Guidelines On Poisoning Management

Ministry of Health
Sultanate of Oman
National Guidelines on
Poisoning Management
Directorate General of Health Affairs

Directorate of Environmental Health
and Malaria Eradication
Poison Control Centre
2006
His Majesty Sultan Qaboos Bin Said
National Guidelines on
Poisoning Management
Edited by
Dr. Salim Said Al-Wahaibi Dr. I. G. Hastie BSc, MD, FRCPC

MPH, COHP, DFE, MD, B Med Sc Ex. Sr. Consultant and Head,
Director, Directorate of Environmental Department of A&E,
Health & Malaria Eradication, Sultan Qaboos University Hospital,
Ministry of Health College of Medicine & Health Sciences
Dr. S. B. Lall MD, DGO, MNAMS, Dr. Nabil Mohsin MD, DTM, MSc
FAMS (Immunology), CES (Nephro.)
Head, Poison Control Centre Sr. Consultant and Head
Directorate of Environmental Health Department of Nephrology
and Malaria Eradication The Royal Hospital
Ministry of Health
CONTENTS Pages
Expert Group Committee I

Authors II - III
Foreword IV
Preface V-VI
Acknowledgements VII
List of acronyms, abbreviations and symbols VIII- IX
Section I : Definitions and General Information on Poisoning 1
Poison,Toxic agents, Toxic effects 3
Toxicokinetics, General mechanisms of toxicity, Exposure 4
Types of exposure 4
Routes of exposure 5
Circumstances of exposure 6
Risk of poisoning 7
Severity of poisoning 7
Symptomatic & specific treatment, Decontamination 7
Out come of treatment 8
Poison Control Centre 9
Central registry of poisoning cases: form 10,11
Section II : Principles of Management of Acute Poisoning 13
General principles of management of acute poisoning 15
Treatment of life threatening poisoning 16
Emergency evaluation and life – saving treatment 17
Toxicological syndromes 23
Antidote treatment 27
Decontamination 31
Enhanced elimination of drugs and toxins 35
High risk factors in poisoning management 38
Care of asymptomatic patient 40
Treatment of anaphylaxis 41
Flow charts : Emergency evaluation & management 42
Referral guidelines 43
Skin or eye exposure 44
Inhaled poison 45
Section III : Management of Venomous Bites & Stings 47
Snake bite 49
Scorpion sting 54
Spider bite 56
Bee & wasp sting and fire ant bite 57
Flow charts : Snake bite 59
Scorpion sting 60
Other insect stings & bites 61
Pictures : Non-poisonous snakes 62
Marine envenomations & injuries 64
Flow chart : Management of marine envenomations & injuries 71
Pages
Section IV: Management of Drug Poisoning 73

Paracetamol poisoning 75
Flow chart : Management of paracetamol poisoning 82
Acetylsalicylic acid & salicylate poisoning 83
Flow chart : Management of acute salicylate poisoning 88
Other nonsteroidal anti-inflammatory drug overdose 89
Anticonvulsant drug overdose 92
Flow chart : Management of carbamazepine poisoning 100
Antipsychotic drug overdose 101
Antidepressant drug overdose 104
Flow chart : Management of tricyclic antidepressant poisoning 109
Antihistamine drug overdose 110
Flow chart : Management of antihistamine poisoning 115
Theophylline overdose 116
Flow chart : Management of theophylline poisoning 121
Iron poisoning 122
Flow chart : Management of Iron poisoning 127
Tables - Toxic doses of some common drugs 128
Potentially fatal doses of some drugs in a child 129
Toxic blood levels of some drugs and alcohols 130
Section V: Management of Household Product Poisoning 131
Pesticide poisoning : Organophosphates & carbamates 133
Flow chart : Management of organophosphate poisoning 138
Pesticide poisoning : Pyrethrins & pyrethroides 139
Rodenticide : Superwarfarins 141
Rodenticide : Zinc Phosphide 143
Poisoning due to herbicide or fungicide 145
Corrossives 147
Flow chart : Management of corrosive poisoning 155
Hydrocarbons 156
Flow chart : Management of hydrocarbon poisoning 160
Tables - Generally nontoxic household items 161
Potentially dangerous household products 162
Pages
Section VI: Management of Poisoning due to Some Plants, 163

164
Lead & Mercury
Datura fastuosa ( benj ) 165
166
Calatropis procera ( ashkhar ) 166
167
Dieffenbachia seguine ( dumbcane ) 167
168
Nerium oleander ( habben ) 168
169
Plants known to cause GIT irritation & dermatitis 170
171
Lead Encephalopathy 172
173
Mercury poisoning 174
175
Section VII: Tables 1 - 23 177-191
178-192
Appendix – 1 Flow chart : Management of food poisoning 192
193
Appendix – 2 Reference Books 193
194
Appendix – 3 Feedback from end-users 194
195
I
Expert Group Committee
Chairman : Dr. Salim Said Al-Wahaibi

MPH, COHP, DFE, MD, B Med Sc.
Director, Directorate of Environmental Health and
Malaria Eradication
Ministry of Health
Dr. S. B. Lall Dr. I. G. Hastie

MBBS, MD, DGO, MNAMS, FAMS BSc, MD, FRCPC
Head, Poison Control Centre Ex. Sr. Consultant and Head
Directorate of Environmental Department of A&E,
Health and Malaria Eradication, SQU Hospital
Ministry of Health
Dr. Nabil Mohsin Dr. K. Omar

MD, DTM, MSc (Immunology), CES MBBS, MCPCP, EMDM
(Nephro.) Consultant, Department of A&E
Sr. Consultant & Head SQU Hospital
Department of Nephrology
The Royal Hospital
Dr. E. Scrimgeour Dr. P. C. Alexander

MD, FRACP, DTM & H MBBS, MD, DCH
Consultant, Infection & Tropical Consultant, Pediatrics
Diseases SQU Hospital
SQU Hospital
Dr. Ragini Vaishnav Dr. Uday Nadkarni

MBBS, MD MBBS, MD, DCH, DNB
Asst. Professor, Department of Sr. Specialist, Pediatrics
Pharmacology, College of Medicine The Royal Hospital
SQ University
Ph. Intisar Al-Busaidi Ph. Sheikha Al-Harthy

BS, Pharmacy M.Pharm.
Pharmacist, Hospital Pharmacy Poison Control Centre
SQU Hospital Directorate of Environmental
Health and Malaria Eradication
Mr. Mattar Al-Riyami Ministry of Health
Poison Control Centre, DEH& ME
Ministry of Health Mr.Khalid Al-Kharousi
Mr.Mohd.Al-Habsi Ministry of Health
Ministry of Health
II
Authors
• Dr. S. B. Lall, MD, DGO, MNAMS, FAMS

Head, Poison Control Centre
Directorate of Environmental Health and Malaria Eradication
Ministry of Health
Section I
Section II: Introduction, Treatment of anaphylaxis , asymptomatic patient, and
flowcharts
Section III: Flowcharts,Pictures of insects
Section IV: Acetylsalicylic acid and salicylates, Anticonvulsants, Non-steroidal anti
inflammatory drugs, Antipsychotics, Tables, Flow charts
Section V: Pyrethroids, Rodenticides, Herbicides and Fungicides, Hydrocarbons,
Flow charts
Section VI: Lead encephalopathy, Mercury poisoning, Plant poisoning
Section VII: Tables. I-23
Proof reading of Guidelines
• Dr. I. G. Hastie, BSC, MD, FRCPC

Ex.Sr. Consultant and Head
Department of A&E, SQU Hospital
Section II: Antidotes, Decontamination, High risk factors in poisoning management,
Flowcharts; Section IV: Paracetamol, Tricyclic antidepressants
• Dr. Nabil Mohsin, MD, DTM, MSc (Immunology), CES (Nephro.)

Sr. Consultant and Head
Department of Nephrology
The Royal Hospital
Section II: Enhanced elimination of drugs and poisons
Section III: Marine envenomations, flowchart
• Dr. K. Omar, MBBS, MSPCP, EMDM

Consultant, Department of A&E
SQU Hospital
Section II: Emergency evaluation and life-saving treatment, Toxidromes,
Flowcharts
Section IV: Anticonvulsants
Section V: Organophosphates and carbamates, Corrosives ,Flow charts
• Dr. E. Scrimgeour, MD, FRACP, DTM&H

Consultant, Infection and Tropical Diseases
SQU Hospital
Section III: Treatment of snakebite, scorpion sting, spider bite, bee and wasp stings
III
• Dr. P. C. Alexander, MBBS, MD, DCH

Consultant, Pediatrics Department
SQU Hospital
Section IV: Iron Poisoning, Flow charts and Table 23
Proof reading of Guidelines
• Dr. Uday Nadkarni, MD, DCH, DNB

Sr. Specialist, Pediatrics Department
The Royal Hospital
Section IV: Antihistamines, Theophylline & flow chart
• Dr. Ragini Vaishnav, MBBS, MD

Asst. Professor, Department of Phamacology
College of Medicine
Sultan Qaboos University
Section IV: Anticonvulsants
• Ph. Intisar Al-Busaidi, BS Pharmacy

Pharmacist
SQU Hospital
Section VI: Poisonous plants and Plants causing GIT irritation or dermatitis
• Ph. Sheikha Al-Harthy, M Pharm

Section IV: Acetylsalicylic acid and salicylates, Tables of preparations
IV
Foreword
Poisoning is an important health problem in every country of the world

and the Sultanate is not an exception. Envenomations, accidental or
intentional exposures to pharmaceuticals & household products and
poisonings due to contaminated food significantly contribute to the
morbidity as indicated by the Annual Health Report as well as by the data
of the Central Registry of Poisoning Cases.
I am pleased to introduce the National Guidelines on Poisoning

Management to all health professionals, especially those working in
Accident and Emergency departments, to ensure prompt and adequate
management of acute poisonings and toxic exposures, and therefore
improving the quality of care and decreasing the morbidity and health
care cost.
These guidelines are expected to be used as standard operating

procedures for the diagnosis, treatment, referral and follow-up of common
poisonings in the country. The expert group involved in the preparation of
the manual has diligently put together the basic principles, facts and their
rich experience in the field, yet tried to keep it simple for quick reference.
I appreciate and congratulate them for their efforts.
The first edition of the manual has been peer reviewed by national experts
and the Chairman of the Consultative Technical Committee for Poison
Monitoring and Control, established by Ministerial Decree No. 102/2003.
I hope it will be used by A&E staff at all health care levels as an

intervention strategy to decrease poisoning-related morbidity, that would
clearly be reflected in future national health statistics.
I wish you all a great success!
Dr. Ali Jaffer Mohammed

H.E. Adviser of Health Affairs and
Acting Director General of Health Affairs
Ministry of Health
V
Preface
National Guidelines on Poisoning Management is a publication of the Ministry of Health,

brought out by the Directorate of Environmental Health and Malaria Eradication, Poison
Control Centre. The need for such guidelines was highlighted in the WHO Training
Course and Workshop on Prevention and Management of Poisoning,held by the
Directorate in May 2002. One of the recommendations included, preparation of standard
guidelines on assessment and treatment of common poisonings encountered in the
country. It should be in the form of a manual, useful as a quick reference for accident
and emergency staff and the focus should be on general principles of treatment, recent
evidence-based shifts in the management protocols and referral guidelines. In addition,
a bedside chart was also felt necessary on "Emergency Evaluation and Management of
Poisoning". As a follow-up of these recommendations, we took the initiative and
responsibility to bring out such a publication for the benefit of staff and students of
Accident and Emergency Departments, at all health care levels.
An Expert Group, constituting experts from the Poison Control Centre, Sultan Qaboos
University Hospital, The Royal Hospital, Khoula Hospital, Al-Nahda Hospital, and Ruwi
Health Centre was created and common poisonings based on the national statistical data
were selected to work on, in a time-framed manner. Each chapter has been contributed
to by experts specialized in that field and then peer-reviewed in the Expert Group
Committee Meetings. The commitment, keen interest and the hard-work of the experts
has been the driving force in the preparation and completion of this document.
Section I of the manual gives definitions of important terms and general information on
poisoning. The definitions have been adapted from the WHO publications on poisoning.
Section II deals with the general principles of management of acute poisonings including
emergency evaluation and life-saving treatment, antidotes, decontamination and
enhanced elimination procedures. Certain high risk factors in poisoning management
such as children, old age, pregnancy, drug abuse and multiple drug overdose, have been
briefly discussed. The information on toxidromes and antidotes is given in tabulated
form as quick reference.
The annual data of the Central Registry of poisoning cases, indicate that venomous bites
and stings contribute 78-80% of the total number of acute poisonings per year.
Therefore, Section III of the manual describes management of snake bite, scorpion and
other insect stings and marine animal envenomations. Emphasis is laid on do's and
don’ts, when and how to use the antivenoms and the referral guidelines. At a glance,
information on management is provided in the form of flow charts and also coloured
pictures of animals and insects for identification. Section IV deals with the management
of poisoning due to pharmaceuticals. Six of the most common drug poisonings were
initially selected by the expert group; however, management of acetylsalicylic acid
(aspirin), other non-steroidal anti-inflammatory drugs and antipsychotic drugs, were later
added to the list. A similar protocol has been followed for each group of drugs.
Information on toxic and potentially fatal doses and toxic blood levels has been
incorporated as tables for easy reference. Common preparations available in Oman,
their formulation and strengths are given for calculation of approximate ingested
amount. Eighteen coloured flow charts for the management of poisonings are included
for ready reference in emergency. In addition, coloured pictures of local poisonous
animals ,insects and plants have been given for quick identification.
VI
The household-products poisoning management is dealt in Section V. Management,

referral and follow-up for common household products, pesticides, rodenticides,
corrosives, and hydrocarbons (petrol/kerosene/solvents) have been included. Tables
enlisting non-toxic and potentially toxic products are given to gauge severity of
poisoning. Section VI provides management guidelines on acute poisoning due to
traditional remedies, containing lead , mercury or poisonous plants as toxic ingredients.
Four most common poisonous plants, which could be ingested accidentally by children
have also been included, with pictures for identification, Arabic names and exposure
management. The last section (VII) has 23 tables, enlisting drugs and chemicals which
cause specific clinical conditions and biochemical changes, and a detailed table on the
doses and indications of therapeutic drugs, apart from antidotes, used in the poisoning
management.
A bedside poster is prepared on "Emergency Evaluation and Management of Poisoning"

that depicts emergency resuscitation with a secondary survey, for a step-wise rapid
guide on assessment and care of a severe poisoning case. A quick reference to the
poster, complemented by consultation of the manual for management, referral and
follow-up is expected to decrease the acute poisoning-related morbidity in the country.
It is indeed pertinent to mention here that the document has been prepared to provide
practical advice for diagnosis and management of most common acute poisonings;
therefore, management of chronic exposures, drug-abuse states and other uncommon
poisonings are out of its scope, for which Poison Control Centre should be contacted.
As per the MOH policy, the draft manual was sent to the Royal Hospital and the Regional
hospitals for comments of the end users. The document has been appreciated as an
excellent piece of work and as a much needed referral support in the A&E Departments
for managing poisoning cases. Their suggestions have been incorporated.
However despite the best concerted efforts of the expert group in preparing the
“ National Guideline on Poisoning Management", there could be some lacunae and
unintentional omissions in this first edition. Please don’t hesitate to send your
comments, suggestions or any corrections to the undersigned, so that changes maybe
incorporated in the revised next edition.
Dr. Salim Said Al-Wahaibi

Director, Directorate of Environmental Health and
Malaria Eradication
Ministry of Health
VII
Acknowledgements
We gratefully acknowledge the painstaking efforts of the Expert Group

members, who despite their busy clinical schedules, participated in all the
expert group committee meetings to plan, critically discuss the subject and
its presentation. We are deeply indebted to the authors, who have
contributed in the preparations of these guidelines. We highly appreciate
the conscientious and tireless work of the editors without whose support it
would not have been possible to bring out this manual.
The continuous cooperation and support of staff from the Poison Control
Centre and from the Pharmacy Department of SQU Hospital is thankfully
acknowledged. We are grateful to the clinicians of A&E Departments at
Regional Hospitals and the Royal Hospital for their valued comments and
advice. We are indebted to the staff of our Drawing Section for their
excellent job in organizing the text and the pictures and also for preparing
the poster on Emergency Evaluation and Management of Poisoning.
Finally, we express our sincere thanks to the secretariat at DEH&ME, for

carrying out the mammoth task of typing work, involved in the preparation.
We thankfully acknowledge the editor Dr. Kent R Olson and Publishers of

the clinical manual “Poisoning and Drug Overdose”, for allowing us to
adapt some of the tables included in the guidelines.
VIII
List of acronyms, abbreviations and symbols used
ABCDEs Airway, breathing, circulation, disability, exposure

ABGs Arterial blood gases
ACLS Advanced cardiac life support
ALT Alanine amino-transferase (hepato cellular enzyme)
ARDS Acute respiratory distress syndrome
ARF Acute renal failure
AST Aspartate amino-transferase (hepatocellular enzyme)
BAL Dimecaprol, British anti-Lewisite
BT Bleeding time
BUN Blood urea nitrogen
BW Body weight
CBC Complete blood counts
CCBs Calcium channel blockers
CCU Coronary care unit
CNS Central nervous system
CPR Cardio pulmonary resuscitation
CTG Cat scan during pregnancy
CV Cardiovascular
CVA Cardiovascular accident
CVP Central venous pressure
CVS Cardiovascular system
ClO Chlorates
Diarrhoea,urination,miosis,bradycardia,bronchospasm &
DUMBBEL
bronchorrhoea,emesis, lacrimation
DMSA Succimer
D5W 5% Dextrose
EDTA Ethylene diamine tetraacetic acid
FFP Fresh frozen plasma
GABA Gamma-aminobutyric acid (inhibitory neurotransmitter in brain)
GCS Glasgow Coma Scale
GIT Gastrointestinal tract
g (gm) gram
HCl Hydrochloric acid
H SO4 Sulfuric acid
HNO3 Nitric acid
HO Hydrogen peroxide
hr (hrs) Hour/Hours
ICU Intensive care unit
IM (im) Intramuscular
INR International Normalized Ratio
IX
List of acronyms, abbreviations and symbols used
INH Isoniazid
IPCS International Program on Chemical Safety
IV (iv) Intravenous
KCl Potassium chloride
KOH Potassium hydroxide
l (L) liter
L/A Long acting
LD50 Lethal dose in 50% animals
LFT Liver function tests
LSD Lysergic acid diethylamide
MSK Musculoskeletal
MDAC Multiple dose activated charcoal
MgSO4 Magnesium sulfate
mg milligram
mcg (µg) microgram
mmol Millimol
mEq MilliEquivalent
NAC N-acetylcysteine
NG Nasogastric
NaCl Sodium chloride
NaHCO3 Sodium bicarbonate
NSAIDS Nonsteroidal anti inflammatory drugs
NaOH Sodium hydroxide
OPs Organophosphates
PEEP Positive pressure ventilation
PRN Repeat as required
PT Prothrombin time
PTT Activated partial thromboplastin time
QID Four times a day
RFT Renal function tests
SC (sc) Subcutaneous
SSRI Selective serotonin reuptake inhibitors
Supp. Suppository
SVT Supraventricular tachycardia
TCAs Tricyclic antidepressants
,4-D Herbicide
VF Ventricular failure
VT Ventricular tachycardia
WBC White blood count
WBI Whole bowel irrigation
Section I
Definitions and
General Information
on Poisoning
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All substances are poisonous, there is none, which is not a
poison, the right dose differentiates a poison from a remedy.
Paracelsus (1493-1541).
Poison
Any agent that is capable of producing a deleterious response in a biological
system, seriously injuring functions or causing death.
Agent
Any substance/object of natural or manmade origin, which may be toxic to a living
organism
Poisoning
Clinical condition produced by exposure to an agent in toxic doses
Product
A substance or preparation placed on the market with a brand name
Contamination
Indicates that the poison has entered the body and may interfere with biological
functions
Toxicity
Ability of an agent to cause injury to the organism. It depends on the dose/ amount
Toxic dose
A dose that results in toxicity.
Toxic Agents
Pharmaceuticals, house hold products, cosmetics, industrial chemicals, pesticides
and other agricultural agents, contaminated food or beverages, poisonous plants,
fungi, poisonous bites or stings, environmental chemicals , warfare chemicals and
substances of abuse can be toxic agents, depending upon the amount of
exposure.
Toxic effects
Local effect
The toxic effect of the agent is limited to the part of the body in contact. For
example, burn, irritation, corrosion, watering and redness of eyes, swelling, local
inflammation, pain, bite, sting, etc.
Systemic effect
The toxic effect of the agent that occurs when it is absorbed in the blood. It can
produce specific signs and symptoms, organ toxicity and functional disability.
3
Toxicokinetics
Absorption, distribution, excretion and metabolism of toxins, toxic doses of
therapeutic agents and their metabolites
Toxicodynamics
Injurious effects of drugs, chemicals, or toxins on organs and vital functions
Volume of distribution (Vd)

It is a hypothetical volume of body fluid that would be necessary if the total amount
of drug were distributed at the same concentration as plasma. Dialysis is usually
not effective for removal of drugs with large Vd. It is calculated from the dose and
peak plasma / blood concentration. Peak levels in blood occur when the rate of
absorption equals the rate of elimination.
Effects on fetus
Almost all toxic substances can harm the unborn baby especially if exposure
occurs during the first three months of pregnancy
General mechanisms of toxicity

1. Interfere with transport or utilization of oxygen
2. Depress or stimulate CNS (central nervous system )
3. Adversely affect ANS (autonomic nervous system)
4. Affect lungs by aspiration
5. Directly toxic to heart and vascular system
6. Cause tissue damage locally
7. Cause delayed effects on liver or kidneys
Hazard
Likelihood that an injury will occur in a given situation or setting. It depends on
dose/amount and inherent toxic nature of the agent.
Exposure
Contact between a living organism and an agent, which may or may not lead to
poisoning.
Types of Exposure
Acute exposure
It is a single contact that lasts for seconds, minutes or hours or it may be several
exposures over a period of less than 24 hours.
Acute on chronic exposure

An acute exposure against a background of chronic exposure of same agent.
4
Chronic exposure
It is contact that lasts for many days, months or years. It may be continuous or
interrupted.
Routes of exposure
The route of entry into the body of an agent varies in different situations. The
amount of poison/chemical that enters the blood in a given time depends on the
route of exposure, and therefore route influences the toxicity of agents.
Ingestion (oral route)
It is an accidental or intentional swallowing of a poisonous agent. Some poisons
can pass through the gut walls and enter the blood vessels. The longer the poison
stays in the gut, the more it will enter the blood. Some are not absorbed from the
gut and therefore do not enter the blood. These are excreted in feaces. Absorption
of chemical/drug/poisonous agents can be reduced by inducing vomiting or by
removing them from the stomach, by binding them with activated charcoal, and by
increasing excretion through feaces with purgatives. There are specific indications,
precautions and contraindications to each procedure.
Inhalation (through lungs)
The poisons in the form of gases, vapors, dusts, fumes, smoke or spray droplets
can be inhaled into the mouth or nose and reach the lungs. The small particles
(< .5µm) are absorbed, bigger particles are trapped in mouth, throat, nose and
may be swallowed. Inhalation is a common route of exposure for industrial and
environmental pollutants
Dermal exposure (through skin)
Absorption through the skin depends on the area of exposure and the duration of
contact. The nature of the chemical, skin injury, burn, temperature and sweat are
other factors affecting the absorption. The poison can be injected in to the skin by
reptiles, insects or marine animals through bites or stings. Poisons or drugs can
also be injected by needle and a syringe, pressure gun or during tattooing.
Injection can be directly into the subcutaneous tissue.
Ocular exposure ( through eyes )
Accidental exposure of the eyes from the splash of corrosive liquids, fumes or toxic
gases can result in local injury to eyes.
Parenteral exposure
Injection of drugs through a dermal, subcutaneous, intravenous or intramuscular
route
Mucosal exposure (through conjunctiva, mouth, vagina, gut,
urethra, rectum)
Exposure via mucous membranes where absorption is fast and may also cause
local effects.
5
Circumstances of exposure
Accidental exposure
It is unintentional exposure to chemicals, (occupational, environmental, fire/smoke)
or exposure due to mishandling and misuse of drugs/products/chemicals or
exposure to poisonous animals, insects, plants, and food / drink. Common in
children below five years and in old age.
Therapeutic error
It is accidental exposure where the poisoning results from a medicine used in error
by a medical personnel or by a lay person.
Over dose toxicity

Occurs with doses above the therapeutic range for a particular patient. It may also
result from decreased drug clearance in renal or hepatic disease
Intentional exposure
Self - poisoning or suicidal attempt is the deliberate intake of poison to kill oneself.
Serious illness or drug dependence are usually involved. Large amounts are
ingested commonly leading to serious outcome. An adverse reaction that is the
unwanted effect of a drug, food or other agent occurring after normal or therapeutic
use of that agent, is also included in intentional exposure. Using poison to harm
another person is intentional and is a criminal assault.
Substance abuse
When someone takes a drug or chemical for pleasure, rather than to treat a
medical condition or prevent illness.
Para suicide
Self - poisoning where the person does not intend to die. The intention is to
threaten or obtain attention of family.
Munchausen by proxy syndrome

The administration of drugs or chemicals to children to produce iatrogenic disease
by mother or caretaker.
Bite
The introduction or possible introduction of toxic agent in the tissues by the biting
parts of an animal
Sting
The introduction or possible introduction of a toxic agent into the tissues by the
stinging device of certain animals and plants
6
Risk of poisoning
The probability of the patient suffering poisoning as a result of exposure to an
agent, if no action is taken to mitigate exposure.
• No risk: No probability
• Minimal risk: Low probability
• Moderate risk: Intermediate probability
• High risk: High probability
Severity of poisoning
Minor severity : Mild, transient and spontaneously resolving symptoms of

poisoning
Moderate severity : Pronounced or prolonged symptoms of poisoning
Severe poisoning : Severe or life threatening symptoms of poisoning
Established poisoning :
A patient shows the signs and symptoms consistent with exposure or has
laboratory confirmation for a particular poisoning
Symptomatic or supportive care

The alleviation of symptoms and signs of poisoning and restoration of normal body
functions by supporting the vital functions of body
Specific treatment
It consists of use of specific antidotes
Antivenom/Antivenin
Antitoxin that counteracts specific venom
Antitoxin
A preparation for parenteral administration that contains an antibody which will
neutralize a specific toxin
Antidote
Any substance that is administered specially to counteract the toxic effects of a
poison
Decontamination
A therapeutic intervention employed to (i) decrease exposure to poison (ii) prevent
local injury and damage (iii) prevent and reduce systemic absorption
Enhanced Elimination
The use of techniques to accelerate removal of toxic substance from the body
7
Outcome of treatment
Full recovery
The return to previous health without any sequelae after treatment
Delayed recovery
Recovery is delayed without sequelae after treatment of acute phase
Sequelae
A persistent disability after recovery from poisoning.
Death
The result of respiratory failure, cardiovascular collapse, seizures, hyperthermia ,
and /or other organ dysfunction.
8
A specialized section established in the Directorate of Environmental Health and

Malaria Eradication, that provides information and advice concerning diagnosis,
prognosis, treatment and prevention of poisoning as well as about the toxicity of
chemicals and the risks they pose to human health. Currently this service is
available between 7:3 To 14: at phone N 2456651 .
However, in the near future the service will extend to 24 hours a day and 7 days a
week. Apart from providing information to the clinicians and other health
professionals, it will also respond to any poison related inquiry from the
community.
A toxicology laboratory has been established in the centre and blood lead analysis
has been standardized with external quality control . The laboratory is ready to
receive blood samples for lead estimation to assist diagnosis and treatment of lead
poisoning.
The poison control centre is also responsible for the Central Registry of
poisoning cases in Oman, with the goal of generating national epidemiological
data on poisoning. The data is being collected on a standard format based on the
globally harmonized software system developed by International Programme on
Chemical Safety (IPCS/WHO ) A sample pro - forma enclosed here , is to be filled
for each poisoning case in the hospitals and health centres. The pro - forma should
be sent to the poison control centre along with the monthly reporting of cases for
the Central Registry of poisoning cases.
Role and Functions

Poison
Control Centre
Poison
Information
Service
Drug Training
Patient Analytical
Information and
Management Toxicology Research
Chemical
Accidents Prevention
Co-ordination Prep./ Resp. Environmental
Toxicology
9
Sultanate of Oman
Ministry of Health
Directorate General of Health Affairs
Department of Environmental Health and Malaria Eradication
S. No.
CENTRAL REGISTRY OF POISONING CASES
HOSPITAL / HEALTH CENTRE / CLINIC …………………………………………………………..
Treated as: A&E …………… Outpatient…………… In-patient ……………Date ...../ ..... / .............
Ward:………….Admission date: …………… Department.……… Unit:…………. HOD:………
Name of Patient: …………………………………..................................... .Phone No:………………………………...
National ID Passport No. Driving License No. Labour Card No.
Address:………………….……………… Hospital No……………………..…… Nationality……………………

Age……… Year/Month......…..........Sex M / F……..…… Weight:……...…Kg. Height:…….……….Cms.
Occupation: None………..…..Housewife. ………………Agricultural. ………..……Industrial ………………..…
Service …..……….Student ……………….….Other ……………….…….Unknown…………
st nd rd
Pregnant : No ….….Yes ………Lactating: No………Yes…..…. Trimester: ………1 …..… 2 …..… 3 …….…
Circumstances of Exposure / Incident

Unintentional
Accidental ….….. Occupational……..….. Environmental….…..Fire / Transport….….. Therapeutic Error……....
Misuse……..….. Food Poisoning ……..….. Other…….…..Unknown……………..
Intentional
Suicide………….…. Abuse …………….….Criminal / Assault ………...….. Adverse drug reaction……………
Other ………….. Unknown ………....
Location:..……….. Home………………..Workplace………….. Hospital……..…..Public place……………

…………. Agricultural…….….. Other……………
Agent Common Name…………………………………………………………… Use………………………

Pharmaceutical………….…… Industrial / Commercial…….……Household……..……Cosmetic………………
Pesticide………………...…… Agricultural (non-pesticide)…………………..
Substance of Abuse………….…… Food / Beverage………………….……
Environmental…………………Warfare……..…….Plant……..…… Fungi………………….
Marine Animal………..……..Insect ………..………Reptile……………… Unknown…………
Type of Animal / Insect / Reptile involved: ………………………………………………………

Site of bite or sting ………………………………Provoked / Not provoked ……………………..
Type of agent Liquid / solid / gas
Quantity gm…………mg…….……litre…………ml…………Other………….Unknown..........
MR - 450
10
Route of Exposure
Ingestion…………….. Inhalation………….. Skin……….….. Parenteral…….….. Ocular……………
Otic……………….….. Sting………….. Bite……..….. Other……….….. Unknown…………….
Duration of Exposure Minutes……..….. Hours……..….. Days….….. Unknown……………
Risk Assessment No risk………….. Minimal risk……….….. Moderate risk……………….

High risk…….….. Established poisoning………………
Management outside hospital Yes……...….. No…………….
Resuscitation…………….. Gastric lavage…..……….. Supportive…..……….. Specific……………..

Skin/Eye washing…………….. Other………..….. Unknown………………….
Presenting symptoms
……………………………………………………………………………………………………………………………………..
……………………………………………………………………………………………………………………………………..
……………………………………………………………………………………………………………………………………..
Examination report:
……………………………………………………………………………………………………………………………………..
……………………………………………………………………………………………………………………………………..
……………………………………………………………………………………………………………………………………..
Investigations asked and carried out:
……………………………………………………………………………………………………………………………………..
……………………………………………………………………………………………………………………………………..
…………………………………………………………………………………………………………………………………...
Treatment given
Supportive: …………………………………………………………………………………………………………………..
Specific antidote: ……………………………………………………………………………………………………………
Severity Minor………….. Moderate……….….. Severe ………………
Outcome Improved………….….. Cured…………….. Sequelae…………………

Expired Yes / No Follow-up: Yes / No
Cause of Death
…………………………………………………………………………………………………………………………………
…………………………………………………………………………………………………………………………………
…………………………………………………………………………………………………………………………………
……………………………………………………………………………………………………………………………………
Doctor's Signature
--------------------------------------------
Agent : A substance/object of natural or man-made origin, which may be toxic to living organism.
Exposure : Contact between a living organism and agent, which may or may not lead to poisoning.
Poisoning : Clinical condition produced by exposure to an agent.
Risk of poisoning : Risk is the probability of the patient suffering poisoning as a result of exposure.
Severity score : Minor –– self resolving. Moderate –– prolonged symptoms. Severe –– life-threatening symptoms.
11
Section II
Principles of Management
of Acute Poisoning
Poisoning
13
14
12
General Principles of Management of Acute Poisoning

• Treat the patient, not the poison.
• Supportive care is the main-stay of management.
• Acute poisoning requires accurate assessment, and prompt therapy.It is
essential to determine if the poisoning:
is life-threatening and already compromising vital functions
poses a potential hazard
is essentially harmless
• In case of a life threatening poisoning, emergency treatment begins with the
initial rapid assessment and resuscitation.
• While assessing the potential toxicity of a substance and the severity of the
poisoning, information regarding the toxic agent (name, amount, route and
duration of exposure and time since exposed, prior treatment received) is
necessary. With the above information, the risk of poisoning is assessed (no
risk, minimal risk, moderate risk or high risk) and accordingly the management
is planned.
• It should be borne in mind that up to 5 % of histories are incorrect with regard to
the substance, quantity and even actual exposure. However, early identification
of the toxic substance (or ingredients and their potential toxicities) can save time
and decrease the risk of toxicity and complications, particularly where a specific
antidote could be life-saving or prevent organ damage. Obtaining the original
toxic substance left over or its container is more reliable for rapid and positive
identification of the poison.
• Call Poison Control Centre for information (Phone No.2456651 )
• Early collection of blood, urine and other body fluid samples to establish
baseline values for monitoring toxic agent (some drugs and metals) and
biochemical parameters is valuable for poisoning management.
• Risk factors such as age, current medications, past history of
medical/psychiatric illness, allergy to drugs, drug abuse and pregnancy should
also be considered.
• A patient, who seems well (asymptomatic) could be exposed to non-toxic
substance, or insufficient amount (too small) to result in poisoning, or the
absorption of toxic substance could be delayed (common with belladonna
alkaloids, antihistamines, diphenoxylate with atropine, phenothiazines and
tricyclic antidepressants). Sustained release preparations have delayed and
prolonged absorption. Delayed symptoms may also be there if only the
metabolites of the substance ingested are toxic (methanol, ethylene glycol,
lithium, etc.)
• Record the events and procedures carefully in a suicidal case.
• Always give advice on prevention of poisoning in case of accidental poisoning
and psychiatric follow-up for intentional poisoning.
• Always fill up proforma for "Central Registry of Poisoning Cases"
15
Treatment of Life-threatening Poisoning
• Emergency evaluation and life-saving treatment

- Primary survey – the ABCDEs
- Secondary survey (diagnosis)
History
Detailed physical examination
Laboratory investigations and X-ray
Toxidrome identification
• Antidote treatment
• Decontamination
- Skin and/or eye

- Gastro-intestinal
Emesis / gastric lavage (limited value)
Activated charcoal (single dose)
Whole bowel irrigation
• Enhanced removal
- Multiple-dose activated charcoal

- Forced diuresis with pH change
- Hemodialysis
- Hemoperfusion (not yet available in Oman)
- Exchange transfusion
• Disposition and/or referral
16
Emergency Evaluation and Life-saving Treatment
Prompt clinical assessment of vital functions and appropriate supportive care is

crucial in the management of acute poisoning. In a comatose patient, the most
common cause of morbidity and death is loss of airway protective reflexes,
resulting in airway obstruction by a flaccid tongue and aspiration of secretions
or vomitus. Breathing difficulty due to ventilatory failure, hypoxia or
bronchospasm caused by some drugs and toxins may further exacerbate the
condition. Other complications contributing to the severity, could be
hypotension, cardiac arrhythmias, seizures, hyperthermia, and organ
dysfunction caused by the toxicant.
Emergency evaluation and life-saving treatment
1. Primary survey and resuscitation – the ABCDEs
2. Secondary survey – history, detailed clinical examination and

laboratory evaluation (establishing diagnosis)
1. Primary survey – the ABCDEs
Check if the patient is conscious. Check the gag reflex. Assess, establish and
maintain vital functions, while resuscitating the patient. Frequently monitor and
record the vital signs (pulse, BP, respiration and core temperature) during
ABCDEs.
A = Airway (with cervical spine control, if neck injury)
• Ensure an open and protected airway by proper positioning (tilt head back
and lift chin up). Suctioning may be required in the presence of secretions
and/or foreign body. Perform definitive airway management (endotracheal
intubation), if the airway is at risk and partially or completely obstructed.
B = Breathing
• Assess breathing (respiratory rate, depth, rhythm, sounds). Normal
respiratory rate in adults varies from 12-18 breaths / minute, any respiratory
rate of >2 or <1 /minute is abnormal in adults (infants normal RR 25-
3 /minute, preschool child, 2 /minute, >3 /min is abnormal).
• Ensure adequate ventilation and oxygenation. Quickly obtain bedside

oximetry and obtain arterial blood gases analyzed. If the patient is not
breathing or breathing inadequately (O2saturation < 9 % and pCO2 > 5 mm
Hg), begin ventilation with a bag-valve-mask (BVM) and give 1 % O2. If the
patient is breathing but O2 saturation is between 9 - 95 % , supplement with
high flow O2 .
17
• Endotracheal intubation, if required.
• Bronchospasm may be treated with nebulized B2 agonist.

