical Toxicologist, Royal Perth Hospital, Perth, WA; VMO Clinical Toxicologist, NSW and WA Poisons Information Centres; Clinical Senior Lecturer, University of Western Australia; Adjunct Clinical Lecturer, University of Notre Dame, WA, Australia

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CONTRIBUTORS

Jason Armstrong MBChB FACEM , Consultant Emergency Physician and Clinical Toxicologist, Sir Charles Gairdner Hospital, Perth, WA; Clinical Senior Lecturer in Emergency Medicine, University of Western Australia; Medical Director, WA Poisons Information Centre; Consultant Clinical Toxicologist, NSW Poisons Information Centre, Australia

Alan Gault MBChB BAO FACEM , Consultant Emergency Physician and Clinical Toxicologist, Sir Charles Gairdner Hospital, Perth, WA; Lecturer, University of Western Australia, Australia

David McCoubrie MBBS FACEM , Consultant Emergency Physician and Clinical Toxicologist, Royal Perth Hospital, Perth, WA; Consultant Clinical Toxicologist, WA and NSW Poisons Information Centres, Australia

Kirsty Skinner MBChB FACEM , Consultant Emergency Physician and Clinical Toxicology Fellow, Royal Perth Hospital, Perth, WA, Australia

Jessamine Soderstrom MBBS FACEM Grad Cert Toxicology , Consultant Emergency Physician and Clinical Toxicologist, Royal Perth Hospital, Perth, WA; Clinical Senior Lecturer, University of Western Australia, Australia

Ioana Vlad MD FACEM , Consultant Emergency Physician and Clinical Toxicology Fellow, Sir Charles Gairdner Hospital, Perth, WA, Australia

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REVIEWERS

David Banfi eld BMed MPH MMedSc DCH FACEM , Emergency Physician and Co-Director, Calvary Health Care ACT, Bruce, ACT; Emergency Medicine Training Clinical Lecturer, Australian National University Medical School, Canberra, ACT, Australia

David Caldicott BSc(Hons)-[NUI] MBBS(Lond) FCEM Dip Clin Tox , Consultant Emergency Physician, Clinical Senior Lecturer, Australian National University, Canberra, ACT; Coordinator of the ACT Investigation of Novel Substances (ACTINOS) Group, Canberra, ACT, Australia

Jon Hayman MBBS FACEM , Director of Emergency Medicine Training, Royal Prince Alfred Hospital, Sydney, NSW; Chair of the Emergency Medicine State Training Council Health Education and Training Institute, NSW; Clinical Senior Lecturer, Faculty of Medicine, University of Sydney, Sydney, NSW, Australia

Paul Jennings BN GradCertAdvNsg AdvDipMICAStud GradCertBiostats GCHPE MClinEpi PhD , Department of Community Emergency Health and Paramedic Practice, Monash University, Melbourne, Vic; Ambulance Victoria, Melbourne, Vic, Australia

Slade Matthews BmedSc(Hons) PhD DipEd GradCertEd(Higher Ed) , Senior Lecturer, Sub-Dean Medical Program Stage 1, School of Medical Sciences (Pharmacology), Sydney Medical School, University of Sydney, Sydney, NSW, Australia

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3.1 Alcohol: Ethanol 140 3.2 Alcohol: Ethylene glycol 143 3.3 Alcohol: Isopropanol (isopropyl alcohol) 146 3.4 Alcohol: Methanol (methyl alcohol) 149 3.5 Alcohol: Other toxic alcohols 152 3.6 Amiodarone 155 3.7 Amisulpride 157 3.8 Amphetamines and other sympathomimetics 159 3.9 Angiotensin-converting enzyme inhibitors 164 3.10 Anticoagulant rodenticides 166 3.11 Anticonvulsants: Newer agents 169 3.12 Antihistamines (non-sedating) 172 3.13 Antihistamines (sedating) 174 3.14 Arsenic 177 3.15 Baclofen 180 3.16 Barbiturates 183 3.17 Benzodiazepines 187 3.18 Benztropine 190 3.19 Beta-blockers 191 3.20 Bupropion 194 3.21 Button batteries 197 3.22 Calcium channel blockers 200 3.23 Cannabinoids (marijuana) 205 3.24 Carbamazepine 208 3.25 Carbon monoxide 211 3.26 Chloroquine and hydroxychloroquine 215 3.27 Chloral hydrate 217 3.28 Clonidine 220 3.29 Clozapine 223

