Toxicology Manual ?? UP PGH

ALGORITHMS
OF COMMON POISONINGS
FOURTH Edition
The printing of Algorithms of Common Poisonings, Third Edition,
is financed by the National Poison Management and Control
Center.
Proceeds from your purchase go to a fund for the development of

future editions of this book as well as other manuals on the
management of poisoning.
Please do not photocopy.
If you would like to order more copies, contact us at 63-2-5241078

or visit our website www.uppoisoncenter.org.
First published 1991

Second edition published 1998
Copyright © 2011, 1998, 1991

by the National Poison Management and Control Center
www.uppoisoncenter.org
Book design by Maria Lurenda S. Westergaard, M.D.
All rights reserved. No part of this publication may be reproduced,

stored in a retrieval system, or transmitted, in any form or by any
means, electronic, mechanical, photocopying, recording, or otherwise, without prior
permission from the National Poison Management and Control Center.
Printed in the Philippines.
ISBN 978-971-8650-24-0
EDITORS
Nelia P. Cortes-Maramba, MD, FPPS, FPSCOT, FPSECP
Professor Emeritus, Department of Pharmacology & Toxicology,
University of the Philippines College of Medicine
Adviser, UP National Poison Management & Control Center
Lynn Crisanta R. Panganiban, MD, DPAFP, FPSCOT

Professor, Department of Pharmacology & Toxicology, University of the
Philippines College of Medicine
Head, UP National Poison Management & Control Center
Joselito C. Pascual, MD, MSc, FRSAP, FPSCOT

Associate Professor, Department of Psychiatry & Behavioral Medicine,
University of the Philippines College of Medicine/Philippine
General Hospital
Consultant, UP National Poison Management & Control Center
Carissa Paz C. Dioquino, MD, MPH, FPNA, FPSCOT

Associate Professor, Department of Neurosciences, University of the
Philippines College of Medicine/ Philippine General Hospital
Maria Lurenda S. Westergaard, MD, MMed

Project Assistant, UP National Poison Management & Control Center
CONTRIBUTORS
Allan R. Dionisio, MD, FPAFP, FPSCOT
Associate Professor, Department of Family & Community Medicine,
University of the Philippines College of Medicine/Philippine
General Hospital
iii
Danilo G. Villamangca, MD, FPCP, DPSCOT
Associate Professor, Department of Pharmacology, Emilio Aguinaldo
College of Medicine
Coordinator, Rizal Medical Center Poison Control Center
Irma R. Makalinao, MD, FPPS, FPSCOT

Professor & Chair, Department of Pharmacology & Toxicology
Nerissa M. Dando, MD, FPPS, DPSCOT

Professorial Lecturer, Department of Pharmacology & Toxicology,
Erle S. Castillo, MD, FPSCOT

Associate Professor, Department of Emergency Medicine, University of
the Philippines College of Medicine/ Philippine General Hospital
Kenneth Y. Hartigan-Go, MD, MD (UK), FPCP, FPSECP,

FPSCOT
President, Philippine Society of Experimental and Clinical
Pharmacology
Aeesha Yahcob-Pingli, MD, DPAFP

Clinical Toxicology Fellow, UP National Poison Management & Control
Center, 2006-2008
iv
CONTENTS
Preface vii
Preface to the Second Edition ix
Preface to the First Edition x
ACRONYMS AND ABBREVIATIONS xii
INTRODUCTION 1
DEFINITION OF TERMS 5
GENERAL MEASURES IN THE MANAGEMENT OF POISONING 9

Readily Available Agents Used as Antidotes 38
OVERDOSE OF COMMON PHARMACEUTICALS 49

Antidepressants
Lithium 51
Selective Serotonin Reuptake Inhibitors - SSRIs 54
Tricyclic antidepressants 58
Antipsychotics
Typical antipsychotics 63
Atypical antipsychotics 69
Barbiturates 74
Benzodiazepines 78
Digitalis 82
Iron / Ferrous sulfate 87
Isoniazid 93
Opiates and Opioids 98
Paracetamol 104
Salicylates 109
Theophylline 115
HOUSEHOLD AND WORKPLACE CHEMICALS 121

Caustic and Corrosive Agents 123
Caustics: Acids 125
Caustics: Alkalis 130
Sodium hypochlorite 135
v
Jewelry cleaning agents (cyanide containing) 138
Kerosene 145
Pesticides
Coumatetralyl / Warfarin 150
N-methyl carbamates 155
Organochlorines 156
Organophosphates 160
Pyrethroids 166
Watusi / Dancing Firecracker 170
SUBSTANCE ABUSE 173

Amphetamines (Shabu) 175
Cannabis (Marijuana) 181
Ethanol 184
ANIMAL TOXINS 191

Ciguatera 193
Cobra bite 198
Paralytic Shellfish 202
PLANT TOXINS 207

Herbal supplements 209
Jatropha seed (Tuba-tuba) 215
Talampunay (Angel’s trumpet, Datura) 218
ANNEX A. Properties of Common Drugs Involved in Poisoning 225

ANNEX B. Approximate Duration of Detectability of Chemicals
in Urine 226
ANNEX C. Specimen Time Collection - Blood and Urine 227
ANNEX D. Common Antidotes - Formulation and Dose 228
ANNEX E. Drugs for Supportive Therapy - Formulation and Dose 230
ANNEX F. Minimum Required Drugs and Devices for the
Management of Poisoning - Assembling a Poison Kit 232
ANNEX G. Rumack-Matthew Paracetamol Nomogram 233
ANNEX H. Units, Concentrations and Conversions 234
IMPORTANT CONTACT NUMBERS 235
vi
PREFACE
In 1989, a study involving 20 tertiary hospitals in Metro Manila was done
to determine the accuracy of response among Emergency Room (ER)
personnel to telephone inquiries on poisoning. Results showed that ER
personnel were giving correct advice in only 38% of calls regarding
poisoning due to isoniazid (INH) and 55% of calls about kerosene
ingestion. It became evident that there was a problem in both diagnosis
and management of poisoning cases.
The National Poison Management and Control Center (NPMCC) has
been working towards upgrading the competencies of health
professionals in the management of poisoning through symposia,
conferences, training programs and fellowships. The Center has also
published various handbooks on poisoning prevention, management
and control. This handbook, fondly called “the Black Book,” remains the
most popular and widely used of the Center's publications.
The practice of toxicology is constantly evolving as it responds to the
changing character and growing number of chemicals being used for
agricultural, industrial, recreational and medical purposes. Although the
list of most commonly encountered poisons has remained consistent
over the past ten years, new products and new toxicants have emerged,
including new designer drugs of abuse.
Over the past decade, clinical practice and research in toxicology
have strengthened support for a number of approaches in the
management of acutely poisoned patients (such as the use of activated
charcoal), and withdrawn support from others (such as forced diuresis).
All these developments present the health care provider with many
challenges, and unfortunately, very little guidance.
This third edition of the Black Book is a major revision of the second.
The editors and contributors reviewed general principles in managing
poisoned patients as well as treatment algorithms for specific poisons.
The algorithms have been revised according to information gleaned from
recent research, current consensus and position statements, as well as
the growing body of local experience in the management of poisoning.
There are sections on new toxicants encountered in the clinics.
The first part of the book describes general measures that apply to
all cases of poisoning. This is followed by algorithms for the
management of specific poisons. Information is presented succinctly.
Steps to be taken in the acute management of poisoning are shown in
vii
flow charts. The design of this book is hinged on enhancing efficiency
through appropriate action within the shortest period of time.
It is our hope that this book will continue to serve as a good resource
for health care providers attending to the acutely poisoned patient.
However, it should be used in the context of holistic care, taking into
consideration underlying medical conditions and psychosocial issues.
We are grateful to be given the opportunity to share our expertise in the
field of toxicology. More so, we continue to thank our families in
supporting us in this endeavor.
The beginning of wisdom is to acquire wisdom; and with all your

acquiring, get understanding. (Proverbs 4:7)
January 2011
viii
PREFACE
TO THE SECOND EDITION
The management of an acutely poisoned patient is a challenge to the
first contact physician because early recognition and management of a
poisoning case contributes greatly to better patient outcome. Thus, it is
important that the physician should have within reach available guides
for the treatment of an acutely intoxicated patient.
The contents of this book have been reviewed and data have been
updated based on the clinical experience and researches conducted by
the toxicology staff of the National Poison Control and Information
Service. The agents discussed are the most commonly encountered
poisons in clinical practice and the treatment guidelines have been used
in effectively managing patients.
The format has been revised to make it more “user friendly” for the
physician who wishes to avail of relevant information quickly, particularly
in the emergency room setting.
The authors and contributors encourage physicians to use these
algorithms as guides to treatment. However, in managing acute
poisoning cases, we should take into consideration the uniqueness of
every patient. Thus, treatment interventions should always be
individualized. Furthermore, the caring physician should always
remember that behind a poisoned patient, whether the nature of
poisoning is occupational, accidental, suicidal or substance abuse, lies a
much deeper problem which deserves equal attention.
We would like to thank our families who have always been supportive
of our endeavors, for their love and understanding during the hours and
days of absence from them because we had to attend to our sick
patients, both in the hospital and in the community.
For wisdom is more precious than rubies, and nothing you desire can
compare with her. (Proverbs 8:11)
August 1998
ix
PREFACE
TO THE FIRST EDITION
This initial guidebook on the management of poisoning focuses on the
most common types we have seen over the last 25 years in the
Philippines. An algorithmic approach to diagnosis and management is
presented. It must be realized, however, that this process can only be
utilized after a thorough history and complete physical examination of
the patient have been undertaken.
The first part of the book deals with general considerations in the
diagnosis and management of poisoning with specific boxed guidelines
for easy recall. The individual poisoning algorithms deal with the general
management followed by a flow chart of the most common
complications. The boxed precautions take into account the adverse
interactions and special conditions to watch out for in the management
of the patient. The annexes include the most common toxidromes one
encounters in the practice of clinical toxicology, the approximate
duration of detectability of chemicals in the urine, and common drug
dosages, among others.
We are grateful for the inputs of all the residents who rotated in
toxicology and the practicing physicians who referred their actual cases
to us. I am grateful most especially to my co-authors.
We hope that the medical officer who faces the dilemma of
diagnosing and managing a poisoning case will find this book a handy
friend. We further hope that he/she will stay cool yet warm at heart
towards troubled patients and their families, and in the process, become
a more knowledgeable physician.
Nelia P. Cortes-Maramba
October 4, 1991
x
NOTICE
The data in this book have been verified with reliable sources, and
treatment modalities discussed have been utilized in clinical practice.
However, new researches, changes in the medical sciences, and
human error should be considered. Readers are advised to confirm
data herein with other sources such as drug information sheets for
dosage, contraindications to administration, and other data relevant
to treatment. Updates may also be available at the NPMCC website:
www.uppoisoncenter.org. The editors are not responsible for errors or
omissions in patient management due to inaccuracies or
incompleteness of the information that may be present in this book.
xi
ACRONYMS and
ABBREVIATIONS
AACT American Academy of Clinical Toxicology
ABG Arterial blood gas extraction and analysis
ACE Angiotensin-converting enzyme
ALD Acute lethal dose
ALT Alanine aminotransferase, also known as serum glutamic pyruvic
transaminase (SGPT)
APTT Activated partial thromboplastin time
ARDS Acute respiratory distress syndrome
ASA Acetylsalicylic acid
AST Aspartate aminotransferase, also known as serum glutamic
oxaloacetic transaminase (SGOT)
BAL British anti-Lewisite
BID Bis in die, two times a day
BP Blood pressure
BUN Blood urea nitrogen
cap Capsule
CBC Complete blood count
CHF Congestive heart failure
CNS Central nervous system
COPD Chronic obstructive pulmonary disease
CPK Creatine phosphokinase
CVA Cardiovascular accident
CVP Central venous pressure
CVS Cardiovascular system
CXR Chest x-ray
CXR-PA Chest x-ray posteroanterior view
DB Direct bilirubin
DBP Diastolic blood pressure
DMPS 2,3 Dimercapto-1-propane sulphonate
DMSA Dimercaptosuccinic acid
DOC Drug of choice
DTPA Diethylene triamineopiate pentaacetic-N-N-N-N-N acid
ECG Electrocardiogram
EDTA Disodium edetate
EAPCCT European Association of Poisons Centres and Clinical Toxicologists
EEG Electroencephalogram
ELISA Enzyme-linked immunosorbent assay
FBS Fasting blood sugar
FPN Ferric chloride, perchloric acid and nitric acid (Forrest test;
xii
phenotiazine screen)
GABA Gamma-amino butyric acid
GI Gastrointestinal
GIT Gastrointestinal tract
HPLC High-performance liquid chromatography
h, hr, hrs
Hour/s
IB Indirect bilirubin
ICU Intensive Care Unit
INH Isoniazid
IV Intravenous
IM Intramuscular
KBW Kilogram body weight
LD Loading dose
LFTs Liver function tests
MAO Monoamine oxidase
mcg Microgram
MD Maintenance dose
mEq Milliequivalent
mg Milligram
mins Minutes
mL Milliliter
mmol Millimole
mcmol Micromole
NAPA N-acetyl penicillamine
NAC N-acetyl cysteine
ng Nanogram
NGT Nasogastric tube
NPO Non/nil/nihil per os/orem, nothing by mouth
NPCIS National Poison Control and Information Service. NPCIS and the PGH
Poison Control and Information Unit were merged in January 2005,
creating the NPMCC.
NPMCC National Poison Management and Control Center
NSAIDs Non-steroidal anti-inflammatory drugs
NSS Normal saline solution
OPIDN Organophosphate induced delayed neuropathy
PAT Paroxysmal atrial tachycardia
PEEP Positive end-expiratory pressure
PCP Phencyclidine
PEG Polyethylene glycol
PEN Penicillamine
PGH Philippine General Hospital
PO Per os/orem, by mouth
PPA Phenyl propanolamine
PRN Pro re nata (take as needed)
xiii
PSP Paralytic shellfish poisoning
PT Protime (prothrombin time)
PTT Partial thromboplastin time
PVC Premature ventricular contraction
QD Quaque die, once a day
QID Quater in die, four times a day
RBC Red blood cell
RBS Random blood sugar
RR Respiratory rate
RUQ Right upper quadrant
SBP Systolic blood pressure
SC Subcutaneous
SR Sustained release
SSRI Selective serotonin re-uptake inhibitor
SV Supraventricular
T4 Thyroxine
TB Total bilirubin
TCAD Tricyclic antidepressant
TIA Transient ischemic attack
TID Ter in die, three times a day
TR Therapeutic level
TX Toxic level
UP University of the Philippines
xiv
INTRODUCTION
Establishing a Network for Poison Management and Control
In 1975, the science of toxicology was introduced in the Philippines with

the establishment of a poison control center at the Philippine General
Hospital (PGH). This was in response to the increasing incidence of
poisoning due to indiscriminate use of pesticides. Activities of the Center
focused on the management of acute poisoning cases and research.
The true picture of poisoning in the country was unknown during those
years. There were very limited data on poisoning cases from other
hospitals in the different regions.
The number of poisoning cases seen at the PGH from 1984-1989
only averaged 190 per year. The 1987 statistics from the Department of
Health (DOH) reported 279 poisoning cases with an incidence of
0.5/100,000 population. In 25% of these cases, the type of poison was
not specified or identified. The limited poisoning data for the country was
mainly due to underreporting and misdiagnosis of cases.
Health professionals handling poisoning cases did not have any
access to an information system nor training in toxicology through which
they would be able to gain knowledge on poisoning and its appropriate
management. At that time, the University of the Philippines (UP) College
of Medicine was the only institution that included the teaching of
toxicology in its curriculum. Activities to improve public and health sector
awareness of the hazards of chemicals and their toxicities were limited.
Furthermore, a standardized system of data collection, monitoring and
evaluation of poisoning cases did not exist.
This situation highlighted the urgency of setting up a national poison
control center and its network of satellite centers to take responsibility
and assume the lead role for all matters related to poisoning in the
country.
In 1991, the Poisons Control and Information Service Network
(PCISN) was created through a grant from the International Development
Research Centre (IDRC) of Canada. Additional support was received
from the Gesselschaft fur Technische Zusammenarbeit (GTZ). The UP-
PGH Poison Control Center was renamed to become the National Poison
Control and Information Service (NPCIS) with the Philippine General
Hospital serving as the training and service hospital, and the
Department of Pharmacology coordinating related efforts of other
1
clinical departments, namely Family Medicine, Emergency Medicine
Services, Internal Medicine, Pediatrics, Surgery, and Psychiatry. The
main objectives of the project were to advocate for poisoning prevention,
and to improve the management of poisoning cases.
With the establishment of NPCIS, a memorandum of agreement on
partnership was signed by the Department of Health Secretary (then Dr.
Antonio Periquet) and the Chancellor of UP Manila (Dr. Ernesto Domingo)
in June 2, 1992. The memorandum of agreement was reaffirmed on
September 25, 1992 by the new Health Secretary who assumed office a
few months later, Dr. Juan Flavier. Through this partnership, satellite
poison centers were established in different regions of the country.
The NPCIS thus became the focal point of a nationwide network that
has since been involved in managing poisoning cases, conducting health
assessment activities on the health effects of chemical exposure among
high-risk communities, conducting training courses and research that
are relevant for policy formulation.
The NPCIS was recognized as a unit of the College of Medicine during
the term of Dean Ramon L. Arcadio on March 21, 2003. Soon after, the
PGH-Poison Control and Information Unit (PICU) was created by then
Director Juan Pablo R. Nañagas.
On January 27, 2005, the Board of Regents of the University of the
Philippines approved the merging of the NPCIS and the PGH-PCIU. The
unit was named National Poison Management and Control Center
(NPMCC).
From 2002 to 2007, the NPMCC managed 4,263 in-patients; an
average of 711 patients a year. During the same period, the Center
assisted in the management of 16,195 poisoning cases through
telephone referrals; an average of 2,699 a year. Although majority of
telephone calls (>90%) were from health facilities, increasing numbers
also came from the general public. These developments point to the
growing awareness of the public regarding poisoning consultation, and
the broadening reach of the Center's poison information service.
The Center continues to be based at the University of the Philippines-
Manila, working with the different clinical departments of the PGH in
managing poisoning cases and training resident physicians and clinical
fellows. It also collaborates with the basic science departments,
particularly the Department of Pharmacology and Toxicology, on the
academic training of clinical fellows, the conduct of postgraduate
courses, and the strengthening of the analytical toxicology laboratory.
2
Poisoning as a Health Problem
The leading causes of poisoning managed at the NPMCC are exposures

to alcohol, kerosene, methamphetamine, sodium hypochlorite, mixed
household pesticide (propoxur and/or pyrethroid), hydrochloric acid,
isoniazid, paracetamol, and ferrous sulfate. In the early 1990s, new
toxicants, such as dancing firecrackers (”watusi”) and jatropha (tuba-
tuba), were added to the list. More recently, poisoning due to cyanide-
containing jewelry cleaning agents, slimming pills, and herbal products,
have been reported.
Alcoholic beverages remain in the top 5 commonly encountered
toxicants. Aggressive advertising and social acceptability significantly
influence alcohol use. Admissions from methamphetamine (”shabu”)
intoxication have decreased through the years, that is, from being the 2nd
or 3rd most commonly encountered toxicant in 2002-2004 to becoming
8th in 2006 and 13th in 2007. There are several reasons for this
development. One is the strict implementation of the law on illegal
substances. Another is the shift in the choice of recreational substance.
Over the past two years, there have been increasing admissions from
newer stimulants such as methylenedioxymethamphetamine (MDMA) or
“ecstasy” as well as older toxicants such as marijuana.
There are two age groups that are at highest risk for poisoning:
young people aged 20 to 35 years (about one third of cases), and
children under 6 years (about a quarter of cases). Accidental poisoning
in children occurs most often because of the accessibility and availability
of toxicants in the home. Children are by nature inquisitive. They can
reach into unlocked cabinets (for example, storage spaces under the
kitchen sink) which are used to store household chemicals like kerosene
or cleaning agents. Often, these toxic substances are stored in
unlabelled bottles that normally contain cola, water or juice. As much as
35% of cases managed by the NPMCC involve accidental exposures
involving children who ingest household chemicals and therapeutic
agents.
Majority of cases (60%) managed by the NPMCC are non-accidental
or intentional in nature. These include suicide attempts and substance
abuse. The reason for self-harm is often relational, that is, conflict
between the patient and a parent, or between the patient and someone
he or she is romantically involved with. There are as yet no local studies
on the impact of economic hardship or workplace stresses on the
incidence of intentional poisoning. Socio-cultural factors that increase
3
the propensity for self-harm, as well as factors that protect against such
behavior, need to be studied.
Slightly more male than female patients consult for poisoning.
Annual data from the 1980s onward show that mortality rates range from
2% to 9%, although the rates are as much as three times higher for males
compared to females.
Strategies in poisoning prevention and control
The NPMCC engages in various strategies to minimize the risks and

occurrence of poisoning. These include training of health personnel in
the early recognition and management of poisoning cases, and the
development of information materials on poisons and poisoning
management. Health advisories are issued to the general public when
there is a sharp rise in the incidence of certain types of poisoning.
In recent years, the NPMCC and other poison centers in the country
have been taking a more active role in chemical safety and poisoning
prevention in industrial and community settings. The work of the poison
control centers goes beyond the corners of the hospitals where these are
located. The staff are involved in responding to chemical incidents and
raising awareness about community exposure to hazardous chemicals.
Lessons from these experiences have been translated into local as well
as national policies.
Challenges ahead
Throughout the years, the NPMCC has realized the importance of

networking and partnership in dealing with the problem of poisoning.
Addressing toxicologic issues is not solely the job of the toxicologist.
Diagnosis, treatment and rehabilitation of the single poisoned patient, a
group of workers exposed to hazardous substances, or a community with
index cases of poisoning, requires a multidisciplinary team. Ensuring a
safe and healthy environment is everybody’s business.
The challenge is not only to preserve the networks that have been
established in the past 35 years, but also to develop new partnerships
between health professionals, policy makers and the general public.
Strength comes in numbers: “A cord of three strands is not quickly torn
apart.”
4
DEFINITION OF TERMS
TOXICITY: inherent ability of a substance to cause injury to biologic
material
RISK: the potential (likelihood) that injury (biological damage) will occur
in a given situation
EXPOSURE: contact with a chemical which may or may not enter the
body
POISON: any agent that is capable of producing deleterious or harmful

effects in a biological system, seriously injuring function or producing
death
POISONING: an event where a living organism is exposed to drugs,

medicaments, chemicals or biological substances that adversely affect
the function of that organism
SELF-POISONING AND PARASUICIDE: refers to the deliberate ingestion

of more than the therapeutic dose of a drug or a substance not intended
for consumption, usually by an adult in a moment of distress. Those who
die are classed as suicides rather than parasuicides regardless of
whether or not this was the intended outcome.
ACCIDENTAL POISONING: non-intentional ingestion, overdose or

exposure to drugs, medicaments or poisonous substances
SUBSTANCE ABUSE: (DSM-IV-TR criteria)

A. A maladaptive pattern of drug use leading to clinically significant
impairment or distress, as manifested by one (or more) of the
following, occurring within a 12-month period:
(1) recurrent drug use resulting in a failure to fulfil major role
obligations at work, school, or home
(2) recurrent drug use in situations in which it is physically hazardous
(3) recurrent drug-related legal problems
(4) continued drug use despite having persistent or recurrent social
or interpersonal problems caused or exacerbated by the effects
5
of the drug
B. The symptoms have never met the criteria for drug dependence.
SUBSTANCE DEPENDENCE: (DSM-IV-TR criteria)

A maladaptive pattern of drug use, leading to clinically significant
impairment or distress, as manifested by three (or more) of the following,
occurring at any time in the same 12-month period:
(1) tolerance, as defined by either of the following:
(a) a need for markedly increased amounts of the drug to
achieve intoxication or desired effect
(b) markedly diminished effect with continued use of the same
amount of the drug
(2) withdrawal, as manifested by either of the following:
(a) the characteristic withdrawal syndrome for the drug
(b) the same (or closely related) drug is taken to relieve or avoid
withdrawal symptoms
(3) the drug is often taken in larger amounts or over a longer period
than was intended
(4) there is a persistent desire or unsuccessful efforts to cut down or
control drug use
(5) a great deal of time is spent in activities necessary to obtain the
drug, use the drug or recover from its effects
(6) important social, occupational or recreational activities are given
up or reduced because of drug use
(7) drug use is continued despite knowledge of having a persistent or
recurrent physical or psychological problem that is likely to have
been caused or exacerbated by the drug
Note: The definitions for substance dependence and substance abuse

exclude acute drug intoxication in the absence of substance dependence
or abuse.
SUBSTANCE WITHDRAWAL: (DSM-IV-TR criteria)

A. The development of a substance-specific syndrome due to the
cessation of (or reduction in) substance use that has been heavy or
prolonged.
B. The substance-specific syndrome causes clinically significant
distress or impairment in social, occupational, or other important
areas of functioning.
6
C. The symptoms are not due to a general medical condition and are not
better accounted for by another mental disorder.
SUBSTANCE INTOXICATION: (DSM-IV-TR criteria)

A. The development of a reversible substance-specific syndrome due to
recent ingestion of (or exposure to) a substance. Note: Different
substances may produce similar or identical syndromes.
B. Clinically significant maladaptive behavior or psychological changes
that are due to the effect of the substance on the central nervous
system (e.g., belligerence, mood lability, cognitive impairment,
impaired judgment, impaired social or occupational functioning) and
develop shortly after use of the substance.
C. The symptoms are not due to a general medical condition and are not
better accounted for by another mental disorder.
7
GENERAL
MEASURES
IN THE MANAGEMENT
OF POISONING
The general approach to the poisoning patient involves the following:
I. Emergency stabilization
II. Clinical evaluation
III. Minimizing absorption of the poison
IV. Enhancing elimination of the absorbed poison
V. Administration of antidotes
VI. Supportive therapy and observation
VII. Disposition
I. EMERGENCY STABILIZATION
As in any other serious medical emergency, life-saving measures should
take priority in poisoning cases. In a suspected or frank case of
poisoning, management is directed towards the immediate life-
threatening problems of airway obstruction, breathing difficulties,
circulatory inadequacy, CNS disturbances, and electrolyte or metabolic
abnormalities.
ABCs of Life Support for Poisoned Patients

A - Airway. Maintain adequate airway
B - Breathing. Provide adequate oxygenation/ventilation
C - Circulation. Maintain adequate circulation
D - Drug- or toxicant-induced CNS disturbances. Treat convulsions, coma
E - Electrolytes. Correct metabolic abnormalities
A. Maintain adequate airway
Assess all patients for airway patency. A patient who is awake is likely to
have an intact airway. However, decreasing sensorium due to worsening
intoxication may compromise airway patency. In patients with
decreased sensorium, the gag or cough reflex may give an indirect
estimate of the patient's ability to keep the airway clear.
If the airway is obstructed, place the patient in supine position. Perform

the chin-lift and jaw-thrust maneuvers to position the tongue away from
the airway. Remove any foreign bodies (dentures, oropharyngeal
secretions).
11
Rule out cervical fracture before attempting endotracheal intubation. If
there is respiratory insufficiency, loss of consciousness, impaired or
absent gag reflex or status epilepticus, endotracheal intubation should
be done by trained or experienced personnel. Once a tube is inserted,
administer humidified air to prevent drying, crusting and sloughing of the
tracheal mucosa. Do bronchial toilet on a regular basis, depending on
the volume of secretions.
B. Provide adequate oxygenation / mechanical ventilation
Inadequate oxygen delivery to the lungs may be due to ventilatory failure,

hypoxia or bronchospasm. In all cases, check ABGs to accurately assess
ventilation. If the patient manifests clinical signs of poor oxygenation, or
pO2 is less than 80 mmHg, give oxygen via nasal cannula, face mask, or
with a mechanical ventilator, depending on the availability of equipment
and the FiO2 level required by the patient. If the patient manifests with
bronchospasm, evaluate the need for bronchodilators.
Common Toxicants that Can Cause Hypoxia

· Alcohol · Opiates · Quinine
· Carbon monoxide · Organophosphates
Modes of Oxygen Delivery with Equivalent FiO2

Nasal cannula 44%
Plastic mask 60%
Rebreathing mask 60 to 80%
Ventilator 100%
IMPORTANT: Oxygen may be contraindicated in the initial management of

watusi poisoning. Watusi is a flammable substance which can explode
in the presence of oxygen. Oxygen may also be contraindicated in the
management of paraquant poisoning because it increases the risk of
pulmonary fibrosis.
C. Maintain adequate circulation
Secure venous access and initiate intravenous infusion of the

appropriate fluids. In case of hypotension (SBP <80 mmHg in patients
under 40 yrs, or SBP < 90 mmHg in patients over 40 yrs), elevate the legs
12
by about 15 cm from the horizontal Recommended IV Fluids
plane to increase venous return to the
Hypotensive patients
heart. Fluid challenge should then be NSS
done using Normal Saline Solution Crystalloid solution
(NSS): 200 mL for adults or 10 mL/kg Adult maintenance
for children. At times, hypotension is D5NSS
resolved when ventilation problems D5AR
are corrected. Pediatric maintenance
D5 0.3NaCl
In severe poisoning cases,
maintenance drips and fluid challenge may be ineffective. For severe
hypotension, insert a central venous line, monitor hydration status, and
infuse plasma expanders to augment intravascular volume. If still
unsuccessful, consider starting dopamine or norepinephrine in D5.
D. Treat CNS disturbances - convulsions and coma
Convulsions in poisoned patients may be due to:

· Direct convulsant effect of the poison (see box)
· Cerebral hypoxia from the respiratory or cardiovascular
depressive effect of the toxicant (e.g., opiates)
· Hypoglycemia
· Severe muscle spasm due to spinal or peripheral effects on the
mechanism controlling muscle tone
· Withdrawal reactions in patients with substance dependence
(e.g., ethanol, diazepam)
· Decreased seizure threshold in an epileptic patient
Toxicants Commonly Associated with Convulsions
· Aminophylline · Isoniazid (INH) · Strychnine
· Amphetamines · Lead · Theophylline
· Carbon monoxide · Lithium · Tricyclic antidepressants
· Cocaine · MAO inhibitors · Withdrawal of narcotics,
· Cyanide · Mefenamic acid diazepam or ethanol
· Ethylene glycol · Organophosphates
· Hypoglycemic agents · Salicylates
13
Treatment of convulsions should be directed towards the etiology,
whether it be metabolic (e.g., electrolyte imbalance, hypoxia,
hypoglycemia) or a secondary effect of the ingested poison. Adequate
tissue oxygenation must be maintained.
Management of Seizures
General management of seizures
Diazepam Adult: 5 mg slow IV push
Pedia: 0.3 mg/kg/dose slow IV push
This may be repeated every 2 to 5 mins up to a
maximum dose of 20 mg. If the dose exceeds 20 mg,
intubation and artificial respiratory support may have to
be done before giving additional doses.
Never dilute diazepam with any fluid.
Lorazepam Adult: 2.5 to 10 mg/dose
Usual dose is 4 to 5 mg/dose
Pedia: 0.05 to 0.1 mg/kg/dose IV up to maximum of
4 mg/dose
Repeat twice at intervals of 15 to 20 mins prn.
Management of uncontrolled seizures
Phenytoin Loading dose:
15 to 20 mg/kg slow IV push
Adult: Give at a rate not to exceed 50 mg/min
Pedia: Give at a rate not to exceed 1 mg/kg/min
Maintenance dose:
Adult: 100 mg PO or IV every 6 or 8 hrs
Pedia: 5 to 7 mg/kg/day in divided doses
Phenytoin should never be diluted in dextrose contain-
ing fluids to avoid crystallization. Flush IV line with
normal saline solution if phenytoin is administered
through a D5-containing solution.
NOTE: Both diazepam and phenytoin are poorly absorbed and are ineffective
when given through the intramuscular route. In emergency situations,
lorazepam is particularly useful since it can be given IV or IM.
Management of seizures of unknown etiology
If seizures are unresponsive to conventional drug therapy, give:
Pyridoxine (B6) therapeutic trial
Adult: 5 g IV
Pedia: 80 to 120 mg/kg/dose IV
In known INH toxicity, pyridoxine should be given in 5 to 10 g
increments until cessation of seizures is achieved.
14
Management of Coma
Coma of unknown etiology
100% oxygen for possible poisoning with asphyxiants (such as
carbon monoxide, hydrogen sulfide) and cyanide
Thiamine (or Vitamin B complex if pure thiamine is not
available) for possible alcohol intoxication to prevent
Wernicke’s encephalopathy
Dose: 100 mg IV, followed by 50-100 mL of D50-50
Glucose for suspected hypoglycemia-induced coma
Adult: 50-100 mL Dextrose 50%
Pedia: 1-2 mL/kg/dose Dextrose 10%
Naloxone for possible opioid/opiate toxicity
Give initial dose of 400 mcg IV every 3 minutes.
If the patient does not respond to up to 2 mg, then
overdose from other drugs should be investigated.
The use of a total dose of 10 mg is seldom
necessary.
For neonates and infants, 10 to 100 mcg/kg/dose
IV, IM, SC to be repeated if necessary after
2 to 3 minutes up to 3 times.
Coma due to opiate overdose
Naloxone In known opiate overdose with altered mental
status and respiratory depression, give 2 mg of
naloxone IV. Exercise caution in giving the drug to
suspected chronic opiate abusers as withdrawal
reaction may occur. Additional IV infusion of
naloxone may be needed depending on the duration
of action of the opiate causing respiratory
depression.
15
E. Correct metabolic abnormalities
Hypokalemia is usually seen in Causes of Hypokalemia

theophylline overdose or in overdose
Alkalinizing agents (NaHCO3)
of other bronchodilators such as
Bronchodilators
salbutamol and terbutaline. These Theophylline
drugs stimulate the Na+/K+pump, Salbutamol
forcing K+ into the cells, thereby Corticosteroids
causing hypokalemia. Forced Diuretics (Furosemide)
alkaline diuresis (with furosemide)
may also produce hypokalemia
Treatment of Hypokalemia
because of K+-H+ exchange.
Treatment of hypokalemia is based Potassium chloride (KCl) solution
on restoring the lower limits of up to 40 mEq/hr
acceptable serum potassium. not to exceed 60 mEq/hr
Hyperkalemia occurs in overdose of Causes of Hyperkalemia

drugs such as beta-blockers and
cardiac glycosides that inhibit the ACE inhibitors
Beta blockers
Na+/K+ pump, allowing K+ to leak into Cardiac glycosides
the extracellular fluid. Angiotensin Carbon monoxide
Conver ting Enzyme inhibitors Cyanide
p r o d u c e h y p e r k a l e m i a b y Oral potassium
angiotensin-aldosterone inhibition. Potassium-sparing diuretics
Hyperkalemia also arises in cyanide
or carbon monoxide poisoning due to Treatment of Hyperkalemia
interference with ATP supply to the
Na+/K+ pump. Intake of oral K+, use of Glucose-insulin infusion
50 mL D50 and
K+-sparing diuretics, toxin induced
10 units of regular insulin
acute renal failure and disruption of Sodium bicarbonate
membrane integrity (rhabdomyolysis) Follow after glucose infusion
can also increase K+ levels. 1 mEq/kg/dose
10% calcium gluconate
+ As an alternative to sodium
Acceptable Serum K Limits bicarbonate
pH K+ level (mEq) 5 to 10 mL slow IV push under
acidosis 4.7 cardiac monitoring
normal 3.7 Dialysis
alkalosis 2.7 For intractable hyperkalemia
16
Hypomagnesemia is commonly observed with the administration of
diuretics, xanthines, aminoglycosides, cardiac glycosides, and in cases
of chronic alcohol abuse. Digoxin-induced hypomagnesemia is due to
the inhibition of the action of Na+/K+ ATPase pumps in the renal tubules.
Hypomagnesemia among alcoholics is primarily due to poor nutrition,
ketosis, gastrointestinal losses (emesis and diarrhea) and
hyperaldosteronism.
Treatment of Hypomagnesemia
Magnesium sulfate
Loading dose: 600 mg of elemental Mg++ in D5W over 3 hrs
Maintenance dose: 600 to 900 mg of elemental Mg++ per 24
hrs IV or IM (Each gram MgSO4 = 99 mg or 4.1 mmol
elemental Mg++)
In emergency situations, the loading dose should not exceed
15 mg/min.
MgSO4 can be administered IM at 200 mg every 4 hrs for 24 hrs
then 100 mg every 4 hrs.
To avoid toxicity, monitor the following parameters:
· Heart rate
· Respiratory rate
· Deep tendon reflexes
· Urine output
ECG monitoring is also recommended.
Hypocalcemia is commonly seen in “watusi” and jatropha seed

ingestion. It may also be a complication of bites and stings of animals
such as sea urchins and spiders.
Treatment of Hypocalcemia
Calcium salt
For parenteral administration of calcium, calcium chloride is
the preferred preparation because it has better and more
predictable retention in the body, compared to calcium
gluconate.
Adult: 2.25 to 4.5 mmol calcium by slow IV push

Repeat as required.
Pedia: 100 to 300 mg/kg/day IV
17
Calcium Preparations with Respective Calcium Contents
Calcium Salt Approximate Calcium Content per g
mg mmol mEq
Calcium carbonate 253 6.3 12.6
Calcium chloride (dihydrate) 273 6.8 13.6
Calcium glubionate (monohydrate) 66 1.6 3.3
Calcium gluconate 89 2.2 4.5
Calcium lactate 184 4.6 9.2
Calcium lactate gluconate (dihydrate) 129 3.2 6.4
Calcium lactobionate (dihydrate) 51 1.3 2.5
Calcium phosphate 388 9.7 19.3
Hypothermia, with a rectal temperature < 30º C, is a complication of an

overdose of several toxicants (see list). In general, only supportive
measures are needed. When the patient's sensorium improves, body
temperature should return to normal. Measures to raise body
temperature rapidly may be harmful. Agents used to induce a rise in
temperature are unnecessary.
Hyperthermia, with a rectal temperature > 40ºC, is a toxic effect of

several agents (see list). Immediately cool the patient to a body
temperature of 39ºC to prevent death or severe brain damage.
Continued cooling below this temperature will lead to “overshoot
hypothermia.” Initial treatment consists of external cooling, sponge bath
using tepid or lukewarm water, fanning, and iced gastric or colonic
lavage. Ice-water immersion may be done provided shivering is
Toxicants Associated with Hypothermia

· Alcohol · General anesthetics · Sedative-hypnotics
· Barbiturates · Opioids · TCADs
· Carbon monoxide · Phenothiazines
Toxicants Associated with Hyperthermia

· Amphetamines · Phenothiazines · Xanthines
· Anticholinergics · Phenytoin Aminophylline
· Antihistamines · Quinidine Theophylline
· Cocaine · Salicylates
· Isoniazid · Sulfonamides
18
controlled with diazepam. Subsequent treatment should be directed
toward the underlying cause.
Hypoglycemia is a common
finding in alcohol intoxication
and salicylate toxicity Treatment of Hypoglycemia
because of prolonged Glucose infusion
glucose utilization and Adult: 50-100 mL Dextrose 50%
depletion of hepatic glycogen Pedia: 1-2 mL/kg/dose Dextrose 10%
stores.
Acid-base abnormalities can also be complications of acute poisoning.