• If the patient is breathing but is unconscious, turn him/her on to one side in-to
the recovery position (exclude neck injury).
C = Circulation
• Assess the circulatory system (pulse rate, rhythm, volume and BP, skin
perfusion and temperature). If pulse is absent, start CPR. Attach to cardiac
monitor and treat any dysrhythmias following the ACLS protocols.
• Start iv line, draw blood samples for routine biochemical, hematological and
suspected toxicity tests.
• Treat hypotension with fluids, 5%dextrose in normal saline

(children – D5 in .25 NS).
• If required, administer vasopressor (Dopamine 5-15µg/kg/min iv infusion).

Titrate based on BP
• Maintain adequate circulation – ensure adequate urine output.
• Treat severe hypertension with Labetalol .2 – .3 mg /kg iv
D = Disability (Nervous system)
• Determine the level of consciousness. A good way of doing this in the

primary survey is AVPU method:
A = Alert V = Responds to verbal stimuli
P = Responds to painful stimuli U = Unresponsive
• Continually assess the level of consciousness.
• Assess pupil size, reactivity and extra ocular movements.
• Check for reflexes and other neurological signs (dystonia, rigidity, dyskinesia)
and rhabdomyolysis.
• Treat seizures promptly with Diazepam (o.1 - .2mg/kg iv slow injection), can
repeat every 1-2 hours as needed. Can use Lorazepam . 5- .1mg/kg iv slow
injection or Midazolam . 5- .1mg/kg iv or im in place of Diazepam, depending
upon the availability. Phenobarbitone (15mg / kg / iv slowly can be used if
convulsions remain uncontrolled with Diazepam.
18
• Coma or stupor is the most common serious complication in acute poisoning.
Consider excluding other causes of coma (trauma, meningitis, encephalitis,
CVA)
- Maintain the airway and assist ventilation, administer oxygen
- Give dextrose iv (5 ml of 5 % in adults and 2 ml/kg of 25% in children)
-Thiamine 1 mg/day (especially in alcoholics) in the iv bottle or given

intra muscularly.
- Naloxone .4mg iv or im, check response in 1-2 minutes, can repeat up to

2 mg iv.
- Monitor core temperature (rectal) and maintain normothermia. Associated

hypothermia should be assessed and treated by rewarming (blankets, warm iv
fluids, warm mist inhalation) slowly to prevent rewarming arrhythmias.
- Do not treat associated bradycardia.
- Do not give excessive fluids
• Patients with life-threatening hyperthermia (temperature > 4 ºC or >1 4ºF),

must be treated immediately.
- Maintain airway and assist ventilation, give oxygen

- Give glucose containing iv fluids, control seizures, agitation
- Start external cooling with tepid (lukewarm) water sponging and
fanning, aim is to bring temperature to 38.6ºC
- Exclude other causes of hyperthermia (drug withdrawal, heat stroke,
thyrotoxicosis, meningitis, encephalitis, or other systemic infections).
- For malignant hyperthermia, give Dantrolene (1-1 mg/kg iv).
- With anticholinergic poisoning, antidote treatment may reduce

hyperthermia.
E = Exposure with environmental control
• The poisoned patient should be completely undressed and examined

thoroughly, particularly for signs of trauma, burns, puncture marks, rash,
petechiae, etc. removal of clothing is also warranted for necessary skin
decontamination.
• Assess and treat anaphylaxis .
19
• Assess and treat rhabdomyolysis by obtaining serum creatinine and
phosphokinase (CPK) levels (elevated levels).
-Treat rhabdomyolysis by administering iv fluids, maintain urine flow to

3-5ml/kg/hr. Mannitol .5g/kg iv can be considered in patients with oliguria.
Alkalinize urine by adding 1 mEq of sodium bicarbonate to each liter of 5%
dextrose.
• Treat dystonia, dyskinesia and rigidity by maintaining airway and ventilation,
and treating associated hypothermia.
• For dystonia, administer Diphenhydramine .5-1mg/kg (25 – 5 mg) im.
• For dyskinesia, give diazepam, if uncontrolled, find the cause
(spider bite/malignant hyperthermia or Neuroleptic syndrome), and treat
accordindly.
2. Secondary Survey – Diagnosis of Poisoning
After the Primary Survey and resuscitation, the patient's assessment involves a
Secondary survey. A focused poisoning survey is performed as follows:
• A careful history
• A detailed clinical examination
• Essential clinical laboratory tests
- History should be obtained preferably from the patient, if possible.
Where it is not possible (e.g. due to unconsciousness or altered level of
consciousness) or when it is likely to be unreliable, coroborative
information may be obtained from contacting friends or relatives, talking
to the person bringing the patient to hospital or to the ambulance
attendants or by contacting the patient's doctor, as applicable.
- A careful history of any underlying medical or psychiatric condition
should be sought as well as information about regular medication use
(prescription, non - prescription, traditional remedy). Some judgment
should be made about the level of patient's suicidal intent (where
applicable) and this should be recorded in the patient's notes.
- Try to obtain label, bottle container of the suspected drug or chemical
(scene residue).
History should be directed towards identifying the following:
• Type of poison (chemical, drug, insect bite/sting, plant)
• Amount / quality
• Route of exposure
• Time since exposure
• Reason for exposure
• Time of onset of symptoms in relation to exposure
• Treatment received outside hospital
20
• Physical examination
A detailed physical examination is of utmost importance and often elicits vital
clues to the nature of poisoning. It is largely directed towards reassessment of
basic life functions (respiration, pulse, BP and core temperature), level of
consciousness, pupil size, and bowel sounds to define toxicological syndrome.
The term toxic syndrome or toxidrome refers to a constellation of physical
findings that, when present, can give the clinician important clues that narrow
the differential diagnosis. This is particularly useful in patients in whom an
adequate history cannot be obtained. A list of common toxidromes is given in
the Table I. Once a toxidrome is identified, the specific management including
antidote treatment can be initiated.
The detailed clinical examination is essential to diagnose poisoning and
should include the following:
- Reassessment of vital functions as mentioned above. Carefully examine
chest for respiratory and cardiovascular functions . Consult tables ( Section
VII ) to assist diagnosis.
- Assess neurological status. The level of consciousness is usually measured
in secondary survey by using Glasgow coma scale (Table II). A GCS of 8 or
less, strongly suggests that patient will not be capable of adequately
protecting his airway. The patient may require continued endotracheal
intubation. Patients who are drowsy or stuporous will often not require
intubation provided they are nursed on their side and continually assessed
e.g., in alcohol or benzodiazepine over dose.
- Assess psychosis, agitation, cognitive function changes
- Assess for any other neurological changes (reflexes, motor dysfunctions,
extra ocular movements, etc.) Consult tables ( Section VII) to know the
possible causes.
- Examine carefully pupil-size, reaction, nystagmus, fundus.
- Examine skin for temperature, dry/moist, colour (pale, cyanosed), bleeding,
rash, piloerection, bullae, burn injury, sting / bite marks, needle tracks.
- Examine gastrointestinal system starting from the mouth (oral mucosa burn,
breath odour) abdominal tenderness, bowel sounds, abdominal distension,
check or inquire about colour of stool.
- Examine genitourinary system for distension of bladder, and check for urine
output, colour of urine.
- Record body weight of the patient
- Check for any Medi-Alert bracelet or card with the patient
21
• Laboratory Investigations
Appropriate use of the laboratory is important in managing poisoned patients.
General laboratory tests as a rule are more useful than 'toxicology screens'.
Physicians should be familiar with the laboratory at their own institutes and
know its capabilities and limitations. Routine laboratory tests include CBC,
blood glucose, ABGs, serum electrolytes, INR, blood urea, serum
creatinine, urine tests and LFT.
Mostly, a thorough and appropriate history, detailed physical examination and
routine laboratory investigations provide sufficient clue to the diagnosis.
Specific laboratory tests as required and as per the facility available, can be
used as adjuncts.
In general, the greatest use comes from tests for Paracetamol, Theophylline,
Lithium, Digoxin, Ethanol, Ethylene glycol, Methanol, Iron, Salicylates,
Carbamazepine, Valproic acid, Phenytoin, Phenobarbitone and levels of
Carboxyhemoglobin, Methemoglobin and Cholinesterase.
Radiological support in diagnosis
Certain drugs are Radiopaque and a plane abdominal X-ray film may provide
useful information . Radiopaque drugs/substances include:
Iron and other heavy metals (As, Pb, Hg)
Calcium carbonate
Potassium
Phenothiazines
Chloral hydrate
Enteric coated tablets
Button battery
Radiographs can also be useful in differential diagnosis. Non cardigenic
pulmonary edema on a chest radiograph suggests opiate or salicylate
overdose, pulmonary aspiration, irritant gases or smoke inhalation, mercury
vapour inhalation, or other metal fumes.
3. Care of an alert patient with stable vital functions, but
symptomatic
Start with secondary survey. Continue supportive treatment. Diagnose the case
by proper history and investigations and treat accordingly .
It must be emphasized that nothing replaces the supportive care and
continual assessment of the patient. Quality Supportive Care has saved
more poisoned patients than any antidote.
4. Care of asymptomatic patient (refer page 37)
5. Treatment of anaphylaxis (refer page 38)
6. Care of inhalation, eye or skin exposure (refer pages 41,42)
7. Treatment of bites and stings (refer pages 43 – 66)
22
Table I : Toxicological Syndromes
TOXIDROME DRUGS/CHEMICALS CLINICAL MANIFESTATIONS
CHOLINERGIC Organophosphates, Carbamates, “ DUMBBELSS”

Mushrooms (some), Edrophonium Defaecation, urination, miosis,
bradycardia, bronchospasm,
bronchorrhoea , emesis,
lacrimation, secretions, seizures.
ANTI-CHOLINERGIC Antihistamines, Antiparkinsonian Tachycardia, hypertension,

drugs, Anti-spasmodics, Atropine, elevated temperature, flushed
Anti-psychotics, Anti- skin, mydriasis, urinary retention,
depressants, many plants decreased bowel sounds,
(Jimson Weed, Amanita muscaria) seizures, dysrhythmias, delirium
with mumbling speech.
SYMPATHOMIMETIC Cocaine, Amphetamine, LSD, CNS excitation, hypertension,

Metamphetamine, over-the- tachycardia, mydriasis,
counter decongestants hyperpyrexia, diaphoresis,
(Phenylpropanolamine, Ephedrine delusions, paranoia ,
etc.) dysrhythmias, seizures.
SEDATIVE Benzodiazepines, Barbiturates, Coma, respiratory depression,

HYPNOTIC Alcohols, Choral hydrate hypotension, bradycardia,
hypothermia.
OPIOID Heroin, Morphine, Codeine, CNS depression

Pethidine, Propoxyphene Miosis (except pethidine)
Hypotension
Coma , decreased bowel sounds
Respiratory depression
Non-cardiogenic pulmonary
oedema
SEROTINERGIC SSRI’s (Fluoxetine, Paroxetine, Neuropsychiatric manifestations

Sertraline) Clomipramine etc. (agitation, confusion, seizures)
Autonomic manifestations
(hyperthermia, diaphoresis,
diarrhoea, tachycardia,
hypertension, salivation)
Neuro-muscular manifestations
(ataxia, rigidity, tremor,
hyperreflexia, myoclonus)
23
TOXIDROME DRUGS/CHEMICALS CLINICAL MANIFESTATIONS
ANION-GAP Salicylates, Alcohol, Hyperventilation, vomiting,

METABOLIC Methanol, Ethylene Glycol, dehydration, hyperthermia, CNS
ACIDOSIS Paraldehyde. depression, ataxia, nystagmus,
Inhalation of solvents pulmonary oedema, renal failure, visual
(“glue-sniffing”) complaints, seizures.
WITHDRAWAL OF Alcohol, Opioids, Tachycardia, diarrheoa, vomiting,
SUBSTANCES OF Barbiturates, Chloral Hydrate mydriasis, pilo-erection, lacrimation,
ABUSE yawning, agitation, seizures.
IRRITANT GAS Ammonia Rhinorrhoea, upper airway oedema,

Formaldehyde coughing, dysphonia, stridor,
Chlorine laryngospasm, lacrimation.
Sulphur dioxide hypoxemia, myocardial ischaemia,
Hydrogen chloride tachydysrhythmias.
Phosgene Agitation, anxiety, confusion, seizures,
Nitrogen Dioxide coma.
ASPHYXIANTS Carbon dioxide, Carbon Tachypnoea, respiratory depression,

monoxide, Cyanides, respiratory arrest.
methaemoglobin – forming Tachycardia, dysrhythmias, cardiac
compounds (Amyl nitrite, arrest.
aniline etc), Sulfides, Azides. Central & peripheral cyanosis
(methaemoglobin forming compounds)
Headache, dizziness, confusion,
agitation, seizures, coma.
CNS excitation followed by CNS
depression.
CORROSIVES Acids (HCl, H2SO4, HNO3) Laryngospasm, bronchospasm, edema

of upper and lower airways
Bases (NH4OH, KOH, NaOH) (inhalataion)
Drooling, difficulty in swallowing,
Oxidizers (ClO2, H2O2) oesophageal injury leading to
perforation with pneumo-mediastinum.
Phosphorous (White, Red, (Ingestion)
Black) Ingestion of concentrated hydrogen
peroxide can cause fatal oxygen gas
(air) embolism.
Chemical burns of skin and mucous
membranes and when the eyes are
affected can lead to blindness.
Oxidizers – met haemoglobinaemia ,
cyanosis.
Hypoxaemia and hypovolemia may
lead to myocardial ischaemia , cardiac
arrest.
Torsion – head and Amantidine , Antihistamines, Dysphonia, oculogyric crisis , rigidity ,
neck syndrome H2 Blockers , Levodopa , tremors, torticollis
Metoclopramide ,
Phenothiazines ,
Butyrophenones
24
Table II A: Adult Glasgow Coma Scale
1. Eye opening
Spontaneously 4
To command 3
To pain 2
None 1
2 Best Verbal Response
Oriented 5
Confused 4
Inappropriate words 3
Incomprehensible sounds 2
None 1
3. Best Motor Response
Obeys commands 6
Localizes 5
Withdrawal 4
Abnormal flexion 3
Abnormal extension 2
None 1
TOTAL SCORE 3 – 15
25
Table II B: Pediatric Glasgow Coma Scale
Eye Opening Score

spontaneously 4
to verbal stimuli 3
to pain 2
never 1
Nonverbal Children Best Verbal Response Score
(as in the Glasgow scale)
smiles oriented to sound oriented and converses 5
follows objects interacts
consolable when crying disoriented and converses 4
and interacts
inappropriately
inconsistently consolable inappropriate words 3
and moans; makes vocal
sounds
Inconsolable, irritable and incomprehensible sounds 2
restless; cries
no response no response 1
Best Motor Response Score
obeys commands 6
localizes pain 5
flexion withdrawal to pain 4
abnormal flexion to pain (decorticate rigidity) 3
extension to pain (decerebrate rigidity) 2
no response 1
Minimum score 3 and Maximum score 15

Source :- Lancet 1982;2:45
26
Antidote Treatment
Antidote Poisoning Dosage Cautions

*Snake Anti- Snake bite Allergic reactions,
venoms Anaphylaxis
Available as 10 ml amp./vial
1. Polyvalent Vipers + Puff adders + Dilute 40 ml(4amp) in 5ml/kg Keep resuscitation trolley
Saudi National Cobra normal saline and infuse iv with adrenaline,
Guard (SNG) anti- slowly over 30-60 min. Repeat antihistaminic and
venom if required every 4 – 6 hrs until corticosteroid ready.
coagulopathy persists.
Child: same dose
Available as lyophilized serum

in amp/vial with 10 ml water for
2. Lyophilized Vipers (except horned injection. Add 10 ml of water
Polyvalent anti- viper + Puff adder) with syringe into serum vial,
snake venom shake for 1 min. until the
(Haffkine) reconstituted serum is clear.
First dose: 20 ml (2 vials)
administered iv very slowly (1
ml/min)
Second dose: to be given after
2 hrs.
Further doses to be given
every 6 hrs, if symptoms
persist. Some serum may be
injected locally around the bite
site, to check gangrene.
Child: same dose
*Scorpion Scorpion Sting Available as 1 ml amp. Dilute Allergic reactions
Antivenom five, 1 ml ampuoles in 20-50 Anaphylaxis
ml 0.45 N/S inject iv in 30
(SNG or minutes. Repeat after 2hrs
Pasteur) PRN
Child: Same dose but dilute in
0.25 N/S (until 6 years of age)
*Atropine Cholinergic syndrome Adult:1 – 5 mg iv boluses as
– Organophosphorous required every 5 - 10 min. till None except anticholinergic
or Carbamate toxicity atropinized (drying of syndrome if overtreated.
pulmonary secretions)
Child: 0.05 mg/kg iv bolus
*Calcium CCB overdose Adult: 10% Ca Gluconate 10- Extravasations of CaCl2 can
(gluconate or Hypocalcemia 20ml or 0.2ml/kg of 10% Ca Cl2 cause tissue necrosis. A big
chloride) (Fluoride, oxalate, given as slow infusion over 5 – patent vein to be used under
10% solution ingestion, topical HFl 10 min. Repeat every 15 – 20 close monitoring of heart
acid) minutes PRN. rate. Avoid local
Severe hyperkalemia Child: 100mg /Kg slow iv Oral extravasations. Rapid
Hypermagnesmia Cal. Carb. Antacid for fluoride administration causes
Beta blocker over ingestion. Topical 32.5% Cal. hypotension, bradycardias
dose. Gluc. gel for HFl skin burns. and dysrhythmias.
*Deferoxamine Iron 15 mg/kg/hr iv infusion Rate related hypotension.
max.dose / 24 hrs, not to Prolonged infusion over 24
exceed 6 g. Then alternating hrs can cause pulmonary
infusion with iv fluids 12 hrly. toxicity.End point of therapy
Child: Same dose is loss of vin-rose colored
urine or serum iron <300ug/dl
27
Hypoglycemia Adult: 50%, 50-100ml by iv Tissue extravasations may cause
*Dextrose (Blood Glucose <3.2 push. Repeat PRN. necrosis. May precipitate
mmol/Liter or < 70mg/dl). Child – 25%, 2-4ml/kg Wernicke Korsakoff syndrome in
Emperic therapy of coma. Neonate – 10% Same dose. thiamine depleted patients
Infusion – 5% to 10% (alchoholics/malnourished).
depending on severity – Administer Thiamine in these
titrate Blood Glucose. cases.
Do not give in uncertain diagnosis,
Dicobalt EDTA
Cyanide 300 – 600 mg iv( adults) Allergic reactions, seizures &
arrhythmias
Acute ingestion: The dose Safe, allergic reactions are remote.
Digibind Digoxin can be calculated Watch for hypokalemia and CHF in
according to the ingested pt. at risk.
Digoxin amount. Each vial
binds 0.5 mg digoxin. Ideally, serum levels to be
Inject the calculated dose iv monitored for therapy.
If the dose is unknown,
inject 10-20 vials.
Child: Same dose
Chronic toxicity: 3–6 vials
adult, 1-2 vials child. (give
iv over 30 minutes if
chronic or by rapid bolus, if
life threatening arrhythmia).
Inorganic mercury, arsenic Lead encephalopathy: 4-5 G.I. effects, headache transient
*Dimercaprol and lead encephalopathy or mg/kg deep im every 4 hrs burning, myalgias, anxiety.
( BAL ) Blood lead level > 100 for two days and then Contraindicated if peanut allergy.
microgram/dl 12hrly for five days in In G6PD deficiency it can cause
conjunction with Cal Disod. hemolysis
EDTA. Child : same dose Hepatic or renal impairment.
Arsenic: 3-5 mg/kg im
every 4 hrs for 2 days then
b.i.d tapering dose based
on clinical symptoms.
Mercury: 5 mg/kg im then,
2.5 mg/kg q 8 hrly on day 1
then 2.5 mg/kg q 12 – 24
hrs till clinical
improvement. – maxmimum
for 10 days.
30 mg/kg in 2 – 3 divided Nephrotoxicity (monitor renal
*Edetate Ca Lead encephalopathy or doses deep im injection or function) Transient increases in
disodium Blood lead level > 100 1.5 gm/m2/day by slow transaminases.
microgram/d l continuous 24 hr. iv
infusion (concentration <
0.5%) Start 4 hrs after BAL,
give for 5 days.Child : same
dose
Benzodiazepine 0.1 mg/min to a total dose Seizures in mixed drug overdoses
*Flumazenil CNS toxicity (will not of 1 mg – slow iv titration to especially. TCA’s. Past history of
improve respiratory effect. Repeat in 20 – 120 seizures increases risk.
depression) mins. PRN. Max. Dose 3mg.
Child: Start with
0.01mg/kg/min slow iv Max.
Dose 1 mg.
2
*Leucoverin Methotrexate toxicity 75mg (10 mg/m )every 4 – Only leucoverin for methotrexate.
(folinic acid) 6 hrs iv leucoverin up to Rare case of seizures, repeat
three days Child : same doses required
dose During dialysis for methanol
*Leucoverin & Methanol poisoning Adults: 50 mg toxicity.
Folic Acid Child: 1mg/kg folic acid iv
every 4 hrs for 24 hrs.
28
Toxin induced Available as 10% solution. Generally safe. Irritating to veins
*Methylene Blue methemoglobinemia 1 – 2 mg/kg iv over 5 min. and tissues. Conceals cyanosis.
(over 20%) followed by 30 ml fluid In overdosage may cause
flush. methemoglobinemia esp. with
Child: Same dose G6PD deficiency, so no second
Neonates: 0.3 – 1 mg/kg dose to be given
Repeat every 4 hrs as
necessary.
Salicylate, T.C.A.’s iv bolus – 1 meq/kg B.W. in Avoid pH > 7.55
*Na Bicarbonate Antiarrhymics–Type1 1 min. may repeat PRN.
Phenobarbitone over Infusion – 50 meq in 500 ml Don’t administer Na Bicarbonate
dose,Severe D5W with calcium containing solution
metabolic acidosis at 250 ml - 500 ml/ hr at the same time.
esp. drug induced (rate and bolusing
(methanol, glycols) dependent on pH as well
as Condition of the
patient. In children : same
dose
Paracetamol Solution: 20% (2 gm in 10 Nausea + vomiting
*NAC Toxicity ml) Use metoclopromide
(N – acetyl cysteine) Acute – 150 mg/kg Intravenous: 150 mg/kg in
dose ingested or 150 500 ml D5W, load over 1 hr. Anaphyllactoid reactions which
µg/ml serum levels at Then 150 mg/kg in 500- are infusion rate related. Transient
4 hrs or elevated 1000 ml D5W, over 24 hrs. increase. in INR after 24 hrs.
transaminases 2 x Child: Same dose in 100-
Normal levels or 200 ml D5W
>1000 IU/L Oral: load 140 mg/kg, then
70 mg/kg every 4 hrs for 72
hrs (dilute each dose 1
part to 4 parts juice or
other diluent)
Opioid toxicity 0.05 mg iv in suspected Possible withdrawal otherwise
*Naloxone addicts otherwise 0.4 - 0.8 very safe.
mg iv, then repeat at 2-3
mins upto 2mg or till
response occurs. Pediatric
and adult doses same.
Anticholinergic 0.04 – 0.08 mg/kg iv (max 5 Overdosage causes cholinergic
*Neostigmine syndrome mg dose) may repeat in 30 syndrome (see manual for
– 60 min. to effect.Child : toxidromes)
same dose
Cyanide or hydrogen 300 mg iv in 2 – 3 min (10 Hypotension
Nitrite sodium sulphide mg/kg in children) May Excessive methaemoglobinaemia
repeat ½ above dose in 30
mins
(methaemoglobinaemia of
20 – 30% is target).
Cyanide Thiosulfate 12.5 gm (50 ml) Thiosulfate is non-toxic

*Thiosulphate for adult. Pediatric dose is
0.33 ml/kg/B.W.
Lead, mercury and Adult: 500 mg q.i.d. orally Hypersensitivity
*Pencillamine copper for 2 – 3 months. Reactions (pencillin allergy –
contra-indicated).
Child: 25 mg/kg q.i.d for 2 – No other significant reactions.
3 months.
29
Cholinergic syndrome Adult: 1 – 2 gm in 100 ml Transient
*Pralidoxime (Organophosphate or N/S slow iv over 15 – 30 blurred vision and dizziness.
Carbamate) min.
Child: 20 – 40 mg/kg iv in
30 min. Repeat after 1 hr
PRN or
give maintenance infusion
at the rate of 1 gm in 100
ml N/S, 200 - 500 mg/hr in
adults and 5 - 10 mg /kg/hr
in children till relief of
muscular weakness and
fasciculation.
Heparin infusion 25 – 50 mg iv over 15 min. Rate related hypotensive and

*Protamine overdose (approx. 1 mg/kg/B.W) anaphyllactoid reactions
check activated clotting
time after first dose and in
24 hrs for repeat dosing
0.25--1mg/100 units of
Heparin iv overdose heparin, depending on time
of heparin dose
Child: same dose
Isoniazid over dose 1 gm pyridoxine in 50ml
*Pyridoxine dextrose iv for 1 gm INH None
(Vit. B6) (child 70 mg/kg) .
Max. dose for all patients 5
gm. Max. rate 0.5 gm/min
for emergency control of
seizure otherwise give over
4 – 6 hrs iv.
Ethylene glycol For ethylene glycol 50mg
Poisining iv or im till intoxication
resolved
Comatosed Patient Adult: 100 mg Thiamine Extremely rare cases of
*Thiamine (Wernicke – slow iv or im daily anaphylactoid reactions
(Vit. B1) Korsakoff’s Child: 1-2mg/kg PO, im or (probably . from diluent)
Syndrome – an slow iv per day.
encephalopathy) Maximum dose in severe
cases upto1g
in 12 hrs.
Hypoprothombinemia Adult: Oral 25– 50 mg None.
*Vit. K1 raised INR (Warfarin every 6 – 8 hrs. Im dose causes hematomas.
(Phytonadione) or Superwarfarin Child: Oral 3 – 5 mg OD Anaphylactoid reactions (rate
rodenticides) Adult: SC 10–25 mg related)
Child: SC 1–5mg 6-8 hrly
IV : 10 mg slowly in 10 min
in adults and 0.6mg/kg in
children for life threatening
conditions only.
*Approved by MOH
Note : 1. Activated charcoal powder and polyethylene glycol electrolyte solution are approved by MOH
. 2. Dicobalt EDTA, Digibind and Sodium Nitirite are available at SQUH
30
Decontamination
Decontamination is a therapeutic intervention employed to (i) decrease exposure
to poison, (ii) prevent local injury and damage, and (iii) prevent and reduce
systemic absorption. The procedures include irrigation of skin and eyes, removal of
toxic substance within the GIT by emesis, gastric aspiration and lavage, single
dose activated charcoal, catharsis and whole bowel irrigation
Skin decontamination
Skin exposure to chemicals and corrosives results in immediate pain, redness,

burn or necrosis. Potent toxins (e.g. organophosphates) may be absorbed through
the skin and so removal of clothes, shoes and accessories by gloved personnel
and copious irrigation with water and washing with soap of exposed areas, nails,
skin folds and hair is appropriate, if the history and clinical features support skin
exposure. After thorough washing, skin should be dried gently with clean towel. In
case of burns, blisters should not be opened, the skin should be left intact. The
area be covered with sterile dry dressing and loose bandage. Replace fluid loss by
oral rehydration salts. Treat pain with analgesics. Contact Poison Control Centre
for information on systemic toxicity. Look for signs, refer the patient to regional
hospital, if required.
Eye decontamination
Ocular exposure to toxins can cause local and general effects but the most critical
for emergency management are corrosives including hydrocarbon solvents.
Alkalis are worse than acids as they cause liquefaction necrosis. Continuous
irrigation with water or normal saline is crucial until pH of tears reaches 7.5 - 8.
Remember to remove particulates with wet swabs especially under the tarsal
plates and conjunctival recesses. Place the victim with affected eye open under
the tap or use intravenous tubing connected to a direct stream of water (low
pressure) across the nasal bridge in to the medial aspect of the affected eye. Use
at least one liter of water or saline to irrigate each eye for 15-3 minutes.
Principles
1-Irrigate the skin and eyes copiously for all corrosives (especially alkalis) with
normal saline or water. This may require hours for the eyes and is ideally guided
by pH of lachrymal secretions.
2- After irrigation, check conjunctival and corneal surfaces for evidence of full
thickness injury. A fluorescent and slit lamp examination by an ophthalmologist is
recommended.
31
Gastro-intestinal decontamination
There exists a considerable controversy about the role of gastric emptying
(emesis, gastric aspiration and lavage), activated charcoal and cathartics in the
management of acute poisoning. Studies have shown that gastric emptying may
be of limited benefit and activated charcoal without prior gut emptying is as
effective or even more effective. Moreover, factors such as age of the patient, the
substance ingested, the severity of symptoms, the time since ingestion, the
presence of co-ingestants, all affect the choice of the procedure beneficial for the
patient. Understanding the limitations and benefits of each procedure and then
considering the specific clinical situation will form the basis for a rational approach
to gastrointestinal decontamination. The indications for emesis include (i) the
substance must have strong probability of being in the stomach i.e. the time since
ingestion of toxic liquid substance should not be more than 1 hour and for a solid
(tab, caps, powder) within 2 hours and the patient has not vomited before, (ii) the
patient is conscious or the airway has been protected in unconscious, convulsing
or in suspected CNS depressant or stimulant ingestion, (iii) substance is not
corrosive or hydrocarbon, and finally (iv) the substance is highly toxic and cannot
be managed by other safer techniques (when the dosage is beyond the capacity of
activated charcoal adsorption or not adsorbed by it at all, or the formulation of
concretions or bezoars, which cannot be taken out by gastric lavage.)
Always contact Poison Control Centre, if not sure of the safety of the
procedure in a particular patient.
Do not make the patient vomit if:
• The substance is non-toxic
• More than 2 hours passed since ingestion
• Unknown substance
• Patient unconscious or sleepy
• Seizures
• Ingestion of corrosives or hydrocarbons (kerosene, petrol, solvents)
• CNS depressant or stimulant ingestion
• CVS collapse.
Consider induction of emesis only for early ingestion of iron, lithium,
theophylline, salicylates and sustained release CCB's. Emesis is now
regarded as a pre-hospital treatment for these ingestions. An alternative
hospital strategy for all these toxins is whole bowel irrigation
• Mechanical stimulation of throat may not be effective.
• Never use salt water to induce emesis.
Ipecac. Syrup is used as emetic, if available and indicated

Dose: Adults – 3 ml
Children (1-12 years) – 15ml
Children (6-12 months) – 1 ml
Can repeat after 3 minutes
32
Gastric lavage
Gastric aspiration and lavage should not be routinely considered in the
management of all poisoned patients. Stomach evacuation by lavage is
constrained by the same physical and clinical realities as emesis. It also introduces
another limitation in tablet removal through standard tubes.Virtually,all nasogastric
tubes are unreliable in retrieving tablets and even large or gastric hoses will not
retrieve concretions or bezoars.
Principles
1. The use of lavage should be selective as with emesis and the utility is
approximately the same
2. Consider performing only when naso-gastric tube insertion is required for
activated charcoal or when toxins are not adsorbed by activated charcoal
(lithium, iron, ethanol) or for life threatening ingestions, prior to it’s absorption
(within 1 hr )
3. Airway protection (as for emesis) must be ensured to prevent aspiration, by
endotracheal intubation in unconscious or convulsing patient or in suspected
CNS depressant / stimulent overdose.
4. Adverse effects include epistaxis, esophageal perforation, fluid and
electrolyte imbalance
Activated charcoal
For most toxins, activated charcoal has emerged as the gastrointestinal
decontamination procedure of choice. It adsorbs most organic compounds. A few
studies suggest that clinical outcome with activated charcoal administration alone
may be better than gastric lavage. It is obviously most efficient when administered
early and in sufficient quantity to adsorb ingested toxins. It will not adsorb iron,
lithium cyanide, heavy metal salts and alcohols but will adsorb a wide range of
other toxic substances. Adsorption of hydrocarbons is variable so it should not be
considered for simple hydrocarbon ingestions nor should it be used for acids or
alkalis.
Principles
1. Use for all toxins except iron, lithium cyanide, alcohols, simple hydrocarbons
and corrosives
2. Give by mouth if possible, if not possible, by NG tube. Flavour for children,
water for adults.
3. Assess airway stability and protect against aspiration.
Activated charcoal: Dosage
.5gm – 2gm / kg BW depending on dosage of ingested toxin in mg (1 parts by
weight of charcoal to 1 part ingested toxin). Average dose is 1 gm / kg BW
The greatest risk to the administration of activated charcoal , although rare , is
pulmonary aspiration .
33
Cathartics
All classes of cathartic substances have been used in clinical toxicology yet little
scientific evidence exists as to their efficacy. Virtually all studies are combination
studies with activated charcoal and drug elimination is no better with a cathartic
than activated charcoal alone. Because multiple side effects have been reported
with cathartics, some serious, therefore, their use is no longer recommended
especially with the advent of whole bowel irrigation.
Whole bowel irrigation (WBI)
The hypothesis that drugs can be rapidly flushed through the G.I. tract before
significant absorption, is attractive but not yet satisfactorily proven in all clinical
studies. In addition, there are management difficulties in using the technique as
patients need to remain on a commode or bed pan for four to six hours before
maximum efficacy. This, therefore eliminates the intervention as a definitive
emergency technique – patients require admission in most settings. However, the
safety of the technique has improved with the use of polyethylene glycol and
electrolyte lavage solutions ( CoLyte ) versus balanced electrolytes alone.
Significant fluid abnormalities were reported earlier with normal saline, K
supplementation and Ringer's lactate.
While further studies are necessary, selected toxic ingestions may respond to this
intervention. Characteristics of such ingestions would include substances too
copious for activated charcoal alone, especially when they are past the pylorus and
not amenable to stomach evacuation.
Principles
1. Consider WBI when substances are not absorbed by charcoal (Iron, Lithium,
Heavy metal salts, Sustained release tablets, Drug packets) and where time
is too remote for stomach removal by lavage or emesis.
2. Consider when there is good clinical or radiologic evidence for sustained
release medication in the small bowel or with rising drug levels despite
activated charcoal.
Endoscopic or surgical removal
On very rare occasions, endoscopic or surgical procedures may be indicated
to remove adherent button batteries, lead foreign bodies, iron tablets or illicit
drug packages that can not be removed by other techniques.
Conclusions
1. Through an extensive understanding of the benefits , indications , risks and
complications of the existing decontamination procedures , the clinician can
choose the best suited procedure for the individual patient with a specific
exposure
2. Ipecac – induced emesis is a pre-hospital procedure
3. Gastric lavage has limited value and is superceded by activated charcoal
administration, which has emerged as the choice of decontamination
procedure for most poisoning.
4. Decontamination is no substitute for supportive care
34
Enhanced Elimination of Drugs and Toxins
These techniques are complementary to the general principles mentioned in the
previous pages.
The main methods of enhancing the elimination of toxins are:

• Multiple dose activated charcoal
• Enhanced diuresis and urine alkalinization
• Extracorporeal techniques (mainly haemodialysis) and exchange
transfusion
I- Multiple-dose activated charcoal
Multiple-dose activated charcoal (MDAC) is the most commonly used method for
enhancing the elimination of toxins. MDAC can be beneficial in both the pre-
absorptive and post - absorptive phases of poisoning. MDAC is most effective in
removing drugs with a high charcoal binding capacity, a low intrinsic clearance
(i.e., a prolonged elimination half-life), a small volume of distribution, low protein-
binding, and a nonionized state at physiologic pH (low pKa)
Based largely upon experimental models, MDAC is probably beneficial in the

following intoxications:
• Carbamazepine
• Dapsone
• Phenobarbital
• Quinine
• Theophylline.
For these drugs MDAC clearance is near to that of haemodialysis or
haemoperfusion.
Administration:
As soon as possible after the intoxication.
Dose of MDAC:
• Initial dose: 1 g/kg of activated charcoal with sorbitol. Only the first
dose of activated charcoal should be given with sorbitol.
• Subsequently: .5 to 1 g/kg of activated charcoal in aqueous
suspension every two to four hours.
35
II- Urinary alkalinization and forced diuresis
The urinary excretion of some drugs can be enhanced by increasing the urine
output and, more importantly, altering the urine pH. Drugs, which are likely to
respond to these methods, should have the following pharmacological properties:
• Elimination predominantly and in unchanged form by the kidney
• Distribution predominantly in the extracellular fluid compartment
• Minimum protein binding
• The drug is a weak acid
Indications:
• Salicylates (most effective next to haemodialysis)
• Barbiturates: Phenobarbital, Pirimidone and Barbital
• Cyclophosphamide, Cisplatin, Methotrexate and 5- Flurouracil
• Isoniazid
• Sulfonamides
• Meprobamate and Chlorpropamide
• Lithium
• Herbicide: 2,4-D Chlorphenoxyacetic acid
• Barium, Bromide and Chromium
• Thallium
Dose and preparation:
• Prior to the initiation of therapy, baseline measurements of electrolytes,
blood urea nitrogen, serum creatinine, glucose, arterial (or venous) pH and
urinary pH, and serum drug concentrations should be performed. The
placement of a bladder catheter to accurately measure urine output is
recommended.
• Start intravenous infusion of half-normal saline or five percent dextrose in
water to which 5 to 15 mEq of sodium bicarbonate has been added to
each liter. The goal of forced alkaline diuresis is to achieve a urine flow rate
greater than 3 ml/kg per hour with a urine pH of 7.5 or higher.
• The administration of 2 to 4 mEq/L/ hr of potassium chloride may be
required if the plasma potassium concentration falls during urinary
alkalinization.
• Acetazolamide should not be used to alkalinize the urine because it will
lower the serum pH, possibly worsening clinical toxicity.
• Close monitoring of blood and urine pH, electrolytes, respiratory status,
and urine output is important when diuresis and urinary alkalinization
procedures are performed.
Indications:
• As soon as possible after the intoxication and the arrival of the patient to
the hospital (or health centre).
• If MDAC is indicated for a specific indication such as Phenobarbital,
combination treatment is possible.
36
III- Urine Acidification
Urine acidification (urine pH below 5.5) with ammonium chloride or ascorbic acid
may theoretically increase the excretion of weak basic drugs such as
amphetamine, quinidine, or phencyclidine. However, this intervention is not
recommended because its efficacy has not been established and toxicity can
occur.
IV-Haemodialysis ( HD )
HD is most useful in removing toxins with the following pharmacological

properties:
• Low molecular weight (<5 daltons)

• Small volume of distribution (<1 L/kg)
• Low degree of protein-binding
• High water solubility
These drugs include:
• Aminoglycosides: Gentamycine, Amikacine and Netilmycin

• Barbiturates
• Chloral hydrate
• Alcohols: Ethanol, Methanol, Isopropanol, Acetone and Ethylene glycol
• Theophylline
• Salicylates
• Atenolol and Sotalol
• Procainamide
Indications:
• As soon as possible for intoxications with Methanol, Acetone, Ethylene
glycol, Isopropanol and Aminogycosides. For aminogycoside
intoxications the severity of the intoxication has to be taken into
consideration.
• When MDAC has not or only partially been effective in Theophylline
intoxication; in very severe cases both treatments can be combined.
• When urinary alkalinisation and forced diuresis have not or only partially
been effective; in severe cases both treatments can be combined.
V- Exchange transfusion
Exchange transfusion is rarely indicated but may be useful in the treatment of

massive haemolysis, methaemoglobinaemia, sulfhaemoglobinaemia (eg,
secondary to hydrogen sulphide exposure), or in neonatal drug toxicity.
37
High Risk Factors in Poisoning Management
There are a number of criteria involved in an overall risk evaluation other than the
specific drug and the severity of the clinical syndrome, the latter of which is the
most important consideration.
Extremes of age
Extremes of age (< 2 yrs > 65 yrs) may increase drug toxicity through a smaller
volume of distribution or via greater impact on organ systems especially CNS, CVS
and respiratory systems. In some instances, metabolic responses to specific
toxins may vary with age e.g., ethanol and salicylate induced hypoglycaemia in the
young. While general management principles are similar, consideration of baseline
CVS, renal and hepatic function may require modification of elimination techniques
such as alkaline diuresis (cardiac failure) or haemodialysis (very young child).
Hospitalization is often required for monitoring and more intensive support.
Probably the most important age consideration is the issue of diagnosis, as an
absent or uncertain history often characterizes the very young or the elderly
poisoned patient. In addition, signs and symptoms may be similar in a wide range
of age specific common diseases and so poisoning may not be included in the
differential diagnosis.While children will have the greatest frequency of
presentations of acute accidental exposures than any other age group, the elderly
have the highest morbidity/mortality rates.
Principles
1. Do not over treat innocuous ingestions in children
2. Poisoning should be a consideration in any bizarre or unusual clinical
presentation (falls, confusion etc) while an atypical history in young children
may be abuse and/or depression.
3. Careful CNS, CVS and respiratory monitoring is crucial with emphasis on
homeostasis (adequate tissue substrates) and concurrent diseases.
4. Metabolic assessments, especially glucose need early attention, otherwise
general management principles are acceptable.
5. Consider the effect of multiple drugs and drug interactions in the elderly.
6. Always evaluate the home environment and history behind the ingestion
(specially in extremes of age).
Pregnancy
The major concerns are the altered physiological conditions of the pregnant female
(esp. latter half of pregnancy) and the impact of toxins on the fetus. Except for
obvious cytotoxics / antimetabolites, especially during fetal organogenesis (3 – 8
weeks) most risks to the fetus are due to maternal circulatory/respiratory
depression and/or profound acid/base disturbances. In the third trimester, some
toxins may directly or indirectly lead to premature labour, which will require a
multidisciplinary assessment. Most drugs are present in breast milk and so it is
prudent to briefly limit breast-feeding until toxin elimination.
38
Principles
1. Optimal treatment for the pregnant female is the best treatment for the
fetus. This includes all antidotal and elimination strategies.
2. Fetal evaluation may be appropriate with ultrasound or rarely CTG
monitoring in late pregnancy.
3. There are no scientific recommendations for termination of pregnancy and
very limited information on indications for urgent delivery.
Other diseases/metabolic disorders
Patients with known systemic organ system disorders (especially CV, hepatic,
renal and hematological) and metabolic disorders (thyroid, diabetes, pituitary,
adrenal) are at greater risk for adverse outcomes or protracted recovery.
Individuals with chronic malnutrition may have impaired protective mechanisms for
defense against toxins, internal bleeding and infection. (e.g. depleted liver
glutathione, low Vit.K and depressed circulating antibodies)
Principles
1. Carefully review previous health status and perform thorough physical
examination.
2. Do not screen all organ systems but only those identified by
history/physical, examination, except in life threatening overdoses.
Multiple drugs/agents
A multiple drug overdose is not infrequent in self-poisoning. The toxic syndrome
therefore may be complicated and a mixed clinical picture expressed dependent on
individual drug quantities and potencies, additive, synergistic or even antagonistic
effects. Where this is suspected, the laboratory may be helpful especially, tests on
gastric lavage fluid.
Principles
1. Support and maintain vital functions.

2. Screen for cellular poisons and assess metabolic and acid base status.
3. General decontamination procedures.
4. Maintain a wide differential diagnosis.
Drug Abuse
The drug abuser is considered at high risk for a toxic syndrome primarily because
of habituation. Frequent use may be associated with tolerance and could
accidentally lead to experimentation with multiple drugs and over dosage. Drug
abusers may also have chronic target organ damage and be especially vulnerable
not only to drug effects but also infectious disease. Depressive illness, suicide
attempts and a violent life style are not uncommon.
39
Principles
1. Always consider an infectious disease complication (cellulitis/abscess,

septic thrombophlebitis, viral hepatitis, septic arthritis, osteomyelitis,
endocarditis and septicaemia)
2. Look for target organ damage (CNS, CVS, Hepatic, renal, MSK and
hematopoetic systems)
3. Consider occult trauma
4. Plan - Psycho/Rehabilitative care (Ibn Sina)
Care of Asymptomatic Patient
Causes
• Insufficient amount ingested.
• Delayed effect due to anticholinergic action or sustained
release or concretions formed
• Non-toxic agent
Management
• Perform secondary survey
• Decontaminate (gastric lavage), if substance is potentially
toxic
• Send samples for routine laboratory test.
Consider discharge : Observe till the expected time of onset/

or peak action has passed ( 4-12 hrs, subject to toxin type)
and when vitals are normal and there are no poisoning-
related signs/symptoms.
40
Treatment of Anaphylaxis
Anaphylaxis is characterized by history of exposure to a causative agent
(toxin/drug), nausea, respiratory distress, (bronchospasm, laryngeal oedema,
pulmonary oedema) and associated hypotension, pruritus, and rash. Vomiting,
diarrhoea, abdominal pain may also be present. Anaphylaxis occurs when patients
antigen-specific immunoglobulins E(IgE ) on the surface of mast cells and
basophils are exposed to the antigen, triggoring the release of histamine and
vasoactive substances.
Management
• Maintain airway, breathing, intubate and assist ventilation. Administer

oxygen.
• Administer intravenous fluids (titrate against CVP).
• Administer Epinephrine .3 - .5mg 1:1 solution sc or intramuscularly in
adults, . 1ml/kg, ( 1: 1 ) in children. Can repeat the dose, if required
every 2 -3 minutes as required (no maximum dose) .
• In severe shock, give . 5- .1ml/Kg 1:1 , solution (children
. 5ml/kg/dose 1:1 , ) of epinephrine intravenously slowly or as iv
infusion (1-4 µg/min ), avoid extravasation.
• In case iv access not available, give .5mg in 5ml 1:1 , solution of
epinephrine through endotracheal tube. The dose can be repeated after 1
min if required.
• Give H1 blocker (Diphenhydramine .5-1mg/kg iv) and a H2 blocker
(Ranitidine 5 mg iv slowly in adults and 1mg/Kg/dose iv slowly in children ).
• Nebulized Salbutamol can be tried in refractory bronchospasm.
• Hydrocortisone (3-5mg/kg iv) or methyl prednisolone(1-2mg/kg iv) to treat
bronchospasm.
• In severe hypotension, give Dopamine 5-15µg/kg/min as iv infusion (titrate to
target BP).
Monitor pulse, BP, respiration, ECG, ABG, until recovery.

Severe cases will require prolonged monitoring. Usually recovery is complete.
Discharge the patient with the following advice:
• Identify, if possible, the agent to avoid further reactions.

• Keep cards or bracelet indicating the causative agent.
• Epinephrine preloaded syringe should be kept with the patient for self-use,
for any one, who has suffered a life-threatening anaphylactic reaction.
41
42
Emergency Evaluation and Management
REFERRAL GUIDELINES
• High risk patients ***

• No ICU facility available
• Need for specialized care ( endoscopy, haemodialysis)
• Inadequate laboratory facility for monitoring
• Antidote or other therapeutic modality not available
• Underlying hepatic dysfunction or renal failure or pregnancy
***Any patient with the need for cardio-respiratory support or with persistent seizures
or persistent altered mental status ( Glasgow Coma Scale < 13 ) for > 3 hours or
patient who has ingested a potentially lethal dose and where severe toxicity suspected
43
Skin or Eye
Exposure
Local Systemic
toxicity toxicity
• Remove clothes of patient if needed

• Wash skin with soap and water ( wear gloves )
• Remove contact -lenses
• Irrigate eyes with running water for 15- 0 minutes
• Identify poison contact Poison Control Centre
• Severe burns / severe eye injury/ systemic toxicity refer
to Regional Hospital for specialized care.
44
Inhaled Poison
Unknown Gas / Doubtful Toxic gas

exposure
Asymptomatic *Symptomatic
Observe 6 -12 hrs
Observe 24 hrs Give oxygen
Bronchodilator
Intubate
Asymptomatic
No symptoms
Consider Discharge
discharge
* Consult table : I Symptoms of Regional Hospital

pulmonary oedema for specific
or systemic toxicity treatment
45
Section III
Management of
Venomous Bites
and Stings
47
48
Management of Venomous Bites and Stings
Various types of venomous bites and stings occur throughout Oman. These
usually occur in the community, often in settlements distant from a hospital. Each
section is discussed from management in the initial rural health centre situation, to
that in the referral hospital. Often patients cannot identify the source of the bite,
and management is then empirical.
1. Snake bite
Venomous snake species
Most Omani snakes are harmless. Of the 9 venomous terrestrial snakes, 9 % of
envenomations are by the Saw-scaled Viper ( Echis carinatus ) [Fig 1]. This
aggressive snake occurs throughout Oman, especially in rocky areas. About 9% of
bites are caused by a related species, Burton’s carpet snake (Echis coloratus)
[Fig.2] of hilly regions, or the Horned Viper( Cerastes gasperetti ) [Fig 3.] of
deserts. All three vipers have broad heads and 2-hinged fangs, and the venom
causes impaired clotting. Only in Dhofar are found the non-aggressive Arabian
cobra (venom is neurotoxic) and the indolent Puff adder ( impaired clotting ), but
bites have never been reported in this region.
Snake bite
Many bites even by venomous species are without envenomation. The usual
appearance of a bite by a non-venomous species or by a venomous snake without
venom injection, is two or more fang (tooth) marks, mild local tenderness and
some swelling, but no bruising, blistering or systemic effects.
Envenomation (Viper bite)

The signs of envenomation may be delayed for 3-4, hours, which include severe
local pain, progressive swelling, erythema, petechiae, ecchymosis, bruising and
haemorrhagic blistering around the bite site. The limb may swell to twice its normal
size within few hours. The systemic effects may include nausea, vomiting,
weakness, parasthesias, diaphoresis, signs of impaired clotting (petechiae,
epistaxis, hemoptysis, hematuria), hypotension, hypovolemic shock, pulmonary
edema and cardiovascular collapse.
Envenomation (Cobra bite)

Locally minimal swelling and inflammation may occur. The systemic symptoms
may be delayed for 12 hours or more which include nausea, vomiting, euphoria,
confusion, ptosis, diplopia, disarthria, muscle fasciculations, weakness and
respiratory arrest.
49
Immediate management by paramedics at the place of bite
Reassure the patient, immobilize limb in splint and light bandage. Do not apply
tourniquet, ice, cut or suck the wound or give aspirin. Wash the area with soap and
water and remove constrictive clothing or jewelry. Send patient to the nearest
hospital as soon as possible. If the snake has been killed (make certain it is dead),
send it in a plastic bag with the patient.
Figure 1:
Saw-scaled viper
(Echis carinatus sochurki)
Figure 2:
Burton’s carpet snake (Echis
coloratus)
Figure 3:
Gasperetti’s horned viper
(Cerastes gasperetti)
Poisonus Vipers with hinged front fangs are vasculotoxic

Credits: Dr Andrew Gardner, John Gasperetti.
50
4 5
Fig 4- 5 Snakes of Dhofar Region – Puff-adder ( Vasculotoxic )

& Arabian Cobra ( Neurotoxic )
Immediate management in hospital
Regardless of the species, prepare for both local and systemic effects. Reassure
the patient, note any signs of local or systemic envenomation, make basic
observations i.e. pulse, blood pressure, respiration, draw blood for complete
blood counts, 2 min clotting test, platelet count, PT, fibrinogen, CPK, ABG, serum
creatinine and blood typing. Test urine dipstick for occult blood. Commence fluid
balance chart, documenting urine output.
• Monitor local swelling hourly with measurements of limb girth, local
ecchymosis and circulation
• Obtain consultation from surgeon for wound management
• Give tetanus prophylaxis
• Administer broad spectrum antibiotic
20 minute clotting test

Place 2 ml blood in clean dry glass test tube, leave for 2 minutes at room
temperature. Invert, if no clot (a positive test) antivenom is urgently required.
Snake identification: Compare snake with identification photographs in this manual.
If snake was observed but not killed, show patient photographs (they frequently
identify the Saw-scaled viper).
• Consult expert in management of snake bite as required.
• In cobra bite, monitor for respiratory muscle weakness, maintain airway and
assist ventilation if required.
51
Decide if the patient needs antivenom?
NO antivenom : Two or more fang marks, mild local tenderness, slight local
swelling, no systemic effects, normal 2 minute clotting test and normal
coagulation profile, or if the bite is by identified non-venomous snake, observe the
patient for several hours. If clotting factor tests remain normal and no further
evidence of envenomation, do not give antivenom and discharge following
approval of consultant. Always, admit for observation if in doubt, particularly if the
patient is a child.
GIVE antivenom :
• Local and systemic effects of envenomation including immediate pain
followed by increasing swelling, blistering or bruising, and signs of impaired
clotting with ecchymoses, epistaxis, haematuria.
• Regardless of clinical signs, if the 2 minute clotting test is positive.
• Neurological signs including ptosis in cobra bites.
Attention :
Despite a day or more delay after envenomation, antivenom should be given.
Use Saudi Arabian National Guard (SNG) polyvalent snake anti-venom, which is
available as 1 ml amp./ vial. Check that antivenom is clear, replace if cloudy.
If SNG is unavailable, give Haffkine antivenom (which does not cover Horned
viper bites) available as lyophilized powder with 1 ml as water for injection.
.
Do NOT give test dose

If patient is atopic, first give SC adrenaline, antihistamine, and corticosteroid.
Have 1:1 adrenaline, syringe and needle ready at the bedside
Dose of SNG antivenom

_____________________________________________________________
Envenomation effect Dose of polyvalent snake antivenom
Local swelling only < ½ limb Withold antivenom: observe.

Normal clotting test.
________________________________________________________________
Swelling beyond bite, *4 -1 ml antivenom, diluted in 5 ml /kg of
Impaired coagulation (viper) normal saline, given iv over 3 -6 minutes
Ptosis; neurotoxicity (cobra) or give undiluted directly in severe cases
________________________________________________________________
Marked swelling, * 1 -15 ml antivenom diluted in 5 ml/kg of
Severe systemic signs normal saline, given iv over 3 - 6 min.
or give undiluted directly in severe cases______
* Children need SAME DOSE as adults. Check dilution factor in antivenom advice
note. Use .18% sodium chloride, not normal saline. Avoid fluid overload.
52
● If no response in 1 hr, repeat. Multiple doses 4-6 hrly for 1-7 days may be
needed. Monitor clinical effect with laboratory clotting factor tests.
● Observe all patients during infusion and for 2 hours afterwards.
● If Haffkine’s is available,consult Antidote Treatment Table.
● Cobra bites 4 -1 ml antivenom diluted and give as above, with additional

anticholinesterase e.g. neostigmine, preceded by atropine.
Reactions
Early Reactions
Anaphylaxis : [1 -18 min] (tachycardia, nausea, hypotension, respiratory
distress.)
● 1:1 adrenaline (1mg/ml) solution, give .5 ml -1ml im or sc in adults, and
. 1ml/kg for chidren, repeat every 2 min. if necessary until reaction reversed and
stable. If iv line is set up, infuse 1mg 1:1 adrenaline in 25 ml normal saline, at
rate of 4-2 µg/minute adjusting for response.( for patients in persisting shock )
● Stop antivenom infusion, Call Consultant.
● Give chlorpheniramine maleate iv (1 mg for adults, .35mg/kg/24 hrs. children),
and hydrocortisone 1 -2 mg iv in adults, child < 1year, 25mg, 1-5 yrs 5 mg, 6-
12yrs, 1 mg. Consider H2 receptor blockers if refractory.
Pyrogenic : [1-2 hrs] Fever, rigors, hypotension, febrile fits in children.
● Give paracetamol oral or by suppository.
Late reactions
Serum sickness [5 days-3 wks]: (fever, urticaria, arthralgia)
● Methyl prednisolone 1-4mg/Kg/ 24 hrs iv 4 – 6 hrly in divided doses for 5 days
● Chlorpheniramine maleate oral (1 mg for adults, .1mg/kg children).
Adjunctive treatment in snake bites

● If coagulopathy present, consult haematologist. Fresh frozen plasma may be
needed.
● Treat hypotension with iv fluids
● Antitetanus toxoid.
● Antibiotic: Co-amoxiclav or Erythromycin.
● Treat rhabdomyolysis with iv fluids and sodium bicarbonate.
Envenomation: follow up in hospital

● All patients should be monitored 6-hourly with repeated clotting factor tests
initially two or three times daily until stable. Urine output and repeat serum
creatinine levels must be recorded, as viper venom may be directly nephrotoxic
causing renal impairment immediately or within one or two days.
● If renal impairment develops consult Nephrologist urgently.
● Observe in hospital for 2 to 3 days following clinical recovery and normalisation
of clotting, because delayed absorption of venom can occur, with reappearance
of signs of envenomation after several days.
53
2. Sea-snake bite
About 9 species of venomous sea-snakes occur in Omani marine habitat, but no
instances of envenomation appear to have been documented. . Local sea-snakes
are non-aggressive and have small mouths. Elsewhere, envenomation is known to
cause muscle pain, myoglobinuria, renal failure and neurotoxic effects.
Management Remove patient from water, transport to hospital for supportive
treatment. No antivenom is available in Oman and in the Gulf region.
3. Scorpion sting
Scorpions in Oman
Scorpions are present in most rural environments, but being nocturnal, are
infrequently seen. They are carnivorous, feeding on insects and other arthropods.
Venomous scorpions in Oman include species of the genera Leiurus, Androctonus
[Fig.4], Buthus, and Nebo. Identification is principally of academic interest, and
does not affect management. Scorpions do not bite humans, they sting. The
contents of telson are ejected through the stinger.
Androctonus Scorpion
Scorpion sting
Most scorpion stings in Oman produce immediate, severe, local pain; usually a
single puncture wound with mild or no swelling, and no systemic effects,
ie. no significant envenomation. However, the same species in neighbouring
countries e.g. Saudi Arabia are capable of producing serious envenomation.
No envenomation: management in Health Centre or Out-patient Department

• Reassure patient, remove sting, wash wound.
• Infiltrate wound with long-acting bupivacaine or 1% xylocaine with adrenaline.
• Give tetanus toxoid.
54
• Observe for 1- 2 hours and if no systemic effects, discharge.
• Small children and other patients who appear to be developing systemic effects
should be referred to hospital.
Envenomation
Envenomation causes swelling, adrenergic stimulation with vomiting, diarrhoea,
hypersalivation, sweating and hypertension, muscle fasciculations, opisthotonus,.
priapism in children ,diplopia, and nystagmus
Rarely pancreatitis, myocarditis,paralysis and fits. Fatality is rare.
Management in hospital
• Reassure, obtain basic observations pulse, blood pressure, respiration
(ABCDEs).
• Treat hypertension
• Notify Tropical Medicine consultant or Consultant expert in management
of venomous bites and stings.
• Use Saudi Arabian National Guard or Pasteur polyvalent scorpion
antivenom.
• Check that antivenom is clear, replace if cloudy.
Do NOT give test dose.

If atopic, first give SC adrenaline, antihistamine, and corticosteroid.
Have 1:1 adrenaline, syringe and needle ready at the bedside
Administration of scorpion antivenom

Adult : 2-5 vials diluted in 2 -5 ml, half normal saline, iv over 3 minutes.
Repeat if no improvement after 2 hours.
Child : 2-5 vials diluted in 2 ml of one quarter normal saline, iv over 3 min.
Reactions As above in snake antivenom section.
Monitoring status
• Maintain 4-hourly routine observations.
• Clean wound. Administer augmentin or erythromycin, tetanus prophylaxis, if
indicated
• Treat complications according to standard procedure.
• Do not over sedate.
• Do not use ice packs locally
55
4. Spider bite
Poisonous spiders in Oman include the red back spider (Latrodectus mactans), a
species originally from Australia, which is common in urban gardens. It makes a
sticky, untidy nest under boxes or in sheds, and is nocturnal. Its venom causes
severe generalized myalgia but other systemic effects are rare.
The recluse or fiddle-back spider (Loxosceles), is present in Muscat. It is
nocturnal, and hunts insects. It does not make a distinct web. Bites cause skin
ulceration and necrosis, which may progress to necrotising fasciitis .
Latrodectus mactans bite (red back spider bite)
Clinical presentation
Local pain, systemic effects may appear and include Intense body pain, nausea,
vomiting, sweating, abdominal cramps, muscle spasms, tremors, tachycardia,
hypertension, restlessness.
Loxosceles bite (fiddle-back spider bite)
Burning pain and swelling near the bite.Blue scab forms that turns black, which
drops after few weeks leaving an ulcer that heals in 6-8 weeks. After 24-48 hrs of
bite, fever with chills, nausea vomiting, muscle pain may occur,rarely
unconsciousness and seizures.
Fiddle – back spider Red-back spider
Management of suspected spider envenomation

● Reassure patient, make basic observations. Apply routine cleaning of lesion.
Give supportive management.
● Give tetanus toxoid.
● If offending dead spider is brought with patient, preserve for identification.
● Observe for 2- 4hours until local reaction subsides or systemic signs develop.
● If local inflammation and systemic effects develop, notify Tropical Medicine
Consultant or Consultant expert in management of venomous bites and stings
● Loxosceles bites may require surgical debridement.
● .Anti-venom for Red-back spider bites is not available in Oman. It is produced by
the Commonwealth Serum Laboratories, Melbourne, Australia.
56
5. Hymenoptera stings (bees, hornets, wasps) and
bites (fire-ants)
Hymenoptera venoms contain various amines, peptides such as histamine and
kinins, which cause the local sting reaction. Allergenic venom proteins which elicit
an IgE antibody response, include phospholipases, hyaluronidase etc. The venoms
of Apidae (bees), Vespidae (wasps) and Solenopsis (fire ants) are distinct from
each other. All have been reported in Oman.
Bees ( Apidae ) Wasps ( Vespidae )
Fire ants ( Solenopsis )
Reactions following stings or bites
Bee, Wasp Stings

• Immediate pain and swelling, wheal and itching, which subside in a few
hours.
• Anaphylaxis often within a few minutes, usually, but not always in sensitized
individuals.
• Serum sickness-like symptoms appearing after a few days or a week.
Fire ant bite

• Local redness, swelling, vesiculation, and skin necrosis or hypersensitivity
reactions.
Management
Bee stings usually have the sting embedded attached to the venom gland.
Remove the sting carefully to prevent further venom release by the gland. Wasps
do not leave the stings behind. Clean stung area, apply antipruritic, or
antihistamine ointment as required.
57
Fire ants. Clean bitten area with soap and water. Secondary bacterial infection
may occur and require antibiotics.
Anaphylaxis: Treat with intravenous or intramusclar adrenaline as for anaphylaxis

following use of antisnake venom (see above).
Prevention
• Individuals known to be sensitized should be counselled. They should avoid

contact with offending hymenoptera. Wasp and bee nests around their
residences should be removed.
• They should always carry adrenaline and disposable syringe and needles in
case of unexpected stings or bites. The possession of a medical bracelet
indicating the possibility of anaphylactic reactions is recommended.
• Sting kits containing premeasured doses of 1:1 adrenaline in disposable
syringes are commercially available in some countries.
58
Management of Snake Bite
Consult Poison Control Centre if required
Mnagement of Scorpion Sting
59
Management of Scorpion Sting
60
Management of Insect Stings
61
Non - Poisonous Snakes
‫ دود‬THREAD SNAKE THOMASKS & SNAKE
‫ ــن‬SAND BOA RAT SNAKE
RACER
–-‫ ـن‬-‫ وان‬ ‫ـوان‬ DIADEM SNAKE
62
‫ن – وان‬ - ‫ ن‬- ‫أ‬
RACER SNAKE HOODED MALPO

–
CAT SNAKE SAND OR TREE SNAKE
From ‘Snakes of Arabian Gulf & Oman’

Gallagher 1993
63
Marine Envenomations and Injuries
Oman is a country with long shores and a very rich and varied marine life. A
significant proportion of the population did and still live on fishing. Besides
fishing, diving and snorkelling are becoming increasingly recreational activities
for the inhabitants and the tourists. Nevertheless, specific marine envenomation
and accidents are generally not a frequent encounter. This could be due to
several reasons that include:
• The safety of the Omani waters in spite of their richness.
• Many of the accidents are minor and judged by the victim that a
medical care is not required. These are either not treated or treated at
home.
• Inability to define the biting or stinging animal with precision.
• Some specific accidents are misdiagnosed or undiagnosed such as
ciguatera and scombroid ingestion.
We hope that with more awareness of the medical community, we will be able to
evoke, diagnose and treat more specific diseases related to the marine life.
Accidents due to marine animals can be divided into the following

categories:
1- Intoxications due to toxic stings and bites. Animals involved include:

jellyfish, cone shells, stingrays, sea snakes, urchins, corals and scorpion
fish.
2- Intoxication by ingestion of toxic marine animals such as ciguatera,
tetrodotoxin and scombroid.
3- Traumatic bites and injuries, such as those by sharks, barracuda and
catfish. These are not true intoxications.
The general principles of marine intoxications include:

• Disinfection is important as many of the wounds will be contaminated
with risk of secondary infections.
• In case of stings, applying hot water, vinegar or alcohol are most of
time very beneficial as many of the toxins are thermolabile.
• Symptomatic treatment for pain, burning sensation and anxiety.
• Awareness of the possibility of systemic manifestations and to be ready
for quick aggressive interventions including full resuscitation.
64
Toxic Stings and Bites
I- Jellyfish: Stings occur in Oman mainly from Batinah to Sur. These may occur all
year but there is a seasonal variation with maximum stings between June and
August. The peak is in July.
Symptoms and signs: Locally the site of the sting may be very painful with an
itching and burning sensation. Lacerations may occur in severe cases.
In severe cases systemic manifestations may be present and consist of chest
pain, tachycardia, hypotension, muscular cramps, nausea, vomiting and shock.
Treatment consists of the following:
1. Reduction of the poison effect:
a. Pouring copious amounts of vinegar will reduce the discharge of poison
from the tentacles of the jellyfish. If not available alcohol applied
topically is also beneficial.
b. Removal of the tentacles is essential and should be done carefully.
Removal with bare hands should be avoided. It is better done with a
safety razor or similar instrument. The tentacles should be scraped
gently but quickly and in one direction.
2. Analgesia (and sedation if necessary): Paracetamol, Non-steroidal anti-
inflammatories, Anti-histaminics, topical Xylocaine, or topical Steroids.
3. Treatment of systemic manifestations depends on the severity and may
consist of iv fluids, treatment of shock and resuscitation.
65
II-Cone shells: These can extend a venomous dart from their pointed end which
can penetrate through clothing. Stings are not reported in Oman, probably because
they are mistakenly considered for fish bite or jelly fish sting.
• Symptoms are essentially local with severe pain. Nevertheless the

major risk is paralysis which may occur in severe cases.
• Treatment:
a.Without paralysis: wound disinfection, analgesia, pressure bandage
and immobilization, if necessary.
b. With paralysis: resuscitation and artificial respiration, as the major risk
is respiratory paralysis.
III-Sea worms: Not uncommon in Oman. These may be present mainly in

shallow areas affecting essentially swimmers and fishermen who step with their
feet over their burrowed opening. Called locally “Ghool” which means Snake. In
fact it is not a snake but a worm, though it causes a very painful bite with a
double puncture marks.
• Symptoms: severe sudden pain, oedema of the area or the foot, rarely
the whole limb.
• Treatment: disinfection and analgesics.
66
IV-Sea urchins: They have spines over their body. Venom is contained in
the spine tissue or in the lumen. They occur in Oman, mainly risk to
divers by inadvertent contact.
• Symptoms: The stings of the spine cause pain, burning sensation

and discomfort,sometimes associated with numbness and even
limited paralysis. Secondary infections are common. Rarely severe
general symptoms occur.
• Treatment:
a. The toxin is thermolabile. Immersion or pouring hot water (not
more than 5 °C if it can be tolerated) is very useful. Vinegar and
alcohol are also beneficial. These measures should be
performed as soon as possible. The wound should be
disinfected.
b. Spines removal: these are very brittle so care should be taken
when removing them as they may break. brake. These can be
removed with pincers or carefully by hands. Their removal will
be difficult once they are in the flesh. The healing process may
take about 3-4 weeks.
c. Other aspects may include analgesia and antibiotics. Systemic
manifestations are treated according to the severity and the
affected organ(s) and may require,in extreme cases,
resuscitation.
V-Stingray stings: Sometimes partly buried in shallow waters. They will

sting with a dart on their tail when stepped on. Most commonly
happens in swimmers or fishermen when launching or beaching their
boats from the shores.
67
• Symptoms : are local and systemic. Locally there could be severe
sudden pain and oedema. There could be a wound with variable
loss of tissue. Systemically there could be nausea, vomiting,
muscular cramps, tachycardia and respiratory difficulty.
Secondary infections of the wound may occur.
• Treatment : Hot water wash has the benefit of reducing the effect
of the poison as it is thermolabile. Analgesics and antiseptics are
an essential part of the management. Some wounds may require
surgical debridement and suturing .
Treatment of systemic manifestations follows the general rules
and may require, though rarely, full resuscitation.
VI-Scorpion fish and stonefish: These beautiful fish are usually not
aggressive. Stings occur usually while inadvertently touching them
or during improper handling. The dorsal fin is poisonous.
• Symptoms and signs: Locally the sting site is painful and swollen.
Systemically, the patient may present malaise, fever, and
hypotension and in severe cases cardiovascular collapse and
respiratory distress.
• Treatment : Immobilization of the patient. Since the poison is
thermo labile, pouring hot water on the affected area is beneficial.
Disinfection of the area is important. The treatment of the
systemic manifestations is non specific and may require full
resuscitation.
VII-Catfish: Fishermen are usually the victims while handling the catch from
the nets. Swimmers and divers are rarely affected. The venom is carried by
the dorsal and pectoral spines. Treatment consists of disinfection and
analgesics.
68
Traumatic bites and Injuries
These are relatively common problem in Oman and include:
A-Sharks: Their reputation is worse than reality. Bites may occur while the
fishermen handle the catch thinking the sharks are dead.
The management is not specific and depends on the severity of the injury as
well as the haemodynamic state. It consists of immediate removal of the
victim out of water, pressure bandage and immobilisation if necessary.
Analgesics and sedatives may be administered if necessary and the condition
permits. Otherwise the treatment may include: wound debridement, systemic
antibiotics, intravenous fluids; blood transfusion; treatment of shock;
cardiopulmonary resuscitation and surgery.
B-Barracuda, Moray eels and other non venomous fish injuries : Cause
traumatic injuries, which are managed in a similar way to those caused by
sharks.
C-Coral cuts: despite their delicate appearance, corals can be the cause of
severe wounds. The injuries are usually superficial but are notoriously slow to
heal. Also these cuts are prone to infection.
• Symptoms and signs: Usually local pain, oedema and pruritis that
may persist for weeks.
• Treatment : Thorough cleansing and disinfection of the affected area.
In severe cases the patient may require bed rest, antibiotics and
elevation of the limb.
Intoxication by ingestion of marine animals:
In general, the treatment of these intoxications is not specific (with the
exception of scombroid where antihistaminics are specifically indicated)
and includes:
• Gastric lavage and activated charcoal.
• Symptomatic treatment.
• Shock treatment. The necessity of artificial ventilation should always
be in mind and should be performed when indicated without delay.
The following are some of the specific intoxications.
A -Ciguatera and Tetrodotoxin: Toxicity occurs after ingestion of reef
fish or puffer fish containing toxins. The manifestations are
dermatological, muscular and neurological that may be very serious.
The treatment is gastric lavage, activated charcoal, symptomatic
treatment and resuscitation in severe cases.Recently, treatment with
Gabapentin is suggested.
B- Scombroid Poisoning: It occurs due to the ingestion of inadequately
preserved fish especially tuna or bonito left for few hours at room
temperature or in the sun.
Although there are no firmly documented reports of such poisoning in
Oman. It is quite possible that these are misdiagnosed or overlooked.
69
• Symptoms and signs: These occur minutes after ingestion and are
those of histamine intoxication. These include vasomotor, allergic,
gastrointestinal, dermatological and respiratory manifestations. Shock
may occur in severe cases.
• Treatment : It includes gastric lavage, activated charcoal,
antihistaminics and symptomatic treatment. Severe cases may require
resuscitation.
C- Paralytic Shellfish and crustacean poisoning: Toxic algae infested

oysters, clams, mussels, lobsters, crabs.etc can cause poisoning. The
manifestations may be gastrointestinal; allergic, hepatic or neurological in
the form of paralysis. The treatment is symptomatic and supportive.
D- Green turtles: Ingestion of these turtles may provoke a very severe

and fatal intoxication syndrome that occurs hours or days after ingestion.
It starts with gastrointestinal symptoms and progresses to respiratory
distress with lethargy, skin and tongue ulcers and death in 5 % of cases.
Hunting and eating green turtles is forbidden in Oman as a result of
environmental and marine preservation. This syndrome should not occur
in Oman. Nevertheless the medical community should be aware of this
deadly syndrome especially in the areas where turtles ley eggs such as
Ras al-Had, Ras al-Jins and Massira.
The treatment is symptomatic and often requires full and prompt
resuscitation.
70
Management of Marine Envenomations & Injuries
Traumatic injuries
Toxic stings & bites Toxic ingestions
Jelly fish Paralytic shell fish poisoning: (Toxic
algae in clams, mussels, shrimps,
Mild : Local pain , itching ,burning, lobsters, crabs)
swelling, lacerations
Severe : GIT& CVS manifestations Parasthesias,numbness
Nausea,vomiting,diarrhoea
Muscle paralysis, respiratory
Resuscitate & stabilize
distress, may cause death
Pour vinegar over tentacles, pull
tentacles with pincers, do not rub Resuscitate & stabilize
Gastric lavage,Activated charcoal
Apply ice bags & baking soda paste Alkaline diuresis
Sting rays,sea urchins,cat