CHAPTER 3

SPECIFIC TOXINS

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3.30 Cocaine 225 3.31 Colchicine 229 3.32 Corrosives 232 3.33 Cyanide 236 3.34 Digoxin: Acute overdose 239 3.35 Digoxin: Chronic poisoning 243 3.36 Diphenoxylate–atropine 247 3.37 Gamma-hydroxybutyrate (GHB) 249 3.38 Glyphosate 252 3.39 Hydrocarbons 255 3.40 Hydrofl uoric acid 258 3.41 Hydrogen peroxide 262 3.42 Insulin 265 3.43 Iron 269 3.44 Isoniazid 273 3.45 Lead 275 3.46 Lithium: Acute overdose 279 3.47 Lithium: Chronic poisoning 282 3.48 Local anaesthetic agents 284 3.49 Mercury 288 3.50 Metformin 292 3.51 Methotrexate 295 3.52 Mirtazapine 298 3.53 Monoamine oxidase inhibitors (MAOIs) 300 3.54 New oral anticoagulants 304 3.55 Non-steroidal anti-infl ammatory drugs (NSAIDs) 308 3.56 Olanzapine 311 3.57 Opioids 314 3.58 Organochlorines 319 3.59 Organophosphorus agents (organophosphates

and carbamates) 322 3.60 Paracetamol: Acute overdose 327 3.61 Paracetamol: Modifi ed-release formulations 336 3.62 Paracetamol: Repeated supratherapeutic

ingestion 340 3.63 Paraquat 343 3.64 Phenothiazines and butyrophenones

(antipsychotic agents) 349 3.65 Phenytoin 351 3.66 Potassium chloride 354 3.67 Quetiapine 357 3.68 Quinine 360 3.69 Risperidone 363 3.70 Salicylates 365

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3.71 Selective serotonin reuptake inhibitors (SSRIs) 369 3.72 Strychnine 373 3.73 Sulfonylureas 375 3.74 Theophylline 378 3.75 Thyroxine 383 3.76 Tramadol 385 3.77 Tricyclic antidepressants (TCAs) 387 3.78 Valproic acid (sodium valproate) 391 3.79 Venlafaxine and desvenlafaxine 395 3.80 Warfarin 399

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References Haskell RJ , Stapczynski JS . Duration of hypoglycaemia and need for intravenous glucose

following intentional overdoses of insulin . Annals of Emergency Medicine 1984 ; 13 : 505 – 511 .

Megarbane B , Deye N , Bloch V et al. Intentional overdose with insulin: prognostic factors and toxicokinetic/toxicodynamic profi les . Critical Care 2007 ; 11 ( 5 ): R115 .

3.43 IRON

Ferrous chloride, Ferrous fumarate, Ferrous gluconate, Ferrous phosphate, Ferrous sulfate, Iron amino acid chelates

Iron poisoning is characterised by both local gastrointestinal and dose-related systemic toxicity. Toxicity is determined by the quantity of elemental iron ingested. Most acute overdoses produce minor or moderate gastrointestinal effects only. In large overdoses, systemic toxicity can be prevented by early gastrointestinal decontamination and/or administration of desferrioxamine.

RISK ASSESSMENT • Iron overdose is potentially lethal. • Risk assessment is based on the ingested dose of elemental iron

(see Table 3.43.1 ) and the observed evolving clinical features (see Table 3.43.2 ).