Toxicity with CNS depressants is often associated with mild acidemia due
to mixed respiratory and metabolic acidosis. This is due to a
combination of respiratory depression and cardiogenic shock. In this
situation, correct the respiratory acidosis first for this may obviate the
need for treating the metabolic component.
Salicylate and xanthine poisoning may lead to mixed respiratory alkalosis

and metablic acidosis. In salicylate toxicity, these states are brought
about by respiratory stimulation and Type B metabolic acidosis
(disturbance of hepatic redox state). In aminophylline or theophylline
toxicity, the mixed acid-base disturbance is secondary to
hyperventilation and Type A lactic acidosis (tissue hypoxia).
19
II. CLINICAL EVALUATION
A. History
Elicit the chief complaint and most pertinent symptoms. Remember that
patients with a history of poisoning must be observed at a health care
facility even if they are asymptomatic. Manifestation of symptoms of
poisoning may be delayed by hours or days (see box) .
About 80% of adults who

take, or are exposed to,
Poisons with Delayed Manifestations
poisons are conscious Ethylene glycol 6 hours
on arrival in the hospital Salicylates 12 hours
and a clear history can Paracetamol 36 hours
be obtained. However, Paraquat 48 hours
Methanol 48 hours
some patients may be
Coumatetralyl 72 hours
reluctant to admit what Thyroxine 4 weeks
they have taken.
Depressed sensorium or
massive injury may also prevent them from speaking. The persons who
come in with the patient may also offer some information. Ask
companions or relatives to search the area where the poisoning took
place. Have them look for substances or containers of substances which
may have caused the poisoning.
Gather the following information:
1. Type and amount of poison - Identify the poison in order to

establish its toxicity.
2. Time of exposure - This is especially crucial in caustic ingestion
since the decision regarding nasogastric tube insertion has to be
made. Knowing the time of intoxication will also give an idea of
the poison’s phase of biotransformation at the time of
admission.
3. Mode of exposure - (i.e., oral, inhalational, dermal). Establish
the route of entry in the initial examination.
4. Intake of other substances - Ask about exposure or intake of
other substances which may contribute to the intoxication.
5. Circumstances prior to poisoning - Ask about what the patient
20
was doing prior to the poisoning. Illness occurring while spraying
in a farm may suggest pesticide poisoning. A patient rescued
from a fire may have carbon monoxide and/or cyanide
poisoning. It is also important to note the patient’s emotional
stability. Ask about possible causes of stress at home or at work.
There may also be a history of recent traumatic life events.
6. Past medical history and current medications - Inquire about
whether the patient is currently taking any medication. Ask
about existing heart, liver or lung disease. Ask about psychiatric
consults and medications also. Check if the patient may have
taken other substances which may aggravate the poisoning (e.g.,
barbiturates taken with alcohol, salicylate with warfarin,
marijuana with CNS stimulants/depressants).
7. Any home remedies given - Inquire about home remedies or
immediate treatments given or done by both non-medical and
medical personnel. These measures may either improve or
complicate the condition of the patient.
B. Physical Examination
The physical examination is a valuable tool that can help determine the
extent of poisoning, its complications, and the presence of any
underlying disease.
When history taking yields very little information, pay attention to signs
which, taken collectively with symptoms, can characterize a suspected
toxicant. These toxidromes are groups of manifestations which occur
consistently with particular poisons (see box, next page). For example,
INH toxicity presents with a toxidrome consisting of coma, seizures and
acidosis. Sometimes, however, patients present with ‘partial’
manifestations rather than ‘classic’ clinical findings. Even if the signs
and symptoms of a patient are not entirely characteristic, they may still
be considered as part of a toxidrome and are therefore useful in
establishing etiology.
1. Evaluate general status - Several medical conditions such as

hyper- or hypotension are associated with certain toxicants (see
box, next page).
2. Examine the patient’s skin - Look for needle tracks, bruises,
lacerations. Other dermal findings include:
21
Toxidromes Hypertension
Anticholinergics C Cocaine
Hot as a hare (hyperthermia) T Theophylline
Dry as a bone (dry mucosa) S Sympathomimetics
Red as a beet (flushed skin) (amphetamine, PPA)
Blind as a bat (dilated pupils) C Caffeine
Mad as a hatter (confusion, delirium) A Anticholinergics
N Nicotine
Sympathomimetics
(Cocaine, amphetamines) Hypotension
M Mydriasis
T Tachycardia C Clonidine
H Hypertension R Reserpine and other
H Hyperthermia antihypertensives
S Seizures A Antidepressants
S Sedative-hypnotics
Cholinergics / muscarinic effects H Heroin and other
(Organophospate/carbamate pesiticides) opiates
D Diarrhea, diaphoresis
U Urination Hyperventilation
M Miosis, muscle fasciculations C Carbamates
B Bradycardia, bronchoconstriction, O Organophosphates
bronchorrhea M Methanol
E Emesis E Ethylene Glycol
L Lacrimation T Theophylline
S Salivation, sweating S Salicylates
Nicotinic effects
(Organophospate pesiticides)
Hypoventilation
M Muscle weakness and fasciculations C Clonidine
A Adrenal medulla activity increased O Opioids
T Tachycardia M Heavy metals
C Cramping of skeletal muscles B Beta-blockers
H Hypertension A Aromatic hydrocarbons
T TCADs
Narcotics and Opiates T Theophylline and
M Miosis other xanthines
B Bradycardia S Sedatives
H Hypotension (e.g., barbiturates)
H Hypoventilation Qui Quinidine
C Coma D Digitalis
22
Mydriasis Miosis
A Antihistamines C Cholinergics
Antidepressants Clonidine
S Sympathomimetics O Opiates
(methamphetamine, Organophosphates
cocaine) P Phenothiazines
I Isoniazid Pilocarpine
A Anticholinergics Pontine bleed
S Sedative-hypnotics
· Cutaneous bullae - barbiturates, carbon monoxide

· Diaphoresis - carbamate and organophosphate pesticides,
salicylate, amphetamine
· Jaundice - a delayed manifestation of paracetamol and other
hepatotoxic agents
· Dry skin and hyperpyrexia - atropine and other anticholinergic
agents, TCADs
· Flushing - anticholinergics, alcohol, cyanide
Breath Odors
Bitter almonds Cyanide
Fruity odor Diabetic ketoacidosis
Isopropyl alcohol
Oil of wintergreen Methylsalicylate
Rotten eggs Sulfur dioxide
Hydrogen sulfide
Pears Chloral hydrate
Garlic Arsenic
Organophosphate
Dimethyl sulfoxide (DMSO)
Mothballs Camphor
3. Characterize the odor of the patient’s breath - Certain odors

are associated with drugs or chemicals.
4. Auscultate the lungs - Rales may be indicative of:
· Edema - pesticides, INH, opiates, beta-blockers, TCADs
· Aspiration pneumonia - a primary concern in hydrocarbon
(kerosene) ingestion
23
5. Listen to the heart - Take note of irregular rhythms.
6. Check the abdomen for organomegaly, normality of bowel
sounds and possible gastrointestinal disturbances.
7. Do a complete neurologic examination - The patient’s level of
consciousness can be graded using the Glasgow Coma Scale
(GCS). Although the scale was originally devised for patients
suffering from head injury, until a better method is developed,
the GCS is useful as a descriptive and prognosticating tool for
patients with impaired levels of consciousness.
IMPORTANT POINTS: Neurologic signs can aid in the identification of

etiologic agents. Neurologic manifestations may be due to direct or
secondary metabolic effects of the toxicants.
Remember to consider structural neurologic problems. Trauma to the

head may occur when the patient loses consciousness and falls.
Certain chemicals may mask the effects of other toxicants. A mixed

presentation can manifest when more than one agent is responsible for
the symptoms. Be aware of possible multiple drug intoxication.
Tachycardia Bradycardia
I Iron P Propranolol and other beta-blockers
C Carbon monoxide A Anticholinesterases
Cyanide C Clonidine
O Organochlorines Calcium channel blockers
P Phenothiazine Codeine and other opioids
E Ethylene Glycol E Ethanol
Ethanol D Digitalis
F Free-base cocaine
A Anticholinergics
Antihistamines
Amphetamines
S Sympathomimetics
Salicylates
Solvents
T Theophylline
24
Glasgow Coma Scale
For Adults For Children
Eye Opening
Spontaneous Spontaneous 4
To speech To speech 3
To pain To pain 2
No response No response 1
Best Verbal Response

Oriented conversation Smiles, follows objects/sounds, interacts 5
Confused conversation Cries but consolable 4
Inappropriate words Sometimes inconsolable, moaning 3
Incomprehensible sounds Inconsolable, agitated 2
Best Motor Response

Obeys commands Moves spontaneously or purposefully 6
Localizes pain Withdraws from touch 5
Withdraws from pain Withdraws from pain 4
Decorticate rigidity Decorticate rigidity 3
Decerebrate rigidity Decerebrate rigidity 2
TOTAL SCORE 3 to 15
NOTE: In general, a score of 8 or less is correlated with a poor prognosis.

A score of 3 to 4 has an 85% chance of mortality.
C. Laboratory Examinations
Laboratory tests are usually adjunctive help but in some instances are
important in diagnosis and management. Be aware of possible false
positives or negatives which may adversely affect treatment.
1. Bedside toxicology - Even prior to doing confirmatory analytical

laboratory tests, there are examinations that can be done in the
emergency room setting. These bedside screening tests include
simple examinations per formed on urine samples,
interpretations of which are based on color changes. An
example is the Forrest Test for phenothiazine overdose. A
25
positive test is indicated by the development of a deep purple
color after addition of 6 to 7 drops of 12N sulfuric acid and 2
drops of 10% ferric chloride to 2 mL of the patient’s acidified
urine.
2. Specimen collection
Blood 5 to 10 mL of heparinized and clotted samples
Keep test tubes in ice
Urine 200 mL, preferably the first void
Collect blood and urine for toxicology screening. Place these in a
o
sealed container and store in a freezer (-20 C) if these cannot be
examined right away. The timing of specimen collection is
important for accurate interpretation of laboratory results. The
pharmacokinetic characteristics of a substance dictate when
the samples should be obtained. This is important when
quantitative evaluation is needed. For instance, in cases of
paracetamol toxicity, sampling should not be done earlier than
the fourth hour post-ingestion. This is because the dose-effect
relationship (Rumack-Matthew nomogram) can be
demonstrated only when the blood sample is taken on, or after,
the peak plasma concentration time. When interpreting results,
remember to take into consideration factors such as intake of
other drugs and existing medical conditions. These factors may
alter the effect of the toxicant.
3. General laboratory examinations - General laboratory
examinations must be done rationally
CBC check for anemia and leukocytosis
Urinalysis check urine pH and specific gravity
FBS detect any metabolic abnormalities
BUN, Creatinine
Electrolytes
ABG check for acid-base disturbances and
hypoxemia
ECG detect arrhythmias
LFTs, PT assess hepatotoxicity
activated PTT
Upright CXR check for aspiration pneumonia, pulmonary
edema or perforated ulcer
Abdominal XR use for diagnosing intake of radio-opaque
drugs and ruptured viscus
26
Conditions or Agents Predisposing to
Metabolic Acidosis or Elevated Anion Gap
M Methanol A Aminoglycosides G Grand mal seizures
E Ethanol C Cyanide A Aspirin (salicylates)
T Toluene Carbon monoxide P Paraldehyde
Theophylline I Isoniazid Phenformin
A Alcoholic ketoacidosis Iron
L Lactic acidosis D Diabetic ketoacidosis
Radio-opaque Drugs
C Chloral hydrate
H Heavy metals (arsenic, lead, iron)
I Iodides
P Psychotropics (TCADs, phenothiazines)
E Enteric-coated medications (salicylate)
III. ELIMINATION OF THE POISON

A. External Decontamination
Discard the patient's clothing and thoroughly bathe or shower the patient
when there is dermal exposure to toxic substances. Removal of the
patient's clothing eliminates as much as 70% of the poison.
Contaminated clothes should be put into an impermeable, double
layered bag for later neutralization and disposal. If there is eye
contamination, irrigate the eye with free flowing water for 30 mins. Avoid
the use of neutralizing solutions, as these may cause further injury
because of the resultant exothermic reaction and release of carbon
dioxide, especially in cases of caustic poisoning. It is imperative that
health personnel involved in the decontamination process wear
protective equipment (e.g., gloves, face mask, plastic or vinyl apron) to
prevent contamination. External decontamination should be done in an
area outside of the emergency room to prevent contamination of non-
poisoned patients.
27
B. Empty the Stomach
Induction of emesis and gastric lavage are the two most commonly
employed means of gastric emptying. However, clinical studies have not
shown enough evidence of the effectiveness of these maneuvers in
decreasing gastrointestinal absorption.
1. Induction of Emesis - This is of value only when managing

patients who have ingested poison within one hour. Emesis
must be performed only within one hour of ingestion. Consider
this only when: there are no absolute contraindications; the
amount ingested can lead to toxicity; or anticipated definitive
treatment will be delayed.
Contraindications to Emesis
· Depressed sensorium or impending loss of consciousness
· Impaired gag reflex
· Presence of cardiac disease and aneurysm
· Ingestion of caustics, hydrocarbons, convulsants, arrhythmogenic
agents
· Debilitated, elderly patients or medical conditions such as late preg-
nancy that may be further compromised by the induction of emesis
· Mechanical emesis - Ideally, emesis need not be done in the

hospital, unless the hospital does not have the means to perform
gastric lavage. Clinical indications include:
· ingestion of large pills that do not disintegrate
· ingestions by infants and small children in whom large-
bore tubes cannot be used safely
Instruct the patient to take 1 to 2 glasses of warm water, then
apply pressure on the posterior pharynx with a blunt
instrument.
· Syrup of Ipecac
The use of syrup of ipecac is no longer routinely
recommended for the following reasons: there is no evidence
from clinical studies showing improved outcome with its use;
it can cause prolonged vomiting and this may delay the
administration of activated charcoal; and it may cause
complications including aspiration pneumonia.
28
2. Gastric lavage is recommended in patients who have ingested
potentially life threatening amounts of poison and the procedure
can be done within 1 hour of ingestion. Some studies have
shown that lavage can be of benefit up to 4 hours after ingestion
especially in patients who have ingested drugs that form
concretions or bezoars in the stomach, or those that
substantially decrease gastric motility. Studies show that when
done alone, gastric lavage does not have any benefit even when
it is done within 1 hour of ingestion. There is evidence showing
that the procedure can enhance gastric emptying.
· Insert a nasogastric tube (Fr. 16 for adults or an appropriately
sized tube for pediatric patients).
· Place patient on Trendelenburg position with head turned to
the left while inserting the nasogastric tube. Afterwards,
place patient to the left lateral decubitus position.
· Aspirate gastric contents. Check for presence of blood,
tablets, etc.
· Give lukewarm or tepid water:
Adult: 50 to 60 mL Pedia: 10 to 20 mL
Repeat until return flow is clear.
· Do not perform gastric lavage if the patient:
· has ingested caustics or kerosene unless a more toxic
substance is combined with kerosene, or the ingested
kerosene is > 2 mL/kg
· has depressed sensorium with unprotected airway
· has frank convulsions
· is at risk of hemorrhage or gastrointestinal perforation
· is uncooperative
Risk of aspiration pneumonia should be anticipated when gastric
lavage is performed. Protection of the airway must be a primary
consideration.
C. Administer Single-dose Activated charcoal
Activated charcoal is effective in decreasing absorption of some drugs by

binding these on the surfaces of the charcoal particles. The drug is not
systemically absorbed. The American Academy of Clinical
Toxicology/European Association of Poisons Centres and Clinical
Toxicologists (AACT/EAPCCT) recommend that the administration of
activated charcoal may be considered if the patient has ingested a
29
potentially toxic amount of a poison up to Substances Effectively
one hour following ingestion. There are Adsorbed by
insufficient data to either support or Activated Charcoal
exclude its use if the time of ingestion is Organic Compounds
more than an hour prior to consult. Amphetamines
· Ensure that the patient is in Antidepressants
Trendelenburg and left lateral Antiepileptics
decubitus position. Antihistamines
· To produce effective adsorption, Aspirin
give a ratio of about 10 parts Atropine
charcoal to 1 part poison. Barbiturates
Adult: 50 to 100 g of activated Benzodiazepines
Beta blockers
charcoal in 100 to 200 mL water Chloroquine
Pedia: 1 g/kg in water as 1:3 Cimetidine
dilution, or 30 to 50 g in 100 mL Dapsone
water Digitalis
Furosemide
Substances NOT Glibenclamide
Effectively Adsorbed Glipizide
by Activated Charcoal Indomethacin
Malathion
Cyanide NSAIDs
Alcohol Parace tamol
Lithium Phenol
Iron Phenothiazines
Petroleum distillates PPA
Quinine
Contraindications to Salicylates
the Use of Activated Charcoal Strychnine
· Gastrointestinal tract is not anatomically Tetracyclines
intact - this can cause aspiration or Theophylline
peritonitis
· Unprotected airway - this increases the Inorganic Compounds
risk of aspiration Antimony
· Ingestion of corrosive substances - there Arsenic
is danger of perforation Iodine
Mercury chlorate
Permanganate
Phosphorus
Potassium
Silver
Tin
30
D. Administer cathartic
Cathartics can be used to hasten intestinal elimination of the

unabsorbed toxic agent. Based on clinical studies, the ACCT/EAPCCT
recommend that cathartics should have no role in the management of a
poisoned patient when used alone. However, the experience of the UP-
NPMCC shows that use of cathartics alone have been helpful in
accelerating expulsion of large amounts of poison such as kerosene,
thereby reducing contact time of the poison in the gut.
Sodium sulfate
Adult: 15 g in 100 mL water
Pedia: 250 mg/kg given as 10% solution
Sodium sulfate should be administered after charcoal lavage. If no
bowel movement occurs in 30 minutes to 1 hour, another dose may
be given. If there is still no bowel movement, do not give another dose
of sodium sulfate. Consider giving soap suds enema instead.
Contraindications to the Use of Cathartics

· Caustic ingestion
· Poisoning from drugs/chemicals which are readily absorbable
· In patients with paralytic ileus
· In patients with severe fluid and electrolyte disturbances
· Extremes of age
· In patients with congestive heart failure (do not use sodium-
containing cathartics)
E. Use demulcents/neutralizing agents
Demulcents and neutralizing agents have a very limited role in the

management of poisoned patients.
· Raw egg white (albumin only) is a commonly used demulcent
for mild caustic ingestion and “watusi” poisoning.
Adult: 8 to 12 eggs
Pedia: 4 to 6 eggs
· Sodium bicarbonate
neutralizing agents in iron toxicity and redtide poisoning.
NaHCO3 (8.4%): 1 vial of 8.4% sodium bicarbonate in 250 mL
water makes a 2% solution
31
Baking soda: 1 heaping teaspoon in 100 mL water makes a 5%
solution
· Milk and acetic acid/tannic acid are not recommended as
neutralizing agents.
F. Whole bowel irrigation
This procedure “flushes” the poison down the gastrointestinal tract,

removing and preventing further absorption of the toxicant. A propylene
glycol (PEG) electrolyte solution is used. The recommendation is not to
routinely use this procedure. Studies show that there are no
established indications for the use of whole bowel irrigation, nor is there
conclusive evidence showing that this procedure improves patient
outcome.
IV. ENHANCING ELIMINATION OF

ABSORBED POISONS
A. Multiple-dose activated charcoal
Multiple dose activated charcoal administration is beneficial in:

· enhancing the preabsorptive elimination of drugs which decrease
gastric motility, and sustained-release agents that have erratic
absorption in the gastrointestinal tract
· gut dialysis of drugs that are lipophilic, have low protein binding
capacity, have small volumes of distribution and long half-lives
· interrupting enterohepatic recirculation
Studies have proven the effectiveness of multiple-dose activated
charcoal in poisoning secondary to carbamazepine, dapsone,
phenobarbital, quinine and theophylline.
· Give activated charcoal every 4-8 hours. However, exercise
caution because of the danger of intestinal impaction, gut
obstruction and pulmonary aspiration.
· Ensure that bowel movement is observed daily.
Activated charcoal is contraindicated in poisoning due to caustics and
petroleum distillates.
32
Substances with Enterohepatic Recirculation
· Anticoagulants · Disopyramide · Phenothiazine
· Aspirin · Methamphetamine · Piroxicam
· Carbamazepine · Nadolol · Salicylate
· Cyclosporine · Organochlorine pesticides · Sotalol
· Dapsone · Phencyclidine · Theophylline
· Digoxin · Phenobarbital · TCADs
· Digitoxin · Phenylbutazone
B. Forced diuresis
Forced diuresis is not frequently indicated since many drugs are

metabolized in the liver. In fact, there is no clinical evidence to support its
effectiveness. Therefore, forced diuresis is no longer recommended in
enhancing elimination of the poison. Appropriate rehydration to promote
adequate urine output would suffice.
C. Alkalinization therapy
Alkalinization of the urine ionizes weak acids such as salicylates,

barbiturates, isoniazid, and 2,4-dichlorophenoxyacetic acid. It inhibits
passive renal tubular reabsorption of non-ionized molecules, thus
enhancing excretion.
Sodium bicarbonate
Give NaHCO3 (8.4%) at 1 mEq/kg/dose or 1 mL/kg/dose IV until
urine pH is 7.5-8.5.
D. Acidification therapy
Acidification of the urine ionizes weak bases such as amphetamines,

PCP, phenytoin and theophylline. Although the AACT and EAPCCT no
longer recommend acidification therapy because it can produce
metabolic acidosis, rhabdomyolysis and renal failure, local studies have
shown benefits with the use of this technique in methampethamine
toxicity.
Ascorbic Acid
Adult: 1 g IV q 6 hours until urine pH < 5.5
Pedia: 20 mg/kg IV q 6 hours until urine pH < 5.5
33
E. Dialysis and hemoperfusion Indications for
Hemoperfusion
These procedures are employed in:
· life-threatening poisoning Barbiturates
· electrolyte and acid-base short and medium acting
Disopyramide
disturbances
Glutethimide
· cases involving dialysable toxins Meprobamate
with poor body clearance and high Phenobarbital
plasma toxin concentration Salicylates*
· cases where the patient has Theophylline
underlying kidney or liver problems
Peritoneal dialysis, which is widely *2 to 3 times more efficient
available, is useful if short-term dialysis is than dialysis
required as in severe salicylate toxicity,
and ethylene glycol or methanol ingestion. Hemodialysis is much more
effective than peritoneal dialysis in the elimination of methanol, ethylene
glycol, lithium and isopropanol. Hemoperfusion is effective in poisoning
secondary to barbiturates, carbamazepine, theophylline, glutethimide,
quinidine, and paraquat. Activated charcoal is the most popular
adsorbent used in hemoperfusion.
Toxicants and Indications for Dialysis

Dialysis is Dialysis is dependent on Dialysis is not
indicated patient’s condition indicated
Amanita phalloides Alcohols Iodides Antidepressants

Antifreeze Ammonia Isopropanol Belladona
(glycol type) Amphetamines INH compounds
Heavy metals in Aniline Lithium Benzodiazepines
soluble compounds Barbiturates Meprobamate Chlordiazepoxide
Heavy metals after Boric acid Paraldehyde Dextropropoxyphene
therapy with Bromides Potassium Digitalis
chelating agents Calcium Quinidine Diphenoxylate
Methanol Chloral hydrate Quinine Glutethimide
Diphenylhydantoin Salicylates Heroin and other
Ethclorvynol Strychnine opiates
Fluorides Thiocyanate Synthetic
anticholinergics
34
V. ADMINISTRATION OF
ANTIDOTES
The use of specific antidotes is seldom necessary except when their
administration is beneficial and life-saving. Administration of antidotes
should be dependent on the assessment of the patient’s clinical state,
laboratory results and the pharmacodynamics of the substance.
Antidotes are grouped according to their mechanisms of action as
indicated below.
Chelating Agents
A. Inert Complex Formation BAL - British anti-Lewisite
DMPS - 2,3 Dimercapto-1-
Chelating agents are used in propane sulphonate
heavy metal poisoning. These DMSA - Dimercaptosuccinic acid
chemicals facilitate the formation DTPA - Diethylene triamineopiate
of a stable complex with a 5- or 6- pentaacetic-N-N-N-N-N acid
membered ring, and incorporation EDTA - Edetate calcium disodium
NAPA - N-acetyl penicillamine
of a sulfide bond.
PEN - Penicillamine
Chelators of Choice for Selected Metals

Metal 1st choice 2nd choice Contraindicated
Arsenic DMSA BAL

DMPS
Lead DMSA Ca EDTA BAL*
PEN
Methylmercury DMPS NAPA BAL
DMSA
Cadmium Ca EDTA DMSA BAL
Copper PEN DTPA BAL
DMSA
*Can be used adjunctive with Calcium EDTA in acute lead encephalopathy.
B. Accelerated Detoxification
The use of thiosulfate in cyanide toxicity is a good example of accelerated

detoxification. Thiosulfate enhances rapid detoxification of cyanide to
thiocyanate in the central compartment thereby preventing cyanide
distribution to the cells.
35
C. Reduction in Conversion to More Toxic Compounds
Ethanol is used to inhibit conversion of methanol and ethyl glycol to their

more toxic metabolites. This is also true with the use of phenytoin in
malathion poisoning wherein it prevents the conversion of malathion to
its more toxic metabolite, malaoxon.
D. Competitive Inhibition at Receptor Sites
Naloxone exerts its action by blockade of receptor sites in the central

nervous system, except those in the spinal column. Likewise, atropine
blocks the action of acetylcholine at the muscarinic receptor sites.
E. Bypassing the Effects of the Poison
Administration of oxygen can bypass the effects of cyanide because

oxygen may have a synergistic antidotal action when used with sodium
thiosulfate and sodium nitrite as shown in animal studies. This
mechanism also explains the use of pyridoxine in INH toxicity.
F. Antibodies Interacting with Poisons
Digoxin-specific antibodies (Fab fragments) reverse the binding of

digitalis compounds to cardiac receptors. In snakebites, especially
cobra bites, administration of antivenin neutralizes the venom.
VI. SUPPORTIVE THERAPY AND

OBSERVATION
Supportive care is essential in the management of poisoned patients,
especially when they require intensive care. Be sure to do the
following:
· Give IV fluids for maintenance and replacement of fluid losses.
· When alkaline and acid therapy are employed, test frequently
for blood and urine pH.
· Provide intensive nursing care to avoid aspiration or
development of decubitus ulcers.
· Treat metabolic disturbances: electrolyte imbalance,
hypoglycemia, hypothermia and hyperthermia.
36
· Monitor vital signs.
· Monitor input and output.
VII. DISPOSITION
A poisoned patient should be observed for at least 24 hours, even if he or
she is asymptomatic. This can be done at the emergency room or in the
wards. After such time, re-evaluate and determine whether there is a
need for further observation or if the patient can be sent home.
Refer for psychiatric evaluation if the mode of poisoning is (or suspected

to be) suicidal. While at the hospital, observe suicidal precautions.
Patients who present with violent behavior should be restrained and
placed in an isolation room to minimize unnecessary external stimuli.
For substance abusers, consider referral to support groups or
rehabilitation centers upon discharge. Find out about community
resources or non-govenment organizations which cater to vulnerable
groups such as battered women, unwed mothers, or young people with
emotional problems, and encourage the patient or his/her family to
contact them.
Although the manner of poisoning in children is usually accidental, the

possibility of child abuse should not be discounted. Consider referral to
social services (for example, the Child Protection Unit for PGH patients).
In all cases, family counseling and education should be initiated while

the patient is in the hospital, and continued during out-patient follow-up.
37
38
Readily Available Agents Used as Antidotes*
DRUG INDICATION MODE OF ACTION
Activated charcoal Non-specific adsorbent of poisons EXCEPT Adsorption of drug in gastric and
cyanide, iron, lithium, caustics and alcohol intestinal tracts and interruption
of enterohepatic cycle with
multiple dose (MDAC)
N-acetylcysteine Paracetamol, “watusi” (dancing firecracker), Restores depleted glutathione stores
zinc phosphide, carbon tetrachloride, Protects against renal and hepatic
chloroform, penny royal, cyclophosphamide- failure
induced cystitis
Atropine Organophosphates, carbamates, Competitive inhibition of muscarinic
cholinesterase-inhibiting nerve agents, receptors
scorpion sting in children Reversal of central & peripheral
muscarinic symptoms intoxicated
by Clitocybe or Inocybe mushroom
species
Benzylpenicillin Amanita phalloides Not known; partial protection against
(Penicillin G crystalline, acute hepatic failure; may
sodium salt) displace amatoxin from protein-
binding sites allowing increased
renal excretion; may also inhibit
penetration of amatoxin to
hepatocytes
Bromocriptine Neuroleptic malignant syndrome Dopamine agonist
caused by neuroleptic drugs
or levodopa withdrawal
Readily Available Agents Used as Antidotes* (continued)

Calcium folinate Folic acid antagonists: Bypasses blocked folate metabolism
Leucovorin calcium Methotrexate
(Folinic acid or Trimethoprim
citrovorum factor) Pyrimethamine
Methanol (formate)
Adjunct: Ethylene glycol poisoning
Calcium salts Fluoride ingestion Rapidly complexes with fluoride ion
Black widow spider envenomation Directly antagonistic to the cardiotoxic
Hypocalcemia from oxalate ingestion effects of hyperkalemia
or citrate I.V. (anticoagulant of fresh frozen
plasma/whole blood) Maintains adequate amount of
ionized calcium to prevent
hypocalcemia
Dantrolene sodium Malignant hyperthermia Skeletal muscle relaxant by
Neuroleptic malignant syndrome preventing calcium release from
Phenelzine toxicity endoplasmic reticulum into
myoplasm
Decreases hyperthermia and muscle
rigidity in amphetamine/MAO
toxicity and poisoning with
carbon monoxide
Deferoxamine Iron, chronic aluminum poisoning Chelates ferric ions to form
ferrioxamine and readily excreted
in the urine
Chelates aluminum ion
39
40
Dimercaptopropane Arsenic, methylmercury Forms water soluble chelates with
sulphonate (DMPS)** heavy metals which are
subsequently excreted through
the kidneys
Dimercaptosuccinic Lead, arsenic, mercury Forms water soluble chelates with
acid (DMSA/Succimer) antimony, bismuth heavy metals which are
subsequently excreted through the
kidneys
Digoxin specific Severe digoxin poisoning Forms complexes with digoxin which
antibody fragments** Cardiac glycosides from plant are excreted through the kidneys
and animal products
Edetate calcium disodium Lead Chelation of lead ions and
(Ca EDTA)** endogenous metals (zinc,
manganese, iron, copper)
Ethanol Ethylene glycol, Di- or triethylene Inhibits metabolism of ethylene glycol
glycol, propylene glycol, and other glycols to the more toxic
ethylene glycol butyl ethers glycoaldehyde and glycolate
Methanol Inhibits metabolism of methanol to
formaldehyde and formic acid
Flumazenil Diazepam and other benzodiazepines Direct receptor antagonist in the CNS
Imidazopyridines (zolpidem, zoplicone) GABA receptors

Fomepizole** Ethylene glycol Inhibits metabolism of ethylene glycol
Methanol to gycoaldehyde and glycolate and
Isopropanol competitive inhibitors of alcohol
1,4 Butanediol (1,4-BD) dehydrogenase
Inhibits metabolism of methanol to
formaldehyde and formic acid
Glucagon** Calcium channel blocker or beta-receptor Stimulates formation of adenyl
blocker toxicity cyclase causing intracellular
Cardiac depression caused by Ia and Ic increase in cyclic AMP and
antiarrhythmic drugs; enhanced glycogenolysis and
Empiric use in patients with myocardial elevated serum glucose
depression (bradycardia, hypotension, concentration
low cardiac output)
Heparin Ergotamine Reverses hypercoagulable state by
interacting with antithrombin III
to produce a heparin/antithrombin-
thrombin complex
Used in combination with vasodilator
phentolamine or nitroprusside to
prevent local thrombosis and
ischemia
Hydroxocobalamin** Cyanide and cyanide derivatives Forms cyanocobalamin, a non-toxic
(followed by sodium Cyanogenic compounds (E.g. acetonitrile) metabolite that is easily excreted
thiosulfate) Prevention of nitroprusside-induced through the kidneys
cyanide toxicity
41
42
Methylene blue Chemicals producing severe methemoglobi- Reduces methemoglobin to
nemia hemoglobin; at therapeutic doses,
methylene blue is reduced by
nicotinamide adenine dinucleotide
phosphate dependent enzyme
system to leucomethylene blue
which rapidly converts
methemoglobin back to
hemoglobin
Naloxone Narcotics, opioids Pure anatgonist acting as competitive
Nalmefene** Opioids with long duration of action inhibitor at opiate receptor sites
(m, k, q receptors) within the
central nervous system
Neostigmine Anticholinergic drugs with tachycardia Anticholinesterase which causes
Competitive neuromuscular blockers accumulation of acetylcholine at
(non-depolarizing) cholinergic receptor sites
Nitrite, sodium Cyanide, cyanogenic compounds Oxidizes hemoglobin to methemo-
(intravenous) and Nitroprusside-induced cyanide toxicity globin which binds with free
glyceryltrinitrate/ Hydrogen sulfide cyanide and can enhance
nitrogylcerin (ointment endothelial cyanide detoxification
or patch) by producing vasodilatation
Penicillamine Copper, gold, lead, mercury, zinc, arsenic Chelation of metal ions

Propranolol (oral) Beta-adrenoreceptor stimulants Propranolol, a non-selective beta-
Esmolol (IV) Ephedrine, cocaine, theophylline, adrenoreceptor drug and Esmolol,
(NOT compatible caffeine, thyroxine a cardioselective agent, suppress
with sodium Excessive myocardial sensitivity (freons, sympathetic overactivity and rate-
bicarbonate solution) chloral hydrate, chlorinated hydrocarbons) related myocardial ischemia
Pralidoxime** Organophosphates and some carbamates Reactivates phosphorylated
with nicotinic effects including cholinesterase enzymes and
organophosphate nerve warfare agents protects enzyme from further
inhibition when given before
acetylcholinesterase has been
irreversibly bound; must always be
used in combination with atropine
Pyridoxine Isoniazid, theophylline Reverses acute pyridoxine deficiency
Monomethyl hydrazine, hydralazine by promoting GABA synthesis;
Adjunctive therapy in ethylene glycol poisoning promotes the conversion of toxic
metabolite glycolic acid to glycine
Protamine sulfate Heparin Neutralizes heparin by combining with
heparin and forming an inactive
salt
Sodium bicarbonate Iron Prevents conversion of ferrous to
(continued next page) ferric
Cardiotoxic drugs affecting the fast sodium Decreases affinity of cardiotoxic drugs
channel (tricyclic antidepressants, to the fast sodium channel
cocaine, type Ia and Ic antiarrythmic
agents, diphenhydramine)
43
44

Sodium bicarbonate Weak acids Promotes ionization of weak acids
(from previous page) (salicylates, phenobarbital,
chlorpropamide, chlorophenoxy-
herbicides, methotrexate, INH, etc.)
Chlorine gas inhalational poisoning Neutralization of hydrochloric acid
formed when chlorine gas reacts
with water in the airways
Snake anti-venin Cobra bite Neutralizes venom by binding with
circulating venom components and
with locally deposited venom by
accumulating at the bite site
Sodium thiosulfate Cyanide and cyanide derivatives Replenishes depleted thiosulfate
Cisplatin stores by acting as sulfur donor
necessary for the conversion of
CN-O to thiocyanate through the
action of sulfur transferase enzyme
rhodanese
Thiamine Alcohol Reverses acute thiamine deficiency
Wernicke-Korsakoff Syndrome in
alcoholic and malnourished patients Adjunctive in ethylene glycol
Enhances detoxification of glyoxylic
acid