Scombroid poisoning (spoiled tuna,
fish,scorpion fish, stone fish, weever
bonito,mackerel)
Severe shooting pain, local wound
Chest pain, syncope, nausea, vomiting Signs and symptoms of histamine
cramps, respiratory distress release
Stonefish: Headache,seizures,paralysis Antihistaminics (H1&H2blockers)
Epinephrine as needed
Hot water emersion of the part Ciguatera toxin in reef fish&
Manage wound: cleaning, debridement, tetrodotoxin in puffer fish
spine removal, antiseptics
Analgesics,antibiotic,tetanus Parasthesias,ataxia, vertigo,paralysis
prophylaxis GIT &CVS manifestations
Seizures,respiratory arrest
Sea snake bite
Painless small fang marks Gastric lavage,activated charcoal
Weakness,visual disturbances,
paralysis, respiratory distress, renal
failure Referral guidelines
• Give local treatment, refer if
Resuscitate & stabilize Supportive systemic effects
treatment,no antivenom available in
Oman. • If no systemic effects for 4 hrs,
discharge
Shark, Barracuda and Corals
• Resuscitate & stabilize

• Manage the wound
71
72
Section IV
Management
of
Drug Poisoning
73
74
Paracetamol
Poisoning
Paracetamol is widely prescribed drug to treat fever,
headache, toothache and mild to moderate muscular pain.
It is also a constituent of some cold and cough remedies
which are available over-the-counter.
75
Paracetamol preparations available in Oman*
Generic Name Trade Formulation&Strength
Name
Paracetamol, Acetaminophen Panadol Tab. 5 mg, Syrup 125mg/5ml
Adol, Amol 1 mg/ml Pediatric drops

Adol, Chewable Tab 5 mg
Calpol Tab. 25 mg, Suspension 12 mg/5ml
Tylenol 1 ,125.15 mg,Supp. (Infants)

1 ,2 ,3 ,35 mg, Supp. (Children)
Enelfa Tab. 5 mg, Syurp2 mg/ml,

125,25 ,5 mg, Supp
Fevadol Tab. 5 mg,Syrup 125mg/5ml,

2 mg Supp.
Revanin Tab. 5 mg,

Suspention125mg/5ml,Supp. 25 mg
Combined preparations
Tab. Paracetamol 5 mg+3 mg
Paracetamol+ Pseudoephedrine Sinofree
Pseudoephedrine
Cap, Paracetamol, 3 mg+25 mg
Paracetamol+ Chlomezanone Parafon
Chlomezanone
Tab. Paracetamol 5 mg + 65mg
Paracetamol+Caffeine Panadol
Caffeine
Codalgin Tab. Paracetamol 5 mg + 3 mg
Paracetamol+ Codeine Phospate
fort Codeine
Source:
Approved drugs ( Ministry of Health )
Omani National Formulary (Ministry of Health 2003)
SQ University Pharmacy List (2003 )
76
Therapeutic dose
1 -15mg/kg, 4-6 hourly, orally. Maximum daily dose over age 12 years is
4gm/day.
Toxic dose >15 mg/kg in children

6-7g. in adults
4 hr serum level after overdose: ≥ 993 µmol/L or ≥15 µg/ml.
High risk patients for hepatotoxicity
Alcoholics, patients on phenytoin, phenobarbitone, carbamazepine or isoniazid,

fasting and malnourished subjects or patients with liver disease (because of lower
cellular glutathione stores and induction of cytochrome P-45 enzymes in liver), or
patients with inherited differences in hepatic enzyme activity.
Mechanism of Action
In therapeutic doses, its antipyretic and analgesic action is through central

inhibition of prostaglandin synthetase enzyme.
Pharmaco/toxico/kinetics
Paracetamol is >9 % absorbed (time to action varies from 3 -45 min. from liquid
to tablet formulations and 1.4 – 4 hours with suppositories). Peak plasma levels,
almost always occur within 4 hours. Once absorbed the drug is metabolized in
liver by glucuronidation (6 %), sulfation (3 %) and gets excreted as unchanged
(4-7%) and as harmless metabolites. However, about 4% of any given dose is
metabolized by hepatic cytochrome P-45 mixed function oxidase system to a
toxic intermediate metabolite, N-acetyl-p-benzoquinone imine (NAPQI), which is
normally detoxified by conjugation with reduced glutathione and excreted in urine
as mercapturic acid and cysteine conjugates. In overdose poisoning, excessive
quantities of this toxic metabolite are produced, which deplete liver gluthathione
stores to less than 3 % of normal. The unconjugated toxic metabolite binds
covalently with liver macro-molecules causing centrilobular hepatic necrosis.
NAPQI may also oxidize other important cellular-SH-enzymes leading to a
cascade of hepatic cellular events causing neutrophil accumulation, impairment of
microcirculation and tissue hypoxia. NAPQI may also cause renal tubular
necrosis. Multisystem organ failure is usually secondary to fulminant hepatic
failure although specific organ targets may also be damaged by NAPQI.
77
Clinical manifestations depend on the time after ingestion.
Phase 1 (1-24 hours)
Anorexia, nausea, vomiting, malaise. The patient may appear normal.
Improvement in systemic and GIT symptoms but onset of right upper quadrant
pain and elevation of transaminases (AST and ALT), bilirubin, and prothrombin
time.
Manifestations of clinical hepatic disease i.e. nausea, anorexia, vomiting,
jaundice, rising prothrombin time and bilirubin levels, coagulopathy,
hypoglycemia, encephalopathy and metabolic acidosis. Hepatic coma with
hepato-renal failure leading to death in some cases.
Phase 4 (4 day-2 weeks)
If hepatic injury is reversible, resolutions and recovery occurs.
Most cases do not progress beyond Phase 2 and gradually the liver function
tests return to normal. In children with extremely large paracetamol overdose
producing blood levels >8 µg/ml at 15 hours after ingestion, CNS effects
including coma, apnea, hypotension, hypothermia, and metabolic acidosis have
been reported. However, loss of consciousness is not a feature in adults, if it is
present then review diagnosis and consider another drug eg.CNS depressant,
which may have been ingested concomitantly.
Diagnosis and monitoring
• History of ingestion of toxic amounts (>15 mg/kg)
• Toxic risk best determined with a 4 hour post-ingestion plasma levels of
paracetamol (≥1 micromoles/lit or ≥15 µg/ml. If the time of ingestion is
unknown but less than 4 hours may have elapsed, a sample must be
drawn immediately and then repeated in 2-4 hours to assure a peak level.
Use the nomogram (Fig.1 ) to predict the likelihood of toxicity. The
nomogram should not be used to assess chronic or repeated ingestion
toxicity. The decision to admit and treat the patient is made on the basis of
plasma/serum paracetamol levels at 4 hours post ingestion falling in the
toxic range on the nomogram. When the ingestion time is more than 4
hours, the nomogram can still be used to determine toxicity and treatment.
Liver function tests (AST, ALT), CBC, platelets, prothrombin time, bilirubin,
serum electrolytes, glucose, BUN, creatinine should be obtained. Patients
with elevated transaminases and prolonged prothrombin time even in the
absence of detectable serum paracetamol but with history of paracetamol
ingestion will benefit from antidote treatment.
78
Differential diagnosis
In absence of clear cut history of paracetamol ingestion and undetectable serum
paracetamol levels, but with abnormal LFT, exclude poisoning due to other
hepatotoxins (halogenated hydrocarbons), alcoholic hepatitis, viral hepatitis, and
Reye’s Syndrome.
Treatment
Standard primary and secondary surveys with resuscitation and
monitoring according to severity
Decontamination
Gastric evacuation is useful only within one hour of ingestion because of rapid
absorption. Activated charcoal should be given after gastric lavage if patient
presents between 1-4 hours. If sustained release preparation or other drugs
have been co-ingested that delay gastric emptying (opioids, anticholinergics),
activated charcoal can be given even after 4 hours post-ingestion.
Administration of activated charcoal does not interfere with Antidote Treatment.
Antidote treatment
N-acetyl cysteine (NAC) should be given to all patients at risk (4 hours post
ingestion levels of plasma paracetamol >1 µmol/Lit or 15 µg/ml and if
intersection point of post ingestion time vs plasma paracetamol level is at or
above toxicity line on the Nomogram (Figure 1). In alcoholics, malnourished and
patients on enzyme inducers, peak level of 1 µg/ml is considered for NAC
therapy.
Maximum benefit is seen if NAC is started within 8-1 hours; however,it is

effective (less efficacy) even after 12-15 hours of ingestion. In case of co-
ingested drugs that delay gastric emptying, a second sample after 4 hours
should also be considered for establishing the risk of toxicity and treatment.
Oral regime
• NAC is supplied as 120g/1 ml or as 2 % solution (Mucomyst), give 14
mg/kg orally stat, then
• 7 mg/kg every 4 hours for 72 hours (17 doses)
• Dilute each dose with 4 parts water or fruit juice if 2 % preparation is used, to
make a 5% concentrate.
• Repeat dose if patient vomits within 1 hour of administration. Nasogastric
tube is used if vomiting persists.
• Patients may be given metoclopramide (1-2 mg/kg iv before NAC treatment)
79
Intravenous regime
Supplied as 2gm in 1 ml (2 %) Parvolex
15 mg/kg loading dose given in D5W 5 ml over 1 hour in adults and in children
in D5W1 -2 ml, then 15 mg/kg in 1 litre of D5W over 24 hours. (Reduce
volume in small children.)
Intravenous dose may cause hypersensitivity reactions, therefore NAC should
be administered very slowly to prevent these reactions, and if flushing,
hypotensin, bronchospasm occurs, stop infusion, restart after antihistamine
treatment.
Note
• All patients with intentional exposure to paracetamol, more than 15 mg/kg
(>15 tablets of 5 mg each), must be given NAC within 8 hours of
ingestion, to prevent hepatotoxicity.
• Patients presenting after 8 hours of paracetamol ingestion, with abnormal
liver function tests or with fulminant hepatic failure also benefit form NAC
therapy.
• Pregnancy is no contraindication to NAC.
• Patients with history of several doses taken over 24 hours or more, where
nomogram cannot estimate the risk accurately, give NAC treatment if
amount ingested is >15 -2 mg/kg, (6-7gm) in 24 hours or with abnormal
LFT.
Enhanced elimination
There are no techniques, which are superior to the efficacy of the antidote
NAC.While multi-dose charcoal might have theoretical considerations for
sustained release concretions, there is no evidence to support this. Extra
corporeal techniques especially haemodialysis are of use only in managing
target organ failure (hepato - renal) and not for toxin removal.
Observation, Referral
Patients with serum paracetamol levels at 4 hours post ingestion below toxic
levels may be discharged. Delayed presentations under 24 hours may also be
discharged when levels are below treatment requirements on the paracetamol
nomogram.
Later presentations with elevated transaminases should be admitted for antidotal

therapy and monitoring. Patients with hepato-renal failure may require dialysis.
Follow-up
Admitted patients who are recovering from hepatic injury may be followed as
out-patients in the absence of coagulopathy and normal or improving renal
functions. Transaminases should be falling and may take one – two weeks to
return to normal levels.
Psychiatric evaluation is appropriate in most instances.
80
Figure 1: Nomogram
Adapted from Goldfrank’s Toxicological Emergencies-2002
81
Management of Paracetamol Poisoning
Ask &
• Amount ingested (potentially hepatotoxic dose 6-7g in adults & >150mg/kg in child )
Observe • Time since ingestion
• Nausea, vomiting, anorexia, malaise within 24 hrs
• Right upper quadrant pain after 24 hrs
• Manifestations of severe hepatic disease after 72 hrs.
• Risk factors for hepatotoxicity (on anticonvulsants or isoniazid, alcoholic, fasting,
malnourished )
Conduct Primary and Secondary Surveys with Resuscitation & Monitoring
Manage
According to time since ingestion
0- 4 hrs >4 -8 hrs >8-24 hrs 24-96 hrs
Pregnancy
• Do not induce vomiting • Take blood sample for
• Gastric lavage if < 1 hr paracetamol levels & other tests
• Give activated charcoal • Give a loading dose of N- Acetyl
(single dose) cysteine 150 mg/kg iv
• Get >4 hr peak plasma paracetamol level & determine

toxic risk from the Nomogram
• Get AST, ALT, Bilirubin, CBC, Platelets, PT,
INR,Creatinine , Urea, Blood glucose, Electrolytes
Plasma paracetamol levels ≥150µg/ml at 4hrs Plasma paracetamol levels <150µg/ml at 4hrs or
or intersection point of postingestion time vs intersection point of postingestion time vs level below
level above treatment line of the nomogram treatment line
and/or Abnormal AST&ALT ( >1000IU/L) Normal LFT& other investigations
Asymptomatic
No NAC treatment
Give N- Acetyl cysteine (NAC)
Diacharge the patient
IV DOSE REGIME:Amp.2g in 10 ml , 20 % Refer all cases for hospital management

Loading dose : 150 mg / kg in D5W 500 ml in adult
and in 100-200 ml in child, as slow infusion over 1 hr Note
• Maximum benefit of NAC, when given within 8-10 hrs.
Maintenance dose : 150 mg / kg in 1 L D5W in adult &
500 ml in child over 24 hrs
• In high risk patients, consider 100 µg /ml at 4hrs, as
treatment level.
Treat hypersensivity reaction with Antihistaminic • In chronic overdose (>150-200mg/kg or 6-7g, ingested
in 24hrs) take blood sample and give NAC if indicated.
• If extended release preparation poisoning, get 2hrly
levels done for 8hrs and decide for NAC
82
Acetylsalicylic
Acid and
Salicylate
Poisoning
Acetylsalicylic acid is used as the treatment of mild to
moderate pain, as anti inflammatory agent for soft tissue
and joint inflammation, and as an antipyretic drug. Available
over the counter as common analgesic, anti platelet
aggregatory drug for cardiac patients. Salicylate is used as
keratolytic agent in the form of ointment or lotion.
83
Preparations available in Oman
Available
Generic Name Trade Name formulation&
strength
Acetylsalicylic acid Aspirin Tab. 75mg, 1 mg
Acetylsalicylic acid Aspirin, Dispril Tab 3 mg

(soluble)
Lysine acetylsalicylic Aspegic .9gm Inj

acid
Methylsalicylate Oil of winter green Ointment/lotion

5 gm/5ml.
Therapeutic Dose: 4 -6 mg/kg/day (1 mg/kg single dose)
Toxic dose (acute ingestion):
Mild to moderate toxicity 15 -3 mg/kg
Serious toxicity 3 -5 mg/kg
Potentially lethal >5 mg/kg
One teaspoon of Methylsalicylate is equivalent to about 7.5g of Aspirin
Toxic dose (chronic ingestion) >1 mg/kg/day for 2 or more days
Mechanism of toxicity
• Direct stimulation of respiratory centre results in hyperventilation and
respiratory alkalosis. Hyperventilation,sweating and vomiting leads to
dehydration and metabolic acidosis.
• Intracellular uncoupling of oxidative phosphorylation and inhibition of
cellular enzymes lead to hyperthermia and metabolic acidosis.
• Alteration in capillary integrity may cause pulmonary and cerebral
oedema (most often with associated proteinuria).
Toxicokinetics
Acetylsalicylic acid, being a weak acid, is well absorbed in stomach and small
intestine. Soluble ,buffered and effervescent tablets are completely absorbed
within 2-4 hours after ingestion. Enteric coated are absorbed slowly with
delayed peak serum levels at 4-6 hours. Large ingestions may result in
concretion formation; delayed peak levels and prolonged toxicity. The tissue
distribution is greater in acidemia. It is metabolized in liver. Hepatic enzymes
are saturated at toxic levels and then elimination depends on renal function and
urinary pH. Co-ingestion of other drugs which cause acidemia will increase
toxicity.
84
Poisoning could be due to acute accidental or intentional overdose or due to
chronic over medication for 2 or more days.
Acute overdose Chronic intoxication
• Patient is young • Old confused patient

• Accidental exposure in • Usually accidental over medication
children while intentional • There is underlying illness, like joint
in adults pains
• No underlying illness • Serum drug levels are variable
• Serum acetylsalicylic acid • Mortality is >25%
levels correlate with the
dose ingested and are
usually high
• Mortality rate is low
Estimation of severity of Salicylism

History: The severity of poisoning depends on the dose ingested.
Clinical indications of severity: In acute mild intoxication, tachypnoea occurs
early leading to respiratory alkalosis.In moderate intoxication, compensatory
metabolic acidosis develops. Co-ingestion of a sedative hypnotic drug or in
patients with severe intoxication and pulmonary oedema, the initial respiratory
alkalosis is blunted and a respiratory acidosis may predominate. In children,
metabolic acidosis is a predominant feature.
Laboratory indicators of severity :
Serum salicylate levels greater than 9 -1 mg/L are associated with acute
severe toxicity. A level greater than 6 mg/L accompanied by acidosis and
altered mental status is considered serious for chronic intoxication.
Clinical features: Acute overdose
Mild to moderate poisoning
Nausea and vomiting followed by tachypnea, tinnitus and lethargy are the initial
symptoms, ABG determinations reveal mixed respiratory alkalemia and
metabolic acidosis. Low grade fever and dehydration occurs due to
hyperventilation, increased metabolic rate and vomiting
Severe poisoning
Characterized by hyperpnea and respiratory distress, hyperpyrexia, severe
acidosis, hypoglycemia, altered mental states, coma, convulsions, non-
cardiogenic pulmonary oedema , ARDS and arrhythmias. Death is due to CNS
failure and cardio-vascular collapse.
85
Clinical features: Chronic overdose
Similar clinical picture as acute poisoning. However, cerebral and pulmonary
oedema is more common in chronic overdose.
Laboratory monitoring
Stat and serial serum salicylate levels every 2 hours until peak value has been
determined. Then the levels are repeated every 4-6 hours, until it is less than
3 mg/dl. Peak may be delayed following ingestion of enteric coated or
sustained release tablets. In chronic poisoning cases, the levels do not correlate
with patient's clinical status.
Other biochemical tests include serum electrolytes (anion gap calculation)
ABG,(characteristic mixed respiratory alkalemia and metabolic acidosis),
glucose, BUN, creatinine, PT and PTT, platelet and blood count, urine pH, X-ray
chest and ECG.
Treatment
Primary survey and supportive measures
1. Ensure open airway, adequate ventilation to prevent respiratory acidosis.

(Do not use controlled ventilation, as it will interfere with patients need for
compensatory efforts to maintain serum pH). Give oxygen.
2. Treat seizures by administering Diazepam IV (Adults, 5-1 mg, repeated

every 1 to 15 minutes, as needed. Child: .2 to .5mg/kg, repeat every 1
minutes, as needed), or Lorazepam iv (Adult: 2 to 4mg; Child: . 5 to
.1mg/kg), consider Phenobarbital(dose refer table 23), if seizures recur after
diazepam. Treat hyperthermia by external cooling, give dextrose,if
hypoglycemia.Monitor hypotension, dysrhythmia and respiratory depression.
3. Treat metabolic acidosis by administering iv bolus NaCO3 (refer table 23).

Correct pH to 7.4 – 7.5. Even mild academia can facilitate movement of
salicylate into the brain.
4. Correct dehydration with .9% NaCl at a rate of 1 to 2 ml/kg/hr over 1

hour until a good urine flow is obtained. Do not over-hydrate and follow
pulmonary status carefully. Potassium should be added to subsequent fluid.
Monitor urine output, urine pH, and serum potassium.
5. Alkalinize the urine in patients with clinical or laboratory evidence of toxicity

to promote elimination by kidney. Infuse a solution of 132mEq/L sodium
bicarbonate (3 amps) in liter of D5W at 1.5 to 2 times maintenance fluid
requirements (3-4 ml/kg/hr) to achieve a urine ph greater than 7.5. Add KCl (2
to 4 mEq/L), once urine flow is established. Titrate potassium requirements
against urinary pH.
6. Activated charcoal: Administer charcoal as slurry (24 ml water/3 g

charcoal). Usual dose: 25 to 1 gm in adults / adolescents; 25 to 5 gm in
86
children (1 to 12 years); and 1g/kg in infants less than 1 year old. It can be
repeated 3 to 5 hour-interval until serum levels are falling.
7. Gastric lavage: Consider after ingestion of a potentially life-threatening
amount of the drug, if it can be performed soon after ingestion (generally within
1 hour). Protect airway by placement of patient in Trendelenburg and left
lateral decubitus position or by endotracheal intubation. Control any seizures
first. In small overdose (<3 mg/kg), if charcoal can be given gastric lavage is
not necessary,
8. Asymptomatic patients with history of massive dose or enteric coated
tablets ingestion should be monitored carefully for a minimum of 6 hrs. or
longer.
Indications for haemodialysis
• Clinical signs and symptoms are more important than serum salicylate
levels in determining the need for hemodialysis.
• Consider dialysis at lower serum concentration for patients with chronic
salicylism.
• Patients with high blood salicylate level (>8 to 1 mg/dl after acute
overdose, and 5 to 6 mg/dl, after chronic overdose accompanied by
acidosis or lithargy specially in an elderly patient.
• Refractory acidosis, inability to maintain appropriate respiratory alkalosis.
• Acidemia, CNS toxicity (seizures, coma,, depression, persistent confusion,
cerebral oedema).
• Progressive clinical deterioration despite appropriate therapy.
• Pulmonary oedema, or renal failure
Dermal exposure and ingestion of Methylsalicylate

Significant toxicity has been reported after chronic topical use of creams and
ointments containing salicylates or after acute accidental ingestion in children or
elderly.
Treat as above
Decontamination
Remove contaminated clothing and wash exposed area thoroughly with soap
and water. A physician may need to examine the areas, if irritation or pain
persists and for systemic signs of poisoning.
Disposal and follow-up
• History of massive overdose or enteric coated tablets ingestion, even if the
patient is asymptomatic at the time of admission, monitor for 6 hours or
longer.
• Patients to be discharged only after the serial salicylate levels have
decreased to <25mg/dl, no acid based imbalance, no CNS or pulmonary
symptoms.
• Psychiatric evaluation for intentional poisoning.
87
Management of Acute Salicylate (Aspirin) Poisoning
Assess severity by
• Amount ingested
• Clinical features
• Plasma / serum salicylate level
Mild / Moderate Severe
• Dose ingested 150-300 mg/kg • Dose ingested >300mg/kg

• Nausea, vomiting, tachypnea, • Hyperpnea, respiratory distress,
tinnitus, lethargy, hyperpyrexia, confusion coma,
fever,dehydration pulmonary oedema, arrhythmias,
CVS collapse, acute renal failure
Conduct Primary & Secondary Surveys with Resuscitation & Monitoring
Investigate & Confirm Severity

•Get serial salicylate levels (2 hrly till peak)
Mild / moderate severity : Peak levels = > 300mg / L
Severe poisoning : Peak levels = 900 -1000 mg / L
• Get serum electrolytes, anion gap, ABG, blood glucose, BUN,
creatinine, PT, INR, platelets, CBC, LFT, ECG, X- ray chest
•Monitor urine out put, and pH
Diagnostic: Raised plasma salicylate levels, Respiratory
alkalosis, Anion gap, & Metabolic acidosis
• Correct dehydration,Treat hypoglycemia

• Treat metabolic acidosis with iv sodium bicarbonate, correct hypokalemia
• Alkalinize urine
• Gastric lavage within 1 hr of ingestion
• Give activated charcoal 1g/kg & repeat 2-5 hrly till salicylate level start falling or
<250mg/L
• Consider haemodialysis in severe cases
Referral guidelines
• Refer all cases after initial stabilization for hospital management where
plasma/serum levels are done
• Observe nontoxic ingestions and asymptomatic patients for 6 hrs.
88
Other Nonsteroidal
Anti-
Anti-inflammatory
Drug Overdose
Non-steroidal anti-inflammatory drugs (NSAIDs) though chemically
different, have similar pharmacological effects. These drugs are
widely used to relieve pain, pyrexia and inflammation and most are
available over-the-counter. Accidental exposure may not result in
poisoning; however, intentional intake of large doses is known to
cause severe poisoning
89
Commonly available preparations in Oman
Formulations &
Generic Name Trade Name Strength
Ibuprofen Profinal,Brufen, Tablet 4 mg, Syrup

Balkprofenal, Perofen 1 mg/5ml.
Naproxen Naprox, Prozen Tablet 5 mg.
Indomethacin Indocid, Bondon Capsule 75mg.
Diclofenac sodium Olfen, Voltaren, Tablet 5 mg

Diclogesic, Rofenac Tablet 1 mg(L/A)
Injection 25mg/ml, 3ml
ampoule
Diclofenac potassium Cataflam Tablet 5 mg
Tenoxicam Tilcotil Tablet 2 mg
Nabumetone Relifex Tablet 45 mg
Source:
Toxic dose:
Generally, 5-1 times the therapeutic doses.
Mefenamic acid toxicity is reported with 2.4 gm dose.
Mechanism of Toxicity
NSAIDs inhibit the enzyme cylooxygenase, which is required for the synthesis of
prostaglandins.However, the relationship between toxicity and inhibition of
prostaglandins remains uncertain.
• Most cases of overdose of NSAIDs are asymptomatic.
• Some cases may have mild GIT symptoms (nausea, vomiting, abdominal
pain, haematemesis). Patients usually recover fully within 24 hours.
• Toxic doses of Ibuprofen or Naproxen can produce nausea, vomiting,
abdominal pain, diarrhoea, haematemesis, drowsiness, lethargy,
nystagmus, tinnitus, headache, diplopia, hyperventilation, and seizures. In
severe poisoning, hypotension, bradycardia or tachycardia, apnoea, coma,
hypoprothombinemia/ thrombocytopenia, hyperthermia, metabolic acidosis
and acute renal failure may occur.
90
• Overdose of Indomethacin, Diclofenac, Tenoxicam and Nabumetone
produce similar clinical picture as above. May induce acute renal failure in
some cases.
• Mefenamic acid is a relatively toxic drug. Convulsions are the main
feature of acute overdose. Convulsions are usually preceeded by agitation
and twitching of muscles, and vomiting and diarrhoea are common. Rarely
acute renal failure and hypoprothombinemia may occur.
Diagnosis
• History of overdose ingestion.
• Routine laboratory investigations (CBC, electrolytes, glucose, BUN,
creatinine, liver transaminases, prothrombin time and urine for albumin
and RBC).
Treatment: Supportive, no antidote
• Asymptomatic cases: Discharge,follow up in H.C. for 12-24 hours.
• Mild cases: Administer antacids and milk and observe for 4-6 hours. Self
resolving. Health centre follow up.
• Severe cases with CNS and cardiorespiratory depression – emergency
evaluation and ABCDEs. Admit, treat seizures
• Treat dehydration and hypotension with iv fluids; Dopamine, if required.
• Administer Vit. K in patients with elevated prothrombin time.
Decontamination
• Consider gastric lavage only in massive overdose and if seen early.
• Administer activated charcoal with a dose of saline cathartic.
• Consider repeat dose activated charcoal for retard (slow release)
preparations and for Oxicams, which have significant enterohepatic
circulation
• No role of haemodialysis as all these drugs are highly protein bound and
are extensively metabolized
91
Anticonvulsant Drug
Overdose
There are different types of seizures and the treatment varies from
one type to another. Patient may be on single drug or on combined
drug therapy. Phenytoin, Carbamazepine and Lamotrigine are used
to treat partial and generalized seizures.Valproate is used to treat
tonic-clonic seizures and absence seizures More recently,
Gabapentin is second line drug to treat partial seizures. Vigabatrin
is a second line drug for partial seizures and generalized tonic-
clonic seizures. Vigabatrin may also be useful against other seizure
types, with the exception of generalized absences and
myoclonus.Interactions between antiepileptics are complex and
may enhance toxicity of each other.
92
Commonly available preparations in Oman
Generic name Trade name Formulation&strength
Carbamazepine Tegretol, Temporol Tab. 100,200mg

Tab. Controlled release 200,400mg
Syrup 100mg/ml
Clonazepam Rivotril Tab 0.5,2,2.5mg
Ethosuximide Zarontin Cap 250mg

Syrup 250mg/5ml
Phenobarbitone Gardenal Tab. 30mg,
Elixir 15mg/5ml
Inj. 200mg/ml, 1ml ampoule
Phenytoin Epanutin Cap.25, 50,100mg
Suspension 30mg/5ml
Inj. 50mg/ml, 5ml ampoule
Sodium valproate Depakine Tab. 200,500mg

Syrup 200mg/3.5ml (288mg/5ml)
Inj. 400mg/4ml
Diazepam Valium,Valinil,Apo- Tab. 2 mg, 5 mg, 10 mg.
Diazepam,Stesolid Inj. 5mg/ml, 2ml ampoule
Chlormethiazole Heminevrin Iv Infusion 8mg/ml
Lamotrigine Lamictal Tab. 5,25,50mg
Vigabatrin Sabril Tab. 500mg
Gabapentin Neurontin Cap. 300mg
Topiramate Topamax Tab. 25,50,100mg
Zonisamide Zonegran Cap. 100mg
Source:
93
Phenytoin
Therapeutic dose Oral – 3-4 mg/kg up to 2 -5 mg/day
Loading dose 15-2 mg/kg iv (max. 1 gm.)
Therapeutic serum range: 1 -2 µg/ml

Toxic dose 2 mg/kg
Toxic levels Above 2 µg/ml – Nystagmus, Above 3 µg/ml- Ataxia,
slurred speech,tremor, Above 4 µg/ml, Altered levels of
consciousness
Pharmacokinetics:
Absorption is slow and unpredictable. Peak plasma levels vary and half-life
increases with increasing plasma levels.
Mechanisms of action
Inhibition of Na+ channels and reducing their ability to recover. Also known to
increase brain concentration of GABA. Toxic levels usually cause central
nervous system depression.
Propylene glycol is a diluent in parenteral preparations which may cause cardic
arrest when phenytoin is administerd iv rapidly.
Clinical Presentation
Acute overdose or chronic accidental overmedication ,
Nystagmus, ophthalmoplegia, ataxia, dysarthria, tremors, hyper reflexia,
nausea, vomiting, diplopia, hyperglycemia, agitation and irritability. Seizures are
unlikely to occur. Stupor/ coma and respiratory arrest occur in severe poisoning.
Rapid intravenous injection can cause hypotension, bradycardia or cardiac
arrest.
Diagnosis
History of ingestion, epileptic patient with altered mental status and ataxia.
Get repeated serum phenytoin levels to know the peak level.
Other useful tests: Serum electrolytes, glucose, BUN, creatinine, serum
albumin and ECG.
Treatment
Supportive (ABCDEs)
Treat coma
Protect from self-injury of patient due to ataxia
Treat hypotension ( stop drug,give fluids,Dopamine , if required )
No specific antidote
Decontamination
Administer activated charcoal
Multiple - dose AC may enhance elimination
No role for haemodialysis given the extensive protein binding.
94
Carbamazepine
Therapeutic dose Maximum dose in adults 16 mg/day

Maximum dose in child 3 mg/kg/day
Therapeutic serum levels 4-8 mg/L
Toxic dose ( potentially fatal ) >3 mg/kg

Toxic serum levels >1 mg/L (ataxia & nystamus)
>2 mg/L (severe CNS & Cardio- respiratory signs)
Pharmacokinetics
Absorption is erratic, peak levels after large overdose may occur up to 24 hours
post-ingestion. It is largely metabolized to an epoxide, which is also
pharmacologically active. Plasma levels of the parent compound should be
monitored in patients on treatment and with overdose. Carbamazepine
concentrations are not always reliable predictors of toxicity. Levels above 2
mg/L in adults are associated with coma, seizures and cardiotoxicity. Doses of
carbamazepine in children are higher as they eliminate it more rapidly
Inhibition of Na+ channels and reducing their ability to recover. It also has
anticholinergic effects.
Acute mild to moderate overdose
Ataxia, Nystagmus, Ophthlmoplegia, Dystonia, Mydriasis, Sinus tachycardia,
Nausea, Vomiting, Tremors, Dysarthria, Myoclonus
Severe Poisoning
Stupor, Myoclonus, Choreoathetosis, Seizures, Hyperthermia, Hypotension/
Hypertension, Respiratory depression/ arrest, Tachycardia/ Cardiac conduction
abnormalities (AV block, QRS &QT interval prolongation)
In children higher incidence of dystonic reactions, choreoathetosis and seizures
and less ECG abnormalities are observed.
Chronic over dose