• The amount of elemental iron in a ferrous or ferric salt is calculated as follows: — Ferric chloride dose divided by 3.5 — Ferrous chloride dose divided by 4 — Ferrous fumarate dose divided by 3 — Ferrous gluconate dose divided by 9 — Ferrous sulfate (dried) dose divided by 3.3 — Ferrous sulfate (heptahydrate) dose divided by 5.

• Refi nement of the initial risk assessment can be achieved by: — Abdominal X-ray to confi rm or quantify ingestion — An iron level at 4–6 hours post-ingestion.

• Patients presenting with established systemic iron toxicity have a poor prognosis and may not respond to medical therapy.

• Children: the dose ingested is usually less than that expected to cause systemic toxicity (60 mg/kg).

TABLE 3.43.1 Dose-related risk assessment: Iron

Elemental iron dose Effect

< 20 mg/kg Asymptomatic

20–60 mg/kg Gastrointestinal symptoms

> 60–120 mg/kg Systemic toxicity anticipated

> 120 mg/kg Potentially lethal

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Toxic mechanism Local Direct corrosive effect on the gastrointestinal (GI) mucosa manifests with symptoms ranging from vomiting and diarrhoea to haematemesis and melaena. Large GI fl uid losses may contribute to signifi cant hypovolaemia. Systemic toxicity does not occur in the absence of GI symptoms.

Systemic Iron acts as a direct cellular toxin via poorly understood mechanisms. The chief target organs are the cardiovascular system and the liver. CNS toxicity is secondary to cardiovascular instability and metabolic derangements. Severe metabolic acidosis is observed following large overdoses and attributed to lactic acid formation and the liberation of hydrogen ions from the hydration of free ferric ions in the plasma. Coagulopathy is frequently observed and attributed to interference with the coagulation cascade.

Toxicokinetics Absorption of iron from the GI tract is normally fi nely regulated according to the requirements of the body. In overdose these mechanisms are overwhelmed and the bioavailability of iron increases signifi cantly. Absorbed iron shifts intracellularly over a period of hours. Elimination is minimal under normal conditions.

CLINICAL FEATURES Iron toxicity is classically described as having fi ve stages (see Table 3.43.2 ), although this is an over-simplifi cation. Not all patients

TABLE 3.43.2 Classical stages of severe iron poisoning

Time post-ingestion Clinical features

0–6 hours Direct corrosive effect on GI tract characterised by vomiting, diarrhoea and abdominal pain. Fluid losses may be suffi cient to cause hypovolaemic shock

6–12 hours Progressive increase in iron absorption and distribution. Some resolution of symptoms may be observed, giving false hope of recovery

12–48 hours Disruption of cellular metabolism manifested as shock from vasodilation and third-space losses, anion gap metabolic acidosis and hepatorenal failure

2–5 days Acute hepatic failure with jaundice, coma, hypoglycaemia, coagulopathy and elevated aminotransferases. This phase is rare, but has a high mortality

2–6 weeks Delayed sequelae, including cirrhotic liver disease and GI fi brosis/strictures

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experience all stages and the duration of each stage is imprecise and they usually overlap. Iron toxicity is more accurately conceptualised as two overlapping stages with a pathophysiological basis: gastrointestinal and systemic toxicity.

INVESTIGATIONS Screening tests in deliberate self-poisoning • 12-lead ECG, BGL and paracetamol level

Specifi c investigations as indicated • Serum iron concentration:

— Iron levels usually peak at 4–6 hours following ingestion. Following this there is rapid intracellular migration of iron. A clear correlation between iron levels and clinical toxicity is not established, but peak levels > 90 micromol/L (500 microgram/dL) are thought to be predictive of systemic toxicity.

• Arterial or venous blood gas — An anion gap metabolic acidosis is a useful marker of

systemic toxicity. • Abdominal X-ray

— Useful in confi rming ingestion, and planning and monitoring decontamination.