Vitamin C Chemicals causing methemoglobinemia Reduces methemoglobinemia to
(Ascorbic acid) in patients with G6PD deficiency hemoglobin
Vitamin K1 Anticoagulant drugs (coumarin, indanedione Bypasses inhibition of Vitamin K
(Phytomenadione) derivatives) epoxide reductase enzyme
Anticoagulant rodenticides
Vitamin K deficiency (hemorrhagic disease As replacement for Vitamin K1
of the newborn) with coagulopathy
Hypoprothrombinemia from salicylate / white
or yellow phosphorous intoxication
*Maramba, NPC and Panganiban LR: U.P. National Poison Management & Control Center
** Not available in the Philippines
45
REFERENCES
American Academy of Clinical Toxicology (AACT), European Association of Poisons
Centres and Clinical Toxicologists (EAPCCT). Position Statement and Practice
Guidelines on the Use of Multi-Dose Activated Charcoal in the Treatment of Acute
Poisoning. Journal of Toxicology Clinical Toxicology, 1999; 37(6):731-751.
------------------------, Proudfoot AT, Krenzelok EP, Vale JA. Position Paper on Urine
Alkalinization. Journal of Toxicology Clinical Toxicology. 2004; 42(1):1-26.
------------------------. Position Paper: Cathartics. Journal of Toxicology Clinical Toxicology.
2004; 42(3):243-254.
-----------------------. Position Paper: Gastric Lavage. Journal of Toxicology Clinical Toxicology.
2004; 42(7):933-944.
------------------------. Position Paper: Single Dose Activated Charcoal. Journal of Toxicology
Clinical Toxicology. 2005; 43(2):61-88.
Chernow B. (ed.). Essentials of Critical Care Pharmacology, 2nd ed. Baltimore: Williams
and Wilkins. 1989.
Dart RC (ed). Medical Toxicology. Philadelphia: Lippincott Williams & Wilkins. 2004.
Dreisbach RH et al. Handbook of Poisoning, 12th ed. Norwalk: Appleton and Lange.
1987.
Ellenhorn MJ et al. Ellenhorn’s Medical Toxicology: Diagnosis and Treatment of Human
Poisoning, 2nd ed. Baltimore: Williams and Wilkins, 1997.
Flommenbaum N, Goldfrank LR, et al. Goldfrank's Toxicologic Emergencies. New York:
McGraw Hill Companies, Inc., 2006.
Haddad LM, et al. Clinical Management of Poisoning and Drug Overdose. 3rd ed.
Philadelphia: W.B. Saunders Company, 1998.
Hardman JG, Limbird PB, et al. (eds). Goodman and Gilman’s The Pharmacological
Basis of Therapeutics, 10th ed. New York: McGraw-Hill. 2001.
Hartigan-Go K et al. Five Year Retrospective Study on Poisoning Cases Presenting at the
Poison Control Center of the Philippine General Hospital (1983-1987). Acta Medica
Philippina. 1992, 28(2):178-185.
Henry J and Volans G. ABC of Poisoning Part 1: Drugs. British Medical Journal. 1984:
289.
Hoffman RB, Nelson LS, et al. Goldfrank's Manual of Toxicologic Emergencies. McGraw
Hill Medical, New York. 2007.
IPCS/CEC Working Group. Evaluation of Chelating Agents Used in the Treatment of
Poisoning. June 1989.
King K. Treatment of Acute Poisoning. The Medical Journal of Australia. June 10, 1985.
142:632-635.
Klaasen CD, Amdur MO, Doull J (eds.). Casarett and Doull’s Toxicology: The Basic
Science of Poisons, 5th ed. Norwalk: Pergamon Press, Inc. 1996.
Leikin JB, Paloucek FP. Poisoning and Toxicology Compendium. Ohio: Lexi-Comp Inc.
1998.
Meredith T. Antidotes. Medicine International. 1989, 3:2508-12.
Olson KR, ed. Poisoning and Drug Overdose. Norwalk: Appleton and Lange, 1994.
Panganiban, LR, Makalinao IR. Chapter 12 Antidotes. In: Philippine National Drug
Formulary Essential Drug Monograph Volume 2. 3rd ed. Manila. 2006: 608-672.
Pascual JCP, et al. Efficacy of Forced Acid Diuresis in the Treatment of
Methamphetamine Induced Psychosis. 1998 (unpublished).
46
Proudfuoot A and Vale A. Clinical features and the immediate management of substance
abuse. Medicine International. 1989, 3:2409-2503.
Reynolds EF (ed.) Martindale: The Extra Pharmacopoeia, 30th ed. London: The
Pharmaceutical Press. 1993.
Rosen P, et al. Emergency Medicine Concepts and Clinical Practice, 2nd ed. Missouri:
The CV Mosby Company, 1988.
Vicellio P. (ed.) Handbook of Medical Toxicology. Boston: Little Brown Co., 1993.
World Health Organization. International Classification of Diseases (ICD 10). 1990.
47
OVERDOSES
OF COMMON
PHARMACEUTICALS
ANTIDEPRESSANTS: LITHIUM
ANTIDEPRESSANTS:
LITHIUM
Lithium is an indispensable psychotropic that has allowed many patients
with manic-depressive (bipolar) illness to achieve almost full
rehabilitation. It is available in the following formulations: regular release
lithium carbonate tablets and capsules, sustained release tablets and
lithium citrate liquid. Lithium stimulates release of endogenous
serotonin and stabilizes serotonergic neurotransmission.
Lithium is neither protein bound nor tissue bound and predominantly
excreted by the kidneys. Serum half-life is shorter for younger
populations.It has a narrow therapeutic index, and serum levels above
well-defined ranges (0.8 -1.2 mEq/L) can result in toxicity. Elimination is
mainly renal with a half life of 14-30 hours.
The overdose effects of lithium may arise from acute ingestion and
chronic treatment. Single ingestion of 40 mg/kg can raise lithium level at
2 mEq/L. Manifestations usually consist of vomiting, diarrhea, drow-
siness, tremor, muscle twitching, lethargy, tinnitus, nystagmus, slurred
speech, polyuria and polydipsia. Hemoialysis is indicated because of
lithium’s small size, poor protein binding, small volume of distribution
and water solubility.
Specific Precautions
• Decreased lithium clearance and increased lithium levels associated with
the following:
Aldosterone antagonists Naproxen
Angiotensin converting enzyme NSAIDS
(ACE) inhibitors Phenylbutazone
Antipsychotics (high doses) Sulindac
Diclofenac sodium Thiazides
Ibuprofen Xanthine derivatives
Indomethacin
• Lithium when coadministered with antiarrhythmics may potentiate
cardiac conduction effects.
• Activated charcoal should be considered if there is suspicion of
co-ingestion of other substances/poisons. Lithium does not bind or
adsorb to activated charcoal.
• Hemodialysis should strongly be considered with a level more than
4.0 mEq/L following an acute ingestion.
51
Management
Amount taken
HISTORY Time and mode of administration
Acute overdose or acute overdose on top of chronic
maintenance medication
Check vital signs, especially BP, RR and temperature
PHYSICAL Complete physical examination with emphasis on the
EXAMINATION CNS and CVS
General Examinations
CBC BUN CPK (MM)
LABORATORY ABG Creatinine ECG
EXAMINATIONS RBS LFTs
Na+, K+, Cl- Protime
Lithium Assay: serially done with ingestion of
sustained release formulation
ABCs of life support
Maintain vital signs.
Keep patient in a quiet room.
In case of hyperthermia, begin external cooling with
tepid sponging and fanning.
GENERAL Put patient on NPO. Give intravenous fluids to restore
MEASURES intravascular volume at a rate 1.5 to 2 times the
maintenance rate.
Adult: D5 0.9NaCl IV infusion
Pedia: D5 0.3NaCl according to KBW
Give activated charcoal if with suspected co-ingestion
Hemodialysis
For severe symptoms: seizure, coma, alterations in
mental status
SPECIFIC For moderate symptoms: lethargy and confusion in
MEASURES the setting of renal failure.
If hemodialysis is not immediately available, peritoneal
dialysis may first be instituted.
Restore sodium and water balance.
52
REFERENCES
Andisen A. The history of lithium. Biol. Psychiatry. 22:522-524. 1986
Bateman N. Poisoning with psychotropic drugs. Medicine International. 1989. 3:2533.
Carruthers G, Hoffman B. et al. Melmon and Morelli’s Clinical Pharmacology, 4th ed.
McGraw-Hill. 2000.
Dart RC (ed.). Medical Toxicology, 3rd ed. Philadelphia: Lippincott Williams and Wilkins.
2004.
Ellenhorn MJ. Ellenhorn’s Medical Toxicology, 2nd ed. Baltimore: Lippincott Williams &
Wilkins. 1997.
Flomenbaum N, Goldfrank LR, et al. Goldfrank's Toxicologic Emergencies. New York:
McGraw Hill Companies, Inc. 2006.
Basis of Therapeutics,10th ed. New York: McGraw-Hill, 2001.
Schatzberg A. and Nemeroff C. Textbook of Psychopharmacology. American Psychiatric
Press, Inc. 1998.
Shannon MW, Borron SW, Burns MJ (eds). Haddad and Winchester's Clinical
Management of Poisoning and Drug Overdose, 4th Ed. Philadelphia: Saunders. 2007.
Stahl S. Essential Psychopharmacology: Neuroscientific and Practical Applications.
Cambridge University Press. 1999.
53
ANTIDEPRESSANTS: SSRIs
ANTIDEPRESSANTS:
SELECTIVE SEROTONIN
REUPTAKE INHIBITORS
The selective serotonin reuptake inhibitors
(SSRIs) share the ability to inhibit presynaptic
serotonin reuptake. Safety and a favorable side- SSRIs
effect profile, as well as lack of multiple receptor Flouxetine (Prozac)
affinity that mediates adverse events, Fluvoxamine (Faverin)
distinguish SSRIs from the TCADs. These agents Nefazadone (Serzone)
undergo extensive hepatic metabolism to Paroxetine (Seroxat)
clinically inactive compounds, have relatively Sertraline (Zoloft)
large volumes of distribution and are highly Trazadone (Desyrel)
bound to plasma proteins.
The overdose effects of SSRIs tend to be generally parallel and
attributable to excessive synaptic serotonin. Manifestations usually
include nausea, vomiting, diarrhea, tremor, tachycardia, decreased level
of consciousness and seizures. All SSRIs can produce the rare and life
threatening serotonin syndrome with either overdose or therapeutic
doses. Management is supportive.
Central Serotonin Syndrome

• Cognitive/Behavioral
Confusion, disorientation, hallucinations (visual, auditory), agitation,
seizures, coma
• Autonomic nervous system
Hyperthermia, diaphoresis, sinus tachycardia, hypertension, hypotension,
dilated pupils, tachypnea, diarrhea, cyanosis, abdominal cramps,
salivation
• Neuromuscular
Myoclonus, clonus, hypereflexia, muscle rigidity, restlessness, tremor,
ataxia/incoordination, nystagmus, trismus, teeth chattering, opisthotonus,
paresthesias
54
• SSRIs produce cumulative CNS-depressant effects with the following:
Alcohol Anticholinergics
Anesthetics Antihistaminic compounds
• Increased bleeding time has been associated with warfarin when
combined with fluvoxamine and paroxetine.
• Increased diazepam and phenytoin levels can occur with fluvoxamine and
flouxetine.
• SSRIs may elevate the concentration of the following concomitantly
administered drugs:
Carbamazepine Quinidine
Flecainide TCAD
Propafenone
• SSRIs (particularly paroxetine, flouxetine and high doses of sertraline)
can increase the levels of the following antipsychotics:
Clozapine Olanzapine Resperidone
• When following an SSRI with a MAOI, drug half-life and where applicable,
the active metabolite should serve as a guide to the length of the
washout period. A standard recommendation would be to wait at least
five times the half-life of the SSRI or its metabolite, whichever is longer,
before starting the next serotonergic agent.
• Repeated doses of activated charcoal is not indicated in view of the large
distribution of SSRIs.
Management
Amount taken
Time and mode of administration
HISTORY
Acute overdose or acute overdose on top of chronic
Intake of other substances (alcohol, barbiturates)

CBC BUN CPK (MM)
55

Put patient on NPO. Give intravenous fluids.
Adult: D5 0.9NaCl or AR 1 liter x 8 hrs
Pedia: D5 0.3NaCl or AR according to KBW
Hook to cardiac monitor.
Insert nasogastric tube (appropriate size for age).
Do gastric lavage with activated charcoal.
GENERAL Adult: 100 g in 200 mL water
MEASURES Pedia: 1 g/kg to make a slurry
Important: Do not repeat activated charcoal lavage. SSRIs
do not undergo enterohepatic recirculation and they have a
large volume of distribution. Repeat only if there is co-
ingestion of other drugs.
After lavage, give sodium sulfate
Pedia: 250 mg/kg in water to make a 10% solution
May be repeated only once if initial dose does not
result in bowel movement after one hour.
Asymptomatic
Observe for 12 hours
Refer to Psychiatry if non-accidental
SPECIFIC If still asymptomatic, discharge
MEASURES Symptomatic
If with Central Serotonin Syndrome, admit to ICU
Treatment of Specific Problems

Phenytoin 5-7 mg/kg/day IV in 3 divided doses
Lidocaine
CARDIAC
50 mg IV push at 1 mL/min
DYSRHYTHMIAS
then start drip at 1-4 mg/min
Sodium bicarbonate 2 mEq/kg bolus
CENTRAL Cyproheptadine
SEROTONIN Loading dose: 4-8 mg PO followed by 4 mg q 2-4h
SYNDROME Max: 0.5 mg/kg/day
Hydrotherapy
HYPERTHERMIA Cooling measures
56
Intravenous fluids
HYPOTENSION If persistent, consider dobutamine 2 ug/kg/min IV
METABOLIC Sodium bicarbonate

ACIDOSIS 1mEq/kg or based on acid-base deficit
Good urine output (>1 mL/kg/hr)

Intravenous fluids
RHABDOMYOLYSIS Mannitol 2.5 mL/kg every 6 hours
Poor urine output (<1 mL/kg/hr)
Consider dialysis
Diazepam
Adult: 2.5-5.0 mg slow IV push
Pedia: 0.3 mg/kg/dose IV
May be repeated q 2-5 min up to 20 mg.
Be ready to intubate patient before giving additional
doses.
SEIZURES Lorazepam
Adult: 2.5-10 mg/dose repeated twice at intervals
of 15-20 min prn. Usual dose is 4-5 mg/dose.
Pedia: 0.05-0.1 mg/kg/dose IV up to a max of
4 mg/dose repeated twice at intervals of 10-15
min prn.
Compatible with D5W
REFERENCES
2004.
Wilkins. 1997.
Gossel TA and Bricker JD. Principles of Clinical Toxicology, 3rd ed. New York: Raven Press.
1994.
Olson KR (ed). Poisoning and Drug Overdose. Norwalk: Appleton and Lange. 1994.
Schatzberg A and Nemeroff C. Textbook of Psychopharmacology. American Psychiatric
Press, Inc. 1998.
Management of Poisoning and Drug Overdose, 4th ed. Philadelphia: Saunders. 2007.
Cambridge University Press, 1996.
57
ANTIDEPRESSANTS: TRICYCLICS
TRICYCLIC ANTIDEPRESSANTS
The tricyclic antidepressants (TCADs) have anticholinergic, alpha-
adrenergic blocking and adrenergic uptake inhibitory properties.
Imipramine and amitryptiline, the prototype drugs, are readily and
completely absorbed from the gastrointestinal tract with peak plasma
levels at 2 to 6 hours. They undergo first pass metabolism in the liver and
are highly protein bound with large volumes of distribution. These drugs
undergo significant enterohepatic recirculation and are eliminated
mainly through the liver.
Toxicity generally occurs at a dose of 10 to 20 mg/kg in adults or >10
mg/kg in children. Manifestations usually consist of anticholinergic
symptoms, central nervous and cardiovascular presentations.
Management is supportive. The antidote physostigmine, an
antichloinesterase agent, is not used generally because of its
complications of bradycardia, seizures and asystole.
• TCAD toxicity is enhanced when anticholinergic effect of decreased
gastrointestinal motility prolongs absorption of the drug.
• Imipramine may cause teratogenic effects because it crosses the
placenta.
• Drugs that enhance TCAD effects are:
Alcohol Anticholinergics Quinidine
Amphetamines Barbiturates Procainamide
• Acidemia and hypoalbuminemia increase free TCAD drug levels.
• Alkalinization prevents development of arrhythmias.
• Quinidine and procainamide are contraindicated because of their
myocardial depressant effects.
• Repeated activated charcoal is beneficial because TCAD undergoes
enterohepatic recirculation.
• Elimination of the drug using forced acid diuresis and dialysis is not
effective.
58
Clinical Features
• Neuropsychiatric
Coma, myoclonus, choreoathetosis, extrapyramidal reactions, ataxia,
severe agitation with hallucinations, status epilepticus
• Anticholinergic symptoms
Mydriasis, blurred vision, urinary retention, diminished sweating, dry
mucous membranes, decreased intestinal peristalsis, absent bowel
sounds, hypo- or hyperthermia, tachycardia
• Cardiovascular
Hypotension with reflex tachycardia, arrhythmias, ECG changes:
prolonged QRS > 0.12 seconds, prolonged PR interval, SV and ventricular
dysrhythmias, heart blocks
Management
Amount taken
HISTORY Acute overdose or acute overdose on top of chronic

Bedside Toxicology Test

Forrest reagent (Mix equal volumes of the following:
0.2% potassium dichromate, 30% sulfuric acid,
20% perchloric acid, 5% nitric acid). To 0.5-1.0 mL
urine, add 1 mL of the reagent; (+) test: yellow green
change in urine color
Plasma levels of parent drug + active metabolite
LABORATORY especially in chronic poisoning
EXAMINATIONS Analytical Test
Flourescent Polarization Immunoassay (FPIA), TDx
assay
ABG BUN CPK (MM)
RBS Creatinine Serial ECG
Na+, K+, Cl- LFTs Urinalysis
Chest x-ray, plain ab. for radio-opaque material
59

Adult: D5 0.9NaCl 1 liter x 8 hrs
GENERAL
MEASURES
Pedia: 1 g/kg to make a slurry
Adult: 15 g in 100 ml water
Repeat lavage every 6 hours for 48 hours.
< 10 mg/kg, asymptomatic
If still asymptomatic, discharge
> 10 mg/kg, asymptomatic
SPECIFIC Refer to Psychiatry if non-accidental
MEASURES Repeat charcoal lavage
Sodium bicarbonate
1-2 mEq/kg/IV until arterial pH=7.45-7.55
> 10 mg/kg, symptomatic
Repeat charcoal lavage.
Sodium bicarbonate
1-2 mEq/kg/IV until arterial pH=7.45-7.55
Cardiac monitoring
Treat specific symptoms
Symptomatic Asymptomatic
Admit to Discharge
ICU
60
Sodium bicarbonate
1-2 mEq/kg
CARDIAC If unresponsive, give Lidocaine
DYSRHYTHMIAS 50 mg IV push at 1 mL/min
then start drip at 1-4 mg/min
Hydrotherapy
HYPERTHERMIA Cooling measures
Intravenous fluids
HYPOTENSION If persistent, give norepinephrine 2-12 ug/min
consider dobutamine 2 ug/kg/min IV
RESPIRATORY Ventilatory support

INSUFFICIENCY Oxygenation
Good urine output (>1 mL/kg/hr)

Intravenous fluids
RHABDOMYOLYSIS Mannitol 2.5 mL/kg every 6 hours
Poor urine output (<1 mL/kg/hr)
Consider dialysis
Diazepam
doses.
SEIZURES Lorazepam
min prn.
Compatible with D5W
61
REFERENCES
Caruthers G, Hoffman B, et al. Melmon and Morelli’s Clinical Pharmacology, 4th ed. Mc-
Graw Hill. 2000.
2004.
Wilkins. 1997.
Gossel TA and Bricker JD. Principles of Clinical Toxicology, 3rd ed. New York: Raven
Press. 1994.
Hoffman R, Nelson L, et al. Goldfrank’s Manual of Toxicologic Emergencies. New York:
Management of Poisoning and Drug Overdose, 4th Ed. Philadelphia: Saunders.
2007.
Press, Inc. 1998.
Cambridge University Press, 1996.
62
ANTIDEPRESSANTS: TYPICAL
TYPICAL ANTIPSYCHOTICS
The typical (first generation) antipsychotics have a broad variety of
actions and by the same token, an equally broad range of toxicologic
manifestations involving the central and autonomic nervous system.
They have significant antidopaminergic, antihistaminergic (weight gain),
antiadrenergic (cardiovascular) and antimuscarinic cholinergic effects
(dry mouth, blurred vision, and constipation). These agents are often
used for purposes other than psychoses such as sedatives and
preanaesthethics, or to treat the manic phase of bipolar disorder,
nausea, vomiting, migraine and tension headaches. Because of their
varied uses, the term antipsychotics is a misnomer.
These drugs are available in the form of tablets and depot injections.
Most typical antipsychotics have similar pharmacokinetics and are well
absorbed after oral administration. Bioavailability is unpredictable due
to interindividual variability, intestinal metabolism and slow, extensive
and variable first-pass hepatic clearance. Only a small amount is
excreted in the urine unchanged. Their pharmacologic effects are
manifested long after the primary drug has been metabolized due to
their long elimination half-lives (range: 10-40 hours). Depot
antipsychotics have an apparent half-life of 3 weeks.
The typical antipsychotics have a large toxic to therapeutic ratio and
are therefore remarkably safe drugs when used properly. Many hepatic
metabolites are pharmacologically active and may extend the parent
drug’s effect in therapeutic doses or overdose. The fatal dose ranges
from 15 to 150 mg/kg although severe symptoms have been observed
with doses <1 mg/kg. Clinical manifestations of toxicity fall under three
categories: adverse effects, drug interactions and overdose.
63
ANTIPSYCHOTICS: TYPICAL
Typical Antipsychotics
Phenothiazines
Chlorpromazine Hcl Mesoridazine Promethazine
Fluphenazine Perphenazine Thioridazine
Levomepromazine Prochlorperazine Trifluoperazine
Butyrophenone
Haloperidol
Thioxanthene
Droperidol Flupentixol Zuclopenthixol
Chlorprothixine Thiothixene
Substituted Benzamide
Amisulpride Sulpiride Tiapride
Clinical Features
• Extrapyramidal effects
Acute dystonia, akathisia, akinesia (Parkinson-like syndrome), tardive
dyskinesia, diffuse upper motor neuron type of neurologic syndrome
(hyperreflexia, spasticity and extensor plantar responses)
• Neuroleptic malignant syndrome
Fluctuating consciousness, hyperthermia (>38°C), muscular rigidity
(lead pipe), autonomic dysfunction
• Cardiovascular effects
Hypotension (postural), tachycardia
• Drug interactions
CNS and respiratory depression, hypotension
Additive effects may occur when these drugs are combined with others
that have sedative effects, alpha adrenoceptor blocking, and anticholin-
ergic effects (pharmacodynamic interaction)
• Overdose
Mild: sedation, ataxia, slurred speech, hypothermia or hyperthermia,
orthostatic hypotension, miosis, constipation, blurred vision, urinary
retention, minimal extrapyramidal symptoms
Moderate: coma stage 1 or 2, lowered seizure threshold, decreased
vasomotor reflexes, quinidine effect, increased QT and PR intervals,
dystonia, akathisia, akinesia
Severe: Coma stage 2 or 3, hypotension, shock, arrhythmias, conduction
block, renal failure, laryngospasm, hypersalivation, dystonia, stiffness
of extremities
64
• Gastrointestinal absorption of antipsychotics may be modified by food
and decreased by orally administered antacids.
• Antipsychotics produce synergistic effects or enhanced toxicity through
interactions with the following:
Alcohol Narcotics TCADs
Antihistamines Opiates
Anesthetics Sedative-hypnotics
• Antipsychotics can enhance neurotoxicity with lithium and TCAs.
• Drugs contraindicated in the treatment of antipsychotic-induced cardiac
arrythmias:
Amiodarone Disopyramide Quinidine
Bretylium Procainamide
• Drugs contraindicated in the treatment of hypotension in antipsychotic
overdose because of the resultant unopposed alpha and beta-adrenergic
stimulation:
Dopamine Dobutamine Epinephrine
• Ephedrine sulfate, norepinephrine and phenylephrine may be used to
correct the hypotension.
• The antipsychotics are highly protein bound (99%), therefore dialysis,
hemoperfusion and forced acid diuresis are ineffective in overdose.
• Do not give diphenhydramine in the presence of hyperpyrexia in
Neuroleptic Malignant Syndrome.
• In performing bedside toxicology tests, urine pH must be acidic to yield a
positive result and to avoid false negative findings.
Management
Amount taken
PHYSICAL (using low reading thermometer)
EXAMINATION Note changes in sensorium, extrapyramidal signs,
cardiac arrhythmias
65
Toxicological Examination
10 mL clotted blood, 100 mL urine (first void)
Bedside Toxicologic Test
FPN reagent (5 mL of 5%FeCL, 45 mL of HClO4,
50mL of 50% HNO3)
To 1 mL urine, add 1 mL FPN reagent; positive test:
LABORATORY light pink, red, orange, violet or blue color
EXAMINATIONS General Examinations
CBC BUN CPK (MM)
ABG Creatinine ECG
RBS LFTs
Plain abdomen since antipsychotics
(e.g. haloperidol, chlorpromazine) present as
radioopaque materials

GENERAL Insert nasogastric tube (appropriate size for age).
MEASURES Do gastric lavage with activated charcoal.
66
Diphenhydramine:
Adult and Pedia: 0.5-1.0 mg/kg IV push
Biperiden HCl 2 mg per orem OR biperiden lactate
5 mg IV
Diazepam in agitated, febrile patient with impaired
thermoregulatory control
ACUTE For patients with seizure disorder: Lorazepam
DYSTONIC Adult: 2.5-10.0 mg/dose repeated twice at
REACTIONS intervals of 15-20 min prn.
Usual dose is 4-5 mg/dose.
Pedia: 0.05-0.1 mg/kg/dose IV up to max of 4 mg
per dose, repeated twice at intervals of 10-15
min prn
If patient is relieved and no other symptoms are
present, may discharge on oral Diphenhydramine
25-50 mg (Adult) or 1 mg/kg/dose (Pedia) TID
to QID for 3-4 days.
Lidocaine 50 mg IV push (1-2 mg/kg) at 1 mL/min

followed by continuous IV infusion
ARRHYTHMIAS Sodium bicarbonate 1-2 mEq/kg IV bolus for patients
with wide QRS complexes may be given as repeated
doses to achieve a blod pH of 7.5.
ELECTROLYTE
or pH Treat accordingly.
ABNORMALITIES
Intravenous fluids (crystalloid boluses 10-40 mL/kg
normal saline or Ringer’s lactate solution)
HYPOTENSION Norepinephrine 2-12 ug/min
Ephedrine sulfate 10-25 mg slow IV, should not
exceed 150 mg
HYPOXIA Adequate oxygenation

Ventilation
67
Mild: Supportive and symptomatic management.

Diazepam 2.5-5.0 mg IV push
NEUROLEPTIC Moderate to Severe: Supportive and symptomatic
MALIGNANT management.
SYNDROME Dantrolene 1 to 10 mg/kg IV OR 1-2 mg/kg p.o. QID
Also give Bromocriptine if there is no hypotension
2.5-10 mg/dose p.o. TID
THERMOREGULATORY Hyperthermia: cold compress, cooling mattress

DISTURBANCE Hypothermia: warm blanket
REFERENCES
Bateman N. Poisoning with psychotropic drugs. Medicine International. 1989, 3:2533.
Braunwald E et al. Harrison's Manual of Medicine, 15th Ed. New York: McGraw-Hill,
2002.
2004.
1987.
Wilkins. 1997.
Press. 1994.
Jenkins JL and Loscalgo J. Manual of Emergency Medicine. Boston: Little Brown
Company. 1986.
Pascual J. Psychosis, Antipsychotic Agents and Neurologic Issues. In: Jimenez, Vista,
Pascual (eds). Rational Pharmacotherapy of Schizophrenia with Medical Co-
morbidities. Megabooks Company, 2004.
Press, Inc. 1998.
Stahl S. Essential Psychopharmacology of Antipsychotics and Mood Stabilizers.
------------------------. Essential Psychopharmacology: Neuroscientific and Practical
Applications. Cambridge University Press, 1996.
68
ANTIPSYCHOTICS: ATYPICAL
ATYPICAL ANTIPSYCHOTICS
The atypical (second generation)
antipsychotics have better efficacy and Atypical Antipsychotics
less side effects compared to the typical
(first generation) antipsychotics. Their Amisulpride
Aripiprazole
atypia is based on: Asenapine
• these drugs' strong binding affinity Clozapine
at dopaminergic D4, muscarinic, Olanzepine
and serotonin (5-HT2A) receptors Paliperidone
compared to dopaminergic D2 Quetiapine
receptors Risperidone
• dopamine partial agonist activity Ziprasidone
(e.g., aripiprazole, bifeprunox)
• low propensity for causing extrapyramidal effects
Some of these agents are now also used for treating conditions aside
from schizophrenia, such as the manic phase of bipolar disorder, mania,
psychotic agitation, major depression. It is also used as a maintenance
drug for bipolar disorder, and as adjunct to the treatment of resistant
depression.
The atypicality of these drugs also extends to their atypical risk profile
of metabolic syndrome (risperidone, olanzepine, quetiapine),
agranulycytosis (clozapine) and tardive dyskinesia.
These drugs are available in tablet, orodispersable tablet, solution, IM
and slow/extended-release forms. They undergo extensive hepatic
clearance and, like their typical counterparts, have metabolites with
varied pharmacological profiles. Toxicity is strongly correlated with peak
serum concentrations and thus usually occurs within the first 4 to 6
hours. Clinical manifestations of toxicity fall under three categories:
adverse effects, drug interactions and overdose.
69
Clinical Features
• Extrapyramidal effects
Acute dystonia, akathisia, akinesia (Parkinson-like syndrome), tardive
dyskinesia, diffuse upper motor neuron type of neurologic syndrome
(hyperreflexia, spasticity and extensor plantar responses)
• Neuroleptic malignant syndrome
Fluctuating consciousness, hyperthermia (>38°C), muscular rigidity
(lead pipe), autonomic dysfunction
• Drug interactions
CNS and respiratory depression , hypotension
• Overdose
Mild: sedation, ataxia, slurred speech, hypothermia or hyperthermia,
orthostatic hypotension, miosis, constipation, blurred vision, urinary
retention, minimal extrapyramidal symptoms
Moderate: coma stage 1 or 2, lowered seizure threshold, decreased
vasomotor reflexes, quinidine effect, increased QT and PR intervals,
dystonia, akathisia, akinesia
Severe: Coma stage 2 or 3, hypotension, shock, arrhythmias, conduction
block, renal failure, laryngospasm, hypersalivation, dystonia, stiffness
of extremities
• Gastrointestinal absorption of antipsychotics may be modified by food
and decreased by orally administered antacids.
• Atypical antipsychotics produce synergistic effects or enhanced toxicity
thru interactions with the following: alcohol, anesthetics, narcotics,
opiates, sedative-hypnotics, and SSRIs.
• Clozapine and carbamazepine may result in synergistic granulocytopenia.
• Dangerous or lethal combination of atypical antipsychotics can occur with
the following nonpsychotropic drugs: astemizole, erythromycin,
ketoconazole.
• Drugs contraindicated in the treatment of antipsychotic-induced cardiac
arrythmias: amiodarone, bretylium, disopyramide, protease inhibitors,
quinine.
• Hyperglycemia, which can be extreme in some cases and associated with
ketoacidosis, hyperosmolar coma or death, has been reported in patients
treated with all atypical antipsychotics.
• Ephedrine sulfate, norepinephrine and phenylephrine may be used to
correct the hypotension. Epinephrine and dopamine should not be used,
since beta stimulation may worsen hypotension.
• The antipsychotics are highly protein bound (99%), therefore dialysis,
hemoperfusion and forced acid diuresis are ineffective in overdose.
.
70
Specific Precautions (continued)
• Do not give diphenhydramine in the presence of hyperpyrexia in
Neuroleptic Malignant Syndrome.
• Atypical antipsychotics are used with caution in elderly patients with
dementia-related psychosis due to increased risk of CVA and TIA in this
population. Consider these adverse events in treating overdose in the
elderly.
Management
Amount taken
Intake of other substances
PHYSICAL (using low reading thermometer)
EXAMINATION Note changes in sensorium, extrapyramidal signs,
cardiac arrhythmias
CBC BUN CPK (MM)
Plain abdomen since extended release formulation
(e.g. paliperidone) presents as radioopaque material

GENERAL
MEASURES
After lavage, give sodium sulfate.
71

Diphenhydramine:
Adult and Pedia: 0.5-1.0 mg/kg IV push
Biperiden HCl 2 mg per orem OR biperiden lactate
5 mg IV
Diazepam in agitated, febrile patient with impaired
thermoregulatory control
ACUTE For patients with seizure disorder: Lorazepam
DYSTONIC Adult: 2.5-10.0 mg/dose repeated twice at
REACTIONS intervals of 15-20 min prn.
Usual dose is 4-5 mg/dose.
Pedia: 0.05-0.1 mg/kg/dose IV up to max of 4 mg
per dose, repeated twice at intervals of 10-15
min prn
If patient is relieved and no other symptoms are
present, may discharge on oral Diphenhydramine
25-50 mg (Adult) or 1 mg/kg/dose (Pedia) TID to QID
for 3-4 days.
Lidocaine 50 mg IV push (1-2 mg/kg) at 1 mL/min
followed by continuous IV infusion
ARRHYTHMIAS Sodium bicarbonate 1-2 mEq/kg IV bolus for patients
with wide QRS complexes may be given as repeated
doses to achieve blood pH of 7.5
ELECTROLYTE
or pH Treat accordingly.
ABNORMALITIES
Intravenous fluids (crystalloid boluses 10-40 mL/kg
normal saline or Ringer’s lactate solution)
HYPOTENSION Norepinephrine 2-12 ug/min
Ephedrine sulfate 10-25 mg slow IV, should not
exceed 150 mg
Adequate oxygenation
HYPOXIA Ventilation
72
Mild: Supportive and symptomatic management.
Diazepam 2.5-5.0 mg IV push
NEUROLEPTIC Moderate to Severe: Supportive and symptomatic
MALIGNANT management.
SYNDROME Dantrolene 1 to 10 mg/kg IV OR 1-2 mg/kg p.o. QID
Also give Bromocriptine if there is no hypotension
2.5-10 mg/dose p.o. TID
THERMOREGULATORY Hyperthermia: cold compress, cooling mattress

DISTURBANCE Hypothermia: warm blanket
REFERENCES
Bateman N. Poisoning with psychotropic drugs. Medicine International. 1989, 3:2533.
2004.
1987.
Wilkins. 1997.
Basis of Therapeutics,10th ed. New York: McGraw-Hill. 2001.
Press. 1994.
Jenkins JL and Loscalgo J. Manual of Emergency Medicine. Boston: Little Brown
Company. 1986.
Pascual J. Psychosis, Antipsychotic Agents and Neurologic Issues. In: Jimenez, Vista,
Pascual (eds). Rational Pharmacotherapy of Schizophrenia with Medical Co-
morbidities. Megabooks Company, 2004.
Schatzberg A and Nemeroff C. Textbook of Psychopharmacology. American Psychiatric
Press, Inc. 1998.
Management of Poisoning and Drug Overdose, 4th Ed. Philadelphia: Saunders.
2007.
Stahl S. Essential Psychopharmacology of Antipsychotics and Mood Stabilizers.
------------------------. Essential Psychopharmacology. Cambridge University Press. 1999.
73
BARBITURATES
BARBITURATES
Barbiturates have anticonvulsant and euphoriant effects that are
mediated by their action on GABAA receptors which enhance inhibitory
impulses at the synapses. Agents are divided into four categories based
on their half-life: ultra-short, short, intermediate, and long-acting. Short
acting agents tend to be more lipid soluble and more protein bound.
They have more rapid onset of action and shorter duration of activity.
Metabolism of barbiturates occurs in the liver. Enzyme autoinduction
accelerates hepatic inactivation. Renal excretion of the unchanged drug
may be significant for long-acting barbiturates such as phenobarbital.
Acute overdosage with barbiturates depresses the CNS, especially the
reticular activating system, the cerebellum and the hypoxic drive for
respiration. Hypotension results from decreased sympathetic output
and negative inotropic effects on the heart. Hypothermia develops from
a direct effect on the hypothalamus. Other manifestations include
slurred speech, ataxia, nystagmus and confusion. Bullous skin lesions
over pressure areas may appear although these are non-specific fixed
drug eruptions.
The usual therapeutic serum level of phenobarbital is 15-40 ug/mL.
Treatment of acute toxicity with phenobarbital consists of
enhancement of elimination through urinary alkalinization and multiple
doses of activated charcoal. There is no antidote for barbiturate toxicity.
• Co-administration of isoniazid or monoamine oxidase inhibitors increases
the effect of barbiturates.
• Aspirin increases barbiturate blood levels.
• Barbiturates enhance the excretion of the following drugs through the
induction of hepatic microsomal enzymes.
Corticosteroids Oral contraceptives TCADs
Dicoumarin Phenytoin Sulfa drugs
Digoxin Tetracycline Vitamins D and K
• Watch out for aspiration pneumonia and pulmonary edema.
• Withdrawal symptoms may occur in habitual users during detoxification.
Watch out for anxiety, arrhythmias, ataxia, convulsions, delirium, fever,
dysarthria, hyperreflexia, insomnia, nystagmus, paranoia, tremors,
vertigo, weakness, emesis, irritability.
• Breakthrough seizures may occur in patients on maintenance pheno-
barbital treatment.
• Hemodialysis is indicated only for persistent hypotension.
74
BARBITURATES
Estimated Fatal Dose and Duration of Coma
for Commonly Used Barbiturates
Drug Estimated Duration of
Fatal Dose (g) Coma (Days)
Amobarbital 1.5 5
Barbital 2.0 5
Hexobarbital 2.0 2
Mephobarbital 2.0 5
Metharbital 2.0 5
Methohexital 1.0 3
Pentobarbital 1.0 3
Phenobarbital 1.5 7
Secobarbital 2.0 3
Thiopental 1.0 1
.
Management
Amount taken
Time and mode of exposure
HISTORY
Intake of other substances (e.g., alcohol)
History of previous barbiturate intake
History of renal/liver disease
Symptoms of somnolence, vomiting
Hypotension Neurologic examination
Hypothermia (down to CNS depression: Use
30°C) modified GCS for
Signs of circulatory baseline and follow-up
PHYSICAL collapse Pupils initially constricted
EXAMINATION Respiratory depression but hypoxic paralytic
Bullous skin lesions pupillary dilatation may
(”barb burns”) occur
Signs of renal failure Hippus effect: changing
anisocoric pattern
Toxicologic Examination
Serum barbiturate levels
5 mL clotted blood at 1st-2nd hr and 24th hr
LABORATORY General Examinations
EXAMINATIONS CBC Na+, K+, Cl- Urine pH
RBS Protime ECG
Creatinine LFTs CXR
BUN ABG
75
BARBITURATES
ABCs of life support. Maintain vital signs.

GENERAL
MEASURES
For phenobarbital overdose: Repeat q 6 hrs for
48 hrs at ½ initial dose.
result in bowel movement after one hour. During
repeated decontamination with activated charcoal,
sodium sulfate may be given after every 4 doses
to prevent constipation.
For phenobarbital overdose: give 8.4% sodium bicar-
bonate: 1 mEq/kg IV q 6-8 hrs until urinary pH>7.5.