Headache, Diplopia, Ataxia, Hyponatremia, Leukopenia
Diagnosis
History of exposure
Typical symptoms appear within 6 hours of ingestion but may be delayed up to
24 hours post ingestion. Reports of symptoms appearing after 72 hours are also
documented.
• Carbamazepine toxicity should be considered in any child presenting with
seizures, apnea or unexplained change in mental status. Severity of
toxicity is assessed on the basis of clinical status.
95
• Serum carbamazepine levels > 2 mg/L suggest serious toxicity, however
lower levels do not indicate a benign course. Hence, serial monitoring
should be performed, every 4-6 hrly.
• Routine biochemical tests might show elevated liver enzymes.
• Sonogram in acute poisoning may show chemical pancreatitis without
accompanying pain.
• ECG abnormalities would further support diagnosis.
Treatment
• Supportive (ABCDEs)
• Treat seizures, coma, dysrhythymias
• Multiple dose activated charcoal is effective and may increase clearance.
• Na Bicarbonate is of unknown value for treating dysrhythmias.
• No specific antidote
• Physostigmine is not recommended
Caution
• The drug lacks water solubility hence haemodialysis and peritoneal
dialysis ineffective
• Asymptomatic patients should be observed for 6 hrs or more after
overdose exposure.
96
Sodium Valproate
Therapeutic dose Oral 2 -3 mg/kg daily (maximum 6 mg/kg/day)
iv 4 -8 mg (up to 1 mg/kg)
Therapeutic levels 5 -1 mg/L (5 -1 µg/ ml)
Toxic Dose >2 mg/kg
Toxic levels 8 -1 mg/L, > 5 mg/L (drowsiness), >1 mg/L
(coma, metabolic abnormalities). In children 185mg/L
has been associated with coma.
Prolongation of Na+ channel inactivation and GABA enhancement.
Pharmacokinetics
Valproate is extensively metabolized in the liver; some metabolites are as
potent as parent compound.
Mild overdose –self limited drowsiness.Moderately severe poisoning causes
Nausea, vomiting, CNS depression (drowsiness, disorientation, coma
&respiratory failure) occurs in severe poisoning. Rarely hypotension with
tachycardia, pinpoint pupil. Occasionally myoclonic movements or seizures
may occur. Cardiorespiratory arrest seen in severe toxicity.
At very high serum levels (>1 mg/L) there may be an anion gap acidosis,
hypocalcemia,hypernatremia and hyperammonemia. Thrombocytopenia,and
leukopenia can occur after 3-5 days of acute over dose.
Diagnosis
• History of exposure
• Clinical picture of CNS depression and metabolic disturbances
• Serial valproic acid levels are high
Routine biochemical tests, LFT, serum osmolality and osmolar gap, ECG.
Treatment
Supportive (ABCDEs)
• Treat coma, hypotension, and seizures.
• Treat acidosis, hypokalemia , hypocalcemia if severe & symptomatic.
Decontamination
• Activated charcoal
• MDAC- is helpful
• Whole bowel irrigation may be helpful in large ingestion or for sustained
release preparations
• Consider hemodialysis only in patients with serum levels of >1 mg/L
and clinical deterioration despite MDAC.
• Asymptomatic patients should be reassessed 12 – 24 hrs. after ingestion
clinically and by serum levels before discharge.
97
Lamotragine
Therapeutic dose Adults 3 –8 mg/day, Children 2-5mg/kg/day

Therapeutic serum levels 1 – 3 µg/ml
Toxic dose Adult 135 mg, Child 8 mg (19 – 64 mg/kg )
Toxic levels >5 µg/ml
Pharmacokinetics
It is rapidly absorbed by the oral route and has a half-life of 24 hours. It does not
have active metabolites. It may raise the concentration of active metabolites of
carbamazepine.
Inhibition of Na+ channels resulting in neuronal membrane stabilization and
decreased release of glutamate, the excitatory neurotransmitter. It also inhibits
folate metabolism.
Most common are dizziness,headache, ataxia, nystagmus, loss of accomodation,
diplopia, blurred vision, slurred speach, and are self resolving with supportive care.
Seizures and ECG abnormalities (widening of QRS, prolonged PR interval ) are
reported in severe cases. Rhabdomyolysis, hypotension and renal failure seen in
uncontrolled seizures.Drug induced rashes and hypersensitivity syndrome also
reported .
Diagnosis
• History of exposure.
• Epileptic patient with typical clinical features
Laboratory monitoring
• Monitoring of arterial blood gases and/ or pulse oximetry, serum
electrolytes, ECG, CBC, urinalysis, and liver and kidney function tests.
Treatment
• Treat Seizures, Rhabdomyolysis, and Ventricular dysrhythmias.
• Evaluate for hypoxia, acidosis, and electrolyte disorders& treat
accordingly.
• No specific antidote.
Decontamination
• Administer activated charcoal.
• Role of hemodialysis has not been established, however, in patients with
renal failure hemodialysis may be required.
98
Phenobarbitone
Therapeutic dose Adult 1 -32 mg (hypnotic dose)
Therapeutic plasma levels 15-35mg/ml
Toxic dose 5-1 times the hypnotic dose
Toxic levels >6 mg/l
Fatal oral dose 6-1 g
Pharmacokinetics
Vary by agent and group. They are highly lipid-soluble and rapidly
penetrate the brain to induce anaesthesia. Phenobarbiturate has long
elimination half-life (8 -12 hr).
Mild to moderate intoxication
Lethargy, Slurred speech, Nystagmus, Ataxia
Higher doses
Hypotension
Coma, hypothermia (common in patients with deep coma)
Respiratory arrest commonly occurs
Diagnosis
1. History of ingestion
2. Epileptic patient with stupor or coma
3. Skin bullae may be seen
4. Plasma barbiturate levels may be >6 -8 mg /l associated with coma,
>15 mg/l with severe hypotension
5. Other routine tests
Treatment
• Treat coma, hypothermia, and hypotension.
Decontamination
• Consider gastric lavage for large over dose
• Administer activated charcoal with single dose cathartic
• Alkalinization of urine
• Repeat- dose activated charcoal may be tried.
• Consider haemodialysis in prolonged coma, renal failure or intractable
hypotension.
Contact poison control centre for poisoning due to newer drugs
99
Management of Carbamazepine Poisoning
Ask &
Observe • History of ingestion, amount
• Toxic dose > 20 mg/kg
• Toxic serum levels > 10 ml/L
• Unexplained drowsiness/seizures/apnea in a child
Acute Chronic
Typical clinical features appear in 6-24 hrs (long term overdose)
Mild-Moderate Severe • Headache, Diplopia,

Ataxia, Hyponatremia,
• Drowsiness • Stupor Leukopenia
• Ataxia • Seizures Treatment:
• Nystagmus • Respiratory depression • Reduce the dose or stop
• Mydriasis • Cardiac conduction the drug after initiating
• Dystonia abnormalities (AV alternative therapy.
• Tremors Block, QRS & QT • Symptomatic treatment
• Dysarthria Prolongation)
• Tachycardia
Conduct Primary Survey and Resuscitate

Treat Seizures & cardiac arrhythmias continue supportive treatment
Secondary Survey and Diagnosis
Investigate & Confirm Diagnosis Decontaminate

• Serial monitoring of serum levels every 4-6 • Perform gastric lavage, if
hrs, peak may take 72 hours. indicated
• Serum levels more than 20 mg/L suggest • Give multiple dose, activated
serious toxicity charcoal until clinical
• Raised liver enzymes recovery
• Ultrasound evidence of chemical pancreatitis • No role of haemodialysis /
• ECG changes peritonial dialysis
Referral
Guidelines • Refer all severe cases
• If no facility for serum levels monitoring
Note • Asymptomatic patients should be observed atleast for 6 hrs.

• For other antiepileptic drug poisoning, refer manual
100
Antipsychotic
Antipsychotic
Drug Overdose
Phenothiazines, butyrophenones and a large number of newer
drugs are widely used to treat psychosis. Prochlorperazine,
promethazine and droperidol are used as emetics.
101
Antipsychotics available in Oman
Generic Name Trade Name Formulation & Strength
Chlorpromazine Largactil Tablets, 25, 1 mg

Injection, 25mg/ml, 2ml
ampoule
Syrup, 25mg/5ml
Fluphenazine Injection, 25mg/ml, 1ml

decanoate vial
25mg/ml 1 ml vial
Thioridazine Melleril, Tablets, 1, 5mg

Ridazine Retard capsule, 1 mg
Trifluoperazine Stelazine Tablets, 1, 5mg

Suspension, 5mg/ml
Haloperidol Haldol, Tablets and capsule, 1.5,

Serenace 5, 1 mg
Liquid, 2mg/ml
Injection, 5mg/ml
Flupenthixol Clopixol, Injection, 5 mg/ml

acetate Acuphase
Zuclopenthixol Clopixol, Injection, 5 mg/ml
acetate Acuphase
Olanzapine Zyprexa Tablets, 5, 7.5,1 mg
Resperidone Risperdal Tablets, 1, 2, 4mg
Source:
Toxic dose is variable, serious extrapyramidal and anticholinergic effects seen
with therapeutic doses. CNS depression and hypotension can occur with
overdose.
• Orthostatic hypotension due to antiadrenergic effect
• Tachycardia due to anticholinergic effect
• Sedation due to direct CNS depression and anticholinergic effect
• Extrapyramidal dystonia due to central dopamine blockade
• Decreased seizure threshold
• Pupil constriction due to alpha adrenergic blockade
102
• Mild poisoning: Sedation, miosis, orthostatic hypotension, dry mouth, dry

skin, tachycardia and retention of urine.
• Severe poisoning: Coma, seizures, respiratory arrest, hypothermia or
hyperthermia, jaw muscle spasm, torticollis, oculogyric crisis, rigidity,
bradykinesia and pill-rolling tremors. Neuroleptic malignant syndrome
seen in patients on chronic antipsychotic therapy, it may present with
rigidity, hyperthermia, sweating, lactic acidosis and rhabdomyolysis.
Clozapine can cause prolonged confusional state, cardiac toxicity, and
agranulocytosis.
Diagnosis
• History of ingestion and clinical features
• ECG shows QT interval and QRS prolongation
• Dystonias common in children
• X-ray abdomen may show the drug (tablets) in GIT
• Routine biochemical and blood tests
Treatment: Symptomatic, no antidote
Severe poisoning
• Emergency evaluation and resuscitation – ABCDEs, monitor ECG
• Treat coma, hypotension, hyperthermia.
• Treat seizures and dysrhythmias with phenytoin .
• Treat dystonia with Diphenhydramine ( .5-1mg/kg im or iv) or Benztropine
(1-2mg iv or im or . 2mg/kg)
• Do not use sympathomimetics to treat hypotension
• Do not use Quinidine or Procainamide to treat dysrhythmias.
• Alkalinize if wide QRS or QT prolongation.
Mild exposure
• Monitor vitals and ECG for at least 6 hours before discharging the patient
Decontamination
• Do not induce vomiting

• Give activated charcoal
• Gastric emptying is not necessary, if activated charcoal can be given
promptly
• Hemodialysis, not effective
• Repeat dose-activated charcoal not evaluated
Follow-up: Refer to psychiatric clinic
103
Antidepressant
Drug Overdose
Antidepressant drugs are used in the treatment of endogenous
depression of moderate and severe degree.These drugs
include tricyclics and related drugs,selective serotonin re-
uptake inhibitors (SSRIs)and other drugs.
104
Preparations available in Oman
Generic name Trade name Formulation &
Strength
Cyclic Compounds
Amitriptyline Saroten, Tryptizol Tab. 25,5 mg
Clomipramine Anafranil Tab. 1 , 25mg
Imiprex, Tofranil Tab. 25mg

Imipramine
Ludiomil Tab. 25,5 mg
Maprotiline
Doxepin Sinquan Tab. 25mg
Dothiepin Dothiepin Tab. 25,75mg

Mianserin Miansarin Tab. 1 mg
Non– Cyclic Compounds

(SSRIs)
Citalopram Cipram Tab. 2 mg
Fluoxetine Prozac, Salipax Cap. 2 mg
Paroxetine Seroxat Tab. 1, 3mg
Other drugs
Flupentixol Fluanxol Tab. 1,3mg
Source:
105
Tricyclic Antidepressants
Therapeutic dose : 2 - 4 mg / kg / day
Therapeutic serum level : 1 - 26 nanograms / ml
Toxic dose :1 - 2 mg/kg (usually 1 gm or greater in adults)
Toxic level : Delerium > 3 nanogram / ml

Seizures > 1 nanogram / ml
Fatal >4 nanogram / ml
Therapeutic action: 2 – 8 hrs after oral dose with tissue to plasma levels
usually 1 :1 and in myocardium possibly 1 : 1.
1. Stimulate release of catecholamines (norepinephrine)
& serotonin and subsequently block their re-uptake at
post -synaptic receptors.
2. Act as central and peripheral anticholinergics
3. Antagonize potassium and sodium channels in the
brain and myocardium
4. Have direct alpha adrenolytic effects.
Pharmaco/toxico/Kinetics
All have first pass metabolism by the liver and are lipophilic, with a large volume
of distribution to heart, brain, liver and kidney. They are bound to alpha
glycoprotein and are therefore concentration and pH dependent with acidosis
increasing the free drug and therefore toxic effects. Fluctuating tissue and
plasma level limits the use of drug levels. They finally are degraded by the
cytochrome P 45 system in the liver. Genetic variations in P 45 system and
drugs which antagonize this (e.g. SSRI) may increase TCA toxicity. Elimination
half-life varies from 8 – 16 hrs and may be prolonged in the elderly. A small
fraction of the active metabolites are excreted in bile and gastric fluids so an
enterohepatic and enterogastric circulation may contribute to toxicity.
The dominant target organs for adverse effects are:
CNS: Progressively confusion, agitation, hallucinations, delerium, seizures or
lethargy and coma. May have hyperthermia. Myoclonus & extrapyramidal
symptoms may occur.
CVS:
Mild Initially sinus tachycardia and mild hypertension, secondary
to release of catecholamines.
Moderate PR, QT & QRS prolongation and sinus tachycardia, hypotension
Severe Prolongation of QRS complex >12 msec, ventricular arrhythmias
AV blocks. systemic hypotension, acidosis, shock pulmonary oedema
Refractory hypotension is most common cause of death.
106
Anticholinergic syndrome Sedation, delirium, mydriasis, dry skin & mucous
membranes, urinary retention, gastro-intestinal atony and tachycardia.
Note: TCA poisoning may present with all or any of the following three
toxic syndromes depending on dose and the drug :
Anticholinergic,Cardiovascular effects and seizures. The above signs
and symptoms are evident within 2 – 6 hrs. If patient remains
asymptomatic after 6 hrs with no prolongation of QT intervals or sinus
tachycardia, he/she may be discharged.
Diagnosis
The clinical picture of an anticholinergic syndrome with sinus tachycardia
and/or prolonged QRS and QT intervals is strongly suggestive of TCA
overdose. Drug levels are usefull only in confirmation but not for management.
ECG signs of toxicity
1. Sinus tachycardia
2. QRS > 1 msec.
QRS > 16 msec. (Ventricular arrthymias)
3. T axis of 13 ° - 27 °
4. R/S ratio in AVR > .7
5. R wave greater than 3 mm in AVR
6. Right axis deviation > 13 °
Other laboratory tests : Electrolytes,glucose, BUN, creatinine, CPK, urine for
myoglobin, ABGs,CBC, LFT, X-Ray chest
Treatment
A standard primary survey with appropriate resuscitation is always indicated.
With the secondary survey a differential diagnosis should be considered.
The mainstay of treatment for significant cardiac or CNS toxicity is aggressive
alkalinization with NaHCO3 iv bolus (1mEq/kg) to an arterial pH of 7.5 – 7.55.
Additional iv boluses may be required. For cardiac arrythymias refractory to
NaHCO3, the next line drugs are Lidocaine followed by MgSO4 as the third
choice. Lidocaine iv dosing is 1 mg/kg body weight and MgSO4 is 1 gm in 1- 2
minutes iv bolus. Each may be followed by an infusion. (Lidocaine 1 -
mg/min,MgSO4 – 3 mg/min). Do not use procainamide or Type Ia or Ic drugs.
Hypotension refractory to NaCl ( .9% boluses upto 3 ml/kg) and NaHCO3
loading may be treated with vasopressors. There is ongoing controversy over
the best pressor (epinephrine, dopamine or nor-epinephrine). Clinicians should
be guided by their clinical experience with pressors and be prepared to change
drugs if the desired effect is not attained with their first choice. Follow standard
ACLS dosing.
Seizures should be controlled with benzodiazipines and if these fail, give
barbiturates. Refractory seizures are unlikely but may then require
neuromuscular paralysis and general anesthesia.
107
Cardiac arrest with V.F. and asystole may require prolonged CPR, especially in
children with successful final outcomes.
Decontamination
• Oro-gastric lavage may be considered in patients with large and early
presentations and should be considered even late where gastric emptying
is delayed (gastric atony – anticholinergic syndrome). Patients with
significant depressed level of consciousness may require intubation for this
to be safely performed.
• All patients should receive an initial dose of activated charcoal and at least
one further dose in 4 hrs. Further dosing depends on bowel motility which
should be present to avoid complications. MDAC is controversial but
reasonable where persistent toxicity is evident (poor metabolizer). Forced
diuretics, haemodialysis and haemoperfusion are not effective.
Antidotes
Experimental antibodies are now available but very costly. They are in Phase
III trials. Investigations on specific bradycardia agents to prevent arrthymias is
still experimental.
Observation, Referral:
• All patients with history of TCA ingestion should be observed and
monitored for 6 hrs. Most patients develop major toxicity signs within this
time and will require continuous cardiac monitoring and admission to CCU
or to ICU if intubated.
• Patients who have had decontamination and are neurologically and
haemodynamically stable with normal ECG’s and a normal QRS complex
may be discharged (mild sinus tachycardia <12 is acceptable).
• The period of hospital monitoring required for the intermediate patient is
24 hrs. Any significant events in the adequately treated patient will occur
during this time.
Selective Serotonin Reuptake Inhibitors (SSRIs)

These drugs are less sedating and have fewer antimuscarinic and cardiotoxic
effects than tricyclics.
Refer Table I Toxicological syndromes
Treatment
Supportive
Note: Hyponatraemia (usually in elderly &possibly due to inappropriate
secretion of ADH)has been observed with all cyclic drugs more frequently
with SSRIs.Hyponatraemia should be considered in all patients who have
drowsiness,confusion or convulsions and are on antidepressant treatment.
108
Management of Tricyclic Antidepressant (TCA) Poisoning
Amitriptyline, Nortriptyline, Imipramine, Desipramine, Doxepin, Clomipramine
Ask • History of ingestion (suicidal ?)

• Amount ingested
Toxic dose 10-20mg/kg,
10 times therapeutic dose
• Time since ingestion
Asymptomatic Drowsy / delirious, Dry mouth, Seizures, Coma, Hypotension,

Dilated pupils, Sinus Shock, Hypo/hyperthermia AV
tachycardia, Absent bowel Block, Vent.Arrhythmias
sounds,Urine retention
Conduct
Primary Survey with Resuscitation & Monitoring
• Get urgent 12 lead ECG Look for Sinus tachycardia, Prolonged
QRS ( > 0.1 sec) & QT intervals
• Secure iv line. Send blood for electrolytes, glucose, BUN,
Creatinine, CPK, ABGs.
• Drug level only to confirm diagnosis (if available)
• Urine sample for myoglobin if seizures
Normal ECG & QRS complexes If Cardiac and CNS toxicity

Refer or treat in ICU/CCU
• Do gastric lavage within 1 hr of
ingestion (only if large ingestion) • Treat cardiac & CNS toxicity with
• Give single dose activated IV bolus of Sodium Bicarbonate
charcoal 1 mEq / kg, repeat until arterial pH is
• Continue monitoring ECG, Body 7.5-7.55
temperature & Vitals • Treat hypotension (guided clinically)
• Control seizures with Diazepam /
Barbiturate / Neuromuscular blocker
Observe for 6hrs in A& E
If remains asymptomatic Continue treatment & monitoring until
QRS interval < 0.1 sec. Mental status and
BP normal & all signs of toxicity are
Discharge with absent for 24 hrs
psychiatric follow up
Note : Suspect TCA poisoning in any case with lithargy,seizures,coma with QRS
interval prolongation. Differtial diagnosis : Overdose of Antipsychotics, Class I
& II Antiarrhythmics ,Antihistamines,
Cardiac ischemia, Conduction defects, Hyperkalemia
109
Antihistamine
Drug Overdose
Antihistamines (H1 receptor antagonists) are among the most
common medicines prescribed for cold, cough, allergy-related
itching, motion sickness and for sedation. These are also
common over-the-counter drugs, available as combination
preparations with sympathomimetic decongestants, cough
suppressants and expectorants.
110
Antihistamine preparation available in Oman
Generic Name Trade Name Formulation
&Strength
Chlorpheniramine Maleate Zeet, Allerfin,Omvil, Chlorohistol, Piriton, Tab. 2,4,6 mg
Soolan, Tussifen, Polaramine Syrup, 2mg/5ml
Inj. 10mg/ml ampoule
Promethazine hydrochloride Phenergan,Histaslac, Promantine, Tab. 25,10mg
Allergiside, Histalol, Syrup, 5-6mg/5ml
Inj. 25mg/ml ampoule
Hydroxyzine Atarax Tab. 25mg
hydrochloride
Cetrizine hydrochloride Zyrtec, Cetralon,Zeran,Agelmine Tab. 10mg

Syrup, 5mg/5ml
Clemastin Tavegyl Tab. 1mg
Dyphenhydramine Amydramine,Dramalyin Syrup

Benylin
Dyphenhydramine + Menthol Isilin, Koffex
Loratadine Claritine,Tidilor, Tab. 10mg

Syrup, 5mg/5ml
Loratadine + Clarinase Tab. 5mg +120mg
Pseudoephedrine
Triprolidine Actifed, Sedofan Tab.2.5mg Syrup

(Combination with
Pseudoephedrine
and guaiphenisin)
Triprolidine 2.5mg + Sudafed Tab. 2.5mg
Pseudoephedrine 60mg
Pseudoephedrine 30mg + Sinecod Syrup, 10mg/5ml

Triprolidine 1.25 mg +
Codeine Phosphate 10mg
Pheniramine Hydrogen maleateAvil Tab. Retard 75mg

Syrup 3mg/ml
Inj. 22.75mg/ml
Source:
Toxic Dose
• Variable and unpredictable, clinical evaluation more important than
attempting to know the amount ingested.
• First generation drugs are toxic to CNS and can produce severe
anticholinergic effects, while non-sedating newer drugs prone to cause
cardiac toxicity.
• The estimated fatal dose of diphenhydramine is 2 -4 mg/kg.
111
• In general, toxicity occurs after ingestion of 3-5 times the usual daily dose
of antihistamine.Children are more sensitive to toxic effects than adults.
Mechanism of Action
Antihistamine drugs competitively antagonize the effects of histamine at H1
receptor sites. First generation H1 blockers have anticholinergic effects
(antimuscarinic), CNS depressant or CNS stimulant action, hyperthermia and
other peripheral effects. Some drugs also block serotonergic and alpha-
adrenergic receptors and have local aenesthetic effect. The non-sedating newer
drugs lack anticholinergic and CNS effects as these do not penetrate blood brain
barrier. However, these may produce supraventricular and/or ventricular
dysrhythmias or cardiac arrest.
Signs and symptoms resemble anticholinergic syndrome and appear within
3 min – 2 hrs. after ingestion.
CNS effects
Excitation, psychomotor agitation, convulsions (tonic-clonic) are common in
children and drowsiness, sedation, delirium, hallucinations, coma in adults.
Dystonic reactions are seen with some drugs in adults.
Anticholinergic effects
Hyperpyrexia, tachycardia, hypertension, fixed and dilated pupils, blurred vision,
diplopia, dry mouth and urinary retention.
Cardiac effects
Myocardial depression, cardiac arrest, QRS widening (common with
Diphenhydramine overdose), QT prolongation-resulting in Torsades de pointes
(polymorphic ventricular tachycardia) and loss of consciousness common with
overdose of terfenadine or astemizole (now withdrawn in Europe) in patients
taking erythromycin or ketoconazale along with these drugs or in patients with
liver disease.
Gastrointestinal effects
Nausea, vomiting, diarrhoea, or constipation, decreased bowel sounds.
Differential Diagnosis
Poisoning or overdose of belladonna alkaloids, antispasmodics, antipsychotics,
cyclic antidepressants, antiparkinsonian drugs.
Diagnosis and Monitoring
• History
• Clinical signs and symptoms
• ECG monitoring (specially QT and QRS intervals)\
• Arterial blood gases (ABG)
• CBC
• Myoglobin in urine
• Blood levels of drugs not useful
112
• Assays for commonly co-ingested agents such as paracetamol, aspirin must
be considered.
Treatment
Supportive
Emergency measures
• Primary Survey and Resuscitation (ABCDEs).
• Treat hypotension (with iv fluids, Dopamine if needed, dose (refer table 23)
• Treat ventricular tachycardia with Lidocaine (dose see table 23)
• Treat coma (as mentioned in general management).
• Treat seizures with Diazepam or Lorazepam (dose refer table 23)
• Give iv boluses of Sodium Bicarbonate, 1mEq/kg if QRS prolongation is
>1 msec. Maintain serum pH >7.45, can give Magnesium Sulfate in
patients with Torsades de pointes (1-2g iv in adults and 25-5 mg/kg in
children over 1-2 min.). If no response in 1 min, repeat the dose and
follow it with infusion of 1 -3 mg/min in adults and 3 -6 mg/kg per 24 hr
in children. Isoproterenol, cardioversion and overdrive pacing may all be
required in some cases.
• Treat hyperthermia by controlling agitation with diazepam and by sponging
with tepid water and use of fan.
Secondary Survey (History, Physical Examination, Sampling for laboratory
tests)
Decontamination
• Emesis not recommended.
• Gastric lavage - consider in a case of ingestion of large dose and if patient
is brought to A&E within 1 hr of ingestion. Protect airway before the
procedure.
• Activated charcoal given to all symptomatic patients. Dose in adults and
children (refer page 3 )
Antidote Treatment
No specific antidote.The reversible acetylcholinestrase inhibitor( physostigmine),
is not routinely recommended for antihistamine drug overdose/poisoning
because of its own toxicity (seizures, broncho constriction and asystole ). It
should be considered only in cases of severe toxicity (severe delirium, seizures
and supraventricular tachyarrhythmias unresponsive to other measures). In
adults, the dose is 2mg iv slowly over 5 min. in children give . 2 – . 5mg/kg iv
slowly with constant cardiac monitoring and atropine available to reverse
symptomatic bradycardia.
Enhanced Elimination
Haemodialysis, haemoperfusion, peritoneal dialysis and repeat-dose activated
charcoal are not effective in removing antihistamines.
113
Admission or referral criteria
• All patients with cardiac dysrhythmias and/or persistently depressed
mental status beyond 6 hr observation period, seizures not controllable
with Diazepam or Lorazepam.
• Adults who ingested more than twice the recommended daily dose of 2nd
generation nonsedating H1 antagonist and a child who ingested any
amount of these drugs should be admitted for cardiac monitoring for 24
hrs. regardless of symptoms.
Discharge criteria
• Patients who are asymptomatic after an observation period of 6 hours,
and who have not ingested a significant amount of nonsedating
antihistamine drug; however, take an ECG before discharge.
• Admitted patients who have no evidence of CNC or CVS toxicity for the
past 24 hours.
• Consult Poison Control Centre if in doubt.
114
Management of Antihistamine Poisoning
• History of ingestion, amount
Ask & • Toxic dose 3 – 5 times the usual daily dose
Observe • Diphenhydramine toxic dose is 20 – 40 mg/kg
• Excitation, agitation and convulsion in children
• Drowsiness, hallucination, delirium, coma – in adults
• Dilated pupil, blurred vision, dry mouth, dry skin, fever,
tachycardia
• Nausea, vomiting, constipation
• Cardiac arrhythmias, cardiac arrest
Conduct Primary Survey, Resuscitation & Monitoring
• Maintain airway, assist ventilation as required

• Treat coma, seizures, hyperthermia
• Treat diphenhydramine induced arrhythmias with Sod. Bicarbonate
1 – 2 mEq/kg iv bolus. Repeat if required
Secondary Survey, Investigations & Treatment

Conduct
Decontaminate Investigate
• Consider gastric dosage for • Serum electrolytes, glucose, ABG, ECG

massive ingestion < 1hr. • QT & QRS interval prolonged in
• Give activated charcoal Diphenhydramine overdose
Referral
All cases with cardiac arrhythmias & persistently depressed
Guidelines
mental status
Note • Differential diagnosis, Belladonna alkaloids, antispasmodics,

antipsychotics, TCA, antiparkinsonian over dose
• Repeat dose activated charcoal and haemodialysis not effective
• Observe asymptomatic cases for 6 hrs, discharge after taking ECG

115
Theophylline Overdose
Theophylline is used for the treatment of bronchial asthma.

Oral sustained release prepations are commonly used in
chronic cases.
116
Theophylline
Generic name Theophylline
Trade Names Quibron, Theo-dux, Euphylong
Formulation and strength Tab. 1 mg.
Sustained releaseTab. 3 mg. Caps. 25 , 375 mg
Syrup 6 mg./ 5ml.
Therapeutic dose 8-1 mg/kg (oral dose)
Therapeutic serum levels 1 -2 µg/ml (55-111 µmol/L)
Toxic dose > 50mg /kg
Toxic serum levels >2 µg/ml. (>111µmol/L). Patients with levels above
3 µg/ml (166µmol/L) should be observed until levels are reduced to therapeutic
levels.
Estimated serum level Approximate serum level of non-sustained release
products by doubling the theophylline dose in mg/kg. The serum concentration
is in µg/ml (µg/ml x 5.55 = µmol/L)
Individuals older than 6 years and those aged 3 years and younger, are at
increased risk of toxicity.
Mechanism of Action
• Theophylline is a CNS and cardiac stimulant and has diuretic& smooth
muscle relaxant effects
• Theophylline is an antagonist of adenosine receptors and it inhibits
Phosphodiesterase enzyme at high levels, thereby increasing intracellular
cyclic adenosine monophosphate (CAMP). It also stimulates Beta-
adrenergic receptors directly as well as indirectly by releasing
catecholamines.
Toxicokinetics
Oral Oral administration of liquid or non-sustained release preparations
results in rapid absorption (3 min to 1 hour) after therapeutic dose.
• Sustained release Peak concentration occurs at approximately 4 to 6
hours, however, it may take up to 24 hours. Development of seizures and
arrhythmias has been correlated with a more rapid rate of rise
(6.3 µg /ml/hr vs 1.5 µg/ml/hr).
• Protein binding 4 % at therapeutic serum concentrations. Protein
binding in neonates and elderly is decreased, resulting in a larger volume
of distribution.
• Elimination occurs primarily via hepatic metabolism. Only a small
amount (7%) of theophylline is eliminated unchanged in the urine. The
normal elimination half life is 4-6 hours, which may be significantly
increased (2 hours) in liver disease, congestive heart failure and when
co-administered with erythromycin or cimetidine.
117
Acute single overdose (suicidal/accidental/therapeutic overdose)

• Overdose is characterized by nausea, vomiting, abdominal pain, tremors,
anxiety, tachycardia, mild metabolic acidosis, other metabolic effects
include hypokalemia, hypophosphatemia, hypercalcemia,
hypomagnesemia, hyperglycemia, leukocytosis.
• Hypotension, seizures and dysrhythmias are more common and may
develop at serum concentration of 9 -1 µg/ml. Onset of these
symptoms may be abrupt.
• Seizures are usually resistant to anticonvulsant drugs.
• Sometimes seizures may be delayed till 12-16 hours after ingestion of a
sustained release preparation.
Chronic intoxication occurs when excessive doses are administered
repeatedly over 24 hours or longer or when elimination half-life is prolonged.
Symptoms include vomiting, tachycardia and other dysrhythmias. Hypotension
and metabolic effects are not seen. Seizures occur at lower serum levels (4 -
6 µg/ml).
Diagnosis
• History of poisoning/exposure to theophylline
• Tremors, tachycardia, hypotension more common, in acute overdose.
• Hypokalemia strongly suggests acute overdose.
• Other dysrhythmias such as atrial fibrillation, SVT, VT and cardiac arrest
may occur often with chronic intoxication.
• Nausea, vomiting, abdominal cramps and diarrheoa are common in both
• Seizures may develop abruptly.
Laboratory tests
• Serum theophylline levels Theophylline should be monitored every 2-4
hours until two successive levels decline. Thereafter the levels should
be monitored every 4-6 hours until the values are less than 2 µg /ml (16-
18 hours after acute overdose). Levels <9 -1 µg/ml after acute
overdose are not usually associated with severe symptoms as seizures or
ventricular arrhythmias. Severe toxicity, however, occurs at levels 4 -
6 µg/ml in chronic intoxication.
• Monitor serum glucose and electrolytes, BUN, creatinine
• Institute continuous cardiac monitoring and obtain an ECG.
• Liver function tests
118
Treatment
• Emergency measures support airway, breathing and circulation
• Seizure prophylaxis Phenobarbital is indicated in patients at high risk of
seizures. (Acute overdose with theophylline levels >8 -1 µg /ml/and
chronic overdose with levels >4 -6 µg/ml).
• Seizures Administer Diazepam in bolus, which may be repeated every 5-
15 minutes as needed. Administer IV Phenobarbital. (Dose: adult 1 -
2 mg/kg given at 25-6 mg/min. Child 15-2 mg/kg given at 25-
5 mg/min).
• If severe tachycardia
Beta blocking adrenergic receptor agents may be used. (Use
cardioselective agents.)
• Hypotension, tachycardia and ventricular arrhythmias are caused by
increased B-adrenergic stimulation. Can treat with low dose propranolol
. 1- . 3mg/kg iv or esmolol 25-5 mg/kg/min. Precautions are required
for patients with history of asthma.
• Hypotension Give .9% saline 2 ml/kg. If pressors are required

phenylephrine may be given or another similar diriect vasoconstrictor.
Decontamination
Activated charcoal
Administer charcoal as a slurry (3 gm in 24 ml water)
Gastric Lavage
Consider after ingestion of a potentially life-threatening amount of drug and to be
performed within 1 hour after ingestion.Gastric emptying is not necessary for small
ingestions if activated charcoal is given promptly.
Multiple dose activated charcoal

• May enhance the elimination but is not shown to affect the outcome in
clinical trials.
• Consider in severely poisoned patients.
• Persistent vomiting may interfere with activated charcoal administration.
Treat vomiting with Ranitidine 2 -3 gm or .5-1gm/kg every 2-3 hours
Whole bowel irrigration

Useful in patients who have ingested large quantities of sustained release
preparations. Administer a polyethylene glycol (PEG) bowel preparation solution
at 1-2 ml/kg/hr orally or by NGT until rectal effluent is clear and theophylline
levels have declined.
119
Haemodialysis
Theophylline has a small volume of distribution, therefore, can be effectively

removed by hemodialysis. If is indicated in severe cases and/or when symptoms
persist inspite of AC administration.
Indications
1. Theophylline level >9 µg/ml
2. Theophylline level >4 µg/ml. And significant dysrhythmias, hypotension,
seizures, protracted vomiting.
Referral
To tertiary care centre if any doubt of significant toxicity and no facilities for
monitoring the patient or for theophylline levels estimation.
120
Management of Theophylline Poisoning
• Amount ingested-- Toxic dose (>50 mg/kg)
Assess
• Tremors,Tachycardia,Seizures
severity
Acute Single Overdose Chronic Overdose