• Note: Hyperglycaemia and elevated white cell counts are frequently observed in iron poisoning, but do not correlate with toxicity.

MANAGEMENT Resuscitation, supportive care and monitoring • An early priority is the restoration of adequate circulating volume.

Give boluses of 10–20 mL/kg of crystalloid and assess response. • Ongoing fl uid replacement is essential in the face of continuing

gastrointestinal and third-space losses.

Decontamination • Iron is not adsorbed to activated charcoal. • Whole bowel irrigation (WBI) is the decontamination method of

choice and recommended for ingestions > 60 mg/kg confi rmed on X-ray (see Chapter 1.6: Gastrointestinal decontamination ).

• Surgical or endoscopic removal may be considered in potentially lethal ingestions if WBI fails or is impractical.

Enhanced elimination • Not clinically useful.

Antidotes • Desferrioxamine chelation therapy is indicated if systemic

toxicity (shock, metabolic acidosis, altered mental status) is present or predicted by a serum iron level > 90 micromol/L (500 microgram/dL) at 4–6 hours post ingestion. For further details see Chapter 4.4: Desferrioxamine .

DISPOSITION AND FOLLOW-UP • Children thought to have ingested < 40 mg/kg may be managed at

home provided they remain asymptomatic. Larger or symptomatic

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ingestions are evaluated in hospital. The child who remains asymptomatic at 6 hours and has an abdominal X-ray negative for iron may be safely discharged.

• All adults who have deliberately self-poisoned with iron are evaluated in hospital. If the history suggests ingestion of < 60 mg/kg of iron and they remain asymptomatic at 6 hours, further medical observation is unnecessary.

• Symptomatic patients requiring intravenous fl uid therapy or WBI require admission to hospital.

• Those presenting with established systemic iron toxicity or requiring intravenous chelation therapy are admitted to intensive care.

HANDY TIPS • Where serum iron levels are not readily available, a fall in serum

bicarbonate concentration is a good surrogate marker of systemic iron poisoning and, in conjunction with worsening clinical features, would justify desferrioxamine administration.

• Iron supplements are readily accessible to pregnant women and thus are frequently taken in overdose. The fetus is relatively protected unless maternal cardiovascular instability develops. Therapy is directed towards care of the mother and does not differ from the care of the non-pregnant patient.

PITFALLS • Over-treatment of trivial ingestions. • Failure to perform initial risk assessment thus leading to delays in

therapy and irreversible toxicity following large overdoses. • Failure to recognise systemic iron toxicity in the patient who

presents late with minimal elevation in serum iron level.

CONTROVERSIES • Threshold serum iron level that mandates chelation with

desferrioxamine. • Duration and endpoints for desferrioxamine therapy.

Presentations There are numerous over-the-counter vitamin preparations containing relatively small

amounts of elemental iron, usually iron amino acid chelates, ferrous phosphate or ferrous fumarate. The important preparations containing large amounts of elemental iron are:

Ferrous sulfate 325 mg (105 mg elemental iron) slow-release tablets (30) Ferrous sulfate 250 mg (80 mg elemental iron)/folic acid 300 mg combination controlled-release tablets (30) Ferrous sulfate 6 mg/mL oral liquid (250 mL)

References Chyka PA , Butler AY . Assessment of acute iron poisoning by laboratory and clinical

observations . American Journal of Emergency Medicine 1993 : 11 ( 2 ): 99 – 103 . Pearn J , Nixon J , Ansford A et al. Accidental poisoning in childhood: fi ve year urban

population study with 15 year analysis of fatality . British Medical Journal 1984 ; 288 : 44 – 46 .

Singhi SC , Baranwal AK , Jayashree M . Acute iron poisoning: clinical picture, intensive care needs and outcome . Indian Pediatrics 2003 : 40 ( 12 ): 1177 – 1182 .

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