Provide coverage for Strep. pneumoniae, anaerobes.
ASPIRATION Penicillin (aqueous crystalline)
PNEUMONIA 200,000 u/kg in 4 divided doses IV
with or without metronidazole
Droplight
HYPOTHERMIA Warm blanket
PULMONARY
EDEMA Furosemide 1 mg/kg/dose IV
RENAL If urine output < 1mL/kg/hr, consider hemodialysis

FAILURE Check urine myoglobin

DEPRESSION Adequate oxygen
SHOCK Intravenous fluids and vasopressors (if needed)

Dopamine 5-10 mcg/kg/min
76
BARBITURATES
REFERENCES
2004.
1987.
Wilkins. 1997.
Giannini AJ. et al. Handbook of Overdose and Detoxification Emergencies. New York:
Medical Examination Publishing Co., Inc. 1982.
Klaasen CD, Amdur MO, Doull J. (eds.). Casarett and Doull’s Toxicology: The Basic
Science of Poisons, 5th ed. New York: MacGraw-Hill. 1996.
Matthew H and Lawson A. Treatment of Acute Poisonings. 1979.
77
BENZODIAZEPINES
BENZODIAZEPINES
Benzodiazepines are widely used as anxiolytics. Some have additional
muscle relaxant, anticonvulsant and hypnotic properties. They are
classified into long-acting, intermediate-acting and short-acting
substances based on their elimination half-life. Diazepam is a long-
acting substance with a half-life of 24-48 hours; midazolam is a short-
acting substance with a half-life of 2 hours. Like barbiturates, the effect
of benzodiazepines is mediated mainly by binding with GABAAreceptors.
Diazepam is rapidly and nearly completely absorbed from the
gastrointestinal tract whereas absorption after intramuscular injection is
erratic and incomplete. Many benzodiazepines are metabolized to
pharmacologically active intermediates. Diazepam, for example, is
demethylated to active intermediates N-desmethyldiazepam, oxazepam
and temazepam.
All benzodiazepines produce similar clinical features in overdose.
The most significant finding is CNS depression. Other findings include
slurred speech, ataxia and incoordination. Respiratory and
cardiovascular insufficiency may also be seen. Respiratory depression
happens in midazolam overdose, in patients who have taken other
benzodiazepines in extremely large doses, in those who have taken other
CNS depressants such as alcohol, or in patients with pre-existing
pulmonary disease such as chronic bronchitis. Chronic use of
benzodiazepines can lead to drug dependence.
The determination of specific benzodiazepine levels in urine or blood
is not useful. Patients may be symptomatic even if the compound cannot
be detected in the biologic sample due to its conversion to multiple active
metabolites. Urine benzodiazepine screening may be performed as long
as results are interpreted cautiously and correlated with the clinical
status of the patient.
Treatment of acute benzodiazepine overdose is mainly supportive
after gastric decontamination. The use of flumazenil is limited to pure
benzodiazepine overdose settings.
Flumazenil is a competitive antagonist with weak agonist properties
at the benzodiazepine receptor. The risks related to its use outweigh the
benefits in patients who are using benzodiazepines chronically or
acutely in those with seizure disorders. Indications for the use of
flumazenil are limited to pure benzodiazepine overdose in a non-tolerant
patient who has:
78
BENZODIAZEPINES
• CNS depression
• normal vital signs, including oxygen saturation
• normal ECG
• otherwise normal neurologic examination
The expected response to the use of flumazenil is improvement of the
level of consciousness.
Avoid using flumazenil in overdose settings when drugs that can
cause seizures or dysrhythmias may have been ingested (e.g.,
theophylline, carbamazepine, TCADs).
• Many benzodiazepines and their active metabolites have long half-lives.
Therefore, it may take several days before patients recover fully from
overdose.
• Benzodiazepine abstinence syndrome rarely occurs but when it does,
symptoms usually manifest around 5 days after discontinuation of the
drug.
• Diazepam and other benzodiazepines exert a synergistic effect with other
CNS depressants such as barbiturates, ethanol and other sedative-
hypnotics.
• Diazepam increases blood levels and enhances the toxicity of TCADs.
• Flumazenil has no role in unknown overdose presenting with coma.
• The risk in the use of flumazenil outweighs the benefits in patients who
are using benzodiazepines chronically or in those with seizure disorders.
• Forced diuresis and hemodialysis are not effective because diazepam
and other benzodiazepines are highly protein bound.
79
BENZODIAZEPINES
Management
Amount taken
HISTORY
Intake of other substances (e.g., alcohol)
Symptoms of slurred speech, dizziness, somnolence
Hypothermia Neurologic examination

Bronchial hypersecretion Drowsiness, coma
Mental Status Examination Ataxia
PHYSICAL Sensorial changes Nystagmus
EXAMINATION Intermittent Dysarthria
hallucinations Weakness
Behavioral changes
Aggressive
behavior
5 mL clotted blood
100 mL urine (first void)
EXAMINATIONS RBS LFTs CXR-PA
BUN ABG Pregnancy test:
Creatinine ECG benzodiazepines are in
Na+, K+, Cl- pregnancy risk category D

Oxygen inhalation, if necessary.
If within 1 hour from ingestion, insert nasogastric tube
(appropriate size for age).
GENERAL Do gastric lavage with activated charcoal.
MEASURES Adult: 100 g in 200 mL water
Repeat every 6 hrs for 48 hrs at ½ initial dose.
80
BENZODIAZEPINES
(-) Respiratory depression
Observe for 24 hours or until fully awake.
Refer to Psychiatry.
If asymptomatic after observation, discharge.
(+) Respiratory depression
SPECIFIC Ventilatory support, adequate oxygenation
MEASURES Flumazenil
Adult: 0.1 mg/min to a total dose of 1 mg
Pedia: 0.01 mg/kg. May be repeated at 1-2 min
intervals up to a total dose of 1 mg.
If toxicity is due to a long-acting benzodiazepine,
maintenance infusion: 0.2-1.0 mg/hr.
HYPOXIA Adequate oxygenation
HYPOTENSION Fluid challenge
RESPIRATORY
Hyperventilation
ACIDOSIS
Half-lives (hours) of
Commonly Available Benzodiazepines
Drug Half-life Drug Half-life
Alprazolam 10-20 Estazolam 10-25
Bromazepam 7-19 Flurazepam 50-100
Clobazam 10-50 Lorazepam 10-20
Clonazepam 20-30 Midazolam 1-5
Clorazepate 50-80 Nordazepam 24-120
dipotassium Triazolam 1.5-3
Diazepam 30-60 .
REFERENCES
2004.
81
DIGITALIS
digitalis
The active principle of digitalis is derived from plants (leaves of the
foxglove plant, oleander and lily-of-the-valley), and several species of
toads. Digoxin, which is the commonly used digitalis preparation, is
passively absorbed in the small intestines at varying rates depending on
the preparation of the drug. The liquid or encapsulated form is absorbed
more effectively than the tablet form. The peak effects of digoxin occur
at the 3rd to 6th hour and 60 to 80% is excreted mainly in the urine.
Digitalis toxicity causes inhibition of Na+-K+ATPase and consequent
increase in the intracellular concentration of calcium. This leads to
enhancement of contractility and excitability of the myocardium. It also
causes increased neuronal excitability.
Toxicity occurs with ingestion of 0.05 mg/kg. Toxic levels of digoxin
and digitoxin in the blood are >2 ng/mL and >40 ng/mL, respectively. In
cases of chronic intake of digoxin, acute toxicity occurs when the drug
dosage is not adjusted in such conditions as hypothyroidism, hepatic
and renal disease, electrolyte imbalances, alkalosis, hypoxemia,
myocardial disease and cor pulmonale. Treatment is generally
supportive.
• Drug interactions. The following drugs increase digoxin levels:
Amiodarone Macrolide antibiotics
Carvedilol Quinidine
Diltiazem Spironolactone
Indomethacin Verapamil
• The following metabolic imbalances enhance digoxin toxicity:
Hypokalemia Hypernatremia
Hyperkalemia Alkalosis
Hypomagnesemia Hypoxemia
• Repeated administration of cholestyramine or activated charcoal lavage
is beneficial in removing the drug.
• Cardioversion is generally not recommended in cases of digitalis toxicity
because of the possibility of malignant ventricular arrhythmias.
• Use of forced diuresis or dialysis is not effective because of the large
volume of distribution of the drug.
• Digitalis does not have a threshold effect; therefore, the narrow toxic-
therapeutic margin is not well defined. Thus, in chronic intake, predis-
posing factors to toxicity should be taken into consideration.
82
DIGITALIS
Management
Amount taken
Intake of other drugs (calcium channel blockers,
diuretics, etc.)
Presence of disease conditions (cor pulmonale, renal
or hepatic disease, etc.)
Symptoms of acute poisoning:
HISTORY GI disturbances - anorexia, nausea, vomiting,
abdominal pain
Cardiovascular symptoms
CNS manifestations - headache, convulsions, visual
disturbances (yellow halos or xanthopsia)
Symptoms of chronic poisoning:
CNS manifestations - weakness, visual disturbances
Cardiovascular symptoms
Focus on GI, CV and CNS

Acute poisoning Chronic poisoning
Dysrhythmias Dysrhythmias
Extra systoles - PVCs Sinus bradycardia
Ventricular flutter Atrial fibrillation with
PHYSICAL Ventricular fibrillation SVR or junctional
EXAMINATION Tachyarrhythmias escape rhythm
Bradycardia, AV block Ventricular arrhythmias
Mental status changes Accelerated junctional
Drowsiness tachycardia and PAT
Confusion, disorientation with block
Hallucinations
Serum total digoxin levels 6 hrs after ingestion. After
the use of digoxin-specific Fab then only free digoxin
concentrations are meaningul (see p. 86).
LABORATORY Serial ECG Protime Urinalysis
EXAMINATIONS ABG RBS CBC
Serial electrolytes BUN CXR
Na+, K+, Ca++, Mg++ Creatinine T4
Acute poisoning Chronic poisoning
Hyperkalemia Hypokalemia
Hypomagnesemia
Hyperkalemia in severe cases
83
DIGITALIS

Oxygen inhalation, if necessary.
Hook to cardiac monitor
Insert nasogastric tube (appropriate size for age)
For acute poisoning
Gastric lavage with activated charcoal
GENERAL Repeat every 6 hrs for 48 hrs at ½ individual dose.
MEASURES OR Cholestyramine (as alternative to activated
charcoal) 1 gm sachet every 6 hrs
For chronic poisoning
Activated charcoal lavage is not done unless acute
poisoning occurs on top of chronic intoxication.
May give after 4 doses of activated charcoal if there
is still no bowel movement.
Amount ingested
< 0.05 mg/kg > 0.05 mg/kg
Asymptomatic Symptomatic Asymptomatic

Observe for 24h. Repeat Observe for 24h.
Refer to Psych if cholestyramine Repeat
non-accidental. or activated cholestyramine
If still asymptom- charcoal or activated
atic, discharge. lavage.every charcoal
SPECIFIC 6 hours. lavage.
MEASURES Cardiac monitoring. Refer to Psych if
Treat specific non-accidental
problems. If still asymptom-
Give digoxin- atic, discharge.
specific antibody
(Fab fragment)
if available for
severe cases.
Admit to ICU.
84
DIGITALIS
PVCs
Phenytoin 5-7 mg/kg slow IV or Lidocaine 50 mg IV
push (1 mL/min) then drip at 1-4 mg/min
Ventricular fibrillation/flutter/ventricular
CARDIAC tachycardia
DYSRHYTHMIAS Lidocaine 50 mg IV push (1 mL/min)
Symptomatic bradyarrhythmias
Atropine 0.5-2.0 mg IV
AV block - Pacemaker
Supraventricular tachycardia - Carotid massage
See discussion on pp. 14-15.
Hypokalemia
KCl solution up to 40 mEq/hr
Hypomagnesemia
Magnesium sulfate
++
Loading dose: 600 mg of elemental Mg in D5W
over 3 hours
Maintenance dose: 600-900 mg of elemental
Mg++ per 24 hours IV or IM
In emergency situations, the loading dose should
ELECTROLYTE not exceed 15 mg/min
IMBALANCE Magnesium sulfate can be administered IM at 200
mg every 4 hours for 24 hours then 100 mg every
4 hours. Monitor parameters for magnesium
toxicity.
Hyperkalemia
Glucose-insulin infusion
50 mL D50-50 and 10 units regular insulin
Followed by sodium bicarbonate 1 mEq/kg/dose
Hypernatremia
Adjust fluids
HYPOVOLEMIC
SHOCK Fluid challenge
more next page
85
DIGITALIS
Diazepam
doses.
SEIZURES Lorazepam
min prn.
Compatible with D5W
Digoxin-Specific Antibody
Indications for digoxin-specific antibody
• Significant poisoning
Severe hyperkalemia (>5 mEq/L)
Symptomatic arrhythmias not responsive to usual drugs
• Massive oral overdose with high serum levels
Intake of >10 mg in healthy adults or 4 mg in children
Steady state serum concentration >10 ng/mL (6 hrs post-ingestion)
Dosage computation for digoxin-specific antibody
Dose = Total body load (in mg)
0.6 mg
where total body load = (Serum digoxin conc.)(Vd)(weight in kg)
1000
and Vd = volume of distribution = 5.6 L/kg
Note: Each vial of Digibind contains 40 mg of digoxin-specific antibody
fragments that will bind 0.6 mg digoxin or digitoxin.
REFERENCES
Antman EM et al. “Treatment of 150 cases of life-threatening digitalis intoxication with
digoxin-specific Fab antibody fragments.” Circulation. June 1990, 81:6: 1744-1751.
1987.
Wilkins. 1997.
Gossel TA et al. Principles of Clinical Toxicology 3rd ed. New York: Raven Press 1994.
Klaasen CD, Amdur MO, Doull J. (eds.). Casarett and Doull’s Toxicology: The Basic
Science of Poisons, 5th ed. New York: MacGraw-Hill. 1996.
Olson KR, ed. Poisoning and Drug Overdose. Norwalk: Appleton and Lange. 1994.
86
IRON
IRON
Iron is absorbed in the small intestines in the ferrous (+2) state and
further oxidized to the ferric (+3) state. It binds with the storage protein,
ferritin. It is widely distributed in the tissues attached to the globulin,
transferrin.
Serum iron reflects the amount of iron bound to transferrin (normal
concentration of iron = 50-150 mcg/dL; serum transferrin concentration
= 300-400 mcg/dL). Excretion of iron occurs by blood loss or
desquamation of the gastrointestinal mucosa.
Iron toxicity results from direct corrosive effects on mucosal tissue,
and cellular dysfunction. These occur when serum iron levels exceed the
iron-binding capacity of transferrin. Free circulating iron causes damage
to systemic blood vessels. A dose of 20-30 mg/kg of elemental iron can
cause abdominal pain, vomiting and diarrhea; 40 mg/kg is potentially
serious; 60 mg/kg is potentially fatal.
Ferric chloride is a caustic substance. In cases of ingestion, use the
acid protocol.
• Iron tablets (especially the slow-release types) may form concretions in
the stomach and duodenum. This may result in delayed elevation of iron
levels.
• Liquid iron preparations and chewable tablets are not radio-opaque but
are as toxic as the tablet form.
• Activated charcoal does not bind iron effectively.
• Drug-drug interactions:
Antacids decrease absorption of iron.
Ascorbic acid increases absorption of iron.
Iron enhances absorption of tetracycline.
• Hemodialysis removes the iron-deferroxamine complex but not iron itself.
Exchange transfusion removes both free and bound iron.
Antacid decrease iron absorption
Ascorbic acid increases iron absorption
Iron enhances absorption of tetracycline
Amount ingested: >20mg/kg

Mild: TSI= 450- <500 (Observe)
Moderate: 500 - <800 mcg/dl ICU
Severe: 800-1,000 PEG soln
TSI – 4-6 hrs repeat 8-12 hrs 87

IRON
Clinical Features
• Initial period - up to 6 hrs post ingestion
Severe hemorrhagic gastritis with diarrhea and vomiting
Lethargy, pallor tachycardia, hypotension
• Quiescent period - up to 12 hrs
Deceptive improvement and stabilization occur
• Recurrent period - 12 to 48 hrs
Hematemesis, melena, gastrointestinal perforation
Increased lethargy, coma, convulsion
Vasomotor collapse, cyanosis, pulmonary edema
Hepatorenal failure, metabolic acidosis, hypoglycemia
• Late period - 2 to 6 weeks
Gastric scarring, pyloric obstruction
Computation for ingested elemental Fe

Elemental Fe (No. of tabs)(mg of Fe salt per tab)(%elemental Fe)
= weight of patient in kg
(mg/kg)
Salt Elemental Iron (Fe)

Gluconate anhydrous 12.0%
Sulfate crystalline 20.0%
Sulfate anhydrous 36.8%
Fumarate 33.0%
Guidelines for Use of Deferoxamine

Indications for deferoxamine treatment
• Peak serum iron concentration >500 mcg/dL
• Significant clinical manifestations: lethargy, coma, hypovolemia,
metabolic acidosis, coagulopathy
• (+) abdominal radiograph for tablets or capsules despite gastrointestinal
decontamination
• Peak serum iron concentration between 350-500 mcg/dL, AND presence
of persistent vomiting, diarrhea, severe abdominal pain
Indications for deferoxamine treatment termination
• Serum iron concentration below 150 mcg/dL
• 24 hours after return of normal urine color (if vin rose colored initially)
• Absence of radio-opaque formulation (if initially present)
• Resolution of clinical signs and symptoms of systemic iron poisoning
88
IRON
Management
Amount and formulation of elemental iron ingested
HISTORY Time of ingestion
GI, CV, CNS manifestations
PHYSICAL Complete physical examination with emphasis on GI
EXAMINATION and CV systems and CNS - see Clinical Features
10 mL clotted blood for Total Serum Iron (TSI) 3 to 5
hrs post ingestion
Gastric aspirate
EXAMINATIONS CBC including hematorcrit
Typing BUN LFTs
ABG Creatinine Protime
RBS Na+, K+, Cl- Plain abdomen
Fecalysis with occult blood
Insert nasogastric tube (appropriate size for age)
Do gastric lavage using
2% sodium bicarbonate solution: dilute 2 vials
8.4% (10ml/vial) in 1L water
OR baking soda: 1 Tbsp in 1 liter of water
GENERAL Adult: 15 g in 100 ml water
MEASURES Pedia: 250 mg/kg in water to make a 10% solution
If abdominal film is (+) for radioopaque tablets or
capsules, repeat gastric lavage followed by sodium
sulfate. Then repeat abdominal film to check if
opacities have disappeared.
Give antacids: aluminum-magnesium hydroxide or H2
blocker
Refer for emergency endoscopy.
Start 8.4% sodium bicarbonate
1 mEq/kg/dose IV or based on acid-base deficits
89
IRON
Amount ingested <20mg/k

<20mg/kg
Give oral antacid (Al-Mg OH)
I
Adult: 60 mL q 6 hrs
Older child: 30 mL q 6 hrs
Pedia: 15 mL q 6 hrs
Observe for 24 hrs.
SPECIFIC Refer to Psychiatry if necessary.
MEASURES If asymptomatic after observation, discharge.
Amount ingested unknown or > 20 mg/kg
Mild Moderate Severe

TSI=450-<500 TSI=500-<800 TSI=800-1,000
mcg/dL* mcg/dL* mcg/dL*
Observe for 24 hrs.
Give oral antacid
as above. Admit to ICU.
Refer to Psych. Repeat gastric lavage with 1%
If asymptomatic, sodium bicarbonate.
discharge. Follow with sodium sulfate.
Treat specific problems.
Start deferoxamine IV
10-15 mg/kg/hr constant
infusion. Max dose: 6g in 24hrs
Infant: 25mg/kg/hr x12hrs x3d
Substance may form concretions

or bezoars. Start repeated
whole bowel irrigation with
polyethyl glycol (PEG) solution.
*Total Serum Iron (TSI) taken 4 to 6 hrs after ingestion.

Repeat after 8 to 12 hrs to determine if preparation is long
acting or has delayed absorption.
Normal TSI: 80-180 ug/dL or 14-32 umol/L
Deferoxamine Challenge Test

1 – 2g (90mg/kg) IM dose of deferoxamine
Follwed by collection of urine to await a “vin rose” urine color change
Absence does not rule out acute iron toxicity or the need for DFO therapy
N
90
IRON
CEREBRAL
EDEMA 10% Mannitol: 0.5 to 1 g/kg/dose
Vitamin K1 (Phytonadione)
DECREASED
Adult: 10 mg IV up to 60 mg/day
PROTIME
Pedia: maximum of 10 mg/dose
(Secondary to GI bleed)
Iced saline lavage
HYPOVOLEMIC IV fluids
SHOCK Blood transfusion
H2 blocker or proton pump inhibitor
Refer for endoscopy
See discussion on pp. 16-19.

Acidosis
Sodium bicarbonate 1 mEq/kg or based on acid-
METABOLIC base deficits
DERANGEMENTS Hypoglycemia
D50-50 and IV fluids
Hypokalemia/hyponatremia
Potassium/sodium replacement
Check urine output

RENAL
>1 mL/kg: Give IV fluids
FAILURE
<1 mL/kg: Exchange transfusion
Diazepam
doses.
SEIZURES Lorazepam
min prn.
Compatible with D5W
91
IRON
REFERENCES
Wilkins. 1997.
Gruber JE. “Acute Iron Poisoning.” Emergency Medicine Concepts and Clinical Practice.
Vol. II. pp. 2193-2201.
Olson KR, ed. Poisoning and Drug Overdose. Norwalk: Appleton and Lange. 1994.
Sinkinson C, et al. “The dilemmas of acute iron intoxication, Emergency Reports.” The
Practical Journal for Primary Care Physicians. Vol. 10, No. 12. June 5, 1989.
92
ISONIAZID
ISONIAZID
Isoniazid (INH) is rapidly absorbed, mainly in the small intestines.
Among rapid acetylators, peak plasma concentrations occur 1 to 2 hours
after oral dosage. The clinical effects of INH overdose occur 0.5 to 2
hours following acute ingestion. The triad of acute INH toxicity consists
of:
• seizures
• coma
• metabolic acidosis
INH produces acute toxic effects by impairing the synthesis of gamma-
aminobutyric acid (GABA), an inhibitory neurotransmitter in the brain.
This toxicity results from depletion of pyridoxine. Convulsions can be
precipitated by concurrent intake of codeine-containing cough syrups or
if patient ingests the drug on an empty stomach. Concurrent intake of
alcohol can also precipitate more seizures and aggravate the metabolic
acidosis produced by INH.
• Contraindicated drugs: salicylates, adrenergic agents, and MAO inhibitors
• Even in the absence of convulsions or acidosis, vitamin B6 should be
given and urine alkalinization with sodium bicarbonate should be done.
• If there is no pure B6 preparation available and patient develops ana-
phylactoid reaction to the B1 component, epinephrine 0.2 mg SQ and
antihistamine IV may be given.
• Pure B6 can be given safely up to a maximum of 40 g in adults.
• Do not use phenytoin to control INH-induced seizures. INH inhibits the
enzymes that metabolize phenytoin and can produce phenytoin toxicity
(see section on treatment of seizures).
• Epileptic patients should be maintained on phenytoin. If the patient is
already using it, the dose should be decreased.
• Funduscopy should be done on follow-up to detect optic neuritis.
93
ISONIAZID
Management
Amount taken
Seizure dose: 80-120 mg/kg
Adult lethal dose: 6-10 g
Time of ingestion
Intake of other substances (e.g., alcohol, cough syrup)
HISTORY Early symptoms Severe overdose
Nausea Seizures
Vomiting Loss of consciousness
Dizziness
Slurred speech
Visual sensitivity to light
Urinary retention
Early signs Severe overdose

Hyperpyrexia Hypotension
Tachycardia Signs of metabolic
PHYSICAL Hyperreflexia acidosis
EXAMINATION Dilated pupils Coma
Dysarthria
Do complete neurologic examination with funduscopy.
Toxicologic Examinations
Plasma INH levels: 10 mL oxalated or heparinized
blood
Urine: 200 mL for metabolite
Bedside toxicologic test
(10% KCN, 10% Chloramine-T)
LABORATORY To 4 drops urine, add 4 drops KCN and 10 drops
EXAMINATIONS Chloramine-T
Positive test: red color
CBC BUN CPK-MM
ABG Creatinine Urine pH
RBS LFTs
94
ISONIAZID
GENERAL Adult: 15 g in 100 ml water
MEASURES Pedia: 250 mg/kg in water to make a 10% solution
To enhance excretion, give alkalinization therapy with
sodium bicarbonate at 1 mEq/kg IV every 6 hrs until
urine pH > 7.5.
Amount ingested known - see next page

SPECIFIC
MEASURES
Amount ingested unknown
B6 not available B6 available

Do lavage until Pure B6
return flow is clear. Give 80-120 mg/kg IV bolus
Give oral prepara- B6 in combination
tion B6 160-240 Use Vit. B1-6-12 mixture at a dose
mg/kg.* of 80-120 mg/kg of the B6 compo-
nent. Give in divided doses such
that B1 component does not exceed
1 g/dose. Otherwise, anaphylactoid
reaction may occur.
Refer to Psychiatry if non-accidental.

Maintenance drug: Vitamin B6 (oral) 10 mg/kg/day
in 3 divided doses for 3 to 6 weeks.
*INH inhibits B6 absorption, hence the need to double the dose. Make
sure there is no activated charcoal in the gut before giving oral B6. If
pure B6 is not available, give combination B1-6-12 as a single dose.
95
ISONIAZID
Amount ingested unknown - see previous page

SPECIFIC
MEASURES
Amount ingested known
B6 not available B6 available

Pure B6
Do lavage until
Dose should equal the grams of INH
return flow is clear.
ingested (1:1).
Give oral prepara-
B6 in combination
tion B6 two times
Use Vit. B1-6-12 mixture in divided
the amount of INH
doses, 15 minutes apart such that
ingested.*
B1 content does not exceed 1 g
per dose. Otherwise, anaphylactoid
reaction may occur.

Maintenance drug: Vitamin B6 (oral) 10 mg/kg/day
in 3 divided doses for 3 to 6 weeks.
*INH inhibits B6 absorption, hence the need to double the dose. Make
sure there is no activated charcoal in the gut before giving oral B6. If
pure B6 is not available, give combination B1-6-12 as a single dose.
If pH<7.2 or patient is clinically acidotic:

Give sodium bicarbonate 1 mEq/kg or based on
acid-base deficits
ACIDOSIS Repeat ABG after 30 min then compute additional
deficit.
Give sodium bicarbonate until deficit in ABG deter-
mination is corrected but watch out for sodium over-
load from repeated administration.
Hydration: 3 to 4 liters/day
Sodium bicarbonate 1 mEq/kg IV q 6 hrs to maintain
MYOGLOBINURIA urine pH >7.5
or Mannitol 2.5 mL/kg IV q 6 to 8 hrs
RHABDOMYOLYSIS Monitor CPK-MM serially. Continue alkaline diuresis
until CPK-MM trend and urine myoglobin are
negative.
Furosemide 1 mg/kg/dose IV bolus
PULMONARY Monitor urine output. If poor, do peritoneal dialysis
EDEMA (see Renal Failure, above).
96
ISONIAZID
Check urine output. If urine output <1 mL/kg:
RENAL Consider peritoneal or hemodialysis.
FAILURE If peritoneal dialysis is used, incorporate 1 g of Vit.
B6 per liter of dialysate.
Diazepam
doses.
Lorazepam
SEIZURES
min prn.
Compatible with D5W
For epileptic patients: If with prior intake of phenytoin,
give diazepam 5 mg IV. If there is no response after
3 doses, give:
Phenytoin 1.5 to 2.5 mg/kg loading dose
Maintenance dose: 1 mg/kg/dose (half of normal
maintenance dose) given q 8 hrs or TID to avoid
toxicity since INH inhibits metabolism of phenytoin.
REFERENCES
Wason S. et al. Single high dose pyridoxine treatment for isoniazid overdose. JAMA. 246:
10. pp. 1102-1104. September 1981.
97
OPIATES AND OPIOIDS
OPIATES AND OPIOIDS

Opiates refer to a group of naturally occurring compounds derived from
the juice of the poppy Papaver somniferum. “Opioid” is the general term
that refers not only to the naturally occurring form of opium but also the
semisynthetic and wholly synthetic agents commonly prescribed for
relief of intense pain, sedation, preanaesthetic medication and
anaesthesia, anti-tussives and antidiarrheals. In this discussion, the
term “opioid” applies to both opiates and opioids as described above.
The more potent opioids have greater capacity to induce drug
dependence and abuse. This is a major drawback to their use. Opioids
are well absorbed from the gastrointestinal tract, nasal mucosa,
pulmonary capillaries and parenteral injection sites. The orally
administered opioid undergoes first pass hepatic excretion. It is
metabolized by hepatic microsomes and excreted in the urine in the
unchanged form and as metabolites.
The intensity and development of clinical manifestations is
dependent on the onset and duration of drug action. That is, the shorter
the onset and duration of action, the greater the intensity and rapidity of
manifestation of overdose.
Generally, opioid toxicity produces a triad of symptoms:
• Pinpoint pupils
• Respiratory depression
• Coma
The most immediate problem is respiratory depression.
Clinical Features
• Mild to moderate poisoning or overdose
CNS Euphoria, dysphoria, weakness, headache, agitation, nausea,
disorientation, lethargy
GIT Dry mouth, constipation, biliary tract spasm with colicky pain
CVS Capillary dilatation (flushing of the face), tachycardia, bradycardia,
palpitation, syncope, hypotension
GUT Urinary retention
Eyes Pinpoint pupils (uncommon with meperidine and those with mixed
activity)
Allergic Itching, urticaria
• Severe poisoning
Coma, respiratory depression, pulmonary edema, apnea
98
OPIATES AND OPIOIDS
• Forced diuresis is not indicated since the renal clearance of unmetabo-
lized opioid contributes very little to overall opioid metabolic clearance.
• Gastric emptying time is delayed following narcotic ingestion.
• Repeated charcoal lavage may be helpful in cases of diphenoxylate and
meperidine toxicities because they undergo enterohepatic recirculation.
• Co-ingestion or co-injection of the following may potentiate the depres-
sant effect of opioids:
CNS depressants (methanol, ethanol, barbiturates)
Antipsychotics (phenothiazines)
Antidepressants (TCADs)
MAO inhibitors
• Concurrent administration of the following drugs can increase the toxicity
of opioids by decreasing metabolism:
Macrolides, chloramphenicol
Fluoroquinolones
H2 blockers
• Treatment of pulmonar y edema with 1 mg/kg of fur osemide, when
combined with morphine, may potentiate the ability of morphine to
increase venous capacitance causing further hypotension and respiratory
depression.
• Use of naloxone or naltrexone in a chronic abuser of opiates should be
done with caution since it may provoke withdrawal signs and symptoms.
99
OPIATES AND OPIOIDS
100
Commonly Encountered Opiates
DRUG TYPE OF USUAL DOSE ELIMINATION DURATION OF THERAPEUTIC TOXIC LETHAL
ACTIVITY (mg) HALF-LIFE ANALGESIA DOSE DOSE DOSE
(hours) (hours) (mcg/dL) (mcg/dL) (mcg/dL)
Naltrexone Antagonist 30-50 10-96 --- 43.6 ng/mL
Morphine Agonist 10 3 4-5 1-7 10-100 >400
Heroin Agonist 4 rapid 3-4 --- 10-100 >400
Pethidine Agonist 100 3 2-4 30-100 500 1000-3000
Fentanyl Agonist 0.2 4 1-2
Codeine Agonist 60 3 3-4 1-12 20-50 >60
Oxycodone Agonist 4.5 4 3-4 1-10 20-500 ---
Propoxyphene Agonist 100 15 4-5 5-20 30-60 80-210
Pentazocine Mixed 50 3 3-4 10-60 200-500 1000-2000
Nalbuphine Mixed 10 3.5 3-6 197-459 ng/mL
Butorphanol Mixed 2 3 3-4 0.9-1.04 ng/mL
Naloxone Antagonist 1-2 1 — 11.3-34.7 ng/mL (neonates)
OPIATES AND OPIOIDS
Management
Amount taken
HISTORY Intake of other substances (barbiturates, ethanol,
methanol, etc.)
Symptoms (see Clinical Features)
PHYSICAL Emphasis on examination of the CNS, respiratory and

EXAMINATION cardiovascular systems (see Clinical Features)
Blood levels: 10 mL
LABORATORY Urine levels: 200 mL (first void)
ABG BUN Urinalysis
RBS Creatinine ECG
Na+, K+, Cl-
GENERAL Put patient on NPO. Give intravenous fluids.
MEASURES Adult: D5 0.9NaCl or AR 1 liter x 8 hrs
Oral Preparation
Insert NGT (appropriate size for age)
SPECIFIC Pedia: 250 mg/kg in water to make a 10% solution
MEASURES May be repeated only once if initial dose does not
Repeat lavage q 6 hrs for 48 hrs using half of initial
dose for cases of meperidine or diphenoxylate
toxicity.
Parenteral Preparation
Check sensorium
more next page
101
OPIATES AND OPIOIDS
Check sensorium
Awake, Depressed
non-toxic Awake, toxic
Sensorium
Observe 24 hrs.
Refer to Psych Naloxone
if non-acciden- Adult: start 0.2mg IV q3 mins up to
tal. 2mg --if no repsonse most likely not
if w/good response may increase up to 10mg
Neonates & infants: 0.01 mg/kg/dose
Depressed Start naloxone drip
sensorium or Compatible fluids: D5W or 0.9 NaCl
respiration Dose: 2/3 of waking up dose to be
given hourly or 2.5 ug/kg/hr
Incompatibilities: Do not mix with
bisulfite, sulfite or long chain or
high molecular weight anions, or
any solution with an alkaline pH.
Respiratory support:
oxygen, assisted ventilation
If asymptomatic, discharge.
Phenytoin 15 to 25 mg/kg
ARRHYTHMIAS
HYPOTHERMIA
Can also hasten metabolism of opioids
CIRCULATORY Insert CVP line

FAILURE Give IV fluids
HYPOTHERMIA Keep patient warm
Hypoxia
Respiratory support
METABOLIC Assisted ventilation
DISTURBANCES Hypoglycemia
D50-50 for adults; dilute to 10% for children
102
OPIATES AND OPIOIDS
Furosemide 1 mg/kg
PULMONARY
Anti-pulmonary edema regimen
EDEMA
PEEP
RENAL If with poor urine output: Dialysis

FAILURE If with good urine output: Observe
Diazepam
doses.
SEIZURES Lorazepam
min prn.
Compatible with D5W
REFERENCES
Aronow R. Handbook of Common Poisonings in Children. American Academy of
Pediatrics. 1993.
Wilkins. 1997.
Gossel TA, Bricker JD, et al. Principles of Clinical Toxicology, 3rd ed. New York: Raven
Press. 1994.
Henry J and Volans G. ABC of Poisoning, Part 1: Drugs. London: British Medical
Association.
McEvoy GK. AHFS Drug Information. American Society of Hospital Pharmacies. 1993.
Olson KR, (ed). Poisoning and Drug Overdose. Norwalk: Appleton and Lange. 1994.
Viccello P. Handbook of Medical Toxicology. Boston: Little, Brown and Company. 1993.
103
PARACETAMOL
PARACETAMOL
Paracetamol is a widely used analgesic-antipyretic present in many
prescription and over-the-counter medications. While generally safe in
therapeutic doses, in overdose, it can produce hepatocellular necrosis
leading to liver failure and death if untreated.
The term “acute overdosage” refers to a single ingestion, or several
episodes of ingestion occuring within a single 4-hour period. Doses of
150 mg/kg in children and 7.5 gm in adults are generally considered the
lowest dose capable of producing significant toxicity. The toxic dose
during repeated supratherapeutic ingestion (RSI) is still controversial.
In therapeutic doses, the cytochrome P-450 system (mainly, CYP2E1)
produces a small amount of toxic metabolite, N-acetyl-p-benzoquinone
imine (NAPQI), that can be readily detoxified by the reduced glutathione
stores of the liver. In overdoses, however, the reduced glutathione stores
can be overwhelmed and NAPQI will covalently bind to hepatic
macromolecules resulting in hepatocellular necrosis.
• Antidotal therapy with N-acetylcysteine (NAC) is most effective when given
within 10 hours of ingestion of paracetamol. After this time, NAC can still
be used but its effectiveness diminishes.
• Intravenous NAC should only be given to cases with clear clinical indica-
tions because it may cause rate-related anaphylactoid reactions. Patients
with history of asthma or atopy are at higher risk. Intravenous diphenhy-
dramine may be given prophylactically to prevent anaphylactoid reaction.
• Risk of hepatotoxicity is probably increased among chronic heavy
alcoholics.
• The Rumack-Matthew nomogram is applicable only for acute overdosage
presenting within 24 hours of ingestion (see nomogram in Annex G.)
• RSI of paracetamol is defined as more than one ingestion over a period
of more than 8 hours that results in a cumulative dose of >4 gm/day
(>150 mg/kg/day in children). NAC is started if serum paracetamol level
is >10 mcg/mL or serum AST is >50 IU/L.
• NAC is US FDA pregnancy category B. When used in pregnant women, it
crosses the placenta and levels achieved in fetus are similar to maternal
levels.
• Consider liver transplantation for patients who develop liver failure with
hepatic encephalopathy.
104
PARACETAMOL
Clinical Features
Stages Symptoms and Signs
Stage I (0-24 hrs) Asymptomatic, some vomiting, AST may be normal
Stage II (24-72 hrs) Asymptomatic, some RUQ abdominal pain, elevated
AST (>1,000 IU/L)
Stage III (72-96 hrs) Onset of hepatic failure + renal failure, very high AST
(>10,000 IU/L)
Stage IV (day 7-10, Resolution of signs and symptoms, AST returns to
variable) normal in a few weeks
Management
Amount taken
HISTORY Intake of other substances (phenobarbital, ethanol,
rifampicin, barbiturates, diphenydramine, etc.)
Symptoms: vomiting, aspiration, seizures (see Clinical
Features)
PHYSICAL Emphasis on examination of the heart, liver, kidneys.