• Tremors, seizures • Vomiting, tachycardia
• Tachycardia, hypotension • Arrhythmias (AF,STV,VT)
• Nausea, vomiting, abdominal pain • No hypotension
Resuscitate , Stabilize, And Monitor
Investigate and Confirm Diagnosis
Monitor serum theophylline levels 2-4 hours until two successive levels decline. Then
every 4-6 hours until <20 µg /ml
• Therapeutic level: 10-20 µg /ml Toxic level : > 20 µg /ml
• Acute overdose: Seizures / arrythmias may not be observed even at 90-100 µg /ml.
• Chronic overdose :Seizures occur at 40- 60 µg / ml
• Hypokalemia, hypophosphatemia, hyperglycemia observed in acute poisoning, and not
in chronic overdose
• Other investigations: BUN, Creatinine, Liver function tests, ECG
Continue Resuscitation and Monitoring
Decontaminate Treatment
• Gastric Lavage only if large amount ingested and • Treat seizures with iv Diazepam or iv
patient has come within 1 hr Phenobarbitone
• Activated charcoal single dose, but in severe • Treat hypotension, tachycardias, and
cases or in SR preparation poisoning, give ventricular tachycardias with
Multiple dose activated charcoal Propranolol 0.01-0.03 mg/kg iv ( be
• Whole bowel irrigation may help careful in asthmatics)
• Hemodialysis effective in severe cases (serum
level >100 µg/ml)
REFERRAL GUIDELINES:
• If no facility for serum level monitoring
• If cardiac toxicity or seizures
121
Iron Poisoning
Iron preparations are used for treating iron deficiency anaemia.
Also used as a common daily vitamin and iron supplement
during pregnancy, lactation and childhood. It is thought to be
harmless and is available as over-the-counter nutritional
supplement. However, it is one of the common childhood
accidental poisonings. Pills usually look like candy to children.
Intentional poisoning can occur in adults.
122
Iron preparations available in oman
Generic Name
Trade Name Formulations& Strengths
Ferrous Sulphate Ferrous Sulphate Dried Tab. 2 mg
(65mg Iron)
Tab. 3 mg (6 mg Iron)
Syrup, 15 -2 mg/5ml
(3 -4 mg Iron)
Drops 75mg/ .6ml (15mg
Iron)
Inj. 2 mg/ml, 5ml ampoule
(as Iron sucrose)
Combined preparations:
Ferrous Sulphate and Fefol Spansule dried ferrous

Folic acid sulphate 15 mg (47mg
elemental Fe)+ Folic acid
5 mg
Multivitamin +Minerals Materna Tab. (6 mg of elemental
iron)
Multivitamin+Iron Ironorm Cap.
Iron Ferosac Inj. 1 mg/5ml

Drops, 5 mg/5ml
Iron + Folic acid Ferosac F Tab. 1 mg
Different iron salts contain elemental iron as follows:

4
Iron salt Dose Elemental Iron
Ferrous fumerate 2 mg 65mg
Ferrous succinate 1 mg 35mg
Ferrous sulphate 3 mg 6 mg
Ferrous sulphate, 2 mg 65mg

dried
Source
Omani National Formulary (Ministry of Health 2003) , SQ University Pharmacy List (2003 )
123
Identifying features
• Brightly red/brown coloured coated tablets
• Green/yellow/clear spansules
• Dark brown coloured syrups
Toxic Dose
The dose ingested is calculated from the elemental Iron present / Tab or per 5ml.
• Less than 2 mg/kg Non-toxic
• Amount between 2 -3 mg/kg potentially toxic
• More than 4 mg/kg serious toxicity
• More than 6 mg/kg potentially lethal
Mechanism of action
Iron is corrosive, may cause erosion, haemorrhagic necrosis and even
perforation of gastrointestinal mucosa. Systemic toxicity occurs when serum
levels exceed the iron binding capacity of transferrin. Free circulating iron
damages systemic blood vessels, leading to release of ferritin, serotonin,
histamine and also can cause free - radical injury. Additionally coagulative
necrosis and platelet aggregation also occur. Fluid loss from the gastrointestinal
tract results in severe hypovolemia.
Toxicokinetics
Iron is absorbed through the GI mucosal barrier in the ferrous state where it gets
oxidized to ferric state and combines with ferritin. It is released from ferritin to the
globulin transferrin in the plasma to the blood forming sites.
Depends on the dose ingested and time lapsed since ingestion. Clinical
manifestations appear in 4 stages, which may often overlap.
Stage I (Gastrointestinal; occurs within 3 min – 6 hours)
Due to the corrosive effect on gastrointestinal mucosa, abdominal pain, vomiting,
haematemesis, diarrhoea usually bloody, melena, lethargy. Massive fluid or blood
loss may result in dehydration, shock, renal failure, and death.
Stage II (Relative stability, occurs between 4-12 hours)
Victims surviving the stage 1 show improvement in GIT symptoms; however, there
may be subclinical hypoperfusion and metabolic acidosis.
Stage III (Shock and Acidosis, between 6-72 hours)
The stage of systemic toxicity is characterized by pallor or cyanosis, lethargy,
restlessness, disorientation, seizures, shock (hypoperfusion, metabolic acidosis),
coma, coagulopathy, and potential multiorgan failure and death.
124
Stage IV (Hepatic toxicity, between 12-96 hours)
If the victim survives the shock stage,they proceed to hepatic failure
characterized by jaundice, coagulopathy and hepatic coma.
Stage V (Late complication, 2-4 weeks)

Due to pyloric, antral or intestinal strictures, patient may complain of abdominal
pain and vomiting.
Diagnosis and monitoring

• History of ingestion of iron preparation
• Clinical signs and symptoms especially vomiting and diarrhoea
• Elevation of WBC >15 /cml, raised blood glucose >15 mg/dl.
• Visible radio-opaque pills on abdominal X-ray.
• Total serum Iron levels more than 3 µg/dl.
(Normal values of total serum Iron = 50-100 µg/dl)

Potential poisoning = 100-350 µg/dl, potentially serious poisoning = 350-500 µg/dl,
definite serious toxicity = 500-1000 µg/dl and potentially fatal = >1000 µg/dl.)
Peak total serum Iron levels occur between 2-4 hours after ingestion,
therefore determine the levels between 4-6 hours of ingestion as estimations
after 6 hours may not correlate with the severity of toxicity except in case of
sustained release tablets,wherein determination between 8-12 hrs is required.
The total Iron-binding capacity (TIBS) is an unreliable parameter in Iron

overdose.
• Coma, leucocytosis, hyperglycemia and increased anion gap may
indicate Iron levels more than 5 ug/dl.
• Other monitoring tests
• Serum electrolytes
• Creatinine
• Prothrombin time
• LFT
• ABGs
Differential diagnosis
Necessary only in cases where history of iron ingestion is lacking.
• Infections, metabolic or structural causes for GIT symptoms
• Other poisonings (Aspirin, Theophylline, Mushrooms, Organophosphates)
Treatment
Patients with self-limited mild gastro-intestinal symptoms or who remain
asymptomatic for 6 hours are unlikely to develop serious intoxication. Patients
with serious poisoning are managed with supportive care and antidote therapy.
125
Supportive measures
Maintain airway, breathing and circulation. Treat shock with normal saline 2 ml/kg
iv.bolus. Treat coma, seizure, and metabolic acidosis.
Specific antidote
Deferoxamine (Desferrioxamine mesilate injection 5 mg/vial) is the specific
antidote for Iron poisoning
Indications:
• Repeated vomiting
• Metabolic acidosis
• Lethargy and toxic look
• Hypotension
• GI bleeding and signs of shock
The dose is 15mg/kg/hr administered as intravenous infusion for no longer than
24 hours followed by alternating 12 hours of Deferoxamine infusion with a 12-
hour hiatus to allow for excretion of ferrioxamine. The chelated deferoxamine-
iron complex colours the urine reddish (vin rose). Therapy may be stopped
when the urine colour returns to normal or when the serum iron level decreases
to <3 µg/dl.
Prolonged Deferoxamine therapy (>36-72 hours) is reported to cause IgE mediated
anaphylaxis, ARDS and Yersina enterocolitica septicaemia.
Gut decontamination
• Gastric lavage beneficial for liquid iron preparation and for chewed tablets.
For tablets large bore tube is necessary.
• Activated charcoal is not effective.
• Whole bowel irrigation (WBI)
It is safe and effective means of gastro-intestinal decontamination in
severe iron poisoning. Polyethylene glycol in a balanced electrolyte
solution (COLYTE or GO LYTELY) .5 lit/hr in children less than 6 years
and 1-2.2 lit/hr in older children and adults is administered via a gastric
tube until rectal effluent is clear. No more than 4 lit (1 ml/kg) is to be
given at one time. Repeated WBI may be required for removing tablet
concretions or bezoars.
• Endoscopy or surgical gastrotomy rarely done.
Enhanced elimination
Haemodialysis or haemoperfusion not effective. However, to remove
deferoxamine. Iron complex in a patient with renal failure, haemodialysis may
be required.
Follow-up
The survivors of severe iron poisoning should be followed uptil 4
weeks of discharge for symptoms of GI scarring and strictures
(fullness after eating, nausea, constipation).
126
Management of Iron Poisoning
• History of ingestion, time since ingestion and amount ingested
• 20-30 mg/kg -Potentially Toxic
• 40 mg/kg -Seriously Toxic
• >60 mg/kg -Lethal Dose
Ingested Iron
Asymptomatic Only GIT symptoms Systemic Toxicity (Acidosis,

present altered mental status or
haemodynamic instability
History of > 60 mg / kg Obtain abdominal X-ray. Obtain abdominal X-ray acid-

Acid-base status consider base status & consider gastric
ingestion
20-60mg / kg lavage, or WBI lavage or WBI
or unknown
amount
Obtain serum iron 4 hr. Send serum iron&

post-ingestion obtain baseline urine
<500ug / dl or >500ug / dl, Start Deferoxamine 15 mg

unavailable and metabolic / kg / hr. as iv infusion for
Asymptomatic at asymptomatic with acidosis, or 24 hrs. then alternate with
6-8 hrs post- normal acid-base symptoms 12 hourly iv fluids
ingestion status develop or
persistent
Urine coloured
No
yes
Clinically
stable?
Discharge Stop Continue deferoxamine as

antidote clinically indicated and until
yes No serum iron level <300 ug /dl
Refer if no facility for monitoring serum levels
Adapted
Adapted from
form Goldfrank’s
Goldfrank’s Toxicologic
Toxicologic Emergencies
Emergencies 2002
2002
127
Table III: Toxic Doses of Some Common Drugs
Drug Toxic Dose Dialyzable
Acetaminophen 6-7g or >150 mg/kg No

Alprazolam, Diazepam, >15-20 times the therapeutic No
Lorazepam dose
Amlodipine, Nifedipine, >10mg, >120mg, No
Verapamil, Diltiazem >480mg, >360mg
Atenolol, Metoprolol 2-3 times the therapeutic dose Yes
Propranolol No
Captopril, Enalapril >5g, >300mg No
Carbamazepine >20 mg/kg No
Chloroquine >30mg/kg No
Dapsone >300mg/day Yes
Dextromethorphan >10mg/kg No
Diclofenac, Ibuprofen >5-10 times the usual No
Oxyphenbutazone, therapeutic dose
Phenylbutazone, Piroxicam
Digoxin 3mg No
Diphenhydramine, 3-5 times the usual daily dose No
Pheniramine,
Chlropheniramine
Imipramine, Amitriptyline 10-20mg/kg No
Iron >20mg / kg No
Isoniazid 1.5g Yes
Levothyroxine (T4) >3mg No
Lithium >2.4gm Yes
Methyl dopa >2g No
Phenobarbital 5-10 times hypnotic dose Yes
Phenyl propanolamine, 2-3 times, No
Ephedrine, 4-5 times the
Pseudoephedrine therapeutic dose
Phenytoin 20mg/kg No
Procainamide >4g / day Yes
Salicylates 150-200mg/kg Yes
Triiodothyronine (T3) 0.75mg No
Theophylline >50mg/kg Yes
Note: Haemodialysis is also indicated in ethylene glycol and methanol.
128
Table IV: Potentially Fatal Doses of Some Drugs in a Child
Drug Potentially Fatal Dose (mg/kg)
Acetaminophen (Paracetamol) 150

Camphor 100
Carbamazepine 30
Chloroquine 30
Chlorpromazine 25
Codeine 15
Desipramine 15
Diphenoxylate 1.25
Diphenhydramine 25
Imipramine 15
Iron 40-60
Methyl salicylate 200
Phenytoin 20
Quinidine 60
Sulfonylurea (oral hypoglycemic) 1.0
Theophylline 50-60
Thioridazine 20
Verapamil 24
129
Table V : Toxic Blood Levels of Some Drugs and Alcohols
Time Post
Toxic
Substances Specimen ingestion to
obtain specimen Concentration
Acetaminophen Serum After 4 h >150µg/mL at 4 h
Carbamazepine Serum Stat steady-state >10µg/mL
Carboxyhaemoglobin Blood Stat Extrapolate
Digoxin Serum 6-8 h >2µg/mL adult
>4µg/mL child
Ethanol Serum 0.5-1 h >80 mg/dL (800µg/mL)
Ethylene glycol Serum 0.5-1 h >20 mg/dL (200µg/mL)

Iron
Liquid Serum 2h >350 µg/dL (3.5µg/mL)
Tablet Serum 4h >350 µg/dL (3.5µg/mL)
Isopropanol Serum 0.5-1 h >50mg/dL (500µg/mL)
Lithium Serum 8-12 h >1.5 mEq/L
Methanol Serum 0.5-1 h >20 mg/dL (200µg/mL)
Methaemoglobin Blood Stat >30%
Phenobarbital Serum Stat steady-state 40 µg/mL
Phenytoin Serum 1-2 h >20 µg/mL
Primidone Serum Stat >12 µg/mL
Salicylate Serum After 6 h >30 mg/dL (300µg/mL)
Theophylline Serum
Liquid 1h >20 µg/mL
Regular tablet 1-3 h >20 µg/mL
Slow release 3-10 h >20 µg/mL
130
Section V
Management of
Household P
Product
roduct
Poisoning
131
132
Pesticide Poisoning
Organophosphates and Carbamates
Organophosphates (OPs) and Carbamates are widely used pesticides in
household, agriculture, horticulture, and for vector control. Most accidental or
suicidal exposures are due to these two groups of pesticides, generally known
as cholinesterase inhibitors. Household sprays as shown below and many other
commercial products contain hydrocarbon solvents (toluene, xylene, kerosene,
etc.) that can be toxic.
Common insecticide products containing

Organophosphates and Carbamates
Diazenon
Organophosphates
• Pif paf Nest Kill baits (Chlorpyrifos .5%)
• Prioderm antilice lotion (Malathion .5% )
• Kemilban shampoo (Malathion 1.3%)
• Newsingn-6 EC antimite in animals(conc. Diazinon)
Carbamates
• Baygon powder (Propoxur 1%)
Other preparations available and are used in the country.
133
Other preparations available and are used in the country
Organophosphates Carbamates
• Abate (Temephos) • Baygon (Propoxur)
• Basudin (Diazinon) • Ficam (Bendiocarb)
• Dursban (Chlorpyrifos) • Marshall (Carbosulfan)
• Roger Perfekthion • Pirimor (Pirimicarb)
(Dimethoate) • Methomyl
• Sumithion (Fenitrothion)
Contact Poison Control Centre for more information.
Mechanism of Toxicity
Organophosphates inhibit the enzyme acetylcholinestrase, which is responsible
for inactivation of the neurotransmitter acetylcholine, thereby allowing
acetylcholine to accumulate at all cholinergic receptor sites (muscarinic,
nicotinic) and in the CNS, producing typical cholinergic toxidrome. The
inactivated (phosphorylated) enzyme is stable and requires several hours to
days for reactivation unless pralidoxime (2-PAM) the enzyme reactivator is used
early. However, if the treatment is delayed, permanent damage to the enzyme
(aging, dealkylation) occurs. Carbamates also inhibit the enzyme but the
inactivation is short-lived and spontaneous recovery of enzyme occurs.
However, clinical features are similar to OPs.
Toxic Dose
Varies with the type of preparation, route of exposure, rate of exposure. The
products available in Oman belong to mild to moderate toxicity
(LD5 >1 mg/kg).
Toxicokinetics
These pesticides are absorbed via all routes (oral, inhalation, dermal and ocular). Onset of
symptoms is most rapid following inhalation and less rapid after dermal exposure. Some OPs
are highly lipophilic and are stored in fat tissues resulting in delayed and persistent toxicity for
several days after exposure.
Clinical presentation: Cholinergic toxidrome

Peripheral Nervous System
CNS
Muscarinic Nicotinic
• Diarrhoea • Mydriasis • Headache
• Urination • Tachycardia • Giddiness
• Miosis • Weakness • Restlessness
• Bradycardia, • Hypertension, • Slurred speech
Bronchorrhea, • Hyperglycemia • Confusion
and • Fasciculations • Convulsions
Bronchospasm • Tremors, muscle • Coma
• Emesis cramps
• Lacrimation • Weakness/paralysis
• Salivation, of muscles of
secretions, respiration
sweating
134
Hypotension, shock, dysrhythmias, pulmonary oedema and aspiration pneumonitis
may develop. Cause of death is respiratory failure (paralysis of respiratory muscles
and depression of respiratory centre).
Management
Diagnosis
• Characteristic toxidrome
• Garlic-like odour of solvent from mouth/nose
• Cholinesterase levels (RBC and Plasma) decreased (≥25%)
Treatment
General measures
Health care providers must prevent direct contact with the skin or clothing of
contaminated victims (wear chemical-protective clothing and gloves).
A. Airway
Continued oropharyngeal suctioning should be carried out because of excessive
salivation and bronchorrhoea. If airway is at risk – intubate early.
B. Breathing
Oxygenation with high flow O2 (15L/min using a mask with a reservoir bag). If
there is inadequate spontaneous ventilation, commence ventilation using bag valve
mask (Ambu bag) with 1 % O2 followed by endotracheal intubation.
C. Circulation
Attach the patient to cardiac monitor. Treat any dysrrhythmias using ACLS
guidelines. Replace fluids lost by vomiting and/or diarrhoea.
D. Disability
Continuously assess the level of consciousness. Treat seizures promptly.
E. Exposure
In suspected dermal contact, undress the patient, wash with copious water and
mild detergent soap.
Treat seizures, coma, pneumonitis
Decontamination
• Gastric lavage by a large bore orogastric tube until returning fluid is clear
• Give activated charcoal through the tube
• Decontaminate skin (wash the part with water and soap) and irrigate eyes
with water/saline.
135
Specific treatment
Antidotes (Atropine and Pralidoxime)
• Atropine: Counteracts muscarinic effects only. The nicotinic effects
(fasciculations, weakness, paralysis) are not affected.Give Atropine 1-5mg,
iv slowly in adults and . 1- . 5mg/kg IV slowly in children. The dose may
be repeated at 5-1 minutes intervals as needed to achieve and maintain full
atropinization.
Check points for Atropinization
• Clearing of rales or drying of pulmonary secretions at lung bases is a sign of
full atropinization.
• Pupillary dilatation is not a good indicator
• Tachycardia is also not a good indicator as it can be due to nicotinic effect of
OPs, and also secondary to hypoxia.
• Atropine should be administered after maximal oxygenation in presence of
cyanosis to avoid ventricular arrhythmias.
• Atropinization must be maintained for hours or days depending on the
estimated severity of poisoning and response. Can give Atropine infusion
( . 2- . 8 mg/kg/hr), if needed.
• Pralidoxime* (2-PAM): Reactivates the acetylcholinestrase enzyme thereby
counteracts all toxic effects of OPs. However, it is most effective if given as
early as possible (within 24hours of exposure before the aging of the enzyme
occurs). Nevertheless, found useful even if given at a later stage, but
efficacy decreases.
• Adult dose: 1-2gm in 1 ml N/S iv over 15-3 min. May be repeated in 1
hr after the first dose, if weakness or fasciculations have not resolved. Can
give as continuous infusion (2 -5 mg/hr) for 24 hrs, up to maximum of
12g/day.
• Pediatric dose: 2 -4 mg/kg in 1 ml N/S iv over 3 min. Maitenance
infusion at 5 -1 mg/kg./hr after the initial bolus.
*The role of Pralidoxime in Carbamate poisoning is controversial. As per one view,
it is unnecessary because Carbamate enzyme complex is reversible and atropine
is quite effective in counteracting short-lived symptoms.
However, 2-PAM is indicated in Carbamate poisoning in case of:
• severe muscle weakness, fasciculations or paralysis
• excessive requirement of Atropine continues
• mixed OP and Carbamate poisoning suspected
Routine investigations to check response to treatment and prognosis include

ABGs, CBC, electrolytes, urea, creatinine, blood sugar, ECG, X-ray chest.
Special investigation: RBC and plasma cholinesterase levels, if available,
although clinical recovery doesn't exactly correlate with the levels.
136
Disposition and Follow-up
• Refer intentional poisoning for psychiatric consultation

• Follow-up OPs poisoning patient for 1-5 weeks after exposure for
intermediate syndrome or peripheral neuropathy.
Comparison of clinical features of organophosphate

and carbamate poisoning
Clinical feature Organophosphate Carbamate

Onset of symptoms Slow (hrs – days) Rapid (15 min-2 hours)
Duration of poisoning Up to 4 weeks 24 hours
Cholinesterase levels Depressed (≥25%) Transiently low
Antidotes Atropine + 2-PAM Atropine
Long term sequelae Many None
137
Management of Organophosphate Poisoning
Ask and • History of ingestion, name of pesticide, amount and duration since
Observe ingestion.Look for local contamination
• Solvent or garlic like breath odour
• Signs and Symptoms of Cholinergic Syndrome – vomiting, diarrhea,
abdominal cramps, bronchospasm, bronchorrhoea, miosis,
bradycardia, excessive salivation & sweating, dehydration, shock.
• Nicotinic Effects – muscle fasciculations, tremors & weakness
• CNS Effects – agitation, seizures, coma
• Pneumonitis may be present
Urgent Primary Survey and Interventions

Airway: Continue oro-pharyngeal suction. If airway at risk Intubate
Breathing: If spontaneous ventilation, give 100% O2 via non-rebreathing bag. If
inadequate ventilation, then ventilate with Ambu bag followed by intubation
(intubate all comatosed patients)
Circulation: Continuously monitor ,Replace fluids, Treat arryhthmias using
ACLS Guidelines
Disability: Continuously assess level of consciousness, Treat seizures, coma
Secondary Survey and Treatment
Decontaminate Antidote Treatment Investigate

• Gastric lavage for Atropine: 1-5mg iv every 5-10 min to CBC, S. Electrolytes,
large, recent achieve full atropinazation( drying of Urea, Creatinine,
ingestion (< 1 hr) pulmonary secretions) . Paediatric Blood Glucose, ABGs,
• Activated charcoal dose : (0.01- 0.05mg/kg iv) INR, LFT, 12 -lead
through tube Pralidoxime (2-PAM):1-2 gm in 100 ml ECG, X - ray chest
• Decontaminate skin N/S iv over 15-30min (Paediatric RBC and plasma
with soap and plenty dose : 20- 40 mg/kg over 30min) cholinesterase levels If
of water, protecting Repeat if necessary after 1 hr as available, but
yourself required or start maintenance iv treatment does not
• Decontaminate eyes infusion 1 g in 100 ml N/S at 200-500 depend on these levels
with water or saline mg/hr in adults (Paediatric dose: 5-
10 mg/kg/hr). Infuse till relief of
fasciculations/muscular weakness.
Treat associated Pneumonitis
Note • Carbamates produce similar clinical features & require only

atropine as antidote
• Refer all high risk patients to tertiary care
138
Pyrethrins and Pyrethroids
Pyrethrins are naturally occurring insecticides derived from Chrysanthemum
flowers. Pyrethroids are synthetic derivatives of Pyrethrins and are common
household insecticides used for killing insects including, head lice, mites, and
fleas of pets. They are widely used in agriculture for pest control and in public
health for vector control.
Common pyrethroids are Permethrin, Deltamethrin, Cypermethrin,
Fenvalerate, and Cyhalothrin. These are available in variety of brand
named products.
• Pif paf powder

• Xtra
• Tox plus
• Tox (V)
• Raid
• Pif paf low allergenic
• Pif paf odourless
• Baygone (against flying insects)
• Super cobra
• Zap
• PreVent shampoo (anti-lice)
• Chinese chalk
• Raid cockroach and ant killer
• Baygon against crawling insects *
* Pyrethroid is combined with organophosphates, or carbamates or
with piperonyl butoxide
Toxicity
Pyrethroids rarely cause systemic toxicity. The toxic oral dose is 1-2gm/kg, thus
a wide margin of safety. These cause cutaneous and inhalational allergic
139
reactions. The solvent present as vehicle in the formulation may produce its
toxicity.
Toxicokinetics
Pyrethroids are mainly absorbed by respiratory route. The absorption via GIT
and dermal routes are poor. They are rapidly metabolized in the body, and
therefore do not produce direct toxicity.
• History of exposure followed by symptoms involving respiratory,
cutaneous, ocular, gastrointestinal or neurological.
• Inhalation: Patient may present with itchy throat, oral and laryngeal
oedema, precipitation of wheezing and bronchitis in asthmatics.
Anaphylactic reaction or pneumonitis may also occur in hypersensitive
individuals.
• Dermal exposure: Burning, itching, parasthesia and numbness occur at
the site of exposure. There may be erythematous dermatitis with
vesicles/papules and intense pruritis.
• Eye exposure: There is eye irritation, stromal oedema and may be slight
corneal erosion.
• Ingestion: Small dose of dilute preparations do not produce systemic
effects because of limited absorption. Large ingestion of concentrated
solution (>5 ml) can cause nausea, vomiting, diarrhea, abdominal
cramps, dizziness, headache, tremors, seizures, coma and respiratory
arrest.
Diagnosis
• Dermal, respiratory gastro-intestinal or ocular symptoms
• No specific laboratory tests required
Treatment
• Symptomatic
• Treat asthma, anaphylaxis, seizures
• Decontaminate skin and/or eyes
• Do not induce emesis.
• Gastric lavage only indicated in large recent ingestions, after endotracheal
intubation (to avoid vehicle aspiration)
• Activated charcoal, may help in reducing GI absorption, though efficacy
remains unproven.
• Vitamin E oil applied on skin may relieve cutaneous paresthesias and
contact dermatitis.
Disposition and follow-up: Cutaneous, pulmonary and ocular symptoms
resolve with withdrawal from exposure and symptomatic treatment. Discharge
the patient with advise on prevention. Follow-up for large ingestions and
anaphylaxis is necessary.
140
Rodenticides: Superwarfarins
The most common agents to kill rats and mice belong to the Superwarfarins
group of anticoagulants. These are long-acting potent anticoagulants, which
can cause coagulopathy and bleeding in humans after accidental or intentional
ingestion.
Superwarfarin rodenticides available in Oman
Talon (Brodifacoum)
Rat Kill (Brodifacoum)
Ratak, Ramik (Diphacinone, Chlorophacinone )
Mechanism of action and Toxicokinetics
These agents inhibit hepatic synthesis of Vit. K dependent coagulation factors;
II, VII, IX, and X and anticoagulant proteins C and S. As synthesis of new
factors is inhibited, the anticoagulant effect is delayed till the circulating factors
are eliminated.
The main effect is prolongation of prothrombin time (PT). The onset may be
delayed up to 24 hours-4 days after ingestion and peak effect may be after 72
hours or later. The effect may continue for weeks to months after a single small
dose (1mg) ingestion.
Absorption by oral route is good and is highly bound to plasma proteins after
absorption. Metabolism is decreased in elderly and in patients with liver
disease, causing prolonged coagulopathy.
Toxic dose : Varies with each compound.
Clinical features
Patient may present after 24 hrs.-4 days of ingestion of rodenticide pellets/baits
or paste with ecchymoses, subconjunctival haemorrhage, epistaxis, bleeding
gums, hematuria, vaginal bleeding or hematomas (joints). There could be life
141
threatening massive internal hemorrhage presenting as abdominal pain,
hematemesis, melena, hematuria, shock, or intracranial bleeding.
Diagnosis and other laboratory investigations
• History of ingestion, asymptomatic for 24 hours – 4 days
• Prolonged prothrombin time and elevated INR. A normal PT after 48
hours of ingestion rules out the intoxication.
• CBC, blood typing/cross matching
• BT, PTT, platelet counts (to rule out other bleeding defects).
• Urine and stool examination for occult blood
• X-ray abdomen, joints
• MRI and neurosurgical consultation
Treatment
General measures
• Send blood sample for base-line PT, repeat everyday
• Treat shock with blood transfusion and fresh frozen plasma
• Gastric lavage is done only in large ingestions
• Administer activated charcoal with cathartic. Multiple dose activated
charcoal without cathartic is helpful.
Specific treatment
• Give Vit. K1 (Phytonadione) only in cases where PT is significantly
prolonged and signs of haemorrhage. Vit. K1 restores the production of
clotting factors.
Do not give Vit K1 prophylactically.
Do not give Vit K2, K3 or K4.
Dose of Vit. K1
Adults: 5-1 mg sc (in life threatening haemorrhage can give IV)
Child : 1-5 mg sc or orally
Can repeat the doses, monitoring with PT.

As high as 4 mg/kg/day in 3-4 divided doses may be required.
Be careful of drug interaction with other medications.
Deposition and follow-up
• Asymptomatic patients with history of exposure, check PT after 24 hours
and repeat at 48 hrs of ingestion. Instruct to come to A&E, if bleeding.
• In symptomatic hospitalized patients, manage with oral Vit K1, till PT is
normal.
142
Rodenticides: Zinc Phosphide
Zinc phosphide is available as dark gray crystalline powder having rotten fish
smell. It releases phosphine gas in contact with water or in GIT, if ingested.
Fatal dose 4 mg/kg orally

Ambient air level of 5 ppm phosphine gas is fatal
Phosphine is highly toxic to all vital organs. Exact mechanism of action is
unknown. It is metabolic poison at the mitochondria,and may affect the cell
membrane permeability of various ions and cause lipid peroxidation.
Clinical features
Onset of symptoms is within an hour if ingested, delayed with inhalation. Clinical
features include fishy breath odour, blackish vomitus, abdominal pain, diarrhoea,
dysrhythmias, cardiogenic (direct myocardial toxicity) and peripheral vascular
shock (vasodilation and hypotension). Patient may be agitated, anxious, drowsy
or in coma. CNS depression or convulsions secondary to shock can occur.
Pulmonary oedema (delayed adult respiratory syndrome), cyanosis, jaundice
may occur after 48-72 hours.
Death is due to cardiovascular collapse and renal failure.
Diagnosis and other investigations
• History of ingestion or inhalation
• Typical breath odour. Silver nitrate test is positive (blackening of filter
paper dipped in silver nitrate with phosphine in breath)
• Electrolytes, BUN, creatinine, LFT, ABGs, x-ray chest
Treatment
General measures
• Airway and ventilatory support. Administer supplemental oxygen (maintain
PO2 of 6 -7 mmHg). Endotracheal intubation and PEEP may be
required.
• Treat shock with Dopamine iv infusion
• Treat seizures with Diazepam
• Administer Na bicarbonate for metabolic acidosis
• Gastric aspiration and lavage only indicated within an hour of ingestion.
• Activated charcoal administration may help
• Give H2 receptor blocker (ranitidine iv)
• Intravenous administration of Magnesium Sulfate, 3gm bolus followed by
6gm infusion over 24 hours (3-3 mg/min) is useful to control polymorphic
ventricular tachycardias.
143
Disposition and follow-up
Symptomatic patients
• Patients should be observed for 48-72 hours after recovery for delayed
onset of pulmonary oedema
• Monitor LFT, jaundice and renal function
• Asymptomatic patients to be kept under observation for 3-4 days with
monitoring of vitals and routine investigations.
Note: Management of Aluminium phosphide is similar to Zinc phosphide.
For managing poisoning due to other obsolete and prohibited rodenticide

including:
Thalium
Sodium monofluoroacetate
Elemental phosphorous
Arsenic
Phenylureas
Contact Poison Control Centre if required
144
Poisoning due to Herbicide or Fungicide
Class Agent Toxicity on ingestion Treatment
1 Dipyridyls (H) Paraquat (20-37%) Highly toxic, corrosive, • Supportive

Diquat (8-36%) multiorgan toxicity • Low Fl O2 with
( banned) Burning pain, ulceration of PEEP
oral mucosa and pharynx, • Activated
salivation, stridor, aphonia, charcoal with
nausea, vomiting, single dose of
abdominal pain, diarrhoea, saline cathartic
GI bleeding, cough, • Gastric lavage
dyspnoea, CNS depression, may injure the
hypoxia (anxiety, agitation, mucosa further
confusion, seizures, coma, • No hemodialysis
metabolic acidosis),
myocardial ischemia,
cardiogenic shock, acute
renal failure, liver damage,
delayed pulmonary fibrosis,
and respiratory failure.
2 Chlorophenoxy 2, 4-D Cause hypermetabolic state • Supportive
acids (H) 2,45T (tachycardia, hyperpyrexia • Gastric lavage
MCPA diaphoresis, hypertonia, • Activated
Agent orange intense thirst), nausea, charcoal
(2,4- vomiting, abdominal pain, • Alkalinize urine
D+2,45T+TCDD) CNS depression, respiratory • No hemodialysis
( banned) depression, hypoxia,
acidosis, cardiac
arrhythmias, hypotension,
pulmonary oedema,
neuropathy, coma,
convulsions, hepatitis, renal
injury, chloracne
3 Pentachlorop Pentachlorophenol Hypermetabolic state • Supportive
henol and Dinocarp Headache, vomiting, fever • Gastric lavage
weakness, sweating
Dinitrophenol Dinoseb • Activated
(H&F) CVS, CNS and respiratory
symptoms as above. Met Hb
charcoal
Diffuse urticaria, chloracne • Treat
Death due to CVS collapse or methaemoglobina-
hyperthermia. Renal failure emia
4 Glyphosate Round-up Corrosive effect of the • Supportive

(H) surfactant in the compound • Treat as
Local GIT injury, bleeding corrosives
Hypotension, renal failure
5 Sodium Sodium chlorate Methaemoglobinemia • Supportive
chlorate (H) • Does not
respond to
methylene blue
• Sodium
thiosulfate used
145
Poisoning due to Herbicide or Fungicide
Toxicity on
Class Agent Treatment
ingestion
6.Metallic Copper oxychloride Severe GIT irritation
Compounds (H) (Nausea, vomiting, • Supportive
Copper sulphate diarrhoea), haematemesis • D-pentacillamine or
( H & F) Shock, hypoxia, cardio- • BAL or
Copper arsenate (H) respiratory and renal • DMSA
( banned) failure, jaundice
7. Diuron, Fenuron Low systemic toxicity • Supportive
Substituted ureas (H) Monolinuron Methaemoglobinemia after • Methylene blue
Chlortoluron 12-14 hours
8. Thiocarbamates Thiram GIT (nausea, vomiting, • Supportive