EXAMINATION Do a complete Neuro Exam (see Clinical Features)
Blood levels: 5-10 mL
EXAMINATIONS CBC LFTs RBS Creatinine ABG
+ + -
Urinalysis Protime BUN Na , K , Cl ECG
Activated charcoal may be repeated, especially if
antidote (NAC) is not available.
105
PARACETAMOL
Serum levels known - see next page

SPECIFIC
MEASURES
Serum levels unknown
Amount Amount Unknown,

Unknown,
ingested ingested asympto-
symptomatic
>150 mg/kg <150 mg/kg matic
Observe Observe
for 24 hours for 72 hours
20% N-acetylcysteine
(NAC)
Test dose: 0.1 mL in 0.9 Symptomatic
mL D5W IV. If no Continue AST,
hypersenstivity, give: ALT and
Adult: protime
Phase 1: 150 mg/kg in monitoring.
200 mL D5W Give NAC.
to run for 1 hr
Phase 2: 50 mg/kg in
500 mL D5W
to run for 4 hrs Asymptomatic
Phase 1: 100 mg/kg in Monitor AST, ALT, protime
1000 mL D5W daily.
to run for 16
hrs
Adjust IV fluid in the Abnormal Normal
presence of renal failure Give NAC. after 72 hrs
or congestive heart
failure.
Pedia: Refer to Psychiatry if
Use adult dose. non-accidental.
However, IV fluid admin- Discharge
istration must consider
body weight.
Give diphenhydramine
1 mg/kg IV (different
site) prior to giving
initial NAC.
Continue monitoring AST, ALT and protime. If still

not clinically improving, give second course of NAC.
After second course, watch out for signs of
coagulopathy. Check partial thromboplastin time
(PTT). Treat hepatitis and coagulopathy.
Significant decrease in AST and ALT compared to

baseline levels and patient is clinically improving.
106
PARACETAMOL
Serum levels unknown - see previous page
SPECIFIC
MEASURES
Serum levels known - assess risk of hepatotoxicity
Time post-
exposure Plasma levels (ug/ml)
4 hours <100 100-120 >120-200 >200
8 hours <50 50-60 >60-100 >100
12 hours <30 30 >30-50 >50
No Slight Possible Probable

risk risk risk risk
Observe for 72 hours. 20% N-acetylcysteine (NAC)

Monitor AST, ALT and Test dose: 0.1 mL in 0.9 mL D5W
protime daily. IV. If no hypersenstivity, give:
Adult:
Phase 1: 150 mg/kg in 200 mL
Abnormal D5W to run for 1 hr
Give NAC. Phase 2: 50 mg/kg in 500 mL
D5W to run for 4 hrs
00 mg/kg in 1000
mL D5W to run for 16
hrs
Normal Adjust IV fluid in the presence
after 72 hrs of renal failure or congestive
heart failure.
Pedia:
Use adult dose. However, IV
fluid administration must
consider body weight.
Give diphenhydramine 1 mg/kg
IV (different site) prior to giving
initial NAC.
Continue monitoring AST, ALT and protime. If still

not clinically improving, give second course of NAC.
After second course, watch out for signs of
coagulopathy. Check partial thromboplastin time
(PTT). Treat hepatitis and coagulopathy.
Significant decrease in AST and ALT compared to

baseline levels and patient is clinically improving.
Refer to Psychiatry if
non-accidental.
Discharge
107
PARACETAMOL
ACUTE RENAL Adjust IV fluids

FAILURE Hemodialysis
BLEEDING Give Phytonadione 10 mg IV every 6 to 8 hrs if protime

TENDENCIES is <60% activity
HEPATIC Anti-hepatic encephalopathy regimen including

INSUFFICIENCY Vitamin B complex and Phytonadione
Hypoglycemia
Adult: 50 to 100 mL D50-50 IV
Pedia: 2 mL/kg D10W
Acidosis
METABOLIC Sodium bicarbonate 1 mEq/kg or based on acid-
DISTURBANCES base deficit
Hypokalemia
Correlate with ABG and correct appropriately
Hypocalcemia
10% calcium gluconate 10 to 20 mL x 30 minutes
REFERENCES
2004.
Hoffman RS, et al. (eds.). Goldfrank’s Manual of Toxicologic Emergencies. New York:
McGraw-Hill, 2007.
Leikin JB and Paloucek FP (eds.). Poisoning and Toxicology Handbook, 4th edition.
New York: Lexi-Comp. 2008.
Olson KR (ed.). Poisoning and Drug Overdose, 5th edition. New York: McGraw-Hill, 2007.
108
SALICYLATES
SALICYLATES
Salicylates are mainly used for their analgesic and anti-inflammatory
properties. Aspirin (acetylsalicylic acid, ASA), which also has antipyretic
activity, is more commonly used nowadays for its antiplatelet property.
Methylsalicylate (oil of wintergreen), a common component of over-the-
counter analgesic liniments, in its pure liquid form, contains 5 g of
salicylate per teaspoon (5 ml). Salicylic acid, a component of some
lotions, creams, and ointments, is mainly used for its keratolytic effects.
In overdose, the toxic effects of all of these salicylates prominently
manifest as central nervous system (CNS) and metabolic
derangements. Additionally, salicylic acid can produce local caustic
injury to the gastrointestinal tract when ingested.
Poisoning due to salicylates (salicylism) may be acute or chronic.
Acute intoxication is generally seen after a single large accidental or
suicidal intake of >150 mg/kg. Ingestion of >300 mg/kg will most likely
produce an acute severe intoxication. Chronic intoxication is more
commonly a result of repeated overmedication for several days and
generally occurs with ingestion of >100 mg/kg/day for two or more days.
Diagnosis is usually missed because manifestations may be non-
specific and may be attributed to pneumonia, gastroenteritis, or sepsis.
Hence, mortality is higher than in acute overdose.
Ingestion of large amounts of salicylate may produce gastric irritation.
Once absorbed, salicylates cause direct stimulation of the medullary
respiratory center resulting in hyperventilation and respiratory alkalosis
(may not be prominent in children <4 yrs old). Salicylates also cause
uncoupling of oxidative phosphorylation, and inhibition of glucose and
fatty acid oxidation, all of which lead to metabolic acidosis with wide
anion gap. By causing increased vascular permeability, salicylates can
produce cerebral and pulmonary edema. Severe cases may also result in
renal failure.
109
SALICYLATES
Clinical Features
Types Symptoms and Signs
Acute (mild) Nausea, vomiting, tachypnea, tinnitus, lethargy, mixed
respiratory alkalosis and metabolic acidosis, serum
salicylates may fall between 15-40 mg/dL
Acute (severe) Above manifestations accompanied by coma, seizures,
hypoglycemia, hyperthermia, cerebral and pulmonary
edema, renal failure, cardiovascular collapse, serum
salicylates may be >40 mg/dL
Chronic Non-specific manifestations such as confusion,
dehydration, hyperthermia, metabolic acidosis, renal
failure, cerebral and pulmonary edema are more
common than in acute
• Systemic acidemia promotes salicylate entry into the brain, worsening
toxicity.
• Since there is no specific antidote for salicylate poisoning, sodium
bicarbonate administration to treat acidemia and alkalinize the urine,
and supportive therapy are the mainstays of treatment.
• Alkalemia is not a contraindication to bicarbonate therapy.
• Single determinations of serum salicylate level are not sufficient because
of possibility of prolonged or delayed absorption.
• In general, the toxicity of salicylates correlates poorly with serum
concentrations, especially in chronic poisoning.
• In chronic poisoning, decontamination is seldom necessary.
• The indications for hemodialysis are:
• Acute ingestion with serum levels >100 mg/dL with severe acidosis
and other manifestations
• Chronic intoxication with serum levels >60 mg/dL with acidosis,
confusion, lethargy (especially if elderly or debilitated)
• Severe manifestations in any patient
• In small children, if hemodialysis is indicated but unavailable, consider
exchange transfusion.
• Multiple-dose activated charcoal (MDAC) can reduce serum salicylate
half-life but not as effectively as hemodialysis.
• MDAC and/or whole bowel irrigation are also useful for gut decontam-
ination with large ingestions (>30 g).
110
SALICYLATES
Management
Amount and form of salicylate taken
HISTORY Acute or chronic intake
Intake of other substances (e.g., acetazolamide can
worsen acidosis)
Note level of sensorium, presence of respiratory
PHYSICAL
distress, hyperpyrexia, gastrointestinal bleed or
EXAMINATION
perforation
Stat and serial serum salicylate levels: 0.5 mL blood
Bedside Toxicologic Test
FeCl3 test: To 2 mL urine, add 0.5 ml FeCl3. Positive
LABORATORY test: purple color
CBC LFTs RBS Creatinine ABG
+ + -
Urine pH Protime BUN Na , K , Cl ECG
CPK-MM Plain abdomen (for enteric coated tablets)
Chest xray
GENERAL Keep patient in a quiet room.
MEASURES Put patient on NPO. Give intravenous fluids.
If ASA or methylsalicylate If salicylic acid, examine

oropharynx for signs of burns.
more next page
111
SALICYLATES
If ASA or methylsalicylate If salicylic acid, examine

oropharynx for signs of burns.
+ for burns OR If no burns, do

+ signs of GI bleeding endoscopy.
Manage as
Caustic Poisoning + for burns No burns
Give 8.4% sodium bicarbonate 2 mEq/kg IV bolus

followed by continuous infusion of D5W 1 liter +
100 mEq sodium bicarbonate to run at 200 mL/hr.
Pedia: adjust volume to run at 3 to 4 mL/kg/hr
Maintain urinary pH > 7.5

May be repeated only once if initial dose does not result in
bowel movement after one hour.
To prevent enterohepatic recirculation, if possible, give
activated charcoal q 6 hours for 8 doses per NGT at half of
initial dose. Give sodium sulfate cathartic if there is no
bowel movement after 4 doses.
SPECIFIC
MEASURES
Asymptomatic, Asymptomatic, Symptomatic, Symptomatic,
Non-toxic Toxic dose Mild Severe
dose Observe Observe Admit to ICU.
Refer to for 12 hrs. for 12 hrs. Treat acidosis.
Psych if Refer to Refer to Repeat ABG.
non-acciden- Psych if Psych if Consider
tal. non-accid- non-accid- hemo- or
Discharge. ental. ental. peritoneal
If still asymp- dialysis or
tomatic, exchange
If still asymp- If symptom- discharge. transfusion.
tomatic, atic, assess
discharge. if mild or
severe.
112
SALICYLATES
GASTROINTESTINAL
Give proton pump inhibitors IV.
BLEEDING
Temperature > 40 degrees C
Hydrotherapy
HYPERPYREXIA IV fluids
Cooling measures
Protime < 70%: Fresh frozen plasma

Phytonadione
LOW PROTIME Adult: 10 mg IV q 8 hours
Pedia: 1mg/kg IV q 8 hours
Sodium bicarbonate
METABOLIC
1 mEq/kg or based on base deficit to maintain
ACIDOSIS
serum pH > 7.4
Hypoglycemia
Adult: 50 to 100 mL D50-50 IV
METABOLIC
Pedia: 2 mL/kg D10W
DISTURBANCES
Hypokalemia
Correlate with ABG and correct appropriately
NON-CARDIOGENIC Endotracheal intubation with mechanical ventilation,
PULMONARY if warranted. Hyperventilate to prevent iatrogenic
EDEMA respiratory acidosis.
Diazepam
doses.
SEIZURES Lorazepam
min prn.
Compatible with D5W
113
SALICYLATES
REFERENCES
2004.
Hoffman RS, et al. (eds.). Goldfrank’s Manual of Toxicologic Emergencies. New York:
McGraw-Hill, 2007.
Leikin JB and Paloucek FP (eds.). Poisoning and Toxicology Handbook, 4th edition.
New York: Lexi-Comp. 2008.
114
THEOPHYLLINE
THEOPHYLLINE
Theophylline is a methylxanthine derivative which is readily absorbed in
the gastrointestinal tract. Its uncoated tablet or liquid forms reach peak
plasma concentration within 1 to 5 hours. However, the sustained-
release preparation may form concretions in the gastrointestinal tract,
with prolonged and delayed absorption up to 24 hours, thereby
increasing blood theophylline levels for a longer period of time. With
single IV administration, peak serum concentration is obtained after 30
minutes. Its metabolism is age-related and is affected by factors such as
smoking, presence of chronic obstructive lung disease, liver or heart
dysfunction, and a number of drugs such as cimetidine, erythromycin,
rifampicin, phenytoin, and oral contraceptives.
The incidence of theophylline toxicity has declined in the past years
since newer ß-agonists and leukotriene antagonists have replaced
theophylline in the treatment of asthma. Toxicity has three clinically
distinct forms (acute, chronic, and acute on top of chronic) with varying
presentations and treatment. Ingestion of > 10 mg/kg (serum level > 20
ug/mL) of the drug is potentially toxic in acute overdose. However, in
chronic overmedication, toxicity can occur even with low serum
theophylline levels. Clinical presentation centers on the gastrointestinal
tract, cardiovascular and central nervous systems. Management is
generally supportive. Experimental and clinical studies have shown that
multiple-dose activated charcoal administration significantly increases
the elimination of life-threatening amounts of theophylline. In patients
presenting with seizures, IV pyridoxine is recommended.
• For sustained-release preparations, toxicity may develop several hours
after ingestion. Peak plasma levels may be seen >12 hours post
ingestion. This is because the drug forms bezoars in the GI tract.
• With chronic use of theophylline, toxicity may occur even at much lower
blood levels.
• There is decreased clearance of theophylline with concommitant use of
the following enzyme inhibiting drugs:
Allopurinol Cimetidine
Beta blockers (Propranolol) Ciprofloxacin
Caffeine Erythromycin
Contraceptives
more next page
115
THEOPHYLLINE
Specific Precautions (continued)

• Theophylline clearance is decreased under the following conditions:
Concommitant illnesses - CHF, COPD, hepatic cirrhosis, acute
hepatitis, acute influenza, pneumonia
High carbohydrate diet
Old age
• There is increased clearance of theophylline with concommitant use of
the following enzyme inducing drugs:
Carbamazepine Phenobarbital Ethanol (chronic intake)
Isoniazid Phenytoin Marijuana
Rifampicin
• Theophylline clearance is increased under the following conditions:
Concommitant illnesses: hyperthyroidism, cigarette smoking
High protein, low carbohydrate diet
Intake of barbecued meat
Childhood
• Hypoalbuminemia increases unbound theophylline in the blood.
• Administration of an anti-emetic agent may be necessary to control
nausea/vomiting for effective administration of multiple-dose activated
charcoal.
• Whole bowel irrigation has not been found to have additional benefit over
activated charcoal alone in sustained-release theophylline toxicity.
• Hemodialysis is considered if serum theophylline levels in moderately
toxic range are increasing despite activated charcoal administration.
Other indications include:
Seizures
Hypotension
Cardiac arrhythmias
Acute overdose with serum levels > 100 ug/mL
Chronic toxicity and patient is not tolerating the present level
Chronic toxicity in a patient < 60 years of age with serum level >60
ug/mL or patient > 60 years of age with serum level > 40 ug/mL
• Since theophylline-induced hypotension is due to excessive ß-adrenergic
agonism, administration of dopamine, dobutamine, epinephrine to
correct hypotension are not preferred.
• Administration of phenytoin as anticonvulsant has been found to be
ineffective in the treatment of theophylline-induced seizures.
• Rapid IV administration of aminophylline produces severe manifestations
such as dizziness, palpitations, profound bradycardia, PVCs, severe hypo-
tension or cardiac arrest. Therefore, it is best to give IV aminophylline
through an infusion pump. (Note: Cases of poisoning have occurred follo-
wing continued use of IV aminophylline in patients transferred from other
hospitals without proper labeling of the IV bottle.)
116
THEOPHYLLINE
Clinical Features
Blood levels
Acute
Mild: Nausea, vomiting, tremors, anxiety, tachycardia 20-40 ug/mL
Moderate: Metabolic disturbances (hypokalemia, 40-100 ug/mL
hypophosphatemia, hyperglycemia, hypocalcemia,
hypomagnesemia, metabolic acidosis)
Severe: Hypotension, ventricular arrhythmias, seizures > 100 ug/mL
Acute-on-chronic
Same as acute however theophylline concentrations
do not predict high-risk patients
Similar to chronic toxicity, patient is symptomatic even
if theophylline concentration is low.
Chronic 20 ug/mL
Less nausea/vomiting
Seizures prominent even at lower concentrations
Palpitations, tachycardia more common
Less metabolic effects (hypokalemia, hyperglycemia)
Management
Amount taken
HISTORY Acute, acute-on-chronic, or chronic
Symptoms involving the target systems: CNS, CVS, GIT

EXAMINATION CNS, CVS and GIT
Theophylline plasma levels: 10 mL clotted blood
LABORATORY In case of acute oral overdosage with sustained
EXAMINATIONS release preparations, obtain theophylline levels
every 2 to 4 hours since peak plasma levels do not
occur until 12 to 16 or more hours post-ingestion.
CBC BUN ABG
LFTs Creatinine K+, Mg++, Ca++
Urinalysis RBS ECG
CPK-MM Plain abdomen (if sustained release)
117
THEOPHYLLINE

GENERAL Pedia: 1 g/kg to make a slurry
MEASURES Repeat activated charcoal administration every 4 to 6
hours for 48 hours or until theophylline concentra-
tion < 20 ug/mL.
Perform hemodialysis as indicated.
During repeat lavage, may give sodium sulfate after 4
doses of activated charcoal.
SPECIFIC
MEASURES
<10 mg/kg
Acute, <10 mg/kg >10 mg/kg >10 mg/kg
Acute-on- Chronic Symptomatic Asymptomatic
chronic
Cardiac monitoring
Treat specific
problems
Admit
Asymptomatic Symptomatic
Observe for 24 hours.

If still asymptomatic, discharge.
118
THEOPHYLLINE
ACUTE RENAL Urine output < 1 mL/kg/hr: hemodialysis

FAILURE
Tachycardia
Esmolol 500 mcg/kg IV bolus over 1 minute,
followed by 50 mcg/kg/minute continuous infusion
ARRHYTHMIAS Ventricular tachycardia
Lidocaine 50 mg IV push at 1 mL/minute or
cardioversion if patient’s hemodynamic condition
is unstable
Iced saline lavage
GASTROINTESTINAL H2 blocker (Famotidine) or proton pump inhibitor
BLEEDING (Omeprazole/esomeprazole)
Refer for endoscopy
Intravenous fluids (Normal saline at 10-20 mL/kg)

Vasopressors
HYPOTENSION Norepinephrine at 2-12 mcg/minute IV infusion in
D5W
Phenylephrine in D5W (preferred if available)
Hyperglycemia: Plain IVF

Acidosis
Sodium bicarbonate 1 mEq/kg or based on acid-
base deficit
Hypokalemia
Potassium supplementation
Adult: 10-15 mEq/hour IV
Pedia: 0.25-0.5 mEq/kg/hour
Monitor serum potassium and ECG
METABOLIC Hypomagnesemia
DISTURBANCES Magnesium sulfate
In an emergency situation:
Loading dose: 15 mg/minute under continuous
ECG monitoring
In an non-emergency situation:
Dose of elemental magnesium: 600 mg
infusion over 3 hours
Maintenance: 600-900 mg/24 hours
Hypocalcemia
10% calcium gluconate 10 to 20 mL x 30 minutes
119
THEOPHYLLINE
Ondansetron 8 mg in 100 mL normal saline x 20

PERSISTENT minutes
VOMITING Metoclopramide 10 mg or 0.1 mg/kg IV
Diazepam
doses.
SEIZURES Lorazepam
min prn.
Compatible with D5W
Pyridoxine 25 mg/kg/dose IV, repeat as necessary.
REFERENCES
American Academy of Clinical Toxicology (AACT), European Association of Poisons
Centres and Clinical Toxicologists (EAPCCT). Position Statement and Practice
Guidelines on the Use of Multi-Dose Activated Charcoal in the Treatment of Acute
Poisoning. Journal of Toxicology Clinical Toxicology. 37(6):731-751. 1999.
2004.
Lheureux P, Penaloza A, Gris M. Pyridoxine in clinical toxicology: a review. European
Journal of Emergency Medicine. Apr; 12(2):78-85. 2005.
Sessler CN. Theophylline toxicity: clinical features of 116 consecutive cases. The
American Journal of Medicine. Jun; 88(6):567-76. 1990.
Shannon M. Predictors of major toxicity after theophylline overdose. Annals of Internal
Medicine. Dec 15; 119(12):1161-7. 1993.
--------------------. Life-threatening events after theophylline overdose: a 10-year prospective
analysis. Archives of Internal Medicine. May 10; 159(9):989-94. 1999.
120
HOUSEHOLD
AND
WORKPLACE
CHEMICALS
CAUSTICS AND CORROSIVES
CAUSTIC AND
CORROSIVE AGENTS
There is no specific level or dose at which corrosive/caustic agents
produce toxic effects. The concentration or pH of the solution, and
contact time are important factors in their potential for serious injury.
They induce injury through inhalation (corrosive gases and their aqueous
solutions), direct contact with the skin or eye, and by ingestion.
Direct inhalation or aspiration of vomitus (after ingestion of caustics)
may result in respiratory tract damage. The chemical manifestations are
hoarseness, stridor, wheezing, and non-cardiogenic pulmonary edema.
The respiratory damage may result in laryngeal edema and ulceration,
epiglottitis, pneumonitis and impaired gas exchange.
Eye or skin exposure to caustic or corrosive agents usually results in
immediate pain and redness followed by blister formation. Conjunctivitis
and lacrimation are common. Severe burns and blindness can occur.
Establish diagnosis by eliciting history of exposure to a corrosive
agent. Perform a detailed examination of the skin or eye (referral to an
ophthalmologist may be needed). Perform appropriate emergency and
supportive measures.
• Inhalation – Give supplemental oxygen and observe closely for
signs of progressive airway obstruction or non-cardiogenic
pulmonary edema. Careful and constant attention to signs and
symptoms of respiratory distress and airway edema (wheezing,
stridor, voice change) is mandatory and could require prompt
intubation as airway edema may progress over minutes to hours.
Start intravenous fluid (D5NSS for adults or D5 0.3NaCl for
children). Laboratory tests include chest x-ray, ABG, pH of
bronchial aspirate, and continuous pulse oximetry.
• Skin and eyes – Remove all clothing and double bag prior to
disposal. Wash skin and irrigate eyes with copious water (skin)
and free flowing water or saline (eyes) for at least 15 minutes to
remove residual caustics and prevent contamination of other
patients and staff. Refer to an ophthalmologist for specific
management and prevention of complications.
123
Precautions for dermal or skin decontamination
• Soap may be used only in removing adherent xenobiotics.
• Water is NOT used for skin decontamination involving reactive
metallic forms of alkali metals, sodium, potassium, lithium,
cesium and rubidium which react with water to form basics.
• Phenol tends to thicken and become difficult to remove following
exposure to water. High flow water or polyethylene glycol
solution may be used. Lime (calcium oxide or CaO) also
thickens and forms Ca(OH)2 following wetting with water.
124
CAUSTICS: ACIDS
CAUSTICS:
ACIDS
An acid is a proton donor. It generally
causes significant tissue injury at a pH
Common Acids
below 3. Aside from pH, other factors Acetic acid
Permanent wave neutralizers, photo-
that should be considered when graphy stop bath, disinfectants, hat
establishing the degree of injury are: making, printing, dyeing, rayon manu-
concentration, molarity, volume, contact facturing
time and pre-morbid condition of the Boric acid
Roach powders, water softener, germ-
stomach. The acids most commonly icides
encountered in poisoning cases are: Carbolic acid
Disinfectants, pharmaceuticals, dyes,
• Mineral acids (automobile battery plastics manufacturing, preservatives
acids, toilet bowl cleaners and other Formic acid
cleaning agents) Airplane glue-making, tanning, deo-
dorizing tablets, plastic menders,
• Inorganic acids (hydrochloric acid, fumigants, embalming fluids
sulfuric acid) Hydrochloric (muriatic) acid
• Organic acids (acetic acid, formic Bleaching agents, metal and toilet
bowl cleaners, dye and chemical syn-
acid) thesis, metal refining
Fatalities have been recorded with Hydrofluoric acid
ingestion of 30 mL of the following: Glass etching, brick cleaning, etching
chips in semiconductor industry, elec-
sulfuric acid 95% (18 M), nitric acid 69% troplating, leather tanning, rust rem-
(15 M), and hydrochloric acid 36% (12 oval, cleaning of porcelain
M). However, ingestion of less than 5 mL Nitric acid
Engraving, electroplating, metal refin-
of mineral acids is known to have caused ing, fertilizer manufacturing
death. Non-accidental ingestions often Oxalic acid
present with more severe injuries and Tanning, blueprint paper, disinfectants,
household bleach, iron cleaner, leather,
complications. chemical synthesis, anti-rust polish
Ingestion of acids, except for Phosphoric acid
hydrofluoric acid, produces coagulation Metal and toilet bowl cleaner, rust-
proofing
necrosis resulting in eschars which tend
Sulfuric acid
to self-limit further damage. The Automobile batteries, drain cleaners,
stomach, primarily the antrum, lesser chemical munitions, fertilizer manufac-
turing
curvature and pylorus, are the common
Adapted from Haddad LM, Shannon MW,
sites of injury. However, the esophagus Winchester JF. Clinical Management of
may also be affected. Ulceration of Poisoning and Drug Overdose. 1998.
necrotic tissues may lead to perforation,

peritonitis, strictures and stenosis of the
esophagus, stomach or pylorus.
125
CAUSTICS: ACIDS
• The concomitant intake of alcohol relaxes the pyloric sphincter, thereby
promoting antegrade progression of acid and production of small bowel
damage and potential perforation.
• DO NOT insert a nasogastric tube since this increases the risk of perfor-
ation and aspiration pneumonia.
• DO NOT administer activated charcoal.
• DO NOT induce vomiting.
• DO NOT give any neutralizing agent because the reaction can evolve
carbon dioxide which can aggravate chemical injury to the stomach and
cause rupture.
• The administration of water may result in an exothermic reaction (release
of steam and heat), which aggravates the damage caused by the strongly
acidic solution.
• Acids may also produce systemic manifestations:
Boric acid - CNS depression including coma, cardiovascular collapse,
renal failure
Carbolic acid - renal and hepatic injury
Formic acid - metabolic acidosis, formate poisoning
Hydrofluoric acid - hypocalcemia, hyperkalemia, hypoglycemia, cardio-
vascular symptoms, CNS symptoms
Oxalic acid - hypocalcemia, renal failure
Picric acid - renal injury
Tannic acid - hepatic injury
• Skin burns should be treated as thermal burns.
• Endoscopy should be done within 12 hours and no later than 24 hours
after exposure.
Classification of Mucosal Injury

Following Caustic Substance Ingestion
Grade 0 Normal findings on examination
Grade 1 Edema, hyperemia of mucosa
Grade 2a Friability, blisters, hemorrhages, erosions, whitish membranes,
exudates, superficial ulcerations
Grade 2b Grade 2a plus deep discrete or circumferential ulceration
Grade 3a Small scattered areas of multiple ulcerations and areas of
necrosis (brown-black or grayish discoloration)
Grade 3b Extensive necrosis
From Zargar SA, Kochlar R, Mehta S, et al. The role of fiberoptic endoscopy in the management of corrosive ingestion
and modified endoscopic classification of burns. Gastroenterol Endosc. 37:165-169. 1991. As cited in Haddad LM,
Shannon MW, Winchester JF. Clinical Management of Poisoning and Drug Overdose. 1998.
126
CAUSTICS: ACIDS
Management
Amount and concentration taken
Time of ingestion
Symptoms of:
HISTORY Nausea Irritability
Drooling Vomiting
Inability to swallow Stridor
Pain upon swallowing
Buccal/pharyngeal/esophageal/epigastric/abdom-
inal pain
Note signs of:
Acute abdomen Upper airway obstruction
Neurogenic/septic shock Respiratory distress
PHYSICAL Upper GI bleed/ Renal failure
EXAMINATION hematemesis
Examine for burns in the oral cavity:
Local and circumferential; note degree of burn
CBC Prothrombin time
LABORATORY ABG Urinalysis
EXAMINATIONS RBS Urine hemoglobin
Na+, K+, Cl-, Ca+2 Typing (save blood for x-matching)
X-rays: Chest PA upright, abdominal
Use copious amounts of water to decontaminate eyes/
skin exposed to acid spills or vomitus.
In the presence of moderate to severe epigastric or
GENERAL chest pain, give opioid analgesics.
MEASURES Pethidine (Meperidine) prn
Adult: 25-50 mg IM in the first 24 hrs
Pedia: 1 mg/kg/dose IM
If with signs of upper GI bleeding, or burns in the oral
cavity, start famotidine (or other H2 blocker or proton
pump inhibitor).
Adult: 20 mg IV q 12 hrs
Pedia: 0.8 mg/kg/dose IV q 12 hrs
127
CAUSTICS: ACIDS
SPECIFIC
MEASURES
Grade 1 to 2a Grade 2b Grade 3a to 3b

Observe 48 hrs. Admit to ICU. Admit to ICU.
Liquid diet for 48 Maintain on NPO Maintain on NPO
hrs. for 2 to 3 days. for 2 to 3 days.
Give H2 blockers Give IV hydration Give IV hydration
oral or IV. or hyperalimen- or hyperalimen-
Give demulcent tation or jejun- tation or jejun-
or locally acting ostomy feeding. ostomy feeding.
antacids or Give H2 blocker Give H2 blocker
cytoprotective or proton pump or proton pump
agent (sucral- inhibitor IV. inhibitor IV.
fate). Continue pethi-
dine (meperi-
Look for signs of dine) only after
intra-abdominal decision to
perforation or operate is
necrotic gastric made in order
lesions. to avoid mas-
king signs and
Negative symptoms of
perforation.
Positive
Refer for laparotomy: exploration or

debridement of non-viable tissue.

If stable and asymptomatic after observation period,
discharge.
Follow-up c/o surgeon or gastroenterologist.
For repeat endoscopy after two weeks.
128
CAUSTICS: ACIDS
Surgery
ACUTE
If gastrectomy is done, give lifelong Vitamin B12
ABDOMEN
replacement.
Start antibiotics.
INFECTION Cover for anaerobes and gram negative organisms.
Septic shock
Fluids (isotonic saline)
Appropriate antibiotics
Hypovolemic shock
SHOCK
Fluid challenge
Acid-base and electrolyte correction
Neurogenic shock
Pethidine (Meperidine) 1 mg/kg/dose IV
Glottic edema
UPPER AIRWAY
Cricothyroidectomy or tracheostomy
OBSTRUCTION
Hydrocortisone 100 mg IV q 6 hrs
UPPER GI Blood transfusion

BLEEDING Surgery
REFERENCES
Arevalo-Silva C, Eliashar R, et al. Ingestion of caustic substances: a 15-year experience.
Laryngoscope. 116(8):1422-6. Aug 2006.
2004.
Wilkins. 1997.
Flomenbaum N, Goldfrank LR, et al. Goldfrank's Toxicologic Emergencies, 8th ed. New
York: McGraw Hill Companies, Inc. 2006.
Goldman LT and Weigert JM. Corrosive substances: a review. Am J Gastroenterology. 79:
2. 1984.
Gossel TA and Bicker JD. Principles of Clinical Toxicology, 3rd edition. New York: Raven
Press. 1994.
Klassen CD, Amdur MO, Doul J. (eds.). Casarett and Doull’s Toxicology: The Basic
Science of Poisons, 5th edition. New York: MacGraw Hill. 1996.
129
CAUSTICS: ALKALIS
CAUSTICS:
ALKALIS
Alkaline substances are proton acceptors that produce significant tissue
damage at a pH above 11. Aside from pH, other factors that should be
considered when establishing the degree of injury are: concentration,
molarity, volume, contact time and pre-morbid condition of the
gastrointestinal tract. Alkaline agents commonly involved in poisoning
cases are sodium hypochlorite, sodium hydroxide, potassium hydroxide
and ammonia.
The consequences of alkali ingestion are related to the form of the
material. Solid crystalline products commonly cause burns confined to
the oropharynx while liquid products are easily swallowed, causing
predominantly esophageal, as well as gastric burns.
Contact of the substance with proteins and fats in tissues causes
liquefaction necrosis. The solubility of alkalis allows extensive
penetration through layers of tissue which may go on for several days.
Sequelae consist of perforation, strictures and later, the development of
malignancy. The peak risk for perforation occurs during the 2nd -3rd week
of injury, although it may occur much earlier.
• Grade I burns - no/very low risk of stricture formation
• Grade II circumferential burns - stricture formation in 75% of cases
• Grade III burns - high risk for perforation aside from stricture
formation
See also discussion on sodium hypochlorite, page 131.
130
CAUSTICS: ALKALIS
• Chlorine gas is released when an aqueous solution of hypochlorite is
mixed with a strong acid. Chloramine gas is released when an aqueous
hypochlorite solution is combined with ammonia solution. Chlorine and
chloramine gas inhalation can result in immediate burning sensation of
the eyes, nose and throat; airway obstruction with croupy cough, hoarse-
ness and stridor. With massive exposure, chemical pneumonitis (non-
cardiogenic pulmonary edema) may occur.
• The patient’s symptoms are not reliable predictors of esophageal or
gastric damage. In children, the presence of stridor, drooling or vomiting
increases the risk for esophageal injury.
• Endoscopy should be done within 12 hours and no later than 24 hours
after exposure.
• DO NOT insert a nasogastric tube since this increases the risk of reexpo-
sure of the esophagus to alkali, perforation and aspiration pneumonia.
• DO NOT give any neutralizing agent because the reaction can evolve
carbon dioxide which can aggravate chemical injury to the stomach and
cause rupture.
• Steroids can help reduce the severity of symptoms of upper airway
obstruction (stridor, dyspnea, hoarseness, laryngeal edema). However,
there are studies that show no beneficial effects in the reduction of
stricture formation.
Classification of Mucosal Injury

Following Caustic Substance Ingestion
Grade 0 Normal findings on examination
Grade 1 Edema, hyperemia of mucosa
Grade 2a Friability, blisters, hemorrhages, erosions, whitish membranes,
exudates, superficial ulcerations
Grade 2b Grade 2a plus deep discrete or circumferential ulceration
Grade 3a Small scattered areas of multiple ulcerations and areas of
necrosis (brown-black or grayish discoloration)
Grade 3b Extensive necrosis
From Zargar SA, Kochlar R, Mehta S, et al. The role of fiberoptic endoscopy in the management of corrosive ingestion
and modified endoscopic classification of burns. Gastroenterol Endosc. 37:165-169. 1991. As cited in Haddad LM,
Shannon MW, Winchester JF. Clinical Management of Poisoning and Drug Overdose. 1998.
131
CAUSTICS: ALKALIS
Management
Time of ingestion (in relation to meals)
Symptoms of:
HISTORY Irritability Nausea
Inability to swallow Vomiting
Pain upon swallowing Drooling
inal pain
Note signs of:
Acute abdomen Upper airway obstruction
Neurogenic/septic shock Respiratory distress
PHYSICAL Upper GI bleed/ Renal failure
EXAMINATION hematemesis
Examine for burns in the oral cavity:
Local and circumferential; note degree of burn
LABORATORY CBC, platelets Urinalysis
EXAMINATIONS ABG Urine hemoglobin
Creatinine Typing (save blood for x-matching)
Na+, K+, Cl- X-rays: Chest PA upright, abdominal
skin exposed to alkali spills or vomitus.
In the presence of moderate to severe epigastric or
GENERAL chest pain, give opioid analgesics.
MEASURES Pethidine (Meperidine) prn
Adult: 25-50 mg IM in the first 24 hrs
Pedia: 1 mg/kg/dose IM
Start famotidine (or other H2 blocker or proton pump
inhibitor).
132
CAUSTICS: ALKALIS
SPECIFIC Extent of esophageal burn
MEASURES
Grade 1 Grade 2a Grade 2b or 3

Start bland diet. Admit. Admit to ICU.
Observe 48 hrs. Trial of soft diet Maintain on NPO.
Give demulcent as tolerated. Give IV hydration
or locally acting Give H2 blocker or hyperalimen-
antacids. or proton pump tation or jejun-
inhibitor IV/po. ostomy feeding.
Give sucralfate. Continue pethi-
If with risk of per- dine (meperi-
foration, NPO dine) only after
for 2 to 3 days decision to
and feed via operate is
gastrostomy, made in order
jejunostomy or to avoid mas-
TPN. king signs and
symptoms of
Look for signs of perforation.
perforation.
Negative Positive
If improving, treat Refer for surgery.

as 1st degree.

If stable and asymptomatic after observation period,
discharge.
Follow-up c/o surgeon or gastroenterologist.
For repeat endoscopy after two weeks.
133
CAUSTICS: ALKALIS

Surgery
ACUTE
If gastrectomy is done, give lifelong Vitamin B12
ABDOMEN
replacement.
Start antibiotics.
INFECTION Cover for anaerobes and gram negative organisms.
Septic shock
Fluids (isotonic saline)
Appropriate antibiotics
Hypovolemic shock
SHOCK
Fluid challenge
Acid-base and electrolyte correction
Neurogenic shock
Pethidine (Meperidine) 1 mg/kg/dose IV
Glottic edema
UPPER AIRWAY Cricothyroidectomy or tracheostomy
OBSTRUCTION Dexamethasone 1 mg/kg/day or methylpredniso-
lone 2 mg/kg/day
UPPER GI Blood transfusion

BLEEDING Surgery
REFERENCES
Boukthir S, Fetni I, et al. High doses of steroids in the management of caustic esopha-
geal burns in children. Archives of Pediatrics. 11(1):13-7. January 2004.
2004.
Wilkins. 1997.
Goldman LT and Weigert JM. Corrosive substances: a review. Am J Gastroenterology. 79:
2. 1984.
Hoffman RS, et al. (eds). Goldfrank's Manual of Toxicologic Emergencies. New
York: McGraw-Hill Companies, Inc. 2007.
Pelclova D, Navratil T. Do corticosteroids prevent esophageal stricture after corrosive
ingestion? Toxicol. Rev. 24(2):125-9. 2005.
134
CAUSTICS: ALKALI - SODIUM HYPOCHLORITE
CAUSTICS:
ALKALI - SODIUM HYPOCHLORITE
Sodium hypochlorite is generally used as a household bleach at a
concentration of 3 to 6% (usually <5%). Stronger solutions (8% with or
without chlorine) are used for industrial purposes.
At concentrations of 3 to 6%, sodium hypochlorite is a mild to
moderate irritant. It causes eye and skin irritation and can produce mild
oral or esophageal burns. In the stomach, it combines with acids to
produce hypchlorous acid which is an irritant to the mucous membrane
but does not cause stricture formation.
Only minor burns have been reported in children who accidentally
ingest household bleach. However, more serious burns have been
observed with ingestion of higher concentrations of sodium hypochlorite
(5 to 7%). In adults, intentional ingestion of large volumes of sodium
hypochlorite may result in hematemesis and electrolyte imbalance.
• DO NOT insert a nasogastric tube. If patient is received with a nasogas-
tric tube, leave in place to avoid possible perforation.
• If patient ingested industrial strength sodium hypochlorite, use Alkali
Protocol, page 126.
Management
Time of ingestion (in relation to meals)
Symptoms of:
HISTORY Pain upon swallowing Nausea
Inability to swallow Vomiting
Drooling
inal pain
135
Note signs of:

Acute abdomen
PHYSICAL Upper GI bleed/hematemesis
EXAMINATION Skin and eye irritation
Examine for burns in the oral cavity
LABORATORY CBC
EXAMINATIONS Typing (save blood for x-matching)
Na+, K+, Cl-
skin exposed to alkali spills or vomitus.
GENERAL Put patient on NPO. Give intravenous fluids.
MEASURES Adult: D5 0.9NaCl or AR 1 liter x 8 hrs
Give demulcent: raw egg white
Adult: 8 to 12 eggs
Pedia: 4 to 6 eggs
SPECIFIC Mode of exposure

MEASURES
Ingestion Eye irritation Skin irritation

Look for signs of Flush with free- Wash with water
bleeding or flowing water for for 30 minutes.
perforation. 30 minutes.
Check endosco-
py findings.
Negative Positive
Dilute with raw white and water PO. Use Alkali
Give antacids - aluminum- Protocol, page
magnesium hydroxide 2 tbsps q 126.
6 hrs.
Observe for 24 hrs.
136
ABDOMINAL
Pethidine (Meperidine) 1 mg/kg/dose
PAIN
ASPIRATION
Penicillin G 200,000 units/kg/day
PNEUMONIA
REFERENCES
Christesen HB. Prediction of complications following unintentional caustic ingestion in
children. Is endoscopy always necessary? Acta Paediatrica. 84(10):1177-82. October
1995.
2004.
Wilkins. 1997.
137
JEWELRY CLEANER (CYANIDE)
JEWELRY CLEANING AGENTS:

CYANIDE CONTAINING
During the period 2001 to 2006, there was a steady increase in the
number of cases of ingestion of “Silver Jewelry Cleaner” solution. A total
of 210 poisoning cases were referred to the National Poison
Management and Control Center at UP-PGH during this six-year period.
There were only two cases in 2001, but there were 94 cases in 2006. The
increasing number of cases of poisoning can be attributed to the growing
popularity of “silver” jewelry among the youth, and therefore the
increasing use of cleaning agents. Silver jewelry cleaners are readily
available in market stalls and malls, packaged without any label
indicating that the contents are poisonous.
In 2006, the age distribution of the 35 patients admitted at PGH was
as follows: 11 were younger than 6 years of age, 13 were between 6 to 20
years of age, and 11 were older than 20 years. In the same year, jewelry
cleaning agent poisoning accounted for 48% of accidental poisoning
cases and 40% of non-accidental cases admitted at the hospital. Twenty-
nine (29) of these patients (73%) were discharged with improvement,
three went home against medical advice (8%) and three died (8%).
Jewelry cleaning agents retrieved from admitted patients mostly
tested positive for cyanide, with an alkaline pH >10. However, there were
also cases of ingestion of another type of jewelry cleaning agent that was
colored blue and acidic, with pH 2 to 3. The acidic type tested negative
for cyanide content. These cases revealed that not all jewelry cleaners
contain cyanide and the management of cyanide toxicity should be
correlated with its symptoms. Jewelry cleaners containing cyanide
should therefore be managed as Cyanide and Caustic Alkali Poisoning.
Aside from cyanide, jewelry cleaning solution can also contain
sulfuric acid, nitric acid, or phosphoric acid. The cleaning agent can be
bought in white crystalline powder form, packaged in plastic sachets or
pouches, or as a prepared solution in a plastic container. When the
crystalline powder is mixed with water, it appears as a colorless liquid.
Thus it can be mistaken for drinking water especially when placed in
mineral/softdrink/juice bottles.
Cyanide is a highly toxic, rapidly acting agent. It comes in the form of
salts and liquid. At temperatures below 25ºC, hydrogen cyanide or
hydrocyanic acid (HCN) is a colorless or pale-blue liquid. At higher
temperatures, it is a colorless gas. Hydrogen cyanide is very volatile,
138
producing potentially lethal concentrations at room temperature. The
vapor is flammable and potentially explosive. Hydrogen cyanide has a
faint, bitter almond odor and a bitter, burning taste. It is soluble in water
and is often used as a 96% aqueous solution.
In the human body, cyanide combines with the ferric ion in
mitochondrial cytochrome oxidase, preventing electron transport in the
cytochrome system and blocking oxidative phosphorylation and ATP
production. The inhibition of oxidative metabolism puts increased
demands on anaerobic glycolysis, which results in lactic acid production.
It is therefore important to check arterial blood gases for severe acid-
base imbalance.
The body has several endogenous mechanisms that can eliminate
small amounts of cyanide. The majority (60% to 80%) of cyanide is
detoxified by rhodanese, a mitochondrial trans-sulfurase enzyme found
primarily in the liver and skeletal muscle. Rhodanese catalyzes the
transfer of CN- to the sulfur group of thiosulfate to form thiocyanate, a
less toxic metabolite that can be easily removed through the kidneys.
However, the body's thiosulfate supply is very limited, and therefore the
system is quickly overwhelmed. The CNS is very sensitive to the toxic
effects of cyanide. Exposure to hydrogen cyanide can quickly produce
neurologic symptoms.
The toxic dose of cyanide is difficult to quantify and depends on the
chemical form, the route and duration of exposure, and patient specific
factors such as individual susceptibility, differences in metabolism or
underlying medical problems.
139
• Oxygen support should be given to all patients exposed to cyanide
especially those with decreased sensorium. Intubate if sensorium
continues to deteriorate.
• If ingestion is within an hour, egg whites may be given as demulcent.
• During nitrite administration, monitor BP, HR, and signs of severe met-
hemoglobin formation.
• Excessive doses of nitrites or their use in susceptible subgroups of
patients (i.e., glucose-6-phosphate dehydrogenase deficiency) can lead
to life threatening methemoglobinemia. Monitor serum methemoglobin
30 and 60 minutes after giving nitrites or if excessive methemoglobin is
observed. May give vitamin C at 25 mg/kg IV in children or 1g IV in
adults. Induced methemoglobin should be 25% to 30% .
• Clinical sequelae of methemoglobinemia may include a bluish or
brownish discoloration of the skin; increased respiratory rate, decreased
blood pressure; increased heart rate; deterioration in mental status;
evidence of cardiac ischemia or worsening acidosis.
• Hypotension is another effect of nitrite administration, particularly with
higher doses. It is due primarily to vasodilatation, but large doses also
produce myocardial depression in animals. It can be avoided by infusing
sodium nitrite over a period of 5 minutes or more and by giving supple-
mental fluids or pressors.
• Signs of thiocyanate toxicity: nausea, vomiting, muscle cramps, rarely
altered mental status or hypotension. Hemodialysis can remove excess
thiocyanate.
• A patient's failure to improve after antidotal therapy may indicate another
reason for the original clinical findings (e.g., co-exposure, anoxic brain
injury or other diseases).
• Check regularly for metabolic acidosis using serial ABGs, metabolic
panels and serum lactate determinations.
140
Management
Inquire about possible cyanide poisoning.
Exposure to cyanide containing substances
Jewelry cleaner Metal refining
Photography Electroplating
Fumigants Artificial nail remover
Ingestion of Prunus species
Exposure to nitropruside
Combustion of wool, silk, synthetic rubber, poly-
urethane
Rapidity of onset of symptoms (very rapid, especial-
HISTORY ly in inhalation). Patient may be comatose or
with sudden loss of consciousness after exposure.
Fire victim with coma or acidosis
Sudden collapse of laboratory or industrial worker
Amount, time and route of exposure
Intake of other substances, home remedies
Prior co-morbidities or exposure to other substances
Signs and symptoms of:
Loss of consciousness Absence of cyanosis
“Cherry colored” skin “Bitter almond taste”
Cold and clammy skin Seizures or coma
Vital signs: bradycardia and hypertension, OR tachy-
cardia, hypotension and bradypnea
PHYSICAL Funduscopy usually shows veins and arteries with
EXAMINATION similar color due to arteriolization
Rales or rhonchi due to pulmonary edema especially
when associated with frothing of the mouth and
if intubated, increased secretions in the endotrach-
eal tube
Respiratory arrest
Signs of acute abdomen due to caustic injury
Cold, clammy skin, absence of cyanosis, cherry red
skin, occasionally with cyanosis at the terminal
stage
Neuro exam: roving of eyes, dilated pupils with sluggish
reaction, reflexes may be decreased or abnormal,
posturing can be present, muscle tone may be
flaccid, coma
141
Serum cyanide - 5 mL red-top blood in vacutainer,
well sealed
Serum methemoglobin - 5 mL heparinized blood in
vacutainer, immerse tube in ice
LABORATORY Ingested substance - send analysis to National Bureau
EXAMINATIONS of Investigation (NBI)
ABG BUN CKMB
CBC Creatinine Serum lactate
ECG Na+, K+, Cl- EGD
RBS AST, ALT Chest x-ray

Give 100% oxygen support to all patients exposed to
cyanide.
Adult: D5 0.9NaCl x 8 hrs
Do not insert NGT.
GENERAL Monitor capillary blood glucose.
MEASURES Start famotidine (or other H2 blocker or proton pump
inhibitor).
Supportive care
Establish IV access.
Give cyrstalloids and vasopressors to maintain BP.
Give 8.4% sodium bicarbonate 1 mEq/kg IV as
empiric therapy.
Antidote available - see next page

SPECIFIC
MEASURES No available antidote, or will be delayed
First aid while waiting for IV antidote
Nitroglycerin patch 1/4 inch, anterior chest, non-hairy area
Amyl nitrite - wrap pearl-like container in gauze then crush.
Let patient inhale for 30 seconds then give oxygen for
another 30 seconds. Use a new perle every 3 to 5 mins.
Alternative to sodium nitrite
Hydroxocobalamin: 50 g to bind 1 g of cyanide.
Adult: 4 to 5 g diluted to a volume of at least 200 mL
and administered IV over approx. 30 min.
Pedia: 50 mg/kg initial dose is recommended
Give sodium thiosulfate right after hydroxocobalamin.
142
SPECIFIC Possible cyanide exposure
MEASURES
Signs and symptoms If asymptomatic, observe.

compatible with cyanide If patient later develops
poisoning signs and symptoms of
cyanide poisoning, give
sodium thiosulfate.
Presence of any of the With previous signs and

following signs: symptoms but currently
Hypotension asymptomatic
Seizures
Altered mental status or For Hgb=12 g/dL (see
coma table below), give
Respiratory depression single dose sodium
Significant metabolic thiosulfate, 1.65
acidosis mL/kg IV push over
10 min.
For Hgb=12 g/dL (see table below), give sodium

nitrite, 0.33 mL/kg slow IV push for 3 to 5 min
followed immediately by
Sodium thiosulfate, 1.65 mL/kg IV push over 10 min.
If no response, give half dose of sodium thiosulfate.
Reference on the variation of sodium nitrite and sodium

thiosulfate dose with hemoglobin concentration*
Hemoglobin Initial Dose Initial Dose Initial Dose
(g/dL) Sodium Nitrite Sodium Nitrite 3% Sodium Thiosulfate 25%
(mg/kg) (mL/kg) (mL/kg)
7 5.8 0.19 0.95
8 6.6 0.22 1.10
9 7.5 0.25 1.25
10 8.3 0.27 1.35
11 9.1 0.30 1.50
12 10.0 0.33 1.65
13 10.8 0.36 1.80
14 11.6 0.39 1.95
*Leikin JB and Paloucek FP. Poisoning and Toxicology Compendium with Symptoms.
Lexi-Comp. Inc. 1998.
143
Give sodium bicarbonate 1 mEq/kg or compute based

ACIDOSIS on acid-base deficit formula. Repeat ABG after 30 min
then compute additional deficit. Give sodium bicarb-
onate until deficit in ABG determination is corrected.
CAUSTIC
Manage as caustic alkali poisoning
INJURY
HYPOTENSION Fluid challenge
Ascorbic acid 1 g IV (adult) or 25 mg/kg (pedia) and/

METHEMOGLOBINEMIA or methylene blue (USP label) 2 mg/kg PO as single
dose (adult) or 1 mg/kg PO single dose (pedia).
REFERENCES
ATSDR. Medical Management Guidelines for Hydrogen Cyanide (HCN). 2001.
Erdman AR. Cyanide. Medical Toxicology, 3rd ed. Dart, RC (ed.). Lippincott
Williams & Wilkins, USA. 2004.
Hall AH and Rumack BH. Cyanide and Related Compounds. Clinical Management of
Poisoning and Drug Overdose, 3rd ed. Haddad LM et al. (eds.).W.B.Saunders
Company, Philadelphia. 1997.
Leikin JB and Paloucek FP. Poisoning and Toxicology Compendium with Symptoms.
Lexi-Comp. Inc. 1998.
144
KEROSENE
KEROSENE
Kerosene, an aliphatic hydrocarbon, is the leading cause of accidental
poisoning among children aged 6 years old and younger. This is because
kerosene, which is commonly used for cooking fuel, is often stored
inappropriately in soft drink bottles or drinking water containers, and
placed in areas that are within reach of children.
The compound is completely absorbed in the gastrointestinal tract
because of its low molecular weight. It can likewise be absorbed through
inhalation and minimally through the skin.
The toxicity of kerosene is due to its local irritating effect and its
systemic effects on various organ systems. It has a high aspiration
potential because of its low viscosity (35 Saybolt solvent universal).
Thus, close monitoring of the lungs is imperative. The compound can
also depress the central nervous system, particularly the ventilatory
drive, and cause seizures because of hypoxia. Studies have shown that
ingestion of >30 mL with vomiting, present a higher risk for development
of pulmonary toxicity. However, such parameters are not 100%
predictive.
Kerosene naturally volatilizes through the esophagus up to the
pharynx. The insertion of a nasogastric tube and the decision to lavage
are thus dependent on the volume ingested and the length of the
patient's esophagus.
• DO NOT induce emesis (mechanical or chemical) unless a more toxic
poison is incorporated or ingested along with kerosene.
• DO NOT use mineral oil nor olive oil. The thickened consistency of the
hydrocarbon predisposes to the development of lipoid pneumonia and
enhances hydrocarbon absorption.
• Activated charcoal lavage would not be of benefit unless other toxic
substances (like pesticides) are taken concomitantly.
• It is important to wash the perianal area after a bowel movement since
contact with stool containing kerosene can produce 1st to 2nd degree
burns on the skin.
145
KEROSENE
Management
Amount taken
Time of ingestion
HISTORY Symptoms of:
Nausea Mucous membrane irritation
Vomiting CNS effects: initial excitation followed
Diarrhea by CNS depression; seizures
Cough Difficulty of breathing
Emphasis on lung findings; note signs of respiratory
distress
Tachypnea
PHYSICAL Coarse or decreased breath sounds
EXAMINATION Rales, wheezes
Cyanosis
Tachycardia, arrhythmias
Abdominal tenderness
Perianal burns
Changes in sensorium
CBC, platelets Urinalysis
LABORATORY ABG Urine hemoglobin
EXAMINATIONS Creatinine Typing (save blood for x-matching)
Na+, K+, Cl- X-rays: Chest PA upright, abdominal
Prothrombin time

Remove patient’s clothes and do decontamination
GENERAL procedures, especially with history of vomiting.
Give oxygen via nasal cannula.
146
KEROSENE
SPECIFIC Volume ingested
MEASURES
KNOWN UNKNOWN or
UNCONSCIOUS
Pedia: < 1 mL/kg Pedia: < 1 mL/kg Pedia: > 1 mL/kg

Adult: < 60 mL Adult: < 60 mL Adult: > 60 mL
plus other toxic
substances
Defer NGT. Insert NGT. Protect airway.

Lavage with Insert NGT.
activated charcoal. Careful lavage with
Adult: 100 g in water.
200 mL water
Pedia: 1 g/kg to
make a slurry.
Give sodium sulfate.

Pedia: 250 mg/kg as a 10% solution
Repeat if no bowel movement within 1 hour.
Once with bowel movement, clean peri-anal area at
once to prevent chemical burns.
Remove NGT.
Check for the following conditions:
• Unconsciousness
• Seizures
• Pneumonitis by x-ray or clinical
parameters (If with clinical evidence of
pneumonia but none on chest x-ray,
repeat chest x-ray on the 3rd day.)
• Ingestion of other toxic substances
e.g., organophosphate pesticides
(Treat as for toxic substance.)
None of Any of
the above the above
Observe 12 hours. Observe 24 hours. Observe for at
least 3 days.
Treat accordingly.
Refer to Psychiatry if non-accidental. Refer to Psych if
Discharge if with no signs of pneumonia. non-accidental.
147
KEROSENE
Start Penicillin G
ASPIRATION Adult: 1 to 2 million units every 6 hours
PNEUMONIA Pedia: 200,000 u/kg/day
If vomitus is bilous, may require administration of
Clindamycin or Metronidazole.
Antacids - Aluminum-magnesium hydrochloride

30 mL q 6 hours
GASTRITIS H2 blockers - Famotidine
Adult: 20 mg IV q 12 hours
Pedia: 0.8 mg/kg/dose q 12 hours
HYPO- Adult: 10 mg IV up to 60 mg/day
PROTHROMBINEMIA
Pedia: maximum of 10 mg/dose
Diazepam
doses.
SEIZURES Lorazepam
min prn.
Compatible with D5W
148
KEROSENE
REFERENCES
Beamon RF, Siegel CJ, Landers G, Green V. Hydrocarbon ingestion in children: a six-
year retrospective study. JACEP. Oct 1976. 5(10):771-5.
2004.
Goldfrank LR et al. (eds.). Goldfrank's Toxicologic Emergencies, 7th ed. New York:
McGraw-Hill. 2002.
Press. 1994.
Haddad LM, Shannon MW., and Winchester JD. Clinical Management of Poisoning and
Drug Overdose, 3rd ed. Philadelphia: W.B. Saunders Company. 1998.
Klaasen, CD, Amdur, MO, Doull J (eds.). Toxicology:The Basic Science of Poisons, 5th
ed. New York: McGraw-Hill. 1996.
Lifshitz M, Sofer S, Gorodischer R. Hydrocarbon poisoning in children: a 5-year
retrospective study. Wilderness Environ Med. 2003 (Summer); 14(2):78-82.
National Poison Management and Control Center. Annual Statistics. (unpublished) 2006.
Nunn, JA., Martin, FM. Gasoline and Kerosene Poisoning in Children. Journal of the
American Medical Association. 1990; 103: 472-474.
Proudfoot A. Poisoning with household, agricultural and industrial products. Medicine
International. 1989; 3: 2526-2527.
Shotar AM. Kerosene poisoning in childhood: a 6-year prospective study at the Princess
Rahmat Teaching Hospital. Neuro Endocrinol Lett. 2005 Dec; 26(6): 835-8.
Simmank K , Wagstaff L , et al. Prediction of illness severity and outcome of children
symptomatic following kerosene ingestion. Annals of Tropical Paediatrics. 1998; 18
(4): 309-314.
149
PESTICIDES: COUMATETRALYL/WARFARIN
PESTICIDES:
COUMATETRALYL / WARFARIN
Warfarin and related compounds (coumatetralyl and indandiones) are
the active ingredients in rodenticides. However, the concentration of the
active ingredient varies from formulation to formulation. Warfarin is
rapidly absorbed orally. It binds totally to albumin in the circulation and is
degraded in the liver. The inactive metabolites of warfarin are to some
extent conjugated with glucuronic acid, undergo enterohepatic
recirculation, and are excreted in the urine and feces.
Warfarin acts as an anticoagulant by interfering with the hepatic
Vitamin K dependent carboxylation of prothrombin, factors VII, IX, X and
the anticoagulant proteins C and S. Toxicity occurs with the ingestion of 1
to 2 mg/kg of the substance for 3 to 6 days. A single intake of >15 grams
may be lethal. Warfarin toxicity manifests in varied ways like hematuria,
petecchiae, excessive menstrual bleeding or massive hemorrhage.
Maximum depression of clotting factors occurs 36 to 72 hours after
ingestion, therefore, manifestations of bleeding may be delayed 8 to 12
hours after ingestion.
Second generation anti-coagulants or superwarfarins, like
difenacoum or brodifacoum are also used as rodenticides. They may be
absorbed through the intact skin. These may produce early coagulation
defects which last up to 6 to 8 weeks. Thus, bleeding may be persistent,
requiring the continuous administration of antidote, depending on the
volume ingested and the length of the patient's esophagus.
150
• Drugs that potentiate the action of anticoagulant pesticides:
Allopurinol Oral hypoglycemic agents
Aspirin Paracetamol
Cimetidine Propylthiouracil
Clofibrate Quinidine
Disulfiram Sulfonamides
Heparin Thyroxine
Metronidazole Trimethoprim-sulfamethoxazole
NSAIDs
• Drugs that decrease the toxicity of anticoagulant pesticides:
Barbiturates Steroids
Carbamazepine Glutethimide
Cholestyramine Rifampicin
Contraceptives
• Any condition that affects liver function or the availability of Vitamin K
(e.g., alterations in intestinal bacteria or decreased food intake) can
alter the patient’s coagulation status).
• Menadione (Vitamin K3) is not an effective antidote.
• For superwarfarin, single dose of 0.12 mg/kg body weight of brodifacoum
(or 1 mg in adults) can cause anticoagulation lasting for several weeks
or even months. Management consists of:
• Monitoring PTT and protime
• Immediate transfusion with fresh frozen plasma or whole blood if
bleeding has occurred
• Phytonadione IV as supportive treatment
• Continuous follow-up for up to 7 months
151
Management
Amount taken
HISTORY Intake of other substances (alcoholic drinks)
History of bleeding tendencies
Rule out liver disease
Check for signs of hemorrhage
Hemorrhagic shock
Intracranial hemorrhage
PHYSICAL Intraabdominal bleeding
EXAMINATION Epistaxis, gum bleeding, conjunctival bleeding
Petecchial rash, hematomas
Excessive menstrual bleeding
Intraarticular bleeding
CBC with serial hemoglobin and hematocrit
Platelet count, reticulocyte count
Urinalysis
LABORATORY Fecalysis with test for occult blood
EXAMINATIONS Liver function tests
Protime and partial thromboplastin generation time
(if second generation rodenticide)
ECG
Chest x-ray

May be repeated once if initial dose does not result in
bowel movement after one hour. During repeat lavage,
may give after 4 doses of activated charcoal if with no
bowel movement.
152
SPECIFIC
MEASURES <15 g single dose
>15 g single dose
OR <1 to 2 mg/kg
OR >1 to 2 mg/kg
for 3 to 6 days with
for 3 to 6 days
mild or no bleeding
Observe for 72 hours. Daily protime.
Normal Abnormal (-) (+)

protime protime bleeding bleeding
Refer to Psychiatry
if non-accidental. Normal Abnormal
If still asymptomatic, protime protime
discharge.
Vitamin K1
Adult: 10 to 20 mg IV/IM q 8 hrs
Pedia: 1 mg/kg IV/IM (max 5 mg)
If unresponsive to Vitamin K1:
Fresh frozen plasma
10 mL/kg initially then
5 mL/kg q 6 to 8 hours
Fresh whole blood
Plasma concentrate of Vitamin K
dependent factors
Abnormal
protime
Normal
protime
Repeat protime and look

for other causes of
bleeding.
153
EXCESSIVE Vaginal packing

MENSTRUAL BLEEDING Refer to Obstetrics/Gynecology Service
Maintain on NPO.
INTRAABDOMINAL Insert NGT.
BLEED Iced saline lavage
Correct fluid/electrolyte abnormalities
Refer to Surgery.
If there is no hypotension:
20% mannitol
Adult: 75 to 100 mL q 6 hours
Pedia: 2.5 to 5.0 mL/kg/dose
INTRACRANIAL OR dexamethasone
BLEED Adult: 5 to 10 mg IV then 4 mg q 6 hours
Pedia: 1.5 mg/kg/dose followed by 1.5 mg/kg/
day in 4 to 6 divided doses for 5 days then
tapered slowly to discontinuation over the next
5 days.
Refer to Neurology Service.
REFERENCES
2004.
Benitz WE and Tatro DS. The Pediatric Drug Handbook, 3rd ed. St. Louis: Mosby-Year
Book, Inc. 1995.
Wilkins. 1997.
Gossel TA and Bricker JD. Principles of Clinical Toxicology, 3rd ed. New York: Raven Press.
1994.
International Programme on Chemical Safety. Environmental Health Criteria 175: Anti-
coagulant Pesticides. Geneva: WHO. 1995.
Klaassen CD, Amdur MO and Doull J. (eds.) Toxicology: The Basic Science of Poisons,
5th ed. New York: MacGraw-Hill. 1996.
Reigart JR and Roberts JR. Recognition and Management of Pesticide Poisonings, 5th
ed. U.S. Environmental Protection Agency. 1999.
154
PESTICIDES: N-METHYL CARBAMATES
PESTICIDES:
N-METHYL CARBAMATES
Carbamates inhibit the action of cholinesterase, the enzyme responsible
for the breakdown of acetylcholine to acetic acid and choline. Unlike the
inhibition produced by organophosphates, the binding of the carbamyl
moiety with cholinesterase is reversible. Thus the clinical syndrome is
more benign and much shorter in duration.
Currently, a number of agricultural pesticides contain carbamates
such as benomyl, carbofuran and carbaryl. Of the household pesticides,
propoxur is no longer a component of
commonly used mixed pesticides. Commonly Encountered
Clinical manifestations of poisoning N-Methyl Carbamates
resemble those of organophosphate Chemical Hazard Category
poisoning (see page 160) with the Aldicarb Ia
exception of central nervous system Bendiocarb II
effects, such as convulsions. Benomyl IV
Management is essentially the BMPC II
Carbaryl II
same as with organophosphate Carbofuran Ib
poisoning (see page 160) but do not Fenobucarb II
give oximes. Duration of atropinization Formetanate Ib
is usually shorter, that is, 24-48 hours Isoprocarb II
only, except for poisoning with aldicarb, Methomyl Ib
which is long acting. Patients are prone Oxamyl Ib
to develop atropine toxicity because of Propoxur II
the reversible action of carbamates. Thiophanate-methyl IV
REFERENCES
Haddad LM, et al. Clinical Management of Poisoning and Drug Overdose, 3rd ed.
Philadelphia: W.B. Saunders Company. 1998.
155
PESTICIDES: ORGANOCHLORINES
PESTICIDES:
ORGANOCHLORINES
Organochlorine pesticides are also known as chlorinated hydrocarbons.
There are three different types: cyclodienes, dichlorodiphenylethanes
and hexachlorocyclohexanes. Except for lindane, which is used as an
anti-scabicide, organochlorines are either banned or restricted by the
Fertilizer & Pesticide Authority. (See http://fpa.da.gov.ph for a
complete listing).
Organochlorines are potent stimulants of the central nervous
system and the sympathetic system. Cyclodienes such as endosulfan
and chlordane antagonize the neurotransmitter gaba-aminobutyric acid
(GABA) and inhibit Na+-K+ ATPase. Dichlorodiphenylethanes increase the
sensitivity of neurons to small stimuli by reducing the transport of
potassium into the cell, interfering with
the transport of sodium outside the cell, Commonly Encountered
and by inhibiting the actions of ATPase Organochlorines
and calmodulin.
Chemical Hazard Category
Liquid preparations are dissolved in Dichlorophenylethanes
petroleum distillate solvents. Absorption DDT II
is through all routes of entry and Cyclodienes
enterohepatic recirculation occurs Aldrin Ia
during metabolism. Organochlorines Chrlordane II
are stored in fat depot. The half-lives of Dieldrin Ib
these pesticides are relatively long Endrin Ib
(weeks to years). In the environment, Endosulfan II
organochlorines pose potential Heptachlor II
Hexachlorocychlohexanes
problems as persistent organic Lindane II
pollutants.
156
• No antidote has been proven effective.
• DO NOT give sympathomimetic agents (e.g., epinephrine) or a cholinergic
blocker (e.g., atropine) because arrhythmias may occur in a sensitized
heart.
• DO NOT give fatty liquids such as broth, milk, olive oil.
• Phenytoin may be given for the following reasons:
- it enhances cytochrome P450 oxidase system activity, thereby enhan-
cing organochlorine metabolism
- it acts as both an anti-arrhythmic and anti-convulsant agent
Clinical Features
• Dichlorodiphenylethanes
Paresthesia, ataxia, abnormal stepping, dizziness, confusion, headache,
nausea, vomiting, fatigue, lethargy, peripheral tremors
• Cyclodienes
Dizziness, headache, nausea, vomiting, motor hyperexcitability, hyper-
reflexia, myoclonic jerks, general malaise, seizures
• Hexachlorocyclohexanes
Tremors, ataxia, convulsions
Management
Amount taken
HISTORY Time and mode of administration
See Clinical Features
PHYSICAL Note level of sensorium
EXAMINATION Arrhythmias
Hypertension
Signs of aspiration pneumonia
LABORATORY ABG X-ray: Chest PA Ionized Calcium
EXAMINATIONS ECG LFTs RBS
EEG Protime Na+, K+, Cl-
157

Put patient in Trendelenburg position.
If poison is absorbed through skin, inhaled, or ingested
then vomited, remove clothing and sponge bath
GENERAL using alkaline soap.
MEASURES If poison is ingested:
May give after 4 doses of activated charcoal if
with no bowel movement.
Insert foley catheter when necessary

Phenytoin 10-20 mg/kg IV or PO loading dose
then 5-7 mg/kg IV or PO
If there is no response, add a cardioselective beta-
blocker
ARRHYTHMIAS
If there is still no response, give 10% calcium gluco-
nate (with cardiac monitoring)
Adult: 10 ml slow IV
Pedia: 10 ml of 1:5 dilution
DERANGED Vitamin B complex and glucose

LIVER FUNCTION D50/50 + 1 ampule B complex in IV fluid
ELECTROLYTE Hypokalemia or hypocalcemia

IMBALANCE Treat with potassium chloride or calcium gluconate
LOW PROTIME Adult: 10-20 mg IV or IM q 8 hours
Pedia: 1 mg/kg; not to exceed 25 mg in 24 hours
158
Diazepam
doses.
SEIZURES Lorazepam
min prn.
Compatible with D5W
REFERENCES
Managing Hazardous Materials Incidents. Agency for Toxic Substances and Disease
Registry. September 2001.
U.S. Department of Health and Human Services. Toxicological Profile for Endosulfan
Public Health Service, Agency for Toxic Substances and Disease Registry. April 1993.
159
PESTICIDES: ORGANOPHOSPHATES
PESTICIDES:
ORGANOPHOSPHATES
Organophosphates can be absorbed via ingestion, inhalation and
dermal contact. They inhibit the action of cholinesterase, the enzyme
that breaks down acetylcholine to acetic acid and choline. Effects may
appear as early as 10 minutes to as late as two hours post-exposure,
depending on the amount absorbed and route of absorption.
Organophosphates in liquid preparation are usually dissolved in
petroleum distillate solvents like kerosene and xylene. Isopropanol is
another solvent used together with petroleum distillates. In water-based
formulations, the concentration of isopropanol may be higher. These
solvents are sympathomimetic agents and may mask the cholinergic
manifestations of the organophosphate. Note that cholinergic effects
may be muscarinic, nicotinic or central, depending on the amount
absorbed.
Clinical Features*
• Mild - mainly muscarinic
Malaise, vomiting, nausea, diarrhea, sweating, abdominal pain, saliva-
tion, miosis
• Moderate - muscarinic and nicotinic
Symptoms of mild poisoning PLUS dyspnea, decreased muscular
strength, bronchospasm, bronchorrhea, speech impairment, muscle
fasciculation, tremor, motor incoordination, bradycardia, involuntary
urination/defecation, muscular cramps, hypotension/hypertension
• Severe - muscarinic, nicotinic and CNS
Symptoms of moderate poisoning PLUS coma, respiratory paralysis,
extreme hypersecretion, cyanosis, sustained hypotension, extreme
muscle weakness, muscular paralysis, convulsion, behavioral changes
*As a guide to remembering muscarinic and nicotinic effects, see Toxidromes on page
20.
160
Commonly Encountered Organophosphates*
Category Ia Category Ib Category II Category III
Ethoprophos Dichlorvos/DDVP Chlorpyrifos Malathion
Methylparathion Edifenphos Diazinon Primiphos methyl
Mevinphos Methamidophos Dimethoate
Phorate Methidathion Fenitrothion Category IV
Phosphamidon Monocrotophos Fenthion Temephos
Terbufos Omethoate Phenthion
Triazophos Phosalone
Pyrazophos
*Categories are based on WHO Classification. See http://fpa.da.gov.ph to view list of
banned or regulated pesticides.
• Contraindicated drugs
Aminoglycosides Furosemide Sulfonamides
Aminophylline Morphine Theophylline and
Barbiturates Phenothiazines other xanthines
Beta-blockers Succinylcholine
Local anesthetics especially procaine derivatives
• DO NOT give IV atropine if patient is cyanotic as this may cause ventri-
cular fibrillation in a hypoxic patient. Give atropine IM and correct
cyanosis before IV administration.
• Aggressive treatment must be instituted if there is a history of concom-
ittant intake of phenothiazine/haloperidol since these drugs aggravate
organophosphate poisoning and increase mortality.
• In case of under atropinization manifested by cholinergic symptoms,
reatropinize.
• In case of atropine toxicity manifested by behavioral changes, high grade
fever, flushing of the face and tachyarrhythmias, discontinue atropine
temporarily or adjust dose/frequency of administration. Observe and
hydrate patient. Never give any anticholinesterase such as physostig-
mine or neostigmine.
• For arrhythmias, never give beta-blockers nor lidocaine. Give calcium
blockers, phenytoin or bretyllium
• Although furosemide is contraindicated in organophosphate poisoning,
the drug is recommended in cases of pulmonary edema. However,
ensure that respiration is normal and potassium is within acceptable
limits.
• Defer regular diet (solid foods) until patient is fully conscious and atro-
pine dose is already given by oral route. Start with liquid diet.
• Organophosphates may produce organophosphate-induced delayed
neuropathy (OPIDN) weeks or months after exposure.
161
Management
Amount taken
HISTORY Time and mode of exposure
PHYSICAL Note size of pupils, respiration, heart rate, cyanosis,
EXAMINATION depressed sensorium, muscle fasciculations, fine
tremors
Collect 5 mL heparinized blood in vacutainer.
Immerse tube in ice and submit to lab within 24 h.
EXAMINATIONS ABG Na+, K+, Cl- LFTs Urinalysis
CBC BUN Protime ECG
RBS Creatinine Amylase

then vomited, give oxygen, remove clothing and
GENERAL sponge bath using alkaline soap.
Insert foley catheter when necessary
Give phenytoin 10-20 mg/kg IV or PO loading dose
then 5-7 mg/kg in 3 divided doses (not faster than
50 mg/min if IV) for cases of malathion, parathion
or dichlorvos poisoning, even in the absence of
seizures.
162
If pralidoxime chloride is available, this should be given
within the first 36 hours.
Adult: 1 g in 250 mL 0.9NaCl
Pedia: 50-100 mg/kg in 125 mL 0.3NaCl to run 1 hr
In severe cases, give the second dose 1 hr later, and
SPECIFIC
subsequent doses 6 hrs apart.
MEASURES
Pralidoxime is effective in poisoning cases secondary
to: diazinon, dichlorvos, disulfoton, EPN, fenthion, isofluro-
phate, malathion, Metasystox®, methyldemeton, methyl
parathion, mevinphos, parathion, phosphamidon, sarin,
Systox®, TEPP.
Severity of poisoning
Mild Moderate Severe

Normal values for 20-40% depres- 40-60% depres- >60% depres-
RBC cholinesterase: sion of RBC sion of RBC sion of RBC
0.75-0.92 pH cholinesterase cholinesterase cholinesterase
Give atropine every 10-15 min until parameters for

initial atropinization are achieved:
• Pupils >4 mm
• Heart rate 100-140 per min
• Dry mouth
• Hypoactive bowel sounds
Atropine dose: Atropine dose: Atropine dose:

Adult: 1-2 mg IV Adult: 2-3 mg IV Adult: 2-5 mg IV
If atropine cannot be Pedia: 0.01 mg/ Pedia: 0.03 mg/ Pedia: 0.05 mg/
given via the IV route, kg/dose kg/dose kg/dose
Alternative atropine Transfuse 1-2
note that it is also dose recommen-
Give sodium units packed RBC
well absorbed by dation: properly cross-
nebulization or by q 1 hr IV x 6 doses bicarbonate matched.
q 2 hrs IV x 3 doses 1 mEq/kg/dose or
instillation into an q 4 hrs IV x 6 doses based on ABG
endotracheal tube. results
Diazepam
Adult: 2.5-5.0 mg
IV push q 8 h for
3 doses. May
be continued
after 24 hrs if
indicated.
Pedia: 0.3 mg/kg/
dose IV push.
May be repeated
q 6-8 hrs.
163
Maintenance atropinization (after the first 48 hours):

• Pupils >4 mm
• Heart rate >60 per min
• Relatively dry mucosa
• Decreased bowel sounds
Dose and frequency of atropine should be titrated
according to patient’s response.
Reduce amount and frequency of doses by 1-3 mg
q 2-4 hrs.
If dose is being given every 4 hrs and patient is fully
conscious, may give oral atropine.
Tincture of Belladona
30 drops in ½ glass water (1 mg atropine sulfate)
q 6 hrs x 1-2 weeks
Atropine sulfate
Ampule: 1 ampule in ½ glass water
Give atropine until RBC cholinesterase is normal or
depressed by only 20%.
Refer to psychiatry if non-accidental.
Sodium bicarbonate
ACIDOSIS based on ABG results
Antibiotic specific for organism

INFECTION AVOID aminoglycosides and chloramphenicol
Furosemide 1 mg/kg/dose
PULMONARY or Atropine 1 ampule in 2 mL NSS as nebulization
CONGESTION If ARDS sets in, start on PEEP.
164
Diazepam
doses.
Lorazepam
SEIZURES of 15-20 min prn. Usual dose is 4-5 mg/dose.
min prn.
Compatible with D5W
Phenytoin
10-20 mg/kg IV or PO loading dose then
5-7 mg/kg in 3 divided doses given at 25-50 mg/
min.
REFERENCES
2004.
Wilkins. 1997.
Hoffman R, Nelson L, et al. (eds.). Goldfrank’s Manual of Toxicologic Emergencies.
McGraw Hill Medical. 2007.
IPCS/CEC Working Group. Evaluation of Antidotes Used in the Treatment of Poisoning,
Annex VIII. April 1989.
Klaassen CD, Amdur MO and Doull J (eds.). Toxicology: The Basic Science of Poisons,
Viccellio P. Handbook of Medical Toxicology. Boston: Little, Brown ad Company. 1993.
165
PESTICIDES: PYRETHROIDS
PESTICIDES:
PYRETHROIDS
Pyrethroids are synthetic analogues of Commonly Encountered
pyrethrin, a compound derived from the
Pyrethroids
chrysanthemum plant. They are the
active ingredients of household Chemical Hazard Category
pesticides, such as mixed pesticide Non-cyano group
sprays, chalk and coil formulations. Allethrin III
Permethrin II
They are also commonly used in the Pyrethrin I II
agricultural settings and for treatment Resmethrin III
of ectoparisitic disease. Because of Tetramethrin IV
their use pattern, pyrethroid poisoning Cyano group
is at the top of the list of pesticide- Cyfluthrin II
induced poisoning cases. Cyhalothrin II
Fortunately, toxicity to humans is Cypermethrin II
low because the compound has low Deltamethrin II
inhalation and dermal absorption, poor Fenvalerate II
Flucythrinate Ib
bioavailability and it undergoes first-
pass metabolism by the liver. More
severe symptoms attributed to central nervous system effects appear
when pyrethroids are taken orally. It affects sodium channels in nerve
membranes, causing repetitive neuronal discharge and prolonged
negative after-potential.
Common adverse manifestations are allergic reactions to the
insecticide. Other pyrethroids may cause paresthesias after cutaneous
exposure characterized as stinging, burning, itching, tingling and later
can progress to numbness. More severe neurotoxic manisfestations are
seen in second-generation pyrethroids which contain a cyano-group.
• Cypermethrin, cyfluthrin and deltamethrin belong to the cyano-group of
pyrethroids such that poisoning may present as severe neurotoxicity.
• Ragweed pollen cross reacts with chrysanthemum. Patients who are
allergic to pollen may develop hypersensitivity to pyrethrin.
• Atropine should NOT be routinely used in pyrethroid poisoning since the
insecticide is not a cholinesterase inhibitor.
166
Clinical Features
Contact dermatitis, allergic rhinitis, pneumonitis, asthma, anaphylactoid
reaction, paresthesia, abnormal facial sensation, dizziness, headache,
fatigue, vomiting, diarrhea PLUS:
• Cyano group
Mild: weakness, muscle spasm, mild ataxia, salivation, irritability to sound
and touch
Moderate: excitation, tremors
Severe: dyspnea, convulsion
• Non-cyano group
Restlessness, incoordination, tremors, paralysis
Management
Amount taken/used
HISTORY Time and mode of administration/exposure
Symptoms of hypersensitivity or neurotoxic reactions

PHYSICAL Note signs and symptoms of anaphylactoid reaction,
EXAMINATION neurotoxicity and cyanide toxicity.
Serum cyanide levels for second generation
LABORATORY pyrethroids
ABG Na+, K+, Cl- LFTs Protime
CBC with reticulocyte count Chest x-ray PA
167

then vomited, give oxygen, remove clothing and
GENERAL sponge bath using alkaline soap.
Repeat if there is no bowel movement after 1 hour.