(H & F) Ziram diarrhoea) • Activated charcoal
Nabam CNS depression, • Do not give atropine
Meneb respiratory depression, or PAM
Zineb seizures
Mencozeb Extrapyramidal symptoms
Cycloate Peripheral neuropathy
Butylate Alcohol intolerance
( antabuse like reaction)
9. Organic Methyl mercury Not used because of severe Refer to section VI
mercury ( banned) CNS and peripheral
compounds nervous system, and renal
(H) toxicity
H = Herbicide F = Fungicide
Contact Poison Control Centre for details of specific poisoning management.
146
Corrosives
Agents that cause corroding injury to the tissues are termed as corrosives.
Most household washing & cleaning agents, bleaches and disinfectants and
some industrial chemicals are corrosives.
Types/Classifications
A. Acids
Hydrochloric Acid
Nitric Acid
Sulphuric Acid
Hydrofluoric Acid
Acetic Acid
Phosphoric Acid
B. Bases: Strong Alkalis
Ammonium hydroxide
Potassium hydroxide
Sodium hydroxide
Calcium hydroxide
Lithium hydroxide
Barium hydroxide
C. Oxidizers
Chlorine dioxide
Hydrogen peroxide
Dichromates (Sodium Potassium and Ammonium)
Sodium hypochlorite
Potassium permanganate
D. Phosphorous
Black phosphorous
Red phosphorous
White phosphorous
Sources of acids
1. Swimming Pool cleaners
Sodium bisulfite
Sodium hypochlorite
2. Toilet Bowl cleaners
Sodium bisulsite
Hydrochloric acid
Phosphoric acid
147
3. Batteries
Sulphuric acid
4. Metal cleaners
Nitric acid
5. Drain cleaners
Hydrochloric acid
Sulphuric acid
6. Anti-rust agents
Hydrofluroric acid
Oxalic acid
7. Disinfectants
Sources of alkalis
1. Lye – Lime, clinitest tablets, bleaches, oven cleaners, drain cleaners, toilet bowl
cleaners and disinfectants
Sodium hydroxide
Potassium hydroxide
Calcium hydroxide
Lithium hydroxide
Ammonium
2. Disinfectants
Sodium hypochlorite (clorox, bleach)
Calcium hypochlorite
Phosphates
Quarternary ammonium compounds
Phenol
Pine Oil etc.
3. Toilet bowl cleaners

Sodium metasilicate
Soda ash
4. Paint removers
Sodium hydroxide
Phenols
Cresols
5. Hair dyes,tints,bleaches
Ammonia
Hydrogen peroxide
148
6. Alkaline storage batteries /disk batteries
Potassium hydroxide
Lithium hydroxide
7. Photographic developer
Lithium hydroxide
8. Automatic dish washer detergent
Trisodium phosphate
Sodium metasilicate
Sodium carbonate
11. Portland cement

Calcium oxide
12. Low-phosphate detergents
Sodium metasiicate
Routes of exposure
Inhalation of dusts (solids) mists (liquids) or “fumes” (vapours)
Skin & mucous membranes
Ingestion
Toxicodynamics
1. Acids cause coagulative necrosis.
When an acid encounters body tissues, the hydrogen ion dissociates from its
accompanying anion (chloride, nitrate etc). The hydrogen ion denatures
biochemicals in the cells. This produces the burn that is characteristic of
acids. The burn is actually a coagulum. This acid produced coagulum helps
restrict the acid from burning deeper.
2. Bases cause liquefactive necrosis
When a base encounters body tissues the hydroxide anion (OH) dissociates
from its accompanying cation (ammonium, sodium etc). The hydroxide ion
denatures biochemicals in the cells. This produces the chemical burn or tissue
destruction called liquefactive necrosis. Unlike necrosis due to acids, this
necrotic tissue is not a coagulum, a scab. This, therefore, permits deeper
penetration of a base. Generally, bases are injurious at the site of contact and
are not significantly absorbed and distributed throughout the body to produce
systemic toxicity.
3. Laboratory investigations
Lab. studies should include the following
• CBC
• ABG
• Type & Cross-match
149
• Chest and abdominal X-ray studies in :
• suspected perforations
• foreign body localization (e.g. ingested alkaline batteries)
• Endoscopy in all patients regardless of symptoms

4. Oxidizers
When an oxidizer encounters body tissues, it reacts with the tissues,
oxidizing cellular components indiscriminately. The effect is corrosive
chemical burn with rapid tissue destruction. If systemically absorbed, many
oxidizing agents can cause haemolysis and oxidation of haemoglobin to
methaemoglobin.
5. White phosphorous
White phosphorous is a pyrophoric (fire-forming) material, igniting

spontaneously in air.
Most of the tissue damage from white phosphorous is due to its ability to
produce chemical and thermal burns. White phosphorous is also
systemically absorbed and distributed – this can result in kidney and/or liver
damage. There can be rapid cardiovascular collapse due to hypovolaemia
caused by chemical burns and by direct cardiotoxicity with pump failure
(cardiogenic shock) and dysrhythmias. White phosphorous combines with
endogenous calcium to produce hypocalcaemia, manifested by a prolonged
QT interval with a potential for torsades de pointes. Hypocalcaemia also
impairs inotropy resulting in decreased cardiac output.
The corrosive toxidrome

a) Respiratory system
Inhalation of corrosive gases, vapours, mists or dusts can cause irritation and
burns of the airway. The patient may complain of coughing, burning and
difficulty in breathing. Corrosive inhalation can cause laryngospasm,
bronchospasm, and oedema of the upper and lower airway.
Dysphonia, cough and throat tightness all suggest involvement of the upper
airways. Progressive hoarseness, stridor and aphonia herald catastrophic
upper airway obstruction.
b) Cardiovascular system
Corrosives directly affect the cardiovascular system by producing chemical
burns that damage the skin, resulting in hypovolaemia that is due to
evaporative fluid losses, loss of intravascular fluids from damaged blood
vessels, and “third-spacing” of intravascular fluids into oedematous tissues.
Hypoxaemia and hypovolaemia can produce myocardial ischaemia which
may lead to myocardial infarction, tachydysrhythmias and cardiac arrest.
150
Oxidizers can produce true anaemia due to haemolysis or functional anaemia
due to methaemoglobinaemia.
Either anaemia can result in tachycardia.
Significant white phosphorus burns or ingestions can cause hypocalcaemia
that results in a prolonged QT interval, negative inotropy and dysrhythmias.
c) Nervous system
If the corrosive injury causes hypoxaemia and hypovolaemia, these then can
cause CNS dysfunction with anxiety, confusion, agitation, seizures,
decreased level of consciousness, coma and even death.
Oxidizers sometimes cause severe haemolysis and/or methaemoglobinemia

that can result in hypoxic central nervous system effects.
White phosphorous burns or ingestions can result in systemic toxicity that

produces hypocalcaemia which can cause tetany and seizures.
d) Skin and mucous membranes
Corrosives cause chemical burns of the skin and mucous membranes. The
burn severity depends on the concentration of the corrosive and the duration
of contact. The patient usually complains of pain at the burn site. If the eyes
are involved, the patient usually complaints of severe pain and chemical
burns of the eyes can lead to blindness.
Acid chemical burns produce coagulative necrosis of tissues. The
coagulation that is formed is similar in appearance and feel of the eschar of a
thermal burn.
Base burns produce liquefactive necrosis of tissues and these look and feel
slippery and soapy.
e) Gastrointestinal system
Corrosive ingestion can cause severe injury to the oropharyngeal tissues with
difficult breathing, drooling, difficulty in swallowing and catastrophic
oesophageal injury such as oesophageal perforation with
penumomediastinum. Ingestion of a corrosive causes chemical burns of the
G.I. tract with abdominal pain, nausea and even vomiting of bloody stomach
contents. Gastro intestinal tract perforation can occur.
Ingestion of concentrated hydrogen peroxide solutions can produce fatal air
embolism. Vomiting and diarrhoea due to white phosphorous can be
luminous and smoking. Smoking stools are virtually pathognomonic of
significant white phosphorous ingestions.
151
f) Liver
Most corrosives have no direct effect on the liver. White phosphorous is the
only exception where burns or ingestions can produce systemic toxicity
resulting in delayed liver damage and even liver failure.
g) Genito-urinary system
Most corrosives have no direct effect on the kidneys. White phosphorous is
the major exception. Significant white phosphorous burns or ingestions can
produce systemic toxicity resulting in delayed renal insufficiency and even
kidney failure.
Corrosive management
The duration of contact i.e. the time interval between contact with a corrosive
and its decontamination with copious irrigation with water or normal saline, is
the major determinant of the clinical outcome for patients with corrosive
chemical burns.
Primary survey and resuscitation
A = Airway
The airway is at risk because of inhalation or ingestion of corrosives. Suction
the airway as needed. Endotracheal intubation should be done as soon as
possible when there are oropharyngeal burns or oedema, dysphonia, aphonia,
stridor or other signs of impending upper airway obstruction.
B = Breathing
For patients with adequate spontaneous ventilation, consider high flow oxygen
at 15 litres per min via a non-rebreather, reservoir mask. Patients with
inadequate spontaneous ventilation should be initially ventilated with a bag
valve mask using 1 % oxygen, then endotracheally intubated and ventilated.
For bronchospasm, salbutamol by nebuliser should be administered. Positive
end expiratory pressure (PEEP) may improve oxygenation and ventilation that
are impaired by noncardiogenic pulmonary oedema.
C = Cardiovascular
Cardiovascular monitoring is needed for all patients with significant burns. If
dysrhythmias occur, follow ACLS guidelines. An iv infusion of normal saline
should be commenced on all patients with moderate to severe symptoms.
Monitor the patient for shock and treat accordingly.
In the setting of white phosphorous burns or ingestions, a prolonged QT
interval with signs of cardiogenic shock should be treated with intravenous
calcium. 1 % calcium chloride (1 – 3 ml) for adults and .2 – .3 ml/Kg for
children.
D = Disability
The patient’s level of consciousness should be assessed continually. If
seizures develop, despite adequate oxygenation and blood glucose, then treat
the seizures with iv Diazepam (1 mg for adults and .1 mg/kg for paediatric
patients). Any altered mental status, seizure activity inco-ordination or visual
152
changes require 1 % oxygen administration. In the setting of white
phosphorous burns or ingestions, signs of hypocalcaemia such as tetany
should be treated with intravenous calcium .
E = Exposure
For all contacts with corrosive liquids or solids, ensure that the patient is
undressed and adequately decontaminated .
Poisoning treatment paradigm

A = Alter Absorption
Remove the patient from the source of poison. Ensure adequate skin and eye
decontamination, if they came into contact with corrosive liquids or solids.
Skin decontamination involves removal of all clothing, jewellery, shoes etc.
Chemical burn blisters should be broken since the blister contains the
offending corrosive. The patient should then be washed with large quantities
of water for at least 15 mins. Water is sufficient because acids, bases and
most oxidizers are usually water soluble. Pay close attention to exposed skin
in skin folds, the axillae, the genital area and the feet.
Skin decontamination of white phosphorous requires its rapid removal,
because it is embedded in the skin.
Calcium glucanate gel is applied locally for hydrofluoric acid exposure

Eye decontamination is carried out by flushing the eyes with large quantities
of water in sterile saline solution, initially for 2 min and for as long as it is
necessary. The best end point of irrigation is restoration of the conjunctival
sac to a pH of 7.
Respiratory decontamination This is accomplished by removing the patient
from the source of air borne exposure. The most important method of
decontamination is adequate ventilation. Ensure adequate ventilation and
oxygenation.
Gastrointestinal decontamination
Gastric lavage and emesis are contraindicated in caustic ingestion as they
may lead to perforation of the oesophagus or cause an aspiration. Patients
with a caustic injury should not receive any oral fluids until they can
swallow their own saliva. The primary forms of initial management is to
prevent vomiting.
Button battery ingestion may require endoscopic removal
Activated charcoal and cathartics are also contraindicated because they
may lead to complications in addition to the fact that charcoal is a poor
adsorbent of caustic agents.
153
Dilution with water may be carried out with caution and using a small quantity
because of the risk of vomiting and aspiration. Dilution is contraindicated in
patients with acute airway swelling and obstruction or in those with clinical
evidence of oesophageal, gastric or intestinal obstruction. It must be
remembered that after strong acid ingestion dilution with water is
inappropriate. The heat produced by the dilution of concentrated sulphuric
acid with an equivalent volume of water in a closed space results in a
temperature of approx. 8 °C.
Neutralization
Alkalis
There are some experimental data that protein containing diluent such as milk
may be of value when hypochlorite has been ingested.
Acids
Contraindicated because this produces an exothermic reaction as stated.
A = Antidote Adminstration
None for acids and bases.
In the setting of oxidizer poisoning Methylene blue can be used for clinically
significant methaemoglobinaemia.
Dose: Adults and Paediatric ( Methylene blue )
1 – 2 mg/kg IV, slowly over 5 min. The dose can be repeated in 3 –
6 min, if symptoms persists. If no response after two doses do not
repeat again (consider G6PD deficiency)
B = Basics
Continually reassess the patient’s ABC and treat accordingly.
C = Change catabolism - Not applicable
D = Distribute Differently - Not applicable
E = Enhance Elimination - Not applicable.
154
Management of Corrosive Poisoning
• History of ingestion, product type, amount and time since ingestion
Ask &
• Local redness, pain, blistering (mouth, skin, eyes)
Observe
• Drooling, difficult swallowing, abdominal pain, nausea, bloody vomiting
• Hoarseness, stridor, aphonia, dysphonia, wheezing, difficult breathing
• Shock, dysrhythmias
• Coma, Seizures
Airway: Suction, endotracheal intubation as required.

Breathing: If spontaneous ventilation present, give high flow oxygen at 15 L/min.
If not then ventilate with bag and mask using 100% oxygen and intubate.
Circulation: Treat shock with fluids. Treat dysrhythmias using ACLS guidelines.
Disability: Monitor level of consciousness, treat seizures, treat coma.
Get flexible endoscopy done to evaluate GI injury
Conduct Secondary Survey, Investigations & Treatment
• Do not perform gastric lavage

• Do not give activated charcoal
• Can give small quantity of water / milk, if patient can swallow
his saliva & if weak acid/alkali has been ingested
Decontaminate Investigate
• Wash skin and eyes with copious • X-ray chest and abdomen
water for 15-20 mins • CBC, electrolytes, ABGs, Blood Glucose,
• Get ophthamological examination Blood Typing & Cross Matching
• Apply Ca gluconate gel on HFl burns • ECG
Referral Refer all high risk patients (consult manual) and oxidizer
Guidelines ingestions
Note • Household bleaches and disinfectants usually are dilute

solutions and can cause mild self limiting GI irritation
155
Hydrocarbons
Organic compounds containing hydrogen and carbon molecules are hydrocarbons.
These are mostly petroleum distillates or fractions and are mixtures of hydrocarbons.
Turpentine and pine oil are products of pinewood distillation. Hydrocarbons are widely
used as solvents or fuels in petroleum, plastic, agricultural and chemical industries. Also
used in household products as fuels, solvents, degreasers, furniture polish, lighter fluid,
paint-thinners, paint and nail polish removers, typewriter correction fluid, shoe polish,
furniture varnish, household cleaning and disinfecting agents, adhesives and glues,
propellants and refrigerants. Sometimes, incorporated as solvents with pesticides,
camphor, aniline, nitrobenzene or heavy metal compounds.
Common hydrocarbons and risks of toxicity

Risk after ingestion
Compound Inhalation toxicity
Aspiration Systemic Toxicity
Petroleum distillates
1. Aliphatic (low
viscosity)
Gasoline Hypoxia and CNS High-risk Low-risk
Kerosene depression (chemical Local GIT irritation (nausea,
Petroleum ether pneumonitis) vomiting)
Naphtha
Mineral spirits
Lighter gas oil
Mineral seal oil
2. Aliphatic (volatile)
Methane Asphyxia & CNS No risk CNS depression
Ethane depression
Propane
LPG
3. Aliphatic (High
viscosity) No risk No risk No risk
Mineral oil
Motor oil
Petroleum jelly
4. Aromatic (Low - CNS depression, High risk of CNS

viscosity and high convulsions and coma depression, respiratory,
volatility) - Pulmonary oedema cardiac , GIT and renal
Benzene - Respiratory arrest, High risk toxicity
Toluene cardiac arrhythmias
Xylene
5. Chlorinated CNS depression. High risk CNS depression,

hydrocarbons (Low Convulsions, coma, respiratory depression
viscosity, high volatility) respiratory arrest, cardiac cardiac arrhythmias, and
Methylene - chloride arrhythmias hepatic, renal and GIT
Carbon tetrachloride toxicity
Trichloroethylene
Tetrachloroethylene
Wood distillates Low-risk High-risk Low
Turpentine (Mild CNS depression)
Pine oil
Solvent for pesticides, Varies with type of solvent High-risk Specific toxicity of
Camphor, Metals, Used with these additives
Aniline, Nitrobenzene compounds compounds
All compounds, except those with high viscosity, are locally irritant to skin and eyes.
156
Long-term repeated exposure to some aromatic and chlorinated compounds can result in
hematologic (benzene) neuropsychiatric (Toluene) and carcinogenic (benzene) effects
Toxic dose
Varies with the agent and whether it is aspirated, ingested or inhaled. Few ml of
kerosene or diesel can cause severe pneumonitis.
Kerosene or Gasoline exposure
Ingestion High risk of aspiration, no systemic toxicity, as not absorbed from GIT.
• Burning in mouth and throat
• Nausea, vomiting, abdominal pain
• Coughing, gagging, choking, tachypnea, bronchospasm, wheezing, cyanosis,
intercostal and subcostal retraction, rhonchi, rales, tachycardia (indications of
aspiration, appear within 3 minutes of ingestion)
• Lethargy/irritability (due to hypoxia)
• Mild fever
• Absence of above symptoms and signs within 4 - 6 hours of ingestion rules out
chemical pneumonitis due to aspiration.
• In severe cases, pulmonary oedema, haemoptysis, shock, cardiopulmonary
arrest, convulsions are reported
• Persistence or development of fever after 24-48 hours of ingestion suggests
bacterial lung infection.
Investigations
• X-ray chest
Increased bronchovascular markings and bilateral basal and perihilar infiltrates
segmental atelectasis and local air trapping (findings positive between 3 minutes
– 24hours). Lobar consolidation, pleural effusion, pneumothorax and
pneumomediastinum are less common findings. Resolution of pulmonary findings
takes 2-4 weeks.
• ABG, BUN, Serum electrolytes, creatinine, blood glucose, ECG, CBC, LFT
Management
• Asymptomatic patients with history of ingestion must be examined for any
pulmonary involvement, X-ray chest to be taken on admission, patient is
observed for 6 - 8 hours, if remains asymptomatic with normal repeat X-ray
chest, then discharged.
• All symptomatic patients to be admitted in ward or ICU, depending on
severity.
• Take X-ray chest and monitor ABG, ECG, send for other investigations
• Provide basic supportive care (ABC)
Administer supplemental oxygen. Treat bronchospasm.
• Other respiratory treatment modalities such as assisted ventilation and PEEP
should be considered as per standard indications.
• Do not use corticosteroids or prophylactic antibiotics.
Note: Do not induce emesis or do gastric lavage as it will increase
aspiration. Similar protocol to be followed for other aliphatic petroleum
distillate ingestions having risk of aspiration.
157
Acute Exposure to Toluene, Xylene, or Benzene or Halogenated
Hydrocarbons
Toluene and Xylene are very common aromatic solvents and are constituents of
household products. However, workers in refinery and other industries may also
get exposed to toluene or benzene. Exposure can occur through ingestion,
inhalation and skin
These cause CNS depression and may sensitize the myocardium to arrythmogenic
effects of endogenous catecholamines. Aspiration pneumonitis can occur. Cause
mild irritation or chemical burns on skin.
Toxic dose
Toluene and Xylene: 15-2 ml can cause serious toxicity, 6 ml is fatal
Benzene – 1 ml is lethal when ingested. Inhalation of 5 ppm is lethal.
Trichloroethane / Trichloroethylene 5ml/kg and 1 ppm toxic
Carbon tetrachloride: 1 -2 ml toxic
Ingestion
• Vomiting, haematemesis
• Diarrhoea
• Signs and symptoms of aspiration
• Headache
• Dizziness
• CNS depression
Inhalation
• Nausea
• Euphoria.
• Dizziness and blurred vision
• Headache
• Weakness
• Delirium
Exposure to high concentration
• Convulsions
• Coma
• Pulmonary oedema
• Respiratory arrest
• Arrhythmias and death
Renal and hepatic injury occurs with halogenated compounds
158
Chronic exposure: (Inhalation abuse)
Haematologic effects are common with Benzene. Signs of permanent CNS
impairment, neurobehavioural changes, tremors and ataxia, myopathy,
neuropathy, hypokalemia and renal damage common in Toluene abusers.
Glue sniffers can come in A&E with neuropsychiatric symptoms or in coma,
convulsions, arrythmias, cardiopulmonary arrest
Diagnosis
• History of acute exposure or acute on chronic
• Typical CNS effects
• Signs and symptoms of aspiration pneumonitis
• CBC, electrolysis, BUN, creatinine, LFT, ECG, X-ray chest, CPK.
• In Toluene abusers, low urine pH, hypokalaemia, haematuria, proteinuria
(renal tubular acidosis) are characteristic.
Treatment
• Emergency support (ABC)
• Treat coma, seizures, and bronchospasm, as per standard protocol
• Treat arrythmias with propranolol (1-2mg iv) or esmolol (25-1 µg/kg/min iv)
Decontamination
• Irrigate skin and eyes with water
• Do not induce vomiting because of danger of aspiration and abrupt onset of
coma and convulsions
• Gastric lavage only in recent large ingestions (>3 ml within 3 minutes) or in
cases of solvent with toxic additive (camphor, pesticide, heavy metals,
carbon tetrachloride)
• Activated charcoal orally or through nasogastric tube beneficial
• No role of haemodialysis.
Psychiatric follow-up in chronic abusers.
159
Management of Hydrocarbon Poisoning
Kerosene/Petrol Toluene/Xylene/Benzene/Chlorinated HC
Ask & • Haematemesis, diarrhoea
• Burning mouth & throat
• Nausea, vomiting, abdominal pain
Observe • Headache, dizziness
• Cough, choking, tachypnoea, • CNS depression
wheezing, cyanosis • Cough, choking , tachypnoea, wheezing,
• Mild fever cyanosis
Severe: Pulmonary oedema, coma, • Pulmonary oedema, coma, convulsions
convulsions
If Chronic abuser
• Neuro-behavioral symptoms,
tremors, ataxia, myopathy, cardio -
pulmonary arrest
• Treat Bronchospasm & Pneumonitis

• Treat Coma, Seizures, Arrhythmias as necessary
Conduct Seconday Survey, Investigations & Treatment
Decontaminate • Do not do gastric lavage * Investigate

• Skin and eyes • Give activated charcoal • CBC, BUN, Creatinine,
with water through nasogastric tube LFT, ECG, X-ray chest,
CPK, Serum electrolytes
(hypokalemia & low urine
pH in toluene ingestion)
Referral Refer all high risk patients

Guidelines
Note • For all asymtomatic patients, take x-ray chest, observe for
6 hrs, repeat x-ray chest. If normal then discharge
* Consult Poison Control Centre if required
160
Table VI : Generally Non -Toxic Household Items
Personal-use Items Toys

Bath oils
Body conditioner Toy cosmetics
Bubble bath Bath tub floating toys
Cologne (low alcohol content) Caps (or toy guns)
Cosmetics Etch-a-sketch
Hair spray and hair tonic Play-Doh
Hand lotions Silly Putty
Lipstick Teething rings
Petroleum jelly (Vaseline)
Rouge
Shampoo (small amounts)
Shaving cream Art Supplies
Soap Ballpoint pen ink
Sunta lotion Chalk
Thermometer (mercury ingestion, Charcoal
not the glasses) Clay
Toothpaste Crayons (marked A.P., C.P.)
Felt-tip pens
Medications Pencils (graphite)
Antacids Rubber cement
Antibiotic (with some exceptions) Watercolors
Calamine lotion White glue without solvent
Birth control pills
Corticosteroids
Hydrogen peroxide 3%
Mineral oil Miscellaneous
Zinc oxide Candles
Zirconium oxide Cigarettes (small amounts)
Silica gel
Cleaning Product Grease and motor oil
Household bleach Incense
(2-5% sodium hypochlorite) Lubricating oil
Laundry detergent ( dilute liquids) Putty and spackle
Fabric softener
161
Table VII : Potentially Dangerous Household Products
Products Potentially Hazardous Agent
Disinfectants
Cresol, phenol. Hexachlorophene
Cleaning agents and solvents
Sodium hypochlorite >2.5%, oxalic
Bleaches
acid, perborates, and boric acid
Window cleaner Ammonia
Ammonia, turpentine, naphthalene
Carpet cleaner
trichloroethane
Oven cleaner Potassium and sodium hydroxide
Dry cleaning fluids and spot Trichloroethane, petroleum
removers distillates, perchloroethylene
Paints ,varnishes , nail polish Turpentine, xylene, toluene,
remover methanol,
Methylene chlroride, acetone
Emissions from heating or cooling
devices
Nitrogen oxide
Gas stove pilot light
Indoor use of charcoal grill Carbon monoxide
Leak from refrigerator or air - Freon
conditioner
162
Section VI
Management of Poisoning
due to Some plants,
Lead & Mercury
163
164
Datura fastuosa (Datura metel)
Common names: benj, murhana

‫ ه‬Arabic :
Synonyms: Datura Chlorantha (hook), Downy thorn apple, horn of plenty
Family: Solanaceae
Toxic parts
All parts are toxic and contain tropane like alkaloids, atropine, hyoscyamine and
scopolamine. Accidental ingestion of seeds is common in children,
Dermal contact with leaves or flowers can cause dermatitis.
Clinical features
Resemble anticholinergic syndrome (disorientaion, agitation, ataxia, verbal and
auditory hallucinations, seizures, tachycardia, flushed skin, dilated pupils,
hyperpyrexia, urinary retention).
Severe poisoning can lead to respiratory failure, CVS collapse and death. Mild to
moderate poisoning resolves completely after treatment.
Management
Supportive (ABCDEs)
• Treat convulsions and hyperthermia
• Gastric Lavage and activated charcoal with a dose of cathartics, if seeds
have been ingested.
• Physostigmine can be given carefully 1-2mg slow iv injection not exceeding
4mg for refractory seizures.
(Keep atropine ready which may be required in case of over dose of
Physostigmine ).
Indications for Physostigmine
Severe CNS symptoms and seizures not responding to other drugs.
Supraventricular arrhythmias not responding to standard treatment.
165
Calatropis procera
Common name: Ashkhar, shakhr, Ushar, Oshur

Arabic : ‫ ر‬- ‫أ‬
Family: Asclepidaceae
Toxic Parts
All parts are poisonous, specially leaves and the latex. Leaves and stem contain
calatropin and calatropagenin. The latex contains glycosides, usacharin, clatoxin,
calactin and may contain cardenolides. Besides the glycosides, this plant also
contains oxalates, proteolytic enzymes and an unidentified allergen.
Toxicity
The sap (latex) is known to cause skin and gastrointestinal irritation. Ingestion may
lead to symptoms due to cardenolides and include vomiting, depression,
weakness, incoordination, seizures, respiratory paralysis, intestinal stasis and
myocardial toxicity. Calotropis has vesicant latex that may cause severe reaction
on skin, and mucous membranes. Ingestion may cause intense irritation and
burning sensation of the mouth. Pharyngeal or laryngeal, edema may be present.
Large quantities of plant parts are seldom swallowed.
Eye exposure may result in severe keratoconjunctivitis.
Decontamination
Exposed eyes should be irrigated with copious amounts of tepid water for at least
15 minutes. If irritation, pain swelling, lacrymation, or photophobia persists ,the
patient should be examined by an ophthalmologist..
Skin is decontaminated with thorough washing; calamine lotion may be applied
locally.
Treatment
Supportive
Treat seizures
166
Dieffenbachia seguine
Common name: Dumbcane
Arabic : ‫دو
ن‬
Family : Araceae
Toxic Parts
The plant belongs to the family Araceae. It is an ornamental plant.
All parts of plant are poisonous including the sap. Toxicity is due to crystals of
calcium oxalate and toxic proteins in sap and leaves.
Clinical features
Ingestion is common in children and can cause burning pain in lips, mouth
followed by inflammation of lips, tongue, buccal mucosa, palate, and larynx,
making speech difficult. In severe cases, acute laryngeal oedema may develop and
cause difficult respiration. Sometimes severe retrosternal pain occurs due to
oesophageal inflammation and necrosis. Oropharyngeal oedema may subside in 2-
3 days while inflammation persists longer. Skin contact may cause dermatitis and
contact with eyes leads to marked burning, and inflammation.
Treatment
• Eye and skin decontamination with copious water.
• For ingested leaves or sap, give cold milk, ice, antacids
• Administer antihistamine or steroids in severe respiratory distress
• Analgesics for local pain
• Rarely endotrachial intubation may be required
167
Nerium oleander
Common name: Habban
Arabic : ، ، ،‫ـــن ن‬
Synonyms: Wild oleander, Pink oleander, Lilly of valley
Family: Apocynaceae
Desert rose
Thevetia peruviana ( yellow oleander )
It is wild in wadis near water and is also cultivated.

Toxic parts
All parts of the plant are poisonous. Cardiac glycosides (oleandroside and
nerioside) are present in all parts.
Ingestion
Ingestion of few flowers or seeds (Kernels) by children can be fatal. Even using
wood for cooking and inhalation of smoke can be poisonous.
Ingestion of leaves, flowers or seeds can initially lead to burning sensation in the
mouth, tingling of tongue, dryness of throat, nausea, vomiting and diarrhoea. If
large quantity is ingested, the person/ child may become drowsy, confused, pale,
and cold extremities. All types of dysrhythmias (bradycardia, SVT, heart block,
ventricular ectopics and ventricular tachycardias) along with hypotension have
been reported. Hyperkalemia occurs early as seen in digitalis overdose. Metabolic
acidosis results due to impaired tissue perfusion.
168
Inhalation
Acute haemolysis may occur due to smoke inhalation. Prolonged inhalation can
cause cardiac toxicity.
Dermal exposure
Sap of the plant may cause local skin irritation and inflammation.
Management
Supportive (ABCDEs)
• Gastric Lavage may not be effective.
• Adminster activated charcoal
• Administer Cholestyramine 4gm orally four times a day in adults that may
reduce the absorption of cardiac glycosides in the gut.
• Routine investigations specially serum potassium, ABG and ECG to be
monitored.
• If serum Potassium is >5.5 mEq/L,give .5g/kg glucose with Insulin(o.1u/kg iv)
and administer Sodium bicarbonate (1mEq/kg). Sinus bradycardia, ventricular
ectopics and AV block are treated with iv Atropine, .5-2 mg .
• Follow standard ACLS protocol for other dysrhthmias.
• Avoid quinidine, procainamide or bretylium.
Specific Antidotes. Fab fragments of Digoxin specific antibodies (Digibind) is
indicated for significant poisoning ( severe hyperkalemia and resistant
dysrhthmias).
Dose, refer table on Antidotes
NB: The Yellow oleander (Thevetia peruvina) is more cardio -toxic and can
produce life threatening poisoning if seeds or plant extract is ingested.
169
Table VIII : Plants Known To Cause Gastrointestinal
Irritation & Dermatitis
‫اء‬ Common Botanical Toxic part/

‫ا‬ Names Name
Family
Component Toxicity *
‫"!ت‬ Shiltaat Sisymbri- Cruciferae Isothiocya- The seeds have a hot, sharp
um irio nate in taste and are rubifacient and
seeds vesicants for skin.
‫ي‬ Ffafy, Carica Caricaceae The leaves The milky sap is very irritating,
Fifaiy, papaya and unripe ripe fruits are much less so.The
Faifai, fruit sap may produce conjunctivitis.
Papaya, contain a Papain may produce allergic
Pawpaw milky sap, manifestations. A powder made
from the seeds is irritating to the
which
Skin. Seeds contain the
contains thioglucoside glucotropaeolin.
the The pulp contains the enzyme
proteolytic myrosinase that may release a
enzyme "mustard oil" from the seeds.
papain. Eating the fruit may cause
The roots yellow coloration of the palms
have and soles. An increase in
rubifacient haemorrhagic tendency is not
action. ruled when there is a
coagulation disorder. It can
increase INR if given with
warfarin.
،$'; Handal, Cirullus Cucurbitace- Plant Severe abdominal pain,
،<ّ Murrah, colocynthis ae vomiting, diarrhoea (often
?'ِ ِ Hedeg, bloody and watery), muscular
‫ري‬Q، soori weakness, prostration and
delirium. Severe nasal pain may
result from contact with the
nasal mucous membranes to the
powdered form. A fatal dose is
near 4 to 6 grams.
‫د‬Q Oud Dianthus- Caryophyll Plant Dermatitis.
"Y‫ا‬ alhilbah deserti -aceae
ّ' Madhyad, Convolvulus Convolvula Roots Dermatitis and Purgative effect
Fadhakh, arvensis
،['\، -ceae
]" Olleiq
Hamar Caesalpinia Leguminosae: Leaves The extracts of leaves are used
pulcherrima Caesalpinio Tannins as a laxative and to regulate
iodeae menstruation..May cause
profuse vomiting and diarrhoea
after a 0.5 to 6 hour delay
170
‫اء‬ Common Botanical Toxic part/
‫ا‬ Names Name
Family
Component Toxicity
Pride of Caesalpinia Leguminosae: Seeds & Vomiting, diarrhoea, , drowsiness,
Barbados gilliesii Caesalpinioi pods and vertigo. Symptoms may
odeae especially develop within 30 minutes and
green as well recovery usually occurs after 24
as leaves & hours. Poisonings have resulted
roots contain from ingestion of 5 seedpods.
an irritant
substance of
unknown
composition
Hydrocyanic
acid is found
in the leaves.
‫د‬Q Ud Paeonia Paeoniace

Vomiting and allergic dermatitis.
^"_‫ا‬ alsaleeb officinalis ae
،` Saber, Aloe Aloaceae Barbaloin, an If ingested a purgative action
barbadensis anthracene may result. Irritant action on the
$` Saqal, glycoside with
(Aloe vera) colon, often congestion.Long
$`‫ا‬ Isqil purgative
Aloe, action. term use might cause
Aloe root hypokalemia, inhibition of
intestinal motility, Allergic
contact dermatitis and cases of
severe dermatitis after
application of aloe vera
preparations in an area
previously subjected
to chemical peel or
dermabrasion are reported.
Chronic use of aloe extract can
lower serum glucose levels in
diabetic patients.
May colour alkaline urine red.
Allergic contact dermatitis is
{\_ Lasafa,Ff reported when extract of the
Capparis
{‫ه‬Q‫~آ‬، akouha, Plant plant is applied as a wet
Spinosa Capparaceae
compressor
، shafallah
{ Geygeh, Pergularia Asclepiadacea Contains Abysinians used this plant for
,{"، ghalaqah tomentosa ghalakkinos making poison arrows. Latex
‫ة‬ ,shajarat ide, a rubbed on skin or eyes can
‫د‬Q"‫ا‬ al-jalood cytotoxic cause inflammation and pain,
cardiac and if ingested can cause
glycoside, a stomach cramps and diarrhea.
possible (Note that this plant is used in
anti-tumor traditional medicine for skin
agent and problems and as an
calactin a expectorant).
related
glycoside.
* Patient needs symptomatic treatment
171
Lead Encephalopathy
Lead is a toxic heavy metal. It is used in various industries (batteries, paint, cable
sheathing, pottery, glazing, brass, bronze, steel, ammunition, solder, pipes,
printing, etc.). It may contaminate food, water and soil and get ingested. Some
traditional remedies like Bint Al-Dahab, contain high amounts of inorganic lead.
This is given to children orally as general tonic or for chronic constipation. Such
practice in Oman is common and has been the cause for lead encephalopathy.
Use of Al-kohl locally on the umbilical stump of the newborns has caused severe
neurological toxicity.
• Inorganic lead is not significantly absorbed from skin, but is largely absorbed
through ingestion or inhalation. Local eye application of Al-kohl (eye
cosmetic) may not get absorbed from eyes or skin but can be ingested by
small children through hand-to-mouth activity.
• Ingestion by children of paint chips, soil, fishing weights or Bint al dahab can
result in acute lead toxicity and encephalopathy.
• Chronic oral exposure through food, water, soil, traditional medicines or from
para-occupational sources (from occupational exposure of father) can lead
to accumulation of lead in the body (soft tissues and bones). Iron and
Calcium deficiency increases the absorption of lead in GIT and blood lead
levels. Increase in blood lead levels up to >8 µg/dl after chronic exposure,
can cause acute lead poisoning and may manifest as encephalopathy.
Mechanisms of Toxicity
• A number of enzymes are inhibited (SH-containing, haeme synthesizing,
cellular and mitochondrial)
• Interacts with essential cations (Ca, Zn, Iron)
• Interferes with neurotransmitter release and nucleotide metabolism
Encephalopathy is due to capillary fluid extravasation and loss of neuronal cells in
brain.
Clinical presentation of lead encephalopathy
• History of acute onset
Lethargy, headache
Sudden onset of persistent vomiting
Vertigo
Ataxia
Restlessness
Visual disturbances
Excitement/delirium
Convulsions
Coma
• History of chronic symptoms as constipation, abdominal pain, vomiting,
muscular pain and weakness followed by acute episode as above.
172
Diagnosis
• History of exposure to lead (usually a traditional remedy) and clinical features
• Blood lead levels >8 µg/dl in children and >1 ug/dl in adults
• Abdominal X-ray showing radio - opaque specks in GIT
• Elevated free erythrocyte protoporphyrin or Zinc protoporphyrin (ZPP)
(>35µg/dl)
• Basophilic stippling of erythrocytes
• Anaemia (normocytic, normochromic)
Treatment
Emergency and supportive
• Treat seizures with Diazepam
• IV fluids (monitor carefully), avoid over hydration
• Increased intracranial pressure may benefit from Dexamethasone 1 mg iv
and Mannitol 1g/kg iv- may repeat .5g/kg every 4 hrs. as necessory
Antidote treatment
• Give Calcium Disodium EDTA 3 mg/kg, deep intramuscular (im) injection in
2-3 divided doses (8-12 hourly) or slow iv infusion diluted to 2-4 mg/ml in 5%
dextrose or normal saline, continue treatment for 5 days.
• Some times BAL 4 – 5 mg/kg ( 75mg/m ) is given initially by deep im 4 hrly
for 2 days and then 12hrly along with Calcium Disodium EDTA for 5 days
• An additional course may be considered based on post-treatment lead levels
after 2 days.
• Assess for any rebound increase in blood lead level after 2 weeks of
treatment.
Decontamination
• Perform gastric lavage
• Activated charcoal may help
• Consider whole bowel irrigation or repeated cathartics, if X-ray still shows
metallic lead flakes/object.
Discharge
• Follow-up for sequelae (epilepsy, dystonia, optic neuropathy, mental
retardation)
• Identify and advise to abate the source of lead
• Call poison centre for follow-up and prevention of exposure
• Blood lead levels <45 ug/dl in children do not require chelation
Note: Facility for blood lead levels is now available at Poison Control Centre,
Directorate of Environmental Health
Instructions for blood sample collection and transportation
Venous blood sample to be collected after thoroughly cleaning the venepuncture site
with spirit swabs (to avoid contamination of sample with lead in the dust deposited on the
skin).
2.0ml of whole blood in BD vaccutainer containing 3.6mg of EDTA (Purple cap)
Discard clotted or haemolyzed sample.
Keep the sample in refrigerator ( do not freeze ) and send it within 12hrs of sample collection
to the laboratory in the Poison Control Centre Ph. 24566510
173
Mercury Poisoning
Mercury (Hg) is used in PDO and in various other industries to manufacture,
caustic soda, chlorine, electrical equipments, thermometers and barometers, silver
and gold extraction, disk batteries, paints, paper, plastic and for dental amalgam.
Mercury salts are also used as antiseptics, antifungal agents and in herbal and
traditional remedies for various skin and intestinal disorders. Large carnivorous
fish such as sword fish may be contaminated with high amounts of organic mercury
due to bioaccumulation.
Toxic forms and routes of exposure
Form Route
Organic Mercury (Methyl mercury) Oral, skin, inhalation
Inorganic Mercury (Mercuric Oral, inhalation
chloride)
Elemental Mercury (Metallic, shining Inhalation
liquid)
Oral Toxic Dose
Methyl Mercury 1 -6 mg/kg lethal (acute oral)

1 µg/kg (chronic daily use)
EPA : No observable effect level = .3µg/kg per day
Mercuric chloride 1- 4 gm (acute, oral) Lethal
Elemental Mercury Orally non-toxic

Mechanism of Action
• Mercury forms covalent bonds with SH-groups of cellular enzymes and
inactivates them .
• Varies with the form of Mercury, route and acute/chronic exposure.
Acute inhalation of Hg vapours
• Chemical pneumonitis (fever, chills, dyspnoea)
• Non cardiogenic pulmonary oedema
• Gingivostomatitis
Acute ingestion of inorganic salts
• Oropharyngeal burns, metallic taste, abdominal pain, haemorrhagic
gastroenteritis, shock
• Acute oliguric renal failure
Chronic exposure to inorganic Mercury
• Tremors, neuropsychiatric symptoms, gingivostomatitis and renal dysfunction.
174
Chronic exposure to organic Mercury
• Paraesthesias (lips, nose, extremities), ataxia, dysarthria, hearing impairment,
constricted visual fields, dementia
• Methyl mercury is a potent teratogen.
Diagnosis
• History of exposure (compound, route, duration)
• Elevated metallic/inorganic Mercury levels in blood and urine (normal urine level
<1µg/dl, blood levels <2 µg/dl) .
• X-ray abdomen
Treatment
Supportive
Vapour exposure
Administer supplemental oxygen (check PO2). Intubate and/or assist ventilation
as required. Maintain PO2 of at least 6 -7 mmHg. PEEP may be necessary.
Mercuric chloride ingestion

Treat shock with iv fluids
Haemodialysis may be required in renal failure
Antidote treatment
• BAL for Mercuric chloride poisoning, if administered early can prevent renal
damage .( 5 mg / kg im then 2.5 mg / kg 8 hrly for one day followed by 2.5 mg /
kg 12 – 24 hrs ) Followed by Pencillamine ( 5 mg qid for adults , 25 mg / kg
qid children ) until improvement , maximum for 1 days
• Do not use BAL for Mercury vapour or Methyl mercury. Can give DMSA, if
available (1 mg / kg oral 8 hourly x 5 days, then 12 hourly x two weeks), or
Pencillamine (2 -3 mg/day in divided doses on empty stomach, oral for 3
months).
Decontamination
• Metallic (liquid) mercury is not absorbed from GIT, do not do gastric lavage
and/or administer activated charcoal.
• Repeat X-ray abdomen , if it shows retention of elemental mercury in gut, can
give cathartic or whole bowel irrigation to prevent chronic intoxication
• For mercuric chloride poisoning perform gastric lavage and administer activated
charcoal
• Arrange for endoscopic examination to check corrosion .
Note: Elemental Mercury is employed in Oman as traditional remedy. Oral

exposure is Not harmful, Mercury spills and vapours are very harmful on
chronic exposure.
175
Section
Section VII
Tables 1-23
177
1. Drugs and chemicals that may cause bradypnea or tachypnea
Bradypnea Tachypnea
Barbiturates & hypnotics Aminophyllin & Theophyllin

Benzodiazepines Aspirin / salicylates
Botulism Carbon monoxide (initially)
Ethanol/Alcohols Chloroquine
Opioids Cocaine
Organophosphates / Carbamates Methanol
Phenothiazines Nicotine
Tricyclic antidepressants OPs / Carbamates
Carbon monoxide (late) Organochlorine
Pentachlorophenol
Phenol
2. Toxicants that may cause hypoventilation or hyperventilation
Hypoventilation Hyperventilation
Barbiturates / hypnotics Amphetamine

Benzodiazepine Anticholinergics
Botulinum toxin Caffeine
Clonidine Camphor
Elapid envenomation Carbon monoxide
Ethanol/Isopropanol Cocaine
Neuro muscular blockers Cyanide
Nicotine Ethanol / Ethylene glycol
Opioids Hydrogen sulfide
OPs / Carbamates Iron
Strychnine Isoniazid
Tetrodotoxin Methanol
Tricyclic antidepressants Methaemoglobinaemia inducers
Paraldehyde
Pentachlorophenol
Salicylate
Theophylline
Hypoventilation = Badypnia or / and Hypopnea → Hypercapnia → ( PCO2

>45mmHg)
Hyperventilation = Tachypnea or / and Hyperpnea ( ↑ tidal volume)
179
3. Some drugs and chemicals causing bronchospasm
Beta blockers Chlorine and other irritant gases

Iodine Hydrocarbon aspiration
Opiates Organophosphates and other
Penicillins anticholinesterases
anticholenesterases
Salicylates Pyrethroids
Tubocurarine Smoke inhalation
Vaccins, sera
Hypersensitivity reaction to food, insect bite
4. Toxic and other causes of Bradycardia or Tachycardia
Bradycardia
Antidysrhythmics
Alpha-adrenergic agonists
Beta-adrenergic antagonists
Calcium channel blockers
Clonidine
Digitalis
Opioids
Sedative hypnotics
Organophosphates / Carbamates
Cerebral oedema (due to trauma / toxic subs / infection )
Tachycardia
CNS stimulants (Theophylline, amphetamine, caffeine, cocaine, camphor)
Anticholinergics
Digitalis
Tricyclic antidepressants
Ethanol and ethylene glycol
Iron
OPs and Carbamates
Phenothiazine
Hyperthermia
Withdrawal syndrome (hypnotics, alcohol, opioids)
180
5. Drugs and chemicals affecting blood pressure
Hypotension
ACE inhibitors
Alpha-adrenergic blockers
Antidysrhythmic agents
Anticholinergics
Arsenic (acute)
Beta adrenergic blockers
Calcium channel blockers
Clonidine
Cyanide
Cyclic antidepressants
Disulfiram
Ethanol / Isoprophyl alcohol / methanol
Iron
Mercury
Nitrates and Nitroprusside
Opioids
OPs and Carbamates
Phenothiazines
Sedative hypnotics
Theophylline
Hypertension
Amphetamine and sympathomimetics
Anticholinergics and tricyclics
Antihistaminics
Cocaine
Cannabis
Lead
Levodopa
Monoamine oxidase inhibitors
Nasal decongestants
Ethanol and hypnotic withdrawal
Organophosphates (early stage)
181
6. Toxic causes of cardiac dysrhythmias
ORS
Tachycardia A-V block Ventricular Arrhythmias
prolongation
Theophylline Digitalis Digitalis Sympathomimetics

Ephedrine Clonidine Beta blockers Digitalis
Pseudoephedrine Beta blockers Chloroquine Theophylline
Caffeine Antiarrhythmics Antiarrhythmics Tricyclics
Carbon monoxide Tricyclics Tricyclic Phenothiazines
Cyanide Calcium channel antidepressants Astemazole and terfenadine
Hydrogen sulfide blockers Carbamazepine Chloroquine
Methaemoglobinaemia Lithium Diphenhydramine OPs and Carbamates
Atropine Opiates Phenothiazine Antiarrhythmics
Phenothiazines Propoxyphene Hyperkalemia Thallium
Tricyclics Oleander (plant) Oleander (plant) Arsenic
Antihistamines Carbamates
Withdrawal of
sedatives or ethanol
Thyroxine
Vasodilators
7. Some drugs and toxins causing hypotension with bradycardia

or tachycardia
Hypotention with relative Bradycardia Hypotension with Tachycardia

Clonidine and methyldopa Fluid loss
Oxymetazoline GIT irritants
Beta blockers (mainly propranolol) Iron
Encainide and flecainide Snake envenomation
Quinidine, procainamide, and disopyramide Hyperthermia
Propoxyphene Arsenic (acute)
Tricyclic antidepressant Βeta2-stimulants (eg metaproterenol,
Barbiturates terbutaline)
Diltiazem ,Verapamil Anticholinergics
Organophosphate and carbamates Nitrites and Sodium nitroprusside
Hypothermia Prazosin,alpha adrenergic blockers
Cervical spinal cord trauma Phenothiazines
Theophylline
Tricyclic antidepressants
ACE inhibitors
Zinc phosphide
Ethanol,Methanol
182
8. Drugs and chemicals that may cause coma or stupor
Drugs Chemicals
Anticholinergics Carbon monoxide
Antihistamines Cyanide
Barbiturates Hydrogen sulfide
Benzodiazepines Methemoglobinemia (nitrobenzene)
Carbamazepine Benzene
Phenothiazines Solvents
Tricyclic antidepressants Ethanol
Valproic acid Ethylene glycol
Clonidine
Quinine
Quinidine
Opiates
Salicylates
Disulfiram
Hypoglycemic agents
Lithium
Phenylbutazone
9. Toxic and other causes of pupil-size changes
Miosis Mydriasis
• Cholinergic agents • Anticholinergic drugs

(OPs and carbamates, (Atropine and related drugs,
Pilocarpine) Tricyclic antidepressants,
Antihistamines)
• Sympatholytic agents
(Clonidine,) Nasal - • Sympathomimetics
decongestants) (Amphetamines,
Cocaine,
• Others Dopamine)
Opiates
Phenothiazines
Valproic acid
Heat stroke
Pontine infarct
Sub arachnoid haemorrhage
Nicotine can cause mydriasis as well as miosis.
183
10. Toxic and other causes of convulsions
Pharmaceuticals Pesticides Drugs of Others

abuse
Antihistamines Carbamates Amphetamine Withdrawal syndrome of

Carbamazepine Organophosphates Cocaine Ethanol and sedatives
Carbon monoxide DEET Methanol Fever
Cyclic antidepressants Phenols Hypoxia
Hypoglycemics Infection
Isoniazid Metabolic causes
Lithium Cerebral haemorrhage
Mefenamic acid Head injury
Metronidazole Brain tumour
Phenothiazines Lead encephalophathy
Propoxyphene Strychnine
Salicylates Camphor
Xanthines Some plant toxins
Theophylline
Caffeine
11. Drugs and agents causing delirium or psychosis
Medicines : Anticholinergic agents, Antihistamines, Beta blockers, Cimetidine and

other H-2 blockers, Levodopa, Lithium, Salicylates, Withdrawal from ethanol or
sedative-hypnotic drugs
Serotonin reuptake inhibitors (SSRIs) , Theophylline, Steroids
Drugs of abuse : Ethanol,Marihuana, Amphetamine, Cocaine

Pesticides : OPs and Carbamates, Herbicides
Other chemicals: Camphor, Turpentine & other volatile oils, Carbon monoxide,
Lead and other heavy metals
12. Some drugs and toxins causing dystonia, dyskinesia &

rigidity
Barbiturates& hypnotics Phenothiazines

Ethanol and other alcohols Tricyclic antidepressants
Hypoglycemic agents Vasodilators
Opiates Carbon monoxide
184
13. Some drugs and toxins associated with rhabdomyolysis
Excessive muscular hyperactivity, Direct cellular toxicity

rigidity, or seizures Carbon monoxide
Clozapine and olanzapine Ethylene glycol
Lithium Other or unknown mechanism
Seizures caused by other agents Barbiturates (prolonged immobility)
Strychnine Chlorophenoxyl herbicides
Tetanus Clofibrate
Tricyclic antidepressants Ethanol
Hyperthermia caused by a variety of
agents
Trauma
14. Some drugs and toxins associated with hypothermia

Dystonia Dyskinesis
Haloperidol and butyrophenones Anticholinergic agents
Metoclopramide Antihistamines
Phenothiazines (prochlorperazine) Caffeine
Rigidity Carbamazepine
Black widow spider bite Ketamine
Lithium Levodopa
Malignant hyperthermia Lithium
Neuroleptic malignant syndrome Serotonin reuptake inhibitors (SSRIs)
Strychnine Tricylic antidepressants
15. Some drugs and toxins associated with hyperthermia
Excessive muscular hyperactivity , rigidity Impared heat dissipation or disrupted

or seizures thermoregulation
Amoxapine Amoxapine
Lithium Anticholinergic agents
Tricyclic antidepressant Antihistamines
Increased metabolic rate Phenothiazines and other antipsychotics
Dinitrophenol and pentachlorophenol Tricyclic antidepressants
(herbicide) Others
Salicylates Exertional heatstroke
Thyroid hormone Malignant hyperthermia
Metal fume fever
Neuroleptic malignant syndrome (NMS)
Serotonin syndrome
Withdrawal from ethanol or sedative-
hypnotic drugs
185
16. Some drugs and toxins causing anaphylactic or
anaphylactoid reactions
Anaphylactic reactions (IgE-mediated) Anaphylactoid reactions (not IgE-

Antisera (antivenins) mediated)
Foods (Nuts, fish, shellfish) Acetylcystine
Hymenoptera and other insect stings Blood products
Immunotherapy allergen extracts Iodinated contrast media
Penicillins and other antibiotics Opiates
Vaccines Tubocurarine
Other or unclassified
Exercise
Sulfites
Tartrazine dye
17. Drugs and chemicals that may cause elevated anion

gap acidosis
Lactic acidosis Other acid anions
Acetaminophen (levels >600mg/l) Alcoholic ketoacidosis
Beta-adrenergic drugs Diabetic ketoacidosis
Carbon monoxide Ethylene glycol
Cyanide Exogenous organic and mineral
Hydrogen sulfide acids
Iron Formaldehyde
Isoniazid (INH) Ibuprofen (propionic acid)
Phenformin (common) and metformin Methanol
(rare) Salicylates (salicylic acid)
Salicylates Valproic acid
Seizures, shock, or hypoxia
Theoplylline
Eq/L
Normal anion gap 8-12 µeq/L
18. Selected causes of alterations in serum glucose levels
Hyperglycemia Hypoglycemia
B2-adrenergic drugs Endocrine disorders (hypopituitarism,
Caffeine intoxication Addison’s disease, myxedema)
Corticosteroids Ethanol intoxication (especially
Dextrose administration paediactric)
Diabetes mellitus Fasting
Excessive circulating epinephrine Hepatic failure
Glucagon Insulin
Theophylline intoxication Oral sulfonylurea hypoglycemic agents
Thiazide diuretics Propranolol intoxication
Renal failure
Salicylate intoxication
Valporic acid intoxication
186
19. Some drugs and chemicals associated with altered serum
sodium levels
Hypernatremia Hyponatremia
Cathartic abuse Diuretics
Lactulose therapy IV fluids therapy
Lithium therapy Psychogenic polydipsia
Severe gastroenteritis (many Syndrome of inappropriate ADH
poisons) (SIADH):
Sodium overdose SSRIs
Valporic acid Amitriptyline
Chlorpropamide
Clofibrate
Oxytocin
Phenothiazines
20. Some drugs and chemicals associated with altered serum

potassium levels
Hyperkalemia Hypokalemia
Alpha-adrenergic agents Beta-adrenergic drugs
Angiotensin converting enzyme (ACE) Caffeine
inhibitors Diuretics (chronic)
Beta blockers Epinephrine
Digitalis glycosides,Nerium oleander Theophylline
Lithium Toluene (chronic)
Potassium Barium carbonate( rodenticide)
Renal failure
Rhabdomyolysis
21. Drugs and chemicals that may cause acute renal failure
Direct nephrotoxic effect Haemolysis

Acetaminophen Arsine
Analgesics (eg ibuprofen, phenacetin) Naphthaline
Antibiotics (eg aminoglycosides) Oxidizing agents (esp. with 6PD
G6PD
Bromates deficiency)
Chlorates Rhabdomyolysis
Chlorinated hydrocarbons Amphetamines and cocaine
Cyclosporin Coma with prolonged immobility
Ethylene glycol (oxalate) Hyperthermia
Heavy metals (eg. Mercury, lead ) Status epilepticus
Strychnine
187
22. Some drugs and chemicals that may cause hepatic
damage
Acetaminophen Phenol
Arsenic Phosphorus
Carbon tetrachloride and other Polychlorinated biphenyls (PCBs)
chlorinated hydrocarbons Pyrrolizidine alkaloids
Copper Thallium
Mercury salts 2-nitropropane
Ethanol Valporic acid
Halothane
Iron
Tables adapted from :

• Poisoning and Drug Overdose by Kent R.Olson et al.1999
• Emergency Toxicology by P.Viccellio et al .1998
• Toxicological Emergencies by Goldfrank et al 1999,2002
• INTOX – databank 2003
• Management of poisoning : A handbook for health care workers J.Henery
& H Wiseman – IPCS / WHO 1997
188
23. Therapeutic Drugs Used in Poisoning Management
DRUGS ADULT DOSE PAEDIATRIC DOSE INDICATIONS

Aminophylline 5mg/kg, slow IV injection over 20 5-10mg/kg, slow IV injection Acute severe asthma not being
minutes (250-500mg) followed by over 1 hour, followed by treated before with theophylline
500mcg/kg/hr 1mg/kg/hr (6m-10yrs) or
0.8mg/kg/hr (10-16yrs)
Amiodarone 150mg IV in 10 min., diluted in 5% 5mg/kg/IV infusion in 5% Cardiopulmonary resuscitation,
dextrose. May repeat x1 dextrose over 20-120 minutes to treat cardiac arrest refractory
Infusion 1 mg/min x6 hrs. with ECG monitoring to defibrillator.Ventricular & atrial
arrhythmias.
Antiemetics
Metoclopramide 10-20mg IV or IM 0.15-0.3mg/kg/dose Q6H IV or Mild nausea and vomiting
IM (should not exceed
500mcg/kg/day). Use with
caution in children, due to extra
pyramidal side effects
Ondansetron 8mg in 50ml of 5% dextrose IV, slow 0.2 mg/kg over 5 minutes then Intractable nausea and vomiting
infusion 0.25-0.5 mcg/kg/minute
if needed
Atropine 3mg IV single dose 0.02-0.5mg/kg (maximum Cardiopulmonary resuscitation to
0.6mg) IV or IM then 0.01-0.05 treat vagal block
mg/kg/dose Q4H-Q6H
Beta2 Agonists
Salbutamol Aerosol inhalation 200mcg 3-4 Aerosol inhalation 100-200mcg Bronchospasm
times/day. Inhalation of nebulised 3-4 times/day. Inhalation of
solution 2.5mg-5mg, to be repeated 4 nebulised solution 1.25mg-5mg,
hourly if needed to be repeated 4 hourly if
needed
Beta Blockers Rapid control of supra
Esmolol 50-200mcg/kg/minute infusion 50-100mcg/kg/minute infusion ventricular or ventricular
(diluted to 10mcg/ml) arrhythmias in theophylline
overdose
Propranolol 1mg IV over 1 minute, if necessary 0.02mg/kg IV, then if necessary Control of tachycardia and
repeat at 2 minutes interval (maximum 0.1mg/kg (over 10 minutes) then ventricular arrhythmias
10mg) 0.1-0.3mg/kg/dose Q3H
Benzatropine 1-2mg IV or IM 0.02mg/kg IV or IM Alternative to
diphenhydramine to treat
acute dystonic reactions
Benzodiazepines
Clonazepam Myoclonic epilepticus
1mg IV over 30 seconds 500mcg IV over 30 seconds
Diazepam 10-20mg at a rate of 0.5ml (2.5mg) per Anxiety or agitation due to

30 seconds, repeated if necessary 200-300mcg/kg or 1mg per year sympathomimetic or
after 30-60 minutes, maximum daily of age upto 12years hallucinogenic drug
dose 30mg intoxication:
Seizures, status epilepticus,
hypertonia and rigidity,
withdrawal symptoms of
drug abuse and alcohol,
febrile convulsions
4mg IV over 2 minutes

Lorazepam 0.05-0.2mg/kg/IV. Over 2
minutes (maximum 2mg) then Status epilepticus
0.01-0.1mg/kg/hr
30-300mcg/kg given in steps of 1-

Midazolam 2.5mg every 2 minutes, slow IV, then 0.15mg/kg/IV over 2 minutes
30-200mcg/kg/hr IV infusion then 1-5mcg/kg/minute infusion Status epilepticus
189
Severe hyperkalemia
Calcium Gluconate 10% solution 0.5ml/kg Symptomatic hypocalcaemia
10% solution 10-20ml slow IV (maximum 20ml) slow IV stat due to intoxication by fluoride or
(maximum 5ml/kg/day IV) oxalate, spider envenomation
Corticosteroids
Hydrocortisone 3-5mg/IV/kg (maximum 500mg) 3-5mg/kg (maximum 100mg) Treatment of anaphylaxis
every 3-6hrs every Q3H-Q6H management of acute asthma
1-4mg/kg initially (maximum 1-4mg/kg/dose stat followed by Treatment of anaphylaxis

Methylprednisolone 500mg) 1mg/kg/dose Q8H
Dantrolene 1mg/kg/minute IV (maximum Malignant hyperthermia
1mg/kg IV 10mg/kg) then 1-2mg/kg/dose
Q6H
Dobutamine 5-20mcg/kg/minute IV infusion Hypovolaemic or cardiogenic
Titrate 2.5-10mcg/kg/minute IV
(Titrate, based on blood shock
infusion
pressure)
Dopamine 5-15mcg/kg/minute IV infusion 5-20mcg/kg/minute IV infusion Hypovolaemic or cardiogenic
(Titrate, based on blood (Titrate, based on blood shock
pressure) pressure)
Epinephrine 0.05-0.1ml/kg/dose of 1 in Anaphylaxis and anaphylactoid
0.3-0.5mg SC or IM. In severe
10,000 IV ( for severe shock) reaction
cases IV infusion 1mg in 250 ml
0.1mg/kg (.01ml/kg of 1 in 1000)
NIS rate, 4 – 20 mcg/min.
x 3 doses 20 minutes apart if
Titrate to effect.
required IM.
Folic Acid 1mg/kg IV 4 hourly Methanol or ethylene glycol
50mg IV 4 hourly
poisoning
Glucose (Dextrose) 2.5ml/kg of 10% dextrose slow Empirical therapy for coma
IV (suspected hypoglycaemia)
50-100ml of 50% dextrose
through IV line
2-4ml/kg of 25% dextrose
through IV line
H1 Receptor Blockers
Chlorpheniramine 10-20mg SC, IM or IV over 1 <1yr 250mcg/kg IV,
minute. 4mg every 4-6 hours, 1-5yrs 2-5mg IV, Pre treatment with antivenin
PO (maximum 24mg/day) 6-12yrs 5-10mg IV To treat extrapyramidal effects
of Metoclopramide
1.25mg/kg 4 times a day Scombroid fish poisoning
Diphenhydramine 25-50mg, every 4-6 hours PO (maximum 300mg/day) IV, IM
2-6years, 6.25mg 4-6 hourly
(maximum 25mg) PO 6-12years Hay fever, urticaria
12.50mg 4-6 hourly (maximum
75mg) PO
0.2mg/kg/day PO
Loratidine
Loraditine 10mg/day PO
H2 Receptor Blockers
Ranitidine 50mg diluted to 20ml and given 1mg/kg/dose IV slow. Q6H- Adjunct to diphenhydramine in
over 2 minutes. May be Q8H. anaphylaxis prophylaxis and in
repeated every 6-8 hrs 2-4mg/kg/dose Q8H-Q12H PO. scombroid fish poisoning.
190
Haloperidol 2-10mg IM or IV initially and 0.01mg/kg (maximum 0.5mg) Management of psychosis,
then every 4-8 hours according daily increased upto psychomotor agitation or
to response (maximum 18mg 0.1mg/kg/dose Q12H IV functional psychosis
daily)
Lidocaine 50-100mg as a bolus over few 1mg/kg (0.1ml/kg of 1%) IV over Ventricular arrhythmias
minutes IV followed by infusion 2 minutes, then 15-
of 4mg/minute for 30 minutes, 50mcg/kg/minute
2mg/minute for 2 hours then
1mg/minute, reduce
concentration further if infusion
continued beyond 24 hours
(ECG to be monitored)
Magnesium Sulphate 50% Magnesium Sulphate, 4g 50% Magnesium Sulphate Cardiac arrhythmias
over 5-15 minutes followed by (2mmol/ml) 0.2ml/kg/dose
IV infusion of 1g/hr x 24 hours (maximum 10ml) Q12H IM or
slow IV
Mannitol 50-200gms over 24 hours 0.25-0.5g/kg/dose IV (2-4ml/kg Cerebral oedema
preceded by initial dose of of 12.5% or 1.25-2.5ml/kg of
500mg/kg by slow IV injection 25%)
Morphine 10-15mg SC or IM every 4 0.1-0.2mg/kg/dose 4 hourly SC Severe pain in bites and stings.
hours. Infusion of 1mg/kg in or IM. Infusion of 1mg/kg in 50ml Pain due to corrosive injury to
50ml of 5% dextrose 1-3ml/hour of 5% dextrose 0.5-1.5ml/hr (10- eye, skin or GIT. Pulmonary
(20-60mcg/kg/hr) 30mcg/kg/hr) oedema due to congestive heart
failure
Phenobarbital 10mg/kg at a rate of not more 20-30mg/kg IM or IV over 30 Control of generalized seizures,
than 100mg/minute (maximum minutes, followed by 10-15mg/kg status epilepticus
1gm) IV infusion. Dilute injection upto 100mg/kg in 24 hours.
1 in 10 with water for injection. Maintenance 5mg/kg (maximum
300mg) daily IV
Phenytoin 15mg/kg at a rate not exceeding 15mg/kg as a loading dose IV Control of generalized seizures,
50mg per minute as a loading over 30 minutes at a rate of status epilepticus, cardiac
dose.max. dose 1g. 1-3mg/kg/minute arrhythmias
Maintenance dose of 100mg
thereafter at intervals of 6-8
hours
Sodium Bicarbonate Base excess X weight Base excess X Metabolic acidosis, some cardiac
10 Weight (for <5kg) arrhythmias
(corrects half the base deficit) 4
Base excess X
Weight (for child <12yrs)
6
(corrects half the base deficit)
Thiamine 100mg, PO, IM or slow IV per 1-2mg/kg, PO, IM or slow IV per Empirical management of
day day comatosed patient
REFERENCES
1. British National Formulary 47, March 2004, Published by British Medical Association and Royal
Pharmaceutical Society of Great Britain
2. Drug Doses, Eleventh Edition 2001-2004, Frank Shann, Royal Children’s Hospital, Australia
191
Appendix -1
Management of Food Poisoning
*
* *
*
* Specific treatment
Adapted from Ellenhorn’s Medical Toxicology -1997
192
Appendix -2
Reference Books
1. Goldfrank L.R. et al. Goldfrank's Toxicologic Emergencies. Seventh Ed. New York:
McGraw-Hill, 2002
2. Ellenhorn MJ. Ellenhorn's Medical Toxicology: Diagnosis and treatment of human

poisoning, Second Ed. Baltimore, Maryland: Williams & Wilkins, 1997
3. Barkin RM, Rosen P. Emergency Pediatrics: A guide to ambulatory care, Sixth Ed.
Philadelphia, Pennsylvania: Mosby, 2003
4. Viccelio P. Emergency Toxicology, Second Ed. Philadelphia

Lippincott-Raven, 1998
5. Olson KR et al. Poisoning & Drug Overdose, Third Ed. New York, McGraw-Hill, 1999
6. Henry JA, Wiseman HM. Management of Poisoning: A handbook for health care workers.
WHO Geneva 1997.
7. Gossel TA and Brick JD. Principles of Clinical Toxicology, Third Ed. London: Taylor &
Francis, 2002
193
Appendix -3
Feedback from end-users
Excellent piece of work.

Very thorough and extensive.
Will be very helpful in managing poisoning cases in A&E.
Sketches and illustrations, excellent.
The Royal Hospital
Manual covers all aspects of poisoning and treatment.

Muscat Region, DGHS
Manual covers all important aspects.

North Batinah, DGHS
Comprehensive and detailed.

Covers common poisonings.
South Batinah, DGHS
Congratulations for bringing out much needed guidelines.

Appreciate detailed explanations.
North Sharquiyah, DGHS
Hearty congratulations for the splendid work in bringing out much needed manual.
South Sharquiyah, DGHS
Manual is valuable.
Musandam, DGHS
Very much needed in emergency departments and will be of great help.

Simplified and easy approach appreciated.
Al-Dakhliya, DGHS
Document is satisfactory.
Al-Dhahira, DGHS
Informative and useful.

Al-Wusta, DGHS
Excellent.
Dhofar, DGHS
194

Guidelines On Poisoning Management

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Guidelines On Poisoning Management

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Ministry of Health

Directorate General of Health Affairs

Dr. Salim Said Al-Wahaibi Dr. I. G. Hastie BSc, MD, FRCPC

Expert Group Committee I

Section IV: Management of Drug Poisoning 73

Section VI: Management of Poisoning due to Some Plants, 163

Expert Group Committee

Chairman : Dr. Salim Said Al-Wahaibi

Dr. S. B. Lall Dr. I. G. Hastie

Dr. Nabil Mohsin Dr. K. Omar

Dr. E. Scrimgeour Dr. P. C. Alexander

Dr. Ragini Vaishnav Dr. Uday Nadkarni

Ph. Intisar Al-Busaidi Ph. Sheikha Al-Harthy

• Dr. S. B. Lall, MD, DGO, MNAMS, FAMS

• Dr. I. G. Hastie, BSC, MD, FRCPC

• Dr. Nabil Mohsin, MD, DTM, MSc (Immunology), CES (Nephro.)

• Dr. K. Omar, MBBS, MSPCP, EMDM

• Dr. E. Scrimgeour, MD, FRACP, DTM&H

• Dr. P. C. Alexander, MBBS, MD, DCH

• Dr. Uday Nadkarni, MD, DCH, DNB

• Dr. Ragini Vaishnav, MBBS, MD

• Ph. Intisar Al-Busaidi, BS Pharmacy

• Ph. Sheikha Al-Harthy, M Pharm

Poisoning is an important health problem in every country of the world

I am pleased to introduce the National Guidelines on Poisoning

These guidelines are expected to be used as standard operating

I hope it will be used by A&E staff at all health care levels as an

I wish you all a great success!

Dr. Ali Jaffer Mohammed

National Guidelines on Poisoning Management is a publication of the Ministry of Health,

The household-products poisoning management is dealt in Section V. Management,

A bedside poster is prepared on "Emergency Evaluation and Management of Poisoning"

Dr. Salim Said Al-Wahaibi

We gratefully acknowledge the painstaking efforts of the Expert Group

Finally, we express our sincere thanks to the secretariat at DEH&ME, for

We thankfully acknowledge the editor Dr. Kent R Olson and Publishers of

List of acronyms, abbreviations and symbols used

ABCDEs Airway, breathing, circulation, disability, exposure

‫آ‪ 3‬ا‪ 12‬و‪ "

Volume of distribution (Vd)

General mechanisms of toxicity

Acute on chronic exposure

Over dose toxicity

Munchausen by proxy syndrome

Minor severity : Mild, transient and spontaneously resolving symptoms of

Moderate severity : Pronounced or prolonged symptoms of poisoning

Severe poisoning : Severe or life threatening symptoms of poisoning

Symptomatic or supportive care

A specialized section established in the Directorate of Environmental Health and

Role and Functions

National ID Passport No. Driving License No. Labour Card No.

Address:………………….……………… Hospital No……………………..…… Nationality……………………

Circumstances of Exposure / Incident

Location:..……….. Home………………..Workplace………….. Hospital……..…..Public place……………

Agent Common Name…………………………………………………………… Use………………………

Type of Animal / Insect / Reptile involved: ………………………………………………………

Duration of Exposure Minutes……..….. Hours……..….. Days….….. Unknown……………

Risk Assessment No risk………….. Minimal risk……….….. Moderate risk……………….

Management outside hospital Yes……...….. No…………….

Resuscitation…………….. Gastric lavage…..……….. Supportive…..……….. Specific……………..

Severity Minor………….. Moderate……….….. Severe ………………

Outcome Improved………….….. Cured…………….. Sequelae…………………

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