Intravenous fluids
ANAPHYLACTOID
Hydrocortisone 100 mg IV q 6 h
REACTION Respiratory support
Bronchodilators (salbutamol, terbutaline)
ASTHMATIC Steroids (beclomethasone, budesonide inhaler)
ATTACK Nebulization
Adequate oxygenation
CONTACT Antibiotic specific for organism

DERMATITIS AVOID aminoglycosides
Topical Vitamin E
PARESTHESIAS Do not give zinc oxide preparations
Atropine
SALIVATION/ Adult: 1 mg IV
BRADYCARDIA Pedia: 0.01 mg/kg/dose prn
168
Diazepam
doses.
SEIZURES/
Lorazepam
TREMORS
min prn.
Compatible with D5W
REFERENCES
Casida JE, et al. Mechanisms of selective action of pyrethroid insecticides. Ann. Rev.
Pharmacol. Toxicol. vol. 23. 1983. pp. 413-38.
2004.
Wilkins. 1997.
Goldfrank LR et al. (eds.). Goldfrank's Toxicologic Emergencies, 7th ed. New York:
McGraw-Hill. 2002.
169
WATUSI
WATUSI
(DANCING FIRECRACKERS)
In 1991, the first documented patient who swallowed an unknown
amount of watusi died in the emergency room complex of the Philippine
General Hospital.
Watusi, dancing firecracker, or “spit devil” is reddish in color, thin like
a matchstick, and measures about ½ to 1 inch long. Chemical analysis
reveals that it has the following components:
Chemical Components and

Toxicity Rating of Watusi
Chemical Toxicity Rating Lethal Dose
Yellow or white phosphorus 6 Super toxic (<5 mg/kg)
Trinitrotoluene (TNT) 4 Very toxic (50-500 mg/kg)
Potassium nitrate 3 Moderately toxic (0.5-5 g/kg)
Potassium chlorate 4 Very toxic (50-500 mg/kg)
.
Summary of Toxicities from TNT,
Potassium Chlorate and Potassium Nitrate
TNT Potassium Potassium
Chlorate Nitrate
Lethal dose 50-500 mg/kg 50-500 mg/kg 0.5 to 5 g/kg
Adult: 12 g Adult: 2-6 g
Child: 5 g
Infant: 1 g
Clinical effects
Hypotension + - +
Nausea/vomiting - + +
Methemoglobinemia + + +
Red cell hemolysis - + +
Aplastic anemia + - -
Subacute hepatic necrosis + - -
.
170
WATUSI
Clinical Stages of Acute Yellow Phosphorus Poisoning
Stage 1
Vomiting with or without hematemesis, severity of symptoms depends on
amount ingested
Stage 2
Relatively symptom-free period
Stage 3
Severe gastrointestinal symptoms, acute degeneration of liver with metabolic
derangements, significant ECG changes mimicking myocardial infarction
• Phosphorous is a protoplasmic poison whose toxicity is enhanced when
dissolved in alcohol, digestible fats and oils like castor oil.
• Skin or mucosal contact with phosphorous produces painful second and
third degree burns.
• Yellow phosphorous is insoluble in water but readily soluble in most oils.
• White phosphorous reacts rapidly with oxygen, easily catching fire at
temperatures 10-15 degrees above room temperature.
Management
Amount ingested
HISTORY Intake of other substances
Characteristic course following ingestion (see clinical
stages)
Evidence of cutaneous or mucosal burns
PHYSICAL Garlic odor in the vomitus or feces
EXAMINATION “Smoking stool” and luminescence of vomitus and
feces
CBC Protime APTT
Reticulocyte count PBS Glucose
Ionized calcium LFTs TB, DB, IB
TP AG ratio BUN Creatinine
LABORATORY Electrolytes Amylase Blood typing
EXAMINATIONS ECG ABG
CPK MB (in massive ingestion)
Urinalysis with uribilinogen
Fecalysis with occult blood
Diagnostic endoscopy
171
WATUSI

Avoid oxygen unless patient is hypoxic.
GENERAL Give raw egg whites
MEASURES Adult: use 8-12 eggs
Pedia: use 6-8 eggs
Do not insert NGT. Do not lavage with NSS solution.
Put patient on NPO initially.
General antidotes
Glucose
Calcium
H2 blockers
Specific antidotes
N-Acetylcysteine (NAC) same dosage schedule as in
Paracetamol Poisoning (see page 102)
Vitamin K1 initially at 1 mg/kg not to exceed 10 mg
in pediatric patients. An empiric dose of 10 mg IV
SPECIFIC may be given to adult patients.
MEASURES Ascorbic Acid in the presence of documented
methemoglobinemia. Give 500-1000 mg every 6
hours for adults and 10-20 mg/kg for pediatric
patients.
Supportive measures
Give Vitamin B complex by the 72nd hour.
Watch out for development of nosocomial infection.
Limit physical activity.
Watch out for multiple target organ damage.
Refer to psychiatry if non-accidental.
REFERENCE
Makalinao IR and Cortes Maramba NP. Watusi Poisoning Monograph: A Comprehensive
Guide to Human Health Effects, Toxicity and Treatment. ISBN 971-8650-08-3. National
Poison Control and Information Service University of the Philippines College of Medicine.
1999.
172
SUBSTANCE
ABUSE
AMPHETAMINES
AMPHETAMINES
(SHABU)
Amphetamine and related stimulant
compounds have power ful CNS
Amphetamine and
stimulant actions in addition to the Related Compounds
peripheral and beta actions common to Amphetamine
sympathomimetic drugs. These Cathinone (khat)
compounds prevent catecholamine Desoxyephedrine
reuptake or cause the direct release of Dextroamphetamine
catecholamines from the presynatic Ephedrine (mahuang)
neuron. Additional hallucinogenic 4-Methyl-2,5-dimethoxyam-
properties are gained by substitutions phetamine (DOM/STP)
Fenfluramine
on the phenyl ring by the methoxyl group Mescaline
(e.g., MDMA, MDA, DOM). Note that 3,4-Methylenedioxyampheta-
appetite suppressants (e.g. mine (MDA)
phentermine, fenfluramine) also belong 3,4-Methylenedioxymetham-
to this group. phetamine (MDMA,ecstasy)
Amphetamines can be taken in the Methamphetamine (shabu)
following modes: snorted, smoked, Methacathinone
ingested or injected. These drugs are Methylphenidate (Ritalin®,
weak bases and are easily absorbed Concerta®)
para-Methoxyamphetamine
across most biologic membranes. Peak (PMA)
plasma concentrations occur in minutes Phenmetrazine
by intravenous route, in about 30 Phentermine (Duromine®)
minutes by the intramuscular or nasal Phenylephrine
route, and within 3-4 hours after Phenylethylamine
ingestion. Phenylpropanolamine
T h e a c u t e t o x i c e f f e c t s o f Propylhexadrine
amphetamine are usually extensions of Pseudoephedrine
its therapeutic actions. The minimum
lethal dose of methamphetamine is 25 mg/kg in adults or 5 mg/kg in
children.
Clinical features include central nervous system, cardiovascular,
gastrointestinal and neuropsychiatric manifestations.
175
AMPHETAMINES
• Amphetamine is seldom used alone. It is usually taken with alcohol,
sedative-hypnotics, and narcotics.
• Drugs sold in the streets as “amphetamines” may contain other substan-
ces like ketamine (sold as ketabo), a variety of sympathomimetic drugs,
phenothiazines, opiates, phencyclidine and adulterants such as corn-
starch, alum, talc, or fibrous materials.
• Amphetamine increases gastric emptying time by as much as 40%.
Emesis or lavage is probably not effective if done more than 4 hours
after ingestion.
• Repeated charcoal lavage will be of benefit since amphetamine under-
goes enterohepatic recirculation.
• Avoid urine acidification therapy in the presence of seizures, hyperther-
mia, myoglobinuria or elevated CPK-MM.
Hyperactivity Rating Scale for Amphetamine Overdose

1+ Restlessness, irritability, insomnia, tremor, hyperreflexia, diapho-
resis, mydriasis, flushing
2+ Hyperactivity, confusion, hypertension, tachypnea, extrasystoles,
mild fever, sweating
3+ Delirium, mania, self-injury, marked hypertension, tachypnea,
arrhythmias, hyperpyrexia
4+ Above symptoms plus: convulsions, coma, circulatory collapse,
or death
Management
Amount taken
Acute or chronic user
HISTORY Previous history of convulsions or psychiatric illness
Symptoms of:
Nausea Headache
Vomiting Excessive sweating
Diarrhea Tremors
Behavioral changes Delirium
176
AMPHETAMINES
Hyperpyrexia Mental status exam:
Hypertension Change in sensorium
Signs of circulatory collapse Hallucinations
PHYSICAL Arrhythmias Paranoid ideations
EXAMINATION Dilated pupils Panic states
Pallor or flushing
Tremors
Collect 200 mL urine for quantitative amphetamine
determination using Fluorescence Polarization
LABORATORY Immunoassay (FPIA)
CBC Na+, K+, Cl- CPK-MM
RBS Creatinine ECG
Urine pH BUN

Keep patient in a quiet, preferably cool room. Avoid all
possible external stimuli.
GENERAL Hook to cardiac monitor.
MEASURES Insert nasogastric tube (appropriate size for age).
Repeat every 6 hours for 48 hours.
May give after 4 doses of activated charcoal if with
no bowel movement.
Ensure adequate hydration to promote urine output
>1 ml/kg/hr.
Give ascorbic acid (observe specific precautions).
0.5-1.5 g q 6 hrs until urine pH < 5.5.
177
AMPHETAMINES
If patient is conscious
Check for:
History of amphetamine withdrawal
Signs and symptoms of withdrawal
High risk for developing withdrawal
If (+) for any of the above:
Admit. Refer to Neurology/Psychiatry Services
Begin treatment for withdrawal.
If (-) for all of the above:
Initiate non-pharmacologic management.
Observe for up to 5-7 days.
Refer to Psychiatry for psychological and pharmaco-
logical support for amphetamine abstinence, long-
term recovery, health maintenance and education.
SPECIFIC
MEASURES If patient is unconscious
Consider empirical Thiamine 100 mg IV/IM then
D50-50 100 mL fast drip IV.
Admit.
Severe amphetamine toxicity
Regains Partially Remains

consciousness conscious unconscious
See box above Determine cause Consider
for treatment of depressed Naloxone 2 mg
of conscious sensorium. IV push
patient. Treat specific May be given
problems every 2 min for
See box above a total of 10 mg
for treatment If with good
of conscious response, treat
patient. as per partially
conscious/
conscious
patient.
If patient remains
unconscious,
determine
cause. Treat
specific prob-
lems.
178
AMPHETAMINES
ACUTE RENAL
Hemodialysis
FAILURE
Beta blocker (Esmolol)
LD: 500 ug/kg/min x 1 min
MD: Infusion at a rate of 50 ug/kg/min x 4 min.
If no response, repeat LD then increase MD at
ARRHYTHMIA increments of 50 ug/kg/min (max. of 200 ug/kg/
min)
Phenytoin
15-20 mg/kg slow IV push at a rate not to exceed
50 mg/min (adult) or 1 mg/kg/min (pedia).
Dilute in normal saline with in-line filter.
Alpha adrenergic blockers
Drug of choice: Prazosin
Adult: LD: 1 mg bid-tid
MD: 3-30 mg/24 hrs, divided bid-qid
HYPERTENSION Pedia: LD: 5 mcg/kg/dose
MD: 25-150 mcg/kg/24 hrs, divided q 6-8 hrs
Alternative Drugs:
Beta blockers, clonidine
For hypertensive crisis:
Nitroprusside infusion in D5W 0.5-0.8 mcg/kg/min
Protect infusion set from sunlight.
HYPERTHERMIA External cooling measures
Hydration
MYOGLOBINURIA Sodium bicarbonate 1 mEq/kg q 6 hrs to maintain
urine pH > 7.5 (if necessary).
Do not use vitamin C.
Diazepam
Pedia: 0.3 mg/kg/dose IV push
PSYCHOSIS May be repeated q 2-5 min up to 20 mg.
doses.
Consider giving antipsychotics.
179
AMPHETAMINES
Diazepam
Adult: 2.5 to 5.0 mg slow IV push
SEIZURES
If needed, repeat q 2 to 5 min up to 20 mg (adult)
doses.
Lorazepam
Adult: 2.5 to 10 mg/dose slow IV push. May be
repeated twice at intervals of 15 to 20 min prn.
Usual dose = 4.5 mg
Pedia: 0.05 to 0.10 mg/kg/dose slow IV push up to
max. 4 mg/dose. May be repeated twice at intervals
of 15 to 20 min prn.
Compatible with D5W as diluent with equal volume
of compatible diluent immediately before use.
Do not give as IV infusion.
REFERENCES
Benitz W and Tatro D. The Pediatric Handbook, 3rd edition. Mosby Year Book Inc. 1995.
Carruthers G, Hoffman B, et al. In: Melmon and Morelli's Clinical Pharmacology,
4th edition. McGraw Hill. 2000.
Dart R. Medical Toxicology, 3rd ed. Lippincott Williams & Wilkins. 2004.
Wilkins. 1997.
Ghodse H. Drugs and Addictive Behaviour: A Guide to Treatment, 2nd edition.
Hardman JG, Limbird PB, et al. (eds.). Goodman and Gilman’s The Pharmacological
Basis of Therapeutics,10th edition. New York: McGraw-Hill. 2001.
Proudfoot A and Vale A. Clinical features and the immediate management of sub-
stance abuse. Medicine International, Vol 3, p 2566. 1989.
Zaloga G. The Critical Care Handbook. Mosby Year Book. 1991.
180
CANNABIS
CANNABIS
(MARIJUANA)
Cannabis is obtained from the tobacco-like preparation of the leaves and
flowers of the Indian hemp plant Cannabis sativa. Various preparations
of cannabis are known by different names in various countries
(marijuana, bhang, ganja, charas, hashish). In the Philippines, it is
commonly known by its street names: “maryjane”, “joint”, “tsongki”,
“weed” or “damo”.
When the plant is fully grown, its upper leaves and flowers are covered
with sticky resin which contains the principal active component, delta-9-
tetrahydrocannabinol (THC). When smoked or ingested, delta-9-THC
binds to cannabinoid receptors (CB1) in the brain, which are present in
high concentration on GABA-ergic interneurons in the hippocampus,
frontal cortex, basal ganglia and cerebellum. This causes the behavioral
and cognitive effects of cannabis.
THC is lipophilic and is rapidly absorbed and metabolized mostly by
the liver to 11-hydroxy-THC (20% more potent than THC) and the lungs.
THC and its metabolites linger for long periods in the fatty tissues of the
body because of their high fat solubility. A single dose may take 30 days
to be eliminated.
Intoxication occurs rapidly when the dried leaves and flowers are
smoked. This is the most common pattern of usage. Oral intake is the
next most common mode of intoxication. The effects of this route of
exposure do not occur immediately but tend to last longer.
Blood levels of delta-9-THC do not correlate well with the psychoactive
effects of the substance. Patients have been observed to maintain
intoxication levels up to 2-3 hours post exposure, even if blood levels of
delta-9-THC have peaked long before this period.
181
CANNABIS
• THC may have stimulant, sedative or hallucinogenic action depending on
the dose and time of consumption. The toxidrome consists of tachycardia
and conjunctival hyperemia combined with evidence of altered mood or
cognitive function.
• CNS features:
Low to moderate usage: Euphoria, state of pleasant relaxation, height-
ening of senses, disorientation, alteration of time and space perception
High dosage: Mild anxiety, paranoia, delusion, hallucination, illusion,
bizarre behavior, cognitive changes in speaking and problem solving,
complex motor function impairment
• Physical signs: hoarseness, pharyngitis, rhinitis, bronchitis, tachycardia,
orthostatic hypotension, “blood shot” eyes (conjunctival hyperemia),
incoordination, slurred speech, fine tremors and ataxia
• Symptoms: precordial pain, fear of dying, pressure in the head, increased
appetite and thirst, nausea, dizziness, dyesthesias, paresthesias, somno-
lence, restlessness
• The long term effects from chronic marijuana use include flashbacks,
panic reactions and amotivational syndrome.
Management
Amount taken
HISTORY Acute or chronic user
Intake of other substances (alcohol, barbiturates,
cocaine)
Emphasis on neurologic and psychiatric examinations
(see clinical features). Check the following:
Hyperemia of conjunctivae
PHYSICAL Irritation of the mucous membrane
EXAMINATION Tachycardia
Problems with short term memory and speech
Difficulty in performing complex tasks
Collect 200 mL urine for cannabinoid determination
EXAMINATIONS CBC Na+, K+, Cl- ECG
RBS Creatinine
Chest x-ray BUN
182
CANNABIS
Keep patient in a quiet preferably cool room. Avoid all
possible external stimuli.
If cannabis is ingested:
GENERAL Do gastric lavage with activated charcoal.
Repeat every 6 hours for 48 hours.

If there is need for a mild sedative: Diazepam PO
Psychosis: Haloperidol 2.5-5.0 mg
BEHAVIORAL Initiate non-pharmacologic management.
CHANGE Refer to Psychiatry for psychological and pharmaco-
logical support for cannabis abstinence, long-term
recovery, health maintenance and education.
Oxygenation
BRONCHITIS
Antiasthmatic drugs
Beta-adrenergic blocking agents

TACHYCARDIA
Propanolol (if no history of asthma)
REFERENCES
Carruthers G, Hoffman B, et al. In: Melmon and Morelli's Clinical Pharmacology,
4th edition. McGraw Hill. 2000.
Ghodse H. Drugs and Addictive Behaviour: A Guide to Treatment, 2nd edition.
Proudfoot A and Vale A. Clinical features and the immediate management of sub-
stance abuse. Medicine International, Vol 3, p 2563-4. 1989.
183
ETHANOL
ETHANOL
Ethanol is a CNS depressant with
Ethanol Content of Common
sedative-hypnotic properties.
Acute overdose may lead to Alcohol-containing Products
respiratory depression, Alcoholic Drinks % Ethanol*
cardiovascular collapse and Beer
death. It is rapidly absorbed from Lager 2-3
the upper gastrointestinal tract Pilsen 5-6
and is distributed in the tissues Strong beer 9-14
according to their water content. Wines 7-12
The pleasurable effects of Fortified wines 15-20
(e.g., champagne)
alcohol are thought to be
Distillates 40-50
mediated via mu opioid receptors (e.g., whiskey, rye,
in the ventral tegmental area bourbon, rhum, gin,
while central effects such as brandy, scotch)
ataxia, sedation and anxiolysis, Local distilled spirits 60-80
are mediated through the GABA- (e.g., tuba, lambanog)
benzodiazepine receptor
complex. Glutamate receptor Other Products
changes such as NMDA Aftershaves 15-80
Cold/allergy medications 5-16
overactivity are central in alcohol
Cough preparations 2-25
withdrawal and together with Glass cleaners 10
reduced GABA-ergic function, Mouth washes 15-25
lead to increase risk of seizure Perfumes or colognes 25-95
and neurotoxicity. *Proof is numerically twice the percent value.
Alcohol is commonly taken
with other drugs, particularly Common Local Terms for
drugs of abuse. The fatal dose is Alcoholic Drinks and their
difficult to ascertain because of Corresponding Volumes
individual tolerance (the result of
of physical dependence and Alcoholic Drinks Volume
Lapad 325 mL
genetic predisposition) but the Bilog 325 mL
equivalent of about 400 mL of Kwatro kantos 325 mL
pure ethyl alcohol consumed in Long neck 740 mL
one hour may be lethal. Beer grande 1000 mL
Patients with blood alcohol Beer (regular) 320 mL
levels of 0.05% (50 mg/100mL)
are considered medically
184
ETHANOL
intoxicated. The rate of metabolism is measured in the blood as 13-15
mg/dL/hour for a non-alcoholic, and greater than 30 mg/dL/hour for a
chronic alcoholic. In cases of intoxication, alcohol follows zero-order
kinetics and metabolism is constant at 100 mg/kg/hour.
Clinical Features
Blood Ethanol
Concentration Clinical Description
(mg/dL)
<50 Talkativeness, subjective feeling of well-being
50-100 Mild intoxication: Decreased inhibition, slurred speech, emotional
instability, incoordination, slight visual impairment, slow reaction
time, increased confidence
100-300 Moderate Intoxication: Ataxia, slurred speech,
muscular incoordination, slight visual impairment,
decreased attention span
diplopia
altered perception, altered equilibrium
300-500 Severe Intoxication:
Vision impairment and double vision
Severe ataxia
Stupor
> 500 Very Severe Intoxication: Coma, respiratory failure
Formula for Calculating Blood Alcohol Level
Plasma Level (mL ingested) x (% alcohol) x (specific gravity ethanol)

(mg/dL) =
(VD) x (weight in kg) x 10
Where VD = Volume of Distribution
= 0.7 L/kg in children
= 0.6 L/kg in adults
Specific gravity ethanol = 800mg/mL
185
ETHANOL
• Ethanol enhances the effects of:
Anticoagulants (coumadin) Hypnotics Sedatives
Antidepresants Insulin Tranquilizers
Antihistamines MAO inhibitors
• Disulfiram-like intolerance to ethanol is associated with:
Acetahexamide Furazolidone Sulfonylureas
Animal charcoal Griseofulvin Thiocarbamates
Calcium carbomide Imidazoles Third generation
Carbon disulfide Metronidazole cephalosporins
Carbitamide Quinacrin Tolazoline
• Alcohol with aspirin increases the likelihood of gastrointestinal bleeding.
• Gastric lavage, induction of emesis and activated charcoal are not
indicated since alcohol is rapidly absorbed from the gastrointestinal
tract. These procedures are indicated only when multiple drug ingestion
is suspected.
Management
Amount taken
Acute or chronic user
HISTORY Intake of other substances (alcohol, barbiturates,
drugs of abuse)
Check for the following:
Vomiting Respiratory depression Seizures
Coughing Aspiration Head trauma
(using low reading thermometer)
Note changes in sensorium, eye movements, pupillary
PHYSICAL size, evidence of head trauma, tremors, breath odor,
EXAMINATION size of thyroid gland
Check for signs of respiratory failure, chronic liver
disease
Blood alcohol level: 5 mL oxalated blood, 100 mL
urine (first void)
EXAMINATIONS CBC, ABG Na+, K+, Mg+, Cl- Amylase
RBS Creatinine CPK MB and MM
++
Chest x-ray BUN Ionized Ca
Urinalysis Urine ketones Liver function tests
186
ETHANOL
ABCs of life support. Respiratory support if necessary.
Maintain vital signs and keep patient warm.
GENERAL Adult: D5 0.9NaCl or AR 1 liter x 8 hrs
MEASURES Pedia: D5 0.3NaCl or AR according to KBW
If patient is conscious
Give thiamine 100 mg IV/IM
then D50-50 100 mL fast drip IV.
Observe for 24 hours. Check for:
History of withdrawal
Signs and symptoms of withdrawal
High risk for developing withdrawal
If (+) for any of the above:
Admit. Refer to Neurology/Psychiatry Services
Begin treatment for withdrawal.
If (-) for all of the above:
Refer to Psychiatry.
If no untoward events within 6 hours, discharge with
SPECIFIC maintenance thiamine 50 mg TID.
MEASURES If patient is unconscious
Give thiamine 100 mg IV/IM
then D50-50 100 mL fast drip IV.
Continue thiamine 100 mg IV q 8 hours.
Admit. Refer to Neurology.
Level of consciousness
Regains consciousness
See box above for treatment of conscious patient.
If no untoward events, discharge with maintenance PO
thiamine 50 mg TID, folic acid 1 mg OD and
multivitamins.
Partially conscious
Determine cause of depressed sensorium.
See treatment of patient who regains consciousness.
Remains unconscious
Naloxone 2 mg IV push. May be given every 2 min for
a total of 10 mg
If with good response, treat as per partially conscious/
conscious patient.
If patient remains unconscious, determine cause.
Consider hemodialysis. Refer to Neurosurgery.
187
ETHANOL
Alcohol Withdrawal Syndrome

A. Cessation of (reduction in) alcohol use that has been heavy and
prolonged.
B. Two (or more) of the following, developing within several hours to a few
days after
1. autonomic hyperactivity (e.g., sweating or pulse rate greater than 100)
2. increased hand tremor
3. insomnia
4. nausea or vomiting
5. transient visual, tactile, or auditory hallucinations or illusions
6. psychomotor agitation
7. anxiety
8. grand mal seizures
C. The symptoms in criterion B cause clinically significant distress or
impairment in social, occupational, or other important areas of
functioning.
D. The symptoms are not due to a general medical condition and not better
accounted for by any another mental disorder.
Specify if:
With perceptual disturbances
From DSM-IV-TR, Diagnostic and Statistical Manual of Mental Disorders. 4th ed.
American Psychiatric Association. 2000.
Treatment for Alcohol Withdrawal Syndrome

Pharmacologic treatment
• Symptom-Triggered Therapy: Start Diazepam 5 to 10 mg q 8 hours,
adjusting dose and frequency based on Clinical Institute Withdrawal
Assessment for Alcohol-Revised (CIWA-Ar) Score
• If there is severe liver dysfunction, drugs metabolized by oxidation (such
as diazepam) are eliminated slowly. In these cases, the “CLOT” benzo-
diazepines Clonazepam, Lorazepam, Oxazepam and Temazepam should
be used (see table on next page).
• Supplementary multivitamins, including thiamine, pyridoxine and folic
acid.
• Maintain euglycemia.
• Potassium, phosphate and magnesium supplements.
Non-pharmacologic treatment
• Reassurance, reality orientation, personal attention, general nursing care
• Frequent monitoring of signs and symptoms using the CIWA–Ar Scale
188
REFERENCES
ETHANOL
Adapted from Haddad, L.M., Shannon, M.W. and Winchester, J.F., Clinical Management of Poisoning and Drug Overdose, 1998.
Caruthers G, Hoffman B, et al. Melmon and
Morelli’s Clinical Pharmacology, 4th ed. Mc-
Graw Hill. 2000.
Dart R. Medical Toxicology, 3rd ed. Lippincott
Williams & Wilkins. 2004.
Drummund DC. Treatment services for alcohol
15-30 mg TID/QID
use disorders In: Gelder M (ed). New Oxford

Glucorinidation
Textbook Psychiatry. Oxford: Oxford University

Intermediate
Oxazepam*
Press. 2000.
Ellenhorn MJ. Ellenhorn’s Medical Toxicology, 2nd
Drugs for Treatment of Alcohol Withdrawal Syndrome
ed. Baltimore: Lippincott Williams & Wilkins.

5-20
1997.
PO
No
Flomenbaum N, Goldfrank LR, et al. Goldfrank's

Toxicologic Emergencies. New York: McGraw Hill
Chlordiazepoxide*
15-20 mg TID/QID
Companies, Inc. 2006.

Ghodse H. Drugs and Afddictive Behaviour: A
Guide to Treatment, 2nd edition. Cambridge
Oxidation
University Press, 2002.

Gossel TA and Bricker JD. Principles of Clinical
IV, PO
Long
6-30
Toxicology, 3rd edition. New York: Raven Press,

Yes
10
1994.
Hardman JG, Limbird PB, et al. (eds). Goodman
1-2 mg BID/QID
Glucorinidation
and Gilman’s The Pharmacological Basis of

Lorazepam*
Intermediate
Therapeutics,10th ed. New York: McGraw-Hill,

IV, IM, PO
2001.
Klassen CD, Amdur MO, Doul J. (eds.). Casarett
5-25
and Doull’s Toxicology: The Basic Science of

No
15
Poisons, 5th edition. New York: MacGraw Hill.

1996.
5-20 mg TID/QID
Lingford-Hughes A. Neuropharmacology of
addiction. Psychiatry. 2:24-28, 2003.
Diazepam
Martin EW. Hazards of Medication. Philadelphia:

Oxidation
JB Lippincott Co. 1978.

20-70
IV, PO
Long
Olson KR (ed.). Poisoning and Drug Overdose, 5th

Yes
33
edition. New York: McGraw-Hill, 2007.

*Not available in the Philippines.
Rosen P, et al. Emergency Medicine Concepts and

Active metabolite
Liver metabolism
Clinical Practice, 2nd edition. Missouri: the C.V.

Half-live (hrs)
Mosby Company. 1988.

Initial dose
Average
Shannon MW, Borron SW, Burns MJ (eds). Haddad

Range
and Winchester's Clinical Management of

Route
Poisoning and Drug Overdose, 4th Ed.

Philadelphia: Saunders. 2007.
Vale A. Alcohol Intoxication and Withdrawal.
Medicine International, vol 3, pp 2543-2545.
1989.
189
animal
toxins
CIGUATERA
CIGUATERA
Ciguatera poisoning is an illness caused by the consumption of toxic
coral reef fish. The toxins involved are produced by planktonic
organisms called dinoflagellates that colonize algae growing on dead
coral. The first dinoflagellate associated with ciguatera was
Gambierdiscus toxicus, but since then, many other species have been
identified. These dinoflagellates are eaten by herbivorous reef fish,
which are, in turn, eaten by carnivorous fish, which are also eaten by
larger carnivores. The toxin accumulates and the larger the fish, the
greater is the amount of toxin accumulated. When such fishes are eaten
by humans, a syndrome characterized by prominent neurologic,
gastrointestinal and cardiovascular manifestations is produced known
as ciguatera poisoning.
There are at least five toxins associated with ciguatera and they may
come in different combinations and proportions in toxic fish. The
manifestations of poisoned patients will therefore vary depending upon
which toxin was predominantly ingested. Ciguatoxin exerts a potent
depolarizing action on nerves and striated muscle by causing the sodium
channels to remain open. Manifestations are mainly muscle weakness,
and myalgia. There also appears to be a cholinergic component to its
actions resembling that of organophosphate and carbamate pesticide
poisoning, resulting in bradycardia and diarrhea. Okadaic acid has a
structure similar to ciguatoxin and also acts to keep sodium channels
open. Its manifestations are additive to ciguatoxin. Scaritoxin also has
manifestations similar to ciguatoxin but, in addition, is associated with
disequilibrium and ataxia 5-10 days after onset of symptoms. Maitotoxin
causes increased intracellular levels of calcium and may manifest as
hypotension and shock. Palytoxin causes severe tonic contractions of
muscles.
These toxins are found in fish muscle but much higher levels can be
found in fish brain, liver, and other internal organs. They are all odorless,
colorless, tasteless, heat stable, and are not destroyed by cooking.
Maitotoxin, however, because it is water soluble, may be removed by
washing the fish several times in salt water.
At the moment, there is no readily available test that can document
the presence of ciguatera toxins in the human body. This is made all the
more difficult by the very low LD50’s of the different toxins, measured in
micrograms rather than milligrams, and therefore requiring highly
193
CIGUATERA
sensitive and expensive equipment.

In acute situations, the diagnosis of ciguatera poisoning is a clinical
one and is based on a history of reef fish ingestion followed by the
matching toxidrome. Laboratory analyses of fish muscle or internal
organs using ELISA or HPLC are accurate and can be performed by the
UP Marine Science Institute (MSI) in Diliman, QC.
Intravenous mannitol is now the treatment of choice in the
detoxification of patients with ciguatera poisoning. The benefits of
mannitol was discovered accidentally when two comatose patients were
given mannitol for suspected cerebral edema and 10 minutes later, both
regained consciousness. Since then mannitol has been used to good
effect, and in some case reports, symptoms have disappeared even
before the mannitol infusion was consumed.
It is not clear what the mechanism of action is. The osmotic effects
alone cannot account for the efficacy of mannitol since other substances
with similar osmotic effects do not produce the same response. Some
theories for the mechanism of action of mannitol are:
• It decreases Schwann cell edema (shown in animal models of ciguatera
poisoning).
• It has hydroxyl radical scavenging properties which can inactivate the
toxins of ciguatera.
• It may cause a competitive inhibition of sodium at the cellular
membrane.
• It sterically inhibits the movement of sodium ions through channels
which have been locked open by the ciguatoxin molecule.
• It dissociates the ciguatoxin molecule from its binding site, perhaps by
osmotic properties.
No randomized control trials have been done and only case series serve
as evidence of the efficacy of mannitol.
Clinical Features - Acute Effects

• Manifestations are delayed and may appear anywhere from 2-12 hours
after ingesting toxic fish.
• Neurologic: paresthesias of the perioral area and extremities, muscle
weakness that occasionally leads to respiratory failure, myalgia, blurred
vision, hypersalivation, diaphoresis, tremor, seizures, ataxia, hot-cold
sensory reversal (pathognomonic)
• Gastrointestinal: Diarrhea, vomiting, abdominal cramps, prolonged
protime and partial thromboplastin time
• Cardiovascular: Bradycardia, hypotension, occasionally circulatory
collapse
194
CIGUATERA
Clinical Features - Chronic Effects
• Chronic effects manifest as protracted pruritus, weakness, hiccoughs,
chronic hypertension, and paresthesias. These symptoms may persist for
months and even years. Alternatively, they may disappear but suddenly
reappear during stressful periods.
• Sensitization to ciguatera toxins occurs and repeat exposure to ciguatoxic
fish as well as to foods and pharmaceuticals containing polycyclic ether
moieties can cause a recurrence of symptoms, especially hypotension.
• For travelers going to places with coral reef where there is known or
suspected ciguatera poisoning:
• Do not eat big reef fish (more than 4lb or 2kg) especially if there is
reported poisoning.
• Avoid eating grouper, snapper and jacks when visiting endemic
regions, and never eat barracuda.
• Avoid fish considered to be harmful by the local population.
• Do not eat scaleless fish or moray eel.
• Avoid the liver, head, gonads, roe, or viscera from any marine fish.
• Beware of eating reef fish after there has been any disturbance of
their environment.
• In endemic areas, avoid eating fish caught in the windward side of the
islands, since wind and waves naturally disturb the reef environment.
• All cases of suspected ciguatera poisoning should be reported to the
local health agency as well as to the National Epidemiology Center of the
Department of Health. The Bureau of Fisheries and Aquatic Resources
should also be involved for long-term monitoring of the affected reefs.
• Mannitol may cause fluid and electrolyte imbalance in a patient already
suffering from vomiting, diarrhea, and dehydration. As with the use of
sodium sulfate, attention must be given to these problems. It also
appears that mannitol given beyond 48 hours post-ingestion may not be
as effective.
• For persistent paresthesias, amitriptyline 25mg twice a day has been tried
with some success. Headache and hot-cold sensory reversal may res-
pond to paracetamol. Indomethacin and other NSAIDs may be given
for joint pains. For pruritus, cyproheptadine 4mg three to four times a
a day has been tried.
• Since sensitization occurs, for the next 6 to 12 months, the patient
should avoid the following foods, chemicals, and medications which may
contain polycyclic ether moieties that can trigger a recurrence of symp-
toms: fish, shellfish, alcoholic beverages, nuts or nut products, seeds or
seed products, mayonnaise, marijuana, opiates, barbiturates, solvents,
glues, epoxies, ethers, resins, herbicides, insecticides, and cosmetics.
195
CIGUATERA
Management
Recent ingestion of fish caught from coral reef
Neurologic, gastrointestinal, and cardiovascular
HISTORY
symptoms several hours after ingestion (see Clinical
Features)
Complete physical examination with emphasis on
PHYSICAL neurologic, gastrointestinal, and cardiovascular
EXAMINATION systems (see Clinical Features)
No specific tests using human biological fluids
If available, freeze specimen of ingested fish and
bring it to UP-MSI or the Bureau of Fisheries and
LABORATORY Aquatic Resources for bioassay of ciguatera toxins
EXAMINATIONS RBC cholinesterase to rule out organophosphate or
carbamate poisoning.
BUN Na+, K+, Cl- CBC
Creatinine LFTs, Protime, PTT Typing
GENERAL If within 2 hours of ingestion, insert nasogastric tube
MEASURES (appropriate size for age).
Diarrhea and dehydration are frequently encountered
with ciguatera poisoning, hence sodium sulfate
should not be given.
Trial of 20% Mannitol, 1g/kg IV over 30 minutes.
May repeat dose within 24 hours if there is no
improvement of symptoms. There is no evidence at
SPECIFIC
the moment that additional doses are helpful.
MEASURES
Before giving mannitol, correct all fluid and electrolyte
abnormalities since mannitol may aggravate these
problems.
196
CIGUATERA
BRADYCARDIA AND
GASTROINTESTINAL Atropine 0.5 mg IV (adult), or 0.01 mg/kg (pedia)
SYMPTOMS
FLUID AND
ELECTROLYTE Treat accordingly.
ABNORMALITIES
Correct dehydration and electrolyte abnormalities

HYPOTENSION Inotropic support with dopamine
Paracetamol and indomethacin can be given for

PAIN headaches, arthralgia, and odontalgia.
Vitamin K 10 mg IV or IM, OD to TID depending on

PROTIME OR PTT
severity of derangment.
DERANGEMENT
Fresh frozen plasma if markedly deranged
Cyproheptadine 4 mg every 6 to 8 hrs (adult) or

PRURITUS OR 15 mg/kg (pedia)
PARESTHESIA Give a trial of amitryptilline 25 mg BID if with persis-
tent pruritus or paresthesia.
RESPIRATORY Intubation and mechanical ventilation in the rare

DEPRESSION event that respiratory paralysis occurs
Diazepam
SEIZURES
doses.
REFERENCES
Lange WR. Ciguatera toxicity. American Family Physician. 35:144-82. 1987.
Sims JK. A theoretical discourse on the pharmacology of toxic marine ingestions. Annals
of Emergency Medicine. 16:1006-1015. 1987.
Swift AEB and Swift TR. Ciguatera. Clinical Toxicology. 31:1-29. 1993.
Wu CH and Narahashi T. Mechanism of action of novel marine neurotoxins on ion
channels. Annual Review of Pharmacology and Toxicology. 28:141-161. 1988.
197
COBRA BITE
COBRA BITE
Snake venom contains neurotoxins which can cause paralysis by
blocking the nicotinic acetylcholine receptors at the postsynaptic motor
endplates and/or affecting the mode of neurotransmitter release at the
pre-synaptic motor end plates. Death is due to respiratory failure as a
result of paralysis of the respiratory muscles.
In the Philippines, there are more than 60 species of snakes, seven
of which are venomous. By far, the most important local snake is the
Philippine cobra (Naja philippinensis).
The Philippine cobra predominantly causes paralysis. Local tissue
injury is uncommon. Neurotoxic signs can appear as late as 24 hours
after the bite. Initial evaluation should focus on the local signs at the bite
area (swelling, blistering and necrosis), neurologic signs (ptosis,
ophthalmoplegia, followed by dysarthria, poor tongue protrusion,
dysphagia, drooling, limb weakness, depressed or absent deep tendon
reflexes), and respiratory distress which is a sign of severe
envenomation. The available antivenom in the Philippines is specific for
cobra bite. Therefore, it should not be used when envenomation is due to
a pit viper.
• Immobilization of the affected limb using pressure bandaging is a useful
technique to reduce venom transport, especially when local necrotic
injury is not evident. The use of a tourniquet, cutting and suctioning of
the wound, or application of chemicals have no value, and in fact can be
detrimental to the patient.
• Patients may develop extreme anxiety and may hyperventilate with con-
sequent paresthesias and numbness. This may be mistaken as enven-
omation.
• When administering the antivenom, extreme caution should be taken in
patients with hypersensitivity to horse serum or have a history of atopy.
• Under no circumstances should a skin test be done unless the antive-
nom must be administered.
• When administering anti-cholinesterases, pre-treatment with atropine
should be done to prevent cholinergic side effects such as bradycardia,
and hypersalivation.
198
COBRA BITE
Management
Time patient was bitten
Type of snake involved. Ideally snake should be killed
and brought in for identification.
HISTORY
Field treatment done, if any
Intake or application of traditional remedies
Concurrent intake of other drugs
Complete physical and neurologic examination
PHYSICAL
Check wound site for edema and/or necrosis
EXAMINATION
Check for signs of envenoming
LABORATORY CBC Prothrombin time Urinalysis - test
EXAMINATIONS ABG Creatinine for hematuria,
LFTs Na+, K+, Cl-, Ca++ myoglobinuria
Platelets CPK (MM) Chest x-ray
Intubate if with signs of respiratory depression.
Place patient on Trendelenburg position. Bite area
GENERAL should be lower than the heart.
Administer oxygen when indicated.
Give anti-tetanus prophylaxis.
Local wound care
No signs of envenoming
Observe for 24-48 hours.
SPECIFIC If with signs of envenoming, see below.
MEASURES
With signs of envenoming
Administer antivenom (see next page)
199
COBRA BITE
If Cobra Antivenom is Available:

• Perform skin test using 0.2 mL of a 1:100 dilution of the serum with NSS.
Inject intradermally on the extremity opposite the bite and read after 15
min. Observe patient constantly after the injection. If no erythema or
pseudopodia of the test wheal occurs, the test is probably negative.
Compare with negative control using NSS 0.2 mL intradermal in the
opposite volar area.
• Administer 0.5 mL IM. In severe cases, give 5-10 ampules (800 IU/amp)
IV over 15 minutes (both adult and pedia) after negative skin test.
Repeat every 1-2 hours until a response is observed. Alternatively,
dilute 5-10 ampules in 500 mL isotonic fluid to run for 1-2 hours.
• If with history of allergy, but condition is life-threatening, administer
diphenhydramine 50-100 mg slow IV prior to anti-venom therapy, then
give slow IV infusion of anti-venom. Discontinue with the first sign of
hypersensitivity reaction and manage the reaction with 1:1000 epineph-
rine 0.5-1.0 mL subcutaneous.
If Cobra Antivenom is NOT Available:

• Pre-treat with atropine 0.6 mg IV.
• Follow with test dose edrophonium chloride 10 mg IV over 1-2 mins.
• If with positive response, start neostigmine 100 ug/kg IV infusion over 4
hrs or 25 ug/kg IV push hourly until reversal of neurotoxic signs is
observed.
• If neostigmine is not available, may give pyridostigmine per NGT, 60 mg
1 tablet twice to four times a day.

ACUTE
Hook to mechanical ventilator
RESPIRATORY
FAILURE Pulmonary toilet
Look for focus of infection

INFECTION Start broad spectrum antibiotics
Debridement
LOCAL TISSUE
Local wound care
NECROSIS
Antibiotics
MYOGLOBINURIA Hydration: 3-4 liters per day
200
COBRA BITE
REFERENCES
Wilkins. 1997.
Watt G. Management of Snakebites in the Philippines. Research paper of the U.S. Naval
Research Unit No. 2. Manila, Philippines (mimeograph, undated).
201
PARALYTIC SHELLFISH
PARALYTIC SHELLFISH
“Red tides” are marine phenomena that usually occur during the rainy
season. They are produced by an overgrowth of dinoflagellates that
contain pigments that are responsible for giving sea water a red-brown
appearance. In the Phillipines, the species of dinoflagellates involved
are Pyrodinium bahamense var. compressum and Gymnodinium
catanella.
These dinoflagellates contain neurotoxins, particularly saxitoxin,
neosaxitoxin, gonyautoxin, and decarboylsaxitoxin. Generally, these
toxins are found in the digestive glands of mollusks which feed on
dinoflagellates.
Paralytic shellfish poisoning (PSP) in human results from the ingestion
of toxin-containing bivalves. Saxitoxin acts on the peripheral and
autonomic nervous system and blocks depolarization at the
neuromuscular junction by increasing sodium permeability in exchange
for potassium efflux. The most common manifestations occurring within
30 minutes include numbness or tingling sensation, weakness and
motor incoordination.
Cases have been encountered where shellfish vendors spray their
produce with pesticides in order to keep away flies and other pests.
Diarrhea and muscle weakness also occur with exposure to
organophosphates, a class of pesticides used frequently in the
Philippines. Organophosphate poisoning is therefore worth ruling out in
cases of PSP by determining RBC cholinesterase levels.
• The toxin is heat stable. Cooking, frying or baking only partially lower
toxicity. In neurotoxic shellfish poisoning, cooking will not lower toxicity.
• Do not give laxative or cathartic if diarrhea is present.
• Avoid use of digitalis.
202
PARALYTIC SHELLFISH
Management
History and intake of shellfish
Time of ingestion
Symptoms
GI: diarrhea, nausea, vomiting, abdominal pain
HISTORY Neurologic: paresthesias of the face, muscle para-
lysis (weakness, dysphagia, ataxia, respiratory
paralysis)
Others: headache, thirst, myalgia, vertigo
PHYSICAL
EXAMINATION Emphasis on neurologic examination
RBC cholinesterase to rule out organophosphate
poisoning
LABORATORY Gastric aspirate
ABG RBS Urine pH
CBC Na+, K+, Cl- , Ca++ ECG
Fecalysis and stool culture

Do gastric lavage with 1.5% sodium bicarbonate.
1 tablespoon baking soda in 1 liter water
OR 2 vials of 8.4% sodium bicarbonate in 1 liter
GENERAL water
MEASURES After 5 min, do gastric lavage with activated charcoal.
Give 8.4% sodium bicarbonate 1 mEq/kg IV q 6 hours
until urine pH > 7.5
203
PARALYTIC SHELLFISH
No respiratory distress
Observe for 24 hours.
SPECIFIC If still asymptomatic, discharge.
MEASURES With respiratory distress
Sodium bicarbonate
1-2 mEq/kg/IV q 6 hours
No respiratory Respiratory
failure failure
Observe for 24 hours. Ventilatory support

If still asymptomatic, Admit to ICU
discharge. Test dose of edrophonium
If respiratory failure 1-2 mg IV
develops, see box If with good response, con-
to right. tinue treatment with
neostigmine 1-3 mg IV
and atropine 0.4-0.6 mg
IV.
If with no response, consi-
der other etiologies.
ELECTROLYTE
Correct potassium and other electrolyte imbalances
IMBALANCES
HYPOVOLEMIC IV fluids
SHOCK Fluid challenge


DISTRESS Oxygenation
204
PARALYTIC SHELLFISH
REFERENCES
Wilkins. 1997.
Makalinao IR. Redtide Poisoning. In So LS et al. (eds). Targeting the Poisoned Patient:
A Manual on Clinical Toxicology. 1997.
205
plant
toxins
HERBAL SUPPLEMENTS
HERBAL SUPPLEMENTS
Herbal medicines are finished labeled medicinal products that contain
plant extracts used in relatively unrefined form to achieve a therapeutic
effect. The Philippine Food and Drug Administration (FDA) requires proof
of safety and efficacy for herbal medicines. On the other hand,
traditionally used herbal products with claimed use for at least 50 years
are not required scientific evidence of safety and efficacy. Herbal
supplements belong to this latter category or if used as food, are
classified as dietary supplements.
Herbal supplements are commonly used for the treatment of anxiety,
back pain, cancer, headache, insomnia, obesity and dermatologic
conditions. They are also sometimes used as alternative substances of
abuse. Herbal medicines have become popular because of the belief
that they are “natural” and therefore safer. Nonetheless, herbal
supplements are repeatedly associated with poisoning.
Herbal supplements are made available in different forms (infusion,
decoction, tincture, and syrup) and can be taken in the following modes:
ingestion, inhalation, injection, or as a topical. Herbs contain compounds
that are not inherently less toxic than their synthesized pharmaceutical
counterparts. Herbal supplements can be adulterated with
pharmaceuticals, contaminated with metals, or are toxic themselves.
Clinical manifestations of toxicity fall under three categories: adverse
effects, drug interactions and overdose. Management is supportive.
Clinical Features
• Gastrointestinal effects
Epigastric discomfort, nausea, vomiting and dehydration, diarrhea and
frank bleeding from the gastrointestinal tract
• Hepatic and renal effects
Hepatorenal syndrome with hematuria and severe electrolyte imbalances
• CNS effects
Cerebral irritation, sedation, confusion, hallucinations, seizure and coma
209
HERBAL SUPPLEMENTS
210
Clinical Toxicity of Selected Herbal Supplements*
NAME COMMON USES ADVERSE DRUG
AND PROPERTIES EFFECTS INTERACTION
Aga Neuralgia, fever, Dizziness, vomiting, May interact with antidepressants, stimulants
Amanita muscaria anxiety, joint pain abdominal pain, movement and antihypertensives
disorders, muscle cramps,
CNS stimulation followed by
deep sleep, confusion, mania,
unconsciousness, coma, death
Aloe Burns, skin diseases Nephritis, GI upset May interact with other laxatives producing
severe diarrhea; may precipitate hypokalemia
if used with diuretics (NOT potassium sparing)
Angel’s trumpet Respiratory diseases Hallucinogenic, anticholinergic May interact with antidepressants, stimulants
Datura brugmansia and antihypertensives
Talampunay (local
name) see p. 170
Betel nut Intoxicating, euphoriant, Bronchoconstriction, May interact with antidepressants, stimulants
Areca catechu, stimulant effects oral cancers and antihypertensives
Pinang, Nganga
(local name)
Chamomile Sedative, antispasmodic Contact irritant, upper airway May interact with histamine relieasing drugs,
obstruction, pharyngeal edema sedatives
Ginger Antinauseant, Prolongs bleeding time through Antiplatelet agents, anticoagulants
Zingiber officenale antispasmodic inhibition of thromboxane
Luya, Agat (local synthetase
name)
Clinical Toxicity of Selected Herbal Supplements* (continuted)
Ginko biloba Dementia, memory GI upset, platelet inhibition Anticoagulants: anticoagulant effect of
impairment, cognitive headache warfarin
decline May decrease anticonvulsant effectiveness
(due to gingkotoxin, a known neurotoxin).
Cautious use with medications known to
decrease seizure threshold
Ginseng Endurance, stress Hypertension, vomiting, epistaxis Headache, mania in patients on phenelzine
Panax resistance May interfere with antihypertensives and with
quinquefolium glycemic control in diabetic patients
Hops Mild sedation may help to Potentiates sedatives
Humulus lupulus decrease male libido
through its anaphrodisiac
effect
Kava Antianxiety, muscle Inebriation, EPS, diffuse Benzodiazepines: excess sedation, lethargy,
Piper methysticum relaxant hepatocellular necrosis disorientation
Kava-kava Alcohol: toxicity
Prolongs effects of some anesthetics
Khat Hallucinogen, CNS Hallucinogenic May interact with antidepressants, stimulants
Catha edulis stimulant and antihypertensives
Bushman’s tea
Licorice Anti-spasmodic, gastritis Metabolic, renal Glycyrrhizin in licorice has MAOI activity
Glycyrrhiza spp. anti-inflammatory May exacerbate K+ loss of diuretics, myopahty
Ma-huang Weight reduction, appetite Sympathomimetic effects, May interact with antidepressants or anti-
Ephedra suppresant, decongestant palpitations, hypertension, hypertensives
Herbal fen-fen bronchodilator, stimulant myocardial infarction, CVA,
Herbal ecstasy mania, psychosis, arrhythmia,
Cloud 9 sudden death
211
HERBAL SUPPLEMENTS
HERBAL SUPPLEMENTS
212
Clinical Toxicity of Selected Herbal Supplements* (continued)
St. John’s Wort Depression, anxiety, sleep Mania Diabetes medications
Hypericum disturbances, viral Contains tannin, so may decrease iron
perforatum infections absorption
Enhances metabolism of oral contraceptives
and TCADs
Decreases levels of theophylline, digoxin, and
protease inhibitors
Enhances effects of SSRIs/SNRIs resulting
to serotonin syndrome
Watermelon frost Pain/healing of mucosal Motor/vocal tics in high doses
lesions
A Chinese herbal medi-
cation containing mercury
Wormwood Appetite stimulant Ataxia, vomiting, diarrhea,
Artemisia diaphoresis, psychosis,
absinthe hallucinations, lowers seizure
threshold
*Adapted from: Forman N. A Guide to Herbal Supplements in the Medical Setting. In: Wyszinki A, Wyszynski B (eds). Manual of
HERBAL SUPPLEMENTS
• Identification of specific poisonous plants by an expert botanist is
essential for optimal therapy. Likewise, the contents of herbal supple-
ments should be ascertained so as to provide the appropriate manage-
ment.
• Management of plant/herbal supplement poisoning is generally sup-
portive.
Management
Plant identification, amount taken
Time of ingestion
Clinical effects: gastrointestinal, hepatic, renal and
central nervous system effects
PHYSICAL
EXAMINATION
LABORATORY CBC Na+, K+, Cl-, Urinalysis
EXAMINATIONS BUN AST, ALT ECG
Creatinine
Do gastric lavage with activated charcoal if within 1 hr
from ingestion
Do soap suds enema if bowel movement occurs after
the second dose of sodium sulfate.
SPECIFIC Provide supportive treatment for dehydration, electro-

MEASURES lyte imbalances and liver abnormalities.
213
HERBAL SUPPLEMENTS
REFERENCES
Cupp M. Herbal remedies: adverse effects and drug interactions. Am Fm Physician
9:1239-124., 1999.
Wilkins. 1997.
Forman N. A guide to herbal supplements in the medical setting. In: Wyszinki A,
Wyszynski B (eds). Manual of Psychiatric Care for the Medically Ill. American
Psychiatric Publishing, Inc. 2005.
Miller LG, Murray WJ (eds). Herbal Medicinals: A Clinician’s Guide. New York,
Pharmaceutical Products Press. 1998.
Weiss RF, Fieldman V. Herbal Medicine. 2nd ed. New York. Thieme. 2000.
214
JATROPHA
JATROPHA SEED
(TUBA-TUBA)
The jatropha seed is commonly known as tuba-tuba, tubang bakod, taba-
taba and taua-taua. It is also known as purging nut, psychic nut or tick
seed. The seed is from the plant Jatropha curcas that belongs to the
family Euphorbiaceae. The shrub grows to about 2-5 meters, is widely
distributed in the country and is commonly used as a hedge.
The seed has a pleasant, pili nut-like taste, which makes it attractive,
especially to children. Unfortunately, the jatropha seed contains ricin or
curcin (toxalbumin), tannic acid and gallic acid which produce its toxic
effects. Mature seeds contain higher concentrations of the toxic
substances, and are therefore more toxic than young seeds.
The main effects of jatropha seeds are gastric irritation, and hepatic
damage. Commonly encountered clinical manifestations are abdominal
pain, nausea, and vomiting. Hypocalcemia and hypoprothrombinemia
are also seen.
215
JATROPHA
• The effects of jatropha seed poisoning is dependent on the number and
maturity of seeds.
• Dehydration, and eventually acute renal failure, can result due to exces-
sive vomiting and therefore must be addressed appropriately.
• Do not give anti-emetics to induce vomiting.
• Do not insert nasogastric tube and defer activated charcoal administra-
tion if patient manifests with gastrointestinal bleeding or severe vomi-
ting.
Management
Number of seeds ingested
Time of ingestion
Nausea, vomiting, abdominal pain, diarrhea
History of liver disease, gastritis

PHYSICAL
Check for signs of upper gastrointestinal bleed,
EXAMINATION
arrhythmias, seizures, dehydration
LABORATORY CBC Na+, K+, Cl- ALT, AST
EXAMINATIONS BUN Ionized calcium Urinalysis: test for
Creatinine Prothrombin time hemoglobinuria
ECG
Do gastric lavage with with activated charcoal if within
1 hour from ingestion and if there are no signs of
GENERAL GI bleeding or severe vomiting.
216
JATROPHA
Treat precipitating factors such as dehydration and/or

ARRHYTHMIAS electrolyte imbalance, such as hypocalcemia.
DEHYDRATION Treat accordingly based on degree of dehydration
ELECTROLYTE Treat electrolyte abnormalities, especially hypocalce-

DISTURBANCE mia
NSS lavage
Give H2 blocker: Famotidine every 12 hours
GASTROINTESTINAL Adult: 20 mg
BLEEDING Pedia: 0.8 mg/kg/dose
Consider emergency endoscopy if with severe abdo-
minal pain and/or upper GI bleeding
HEMOGLOBINURIA Alkalinize urine by giving IV sodium bicarbobate
Vitamin K (Phytonadione)
HYPO-
PROTHROMBINEMIA Adult: 10 mg IV at 1 mg/min, up to 60 mg/day
Pedia: 1 mg/kg, maximum of 10 mg/dose
Diazepam
SEIZURES
doses.
REFERENCES
Abdu-Aguye I, et al. Acute toxicity studies with Jathropa curcas L. Hum Toxicol. 5(4):
269-274. July 1986.
2004.
Wilkins. 1997.
Joubert PH, et al. Acute poisoning with Jatropha curcas (purging nut tree) in children.
S Afr Med J. 65 (18):729-30. May 1984.
Makalinao IR, et al. Jatropha Seed Poisoning. In So LS et al. (eds). Targeting the
Poisoned Patient: A Manual on Clinical Toxicology. 1997. 217
TALAMPUNAY
TALAMPUNAY
(ANGEL’S TRUMPET, DATURA)
Datura metel, locally known as
talampunay, is found extensively
in open, wasted plains in and
about settlements throughout
the Philippines, most especially
in the cooler areas in the
northern parts of the country. It
is a short-lived herb or shrub 0.5
to 2 meters in height, erect,
branched, and can be smooth or
hairy. The leaves are ovate to
oblong-ovate and the trumpet-
shaped flowers are large, white or
nearly purple, axillary and
solitary.
The toxins in the plant are
belladonna alkaloids (atropine,
hyoscyamine, scopolamine)
which can cause strong
anticholinergic ef fects. An
abundant amount of calcium
oxalate in leaves has also been
found. In the Philippines, the use of Datura for the symptomatic relief of
asthma is popular. Preparations in the form of cigarettes and powdered
tea are made from dried leaves and flowers. However, the plant has been
used by drug dependents for its hallucinogenic or mind-altering
properties. The onset of symptoms is between 10 minutes to 6 hours
after the intake of the plant, and usually resolve in 1 to 2 days. Pupillary
dilatation may continue up to 1 week.
218
TALAMPUNAY
• Patients intoxicated with Datura can have a clinically alarming presen-
tation. However, they often recover favorably with supportive treatment.
• Because of the mind-altering effects of datura, patients can present a
danger to themselves or others. Undertake escape and accident
precautions.
• Agitated patients should not be over-sedated. Avoid the use of pheno-
barbital, phenothiazines and haloperidol because of their anticholinergic
properties.
• The use of physostigmine as an antidote for datura poisoning should be
reserved for moderate to severe cases because of the possibility of
seizures and dysrhythmias when inappropriately used.
• Precautions in the administration of physostigmine:
• Give very slowly ( over 3 minutes).
• Do not give merely to “wake the patient up.”
• It should be used only in a setting where advanced life support is
available.
• It should be used only when definitive anticholinergic findings are
present.
• It should always be preceded and followed by good supportive care.
Clinical Features
• Peripheral (muscarinic blockade)
Tachycardia, dry/flushed skin, dry mucous membrane, dilated pupils
(variable), hyperpyrexia, urinary retention, decreased bowel sounds,
hypertension, hypotension (may be late finding)
• Central anticholinergic syndrome
Confusion, disorientation, loss of short-term memory, ataxia, incoordi-
nation, psychomotor agitation, picking or grasping movements, extrapyra-
midal reactions,visual/auditory hallucinations, frank psychosis, coma,
seizures, respiratory failure
• Gastrointestinal
Abdominal pain, nausea, vomiting
• The patient is considered as having moderate to severe toxicity if there
are pronounced hallucinations, agitation, supraventricular arrhythmias,
seizures unresponsive to standard anticonvulsants, ventricular arrhyth-
mias unresponsive to standard anti-arrhythmic agents.
219
TALAMPUNAY
Management
Part of the plant used (leaves, flowers, roots)
Manner of exposure
HISTORY Time of exposure
Anticholinergic toxidrome (see page 22)
EXAMINATION cardiovascular and nervous systems
CBC Na+, K+, Cl- Creatine phosphokinase
LABORATORY Creatinine LFTs Urinalysis, urine pH
EXAMINATIONS Prothrombin time ECG EEG

Do gastric lavage with with activated charcoal if within
GENERAL 1 hour from ingestion and if there are no signs of
MEASURES GI bleeding or severe vomiting.
Mild toxicity
Supportive treatment with benzodiazepines and
SPECIFIC hydration
MEASURES Moderate to severe toxicity
Physostigmine
Adult: Initial dose 1-2 mg IM or IV over 2–5 mins
A second dose maybe repeated in 20-30 mins if
symptoms recur. Max dose should not exceed 4
mg in a half hour.
Pedia: 0.01–0.03 mg/kg slow IV push. Max dose
should not exceed 2 mg.
Watch out for signs of cholinergic excess (bradycardia,
excessive secretions, heart block).
220
TALAMPUNAY
Diazepam
AGITATION
Place patient in a calm, reassuring environment.
Diazepam
SEIZURES
doses.
Cooling blanket, sponge bath
HYPERTHERMIA Hydration
URINARY
Catheterization
RETENTION
REFERENCES
Cortes-Maramba NP. Guidebook on the proper use of medicinal plants.
Manila: National Science and Technology Authority. 1982.
2004.
de Padua LS, et al. Handbook on Philippine medical plants Volume I. Manila. 1977.
Gabel MC. Purposeful ingestion of belladonna for hallucinatory effects. J Pediatr.
72:864-866. 1968.
Greenblatt DJ, et al. Anticholinergics. N Engl J Med. 288:1215-1219. 1973.
Gutierrez HG. An illustrated manual of Philippine material medica Volume I. Metro
Manila: National Research Council of the Philippines. 1980.
Hall RC et al. Angel’s trumpet psychosis central nervous system anticholinergic
syndrome. Am J Psychiatry. 134:312-314. 1977.
Quisumbing E. Medicinal plants of the Philippines. Quezon City: Katha Publishing. 1981.
221
ANNEX
Annex A
Properties of Common Drugs
Involved in Poisoning
Drug pKa Therapeutic Overdose Minimum
Dose Half Life Half Life Lethal Dose
ASA 3.5 0.22-0.28 hours >200mg/kg
Amphetamine 9.8 8- 12 hours 18-24 hours ~100-500mg
Chlorpromazine 9.3 6 hours 75 mg/kg (Pedia)
2 g (Adult)
Clonazepam 1.5 30-40 hours >60 mg
Diazepam 3.3 0.83-2.25 days 48-144 hours 500-5000 mg/kg
Digoxin 1.3-2.2 days 0.05 mg/kg
Digitoxin 4.3-12 days 10 g
Diphenhydramine 8.3 4-8 hours 48 hours 25 g/kg
Ethanol 2-4 hours 4 g/kg
3-6 mL/kg
Haloperidol 8.2 13-35 hours 20-140 mg/kg
Imipramine 9.5 6-18 hours 15-20 mg/kg
Iron 2-3 days 20 mg/kg
Isoniazid 3.5 0.7-4 hours 6+ hours 80-150 mg/kg
Lorazepam 1.3/11.5 10-20 hours 5-15 g/kg
Mefenamic Acid 4.2 2-4 hours
Methamphetamine 10.0 ~100-500 mg
Midazolam 6.2 2-5 hours
Morphine 7.9 2 hours >120-250 mg
(oral)
>30 mg (IV)
Paracetamol 9.5 2 hours 4 hours 140 mg/kg
Pethidine 7.7-8.2 3.2 hours 5-50 mg/kg
Phenobarbital 7.4 6-48 hours 72-120 hours 5 g
Phenytoin 8.3 20-30 hours 36-72 hours 50-5000 mg/kg
Salicylate 3.2 2-19 hours 25-30 hours 200-300 mg
Theophylline 8.75 6-12 hours 6+ hours >10 mg/kg
225
Annex B
Approximate Duration of
Detectability of Selected Drugs
in Urine
Drug/Drug Class Duration (Hours)
Alcohol 12
Barbiturates 900
Phenobarbital
Benzodiazepines 72
Oxazepam
Cocaine 96-144
(as benzoylecgonine)
Heroin 24
Marijuana
Single dose 120
Daily use 240
Chronic daily use 336-720
Methaqualone 112-570
Phencyclidine 200
226
Annex C
Specimen Time Collection Blood
and Urine
Drug Post-Ingestion/ Value & Time to Specimen
Administration Repeat Collection Needed
Carbamazepine 2-4 hours 2-4 hours Serum
TR: 4-10 µg/mL
TX: = 20 µg/mL
Digoxin 2-4 hours 2-4 hours Serum
TR: 0.9-1.2 ng/mL
TX: >1.5 ng/mL
Ethanol 0.5-1 hour TX: 50 mg/100 mL Serum or
ALD: 400 mg/100 mL whole blood
Heavy metals within 24 hours 2-4 hours and during 24 hr urine
chelation and/or whole
blood
(heparinized)
Iron 2-4 hours 2-4 hours Serum
TX: = 350 µg/mL
Isopropanol 0.5-1 hour 2 hours Serum
TX: >150 mg/100 mL
Lithium 2-4 hours TR: 0.6-1.2 mEq/L Serum
TX: >1.2 mEq/L
Methanol 0.5-1 hour TX: >80 mg/100 mL Serum or
whole blood
Paracetamol 4th hour TR: 10-20 µg/mL Plasma or
TX: 200 µg/mL (4th hr) serum
50 µg/mL (12th hr)
Phenobarbital 1-2 hours 2-4 hours Serum
TR: 15-40 µg/mL
TX: >40 µg/mL
Phenytoin 1-2 hours 2-4 hours Serum
TR: 10-20 µg/mL
TX: =20 µg/mL
Salicylates 2-4 hours 2-4 hours Serum
TR: 12-20 µg/mL (free)
TX: >30 µg/mL
Theophylline Ordinary tab/ 1 2 hours Serum
Syrup: 1 hour TR: 10-20 µg/mL
SR: 12-36 hrs TX: 20-35 µg/mL
ALD: >35 µg/mL
227
Annex D
Common Antidotes -
Formulation and Dose
Drug Formulation Dosage
N-acetylcysteine 200 mg/mL Phl: 150 mg/kg in 250 mL D5W IV
25 mL vial x 30 mins-1 hr
Ph2: 50 mg/kg in 500 mL D5W IV
x 4 hrs
Ph3: 100 mg/kg in 1L D5W IV
x 16 hrs
N-acetyl 25 g/bottle PO: 10-20 mg/kg/day in 3 divided
penicillamine doses x 5 days
Antivenom 800 IU/5 mL IV: 5-10 ampules x 10-15 mins
(Cobra anti-venin) 5 mL ampule q 1-2 hrs until (+) response
Atropine 1 mg/mL ampule Neb: 1.5-2 mg q 6 hrs
IV Adult: 0.5-1 mg q 5 mins
Maximum of 5 mg
IV Pedia: 0.01 mg/kg q 5 mins
Bromocriptine 2.5 mg/tab PO: 2.5-10 mg/dose 3 times/day
Calcium 10% 10 mL IV: 10-20 mL x 30 mins
gluconate ampule May follow with 0.5-2 mg/kg/hr
infusion or 10-20 mL/hr
Dantrolene 20 mg/vial IV: 0.8-2.5 mg/kg/dose x 2 hrs
4 times/day up to 10 mg/kg/day
Deferoxamine 500 mg/vial IV infusion: 15 mg/kg/hr
DMSA/ 100 mg/cap PO: 10 mg/kg/dose thrice daily x 5 days
Dimercapto- 200 mg/cap then twice daily x 14 days
succinic Acid
(Succimer)
Edrophonium 10 mg/mL IV: 10 mg x 1-2 mins (pre-tested with
1 mL ampule Atropine 0.6 mg IV)
Ethanol 20% PO/NGT: LD: 800 mg/kg diluted in
juice
MD: 80-130 mg/kg/hr (NA)
150 mg/kg/hr (CA)
Flumazenil 100 mcg/mL IV Adult: 0.5-5 mg or 0.2 mg bolus, then
5 mL and 10 mL 0.1 mg/min until (+) response
ampule IV Pedia: 0.005-0.01 mg/kg
Folic acid 5 mg/capsule PO: 1mg/kg q 4-6 hrs
228
Hydroxocobalamin 4 grams powder IV: 4-5 g diluted to a volume of at least
200 mL D5W x 30 mins
(cyanide poisoning)
Naloxone 0.2 mg/mL IV adult: 200 ug q 3 mins up to 2 mg
1 mL ampule IV pedia: 100 ug/kg/dose
Naltrexone 50 mg/tab PO: 50 mg daily x 7 days
Neostigmine 500 µg/mL IV: 100 µg/kg infusion x 4 hrs or
25 µg/kg IV push hourly (snake bite)
Penicillin G 1M, 5 M units IM/IV Pedia: 200,000 U/kg/day
crystalline IM/IV Adult: 18-24 M U/day
(Amanita phalloides)
Phytonadione 10 mg/mL IM/IV Adult: 10-20 mg q 8 hrs
(Vit K) 1 mL ampule IM/IV Pedia: 1 mg/kg/dose
Pralidoxime 50 mg/mL IV Adult: 1-2 g x 15-30 mins
20 mL vial IV Pedia: 25-50 mg/kg x 15-30 mins
Pyridoxine 100 mg/mL IV: 80-120 mg/kg or 1:1 (INH)
10 mL ampule 25 mg/kg/dose (hydrogen sulfide,
theophylline)
Sodium nitrite 30 mg/mL IV Adult: 10 mL of 30% solution
x 2-4 mins
IV Pedia: 0.2 mL/kg not to exceed
10 mL
Sodium 250 mg/mL IV Adult: 50 mL of a 25% solution
thiosulfate IV Pedia: 1.0 mL/kg not to exceed
50 mL
Thiamine 100 mg/3 mL IM or IV: 100 mg q 8 hrs
in Vit. 1-6-12
preparation
100 mg/mL
ampule
(B-complex)
229
Annex E
Drugs for Supportive Therapy -
Formulation and Dose
Activated Powder, USP PO/NGT Adult: 50-100 g/dose
Charcoal 50 g/pack PO/NGT Pedia: 1 g/kg/dose as a slurry
Aluminum 600 mg/300 mg PO: 1-2 tabs or 5 hydroxide/10 mL
hydroxide or per tablet/
Magnesium 5 mL May increase to 10-30 mL
hydroxide
Ascorbic acid 250 mg/mL IV Adult: 1g IV q 6 hours
2 mL ampule IV Pedia: 25 mg/kg/dose
Chlorpromazine 25 mg/mL IM: 0.5-1.0 mg/kg/dose q 1-4 hours
2 mL ampule until agitation is controlled
Diazepam 10 mg/ampule IV Adult: 5 mg/dose
IV Pedia: 0.3 mg/kg/dose
at a rate of 1-2 mg/min
Diphenhydramine 50 mg/mL IM/IV Adult: 25-50 mg/dose
IM/IV Pedia: 1 mg/kg/dose
Dobutamine 250 mg/20 mL IV: 2.5-10 mcg/kg/min
Dopamine 40 mg, IV: Renovasodilation
80 mg/mL 0.5-2.0 mcg/kg/min
Inotropic/Dopaminergic
2-5 mcg/kg/min
alpha-, beta-dopaminergic
>10 mcg/kg/min
Famotidine 20 mg/2 mL IV Adult: 20 mg IV q 12 hours
ampule IV Pedia: 0.8 mg/kg/dose
Furosemide 10 mg/mL IV Adult: 40 mg/dose
2, 5, 25 mL IV Pedia: 1 mg/kg/dose
ampule Doses >6 mg/kg not recommended
Haloperidol 5 mg, 50 mg/mL IV: 2.5 5.0 mg q 1 hour until
agitation is controlled; usually <10-
15 mg/day
Lidocaine 1%, 2% IV: Loading dose
50 mL vial 1.0-1.5 mg/kg IV given twice over
20 min, then infusion 1-4 mg/min
230
Magnesium 25% IV: Hypomagnesemic seizures/
sulfate 10 mL ampule cardiac arrhythmias
1-2 g q 4-6 hours over 15 mins
then 1-2 g q 4-6 hours
IM/IV: Hypomagnesemia
1 g q 6 hours for 3-5 days
Mannitol 20% IV: 1-2 g/kg IV over 2-6 hours
250, 500 mL
bottle
Omeprazole 40 mg/10 mL IV: 20-40 mg once a day
ampule
Phentolamine 5 mg/mL IM/IV Adult: 5 mg prn
1 mL vial IV Pedia: 0.1 mg/kg prn
Phenytoin 50 mg/mL IV Loading dose:
2 mL ampule 15-18 mg/kg at a rate not to
exceed 50 mg/min
IV Maintenance dose
5-7 mg/kg/day or 300 mg/day
Polyethylene 227.1 g/packet PO: 3-4 L/hr (Adult) x 2-6 hours
glycol 1-2 L/hr (Adolescent)
0.5 L/hr (Child)
Potassium 2 mEq/mL IV: 40 mEq/hour
chloride 20 mL vial
Prazocin 1, 2, 5 mg tablet PO: 1 mg q 8-12 hours, titrate to max
dose of 20 mg/day
Propanolol 1 mg/mL vial IV: 0.5-1.0 mg q 5 min to desired effect
Ranitidine 25 mg/mL IV: 50 mg q 8 hours
2 mL ampule (50 mg/day if with renal disease)
Salbutamol 2.5 mg/nebule Neb: 1 nebule q 6-8 hours
Sodium 8.4% 1 mEq/mL IV: Severe acidosis
bicarbonate 10, 50 mL vial 1 mEq/kg IV or adjust according to
ABG results
Infusion: 2-5 mEq/kg q 4-8 hours
Sodium sulfate Powder, USP PO/NGT Adult: 15-30 g in 100 mL water
PO/NGT Pedia: 250 mg/kg as a 10%
solution
231
Annex F
Minimum Required Drugs and
Devices for the Management of
Poisoning (Poison Kit)
Fluids Devices
D5W D5 AR Aseptosyringe
D5 0.9 NaCl D5 LR Foley catheters
D50-50 Kidney basin
D5 0.3 NaCl Laryngoscope
Low-reading thermometer
Drugs Nasogastric tubes
N-acetyl cysteine ampules (Fr. 16 for adults;
Activated charcoal sachets Fr. 10-12 for children)
Ascorbic acid ampules Oropharyngeal tubes
Atropine ampules Oxygen with nasal catheters and
Baking soda venturi masks
Calcium gluconate 10% Suction apparatus
ampules Gloves, surgical; gloves, gauntlet
Diazepam ampules/tablets (for pesticide poisoning)
and/or Lorazepam KY jelly
ampules IV tubes with venoset/soluset
Diphenhydramine ampules IV catheters (G. 24 to G. 18)
Dobutamine vials
Dopamine vials
Epinephrine ampules
Esmolol ampules
Famotidine/omeprazole
ampules
Furosemide vials
Mannitol 20%
Naloxone ampules
Phenytoin ampules
Potassium chloride vials
Pyridoxine ampules
Phytonadione ampules
Sodium bicarbonate 8.4% vials
Sodium sulfate sachets
Vitamin B complex ampules
Vitamin K1 ampules
232
Annex G
Rumack-Matthew Paracetamol
Nomogram
1000
500
Paracetamol plasma concentration ug/mL
200
150
100
Potential for hepatic toxicity
50
Hepatic toxicity
unlikely
10
0 4 8 12 16 20 24
Hours post-ingestion
The nomogram is useful in the first 24 hours after ingestion. Blood should be drawn at
least 4 hours post-ingestion. Before the 4th hour, the drug is still being absorbed in the
GI tract. Taking the drug level too early can lead to an underestimation of its plasma
concentration. If the paracetamol level falls above the diagonal lines, treatment with N-
acetylcysteine should be given or continued. Below the diagonal lines, treatment need
not be given or should be discontinued. In between the diagonal lines, toxicity is
possible. Observe the patient closely for signs of toxicity and determine if treatment is
necessary. The nomogram is useful for predicting hepatic toxicity, while paracetamol
can also cause kidney failure and electrolyte disturbances. Remember to rule out
toxicity to other organ systems.
233
Annex H
Units, Concentrations and
Conversions
1. Mass
1g = 1000 mg
1 mg = 1000 mcg
1 mcg = 1000 ng
2. Volume
1 dL = 100 mL
1 teaspoon = 5 mL
1 tablespoon = 15 mL
3. Concentrations
1 ppm = 1 mg/L (liquids), 1 mg/m3
1 ppb = 1 mcg/L (liquids), 1 ug/m3
Weight by volume = mg/L, ug/mL, etc.
Percent weight in
volume = g/100 mL
Percent by weight = g/100 g
Percent by volume = mL/100 mL
4. Conversion of molar units to mass units
Use the molecular weight of the substance as the conversion factor.
Example:
Molecular weight of phenobarbital = 232.24
1 mole phenobarbital = 232.24
1 g phenobarbital = 1/232.24 = 0.0043 mole
1 mg phenobarbital = 0.0043 mmole
1 mcg phenobarbital = 0.0043 mcmole
REFERENCES
Goldfrank LR, et al. (eds.) Goldfrank's Toxicologic Emergencies. Connecticut: Appleton
and Lange. 1990.
International Program on Chemical Safety - World Health Organization. IPCS/INTOX
Poisons Centre Trianing Manual. 2006.
234
Important Contact Numbers
POISON CONTROL CENTERS Rizal Medical Center Poison Control
Center
National Poison Management & Pasig City
Control Center Contact Person: Dr. Danilo
Philippine General Hospital Villamangca
Manila Telephone numbers: (062)-5706273
Contact Person: Dr. Lynn R. (062)-6719740
Panganiban
Telephone number(s): (062)- OTHER AGENCIES / UNITS
5241078 (Hotline); (062)-5548400
local 2311 Child Protection Unit
Mobile: 0922-8961541 Philippine General Hospital
Fax number: (062)-5260062 524-1512/524-0712
E-mail address: 554-8400 local 2213/2214
toxinfo@uppoisoncenter.org
Women's Desk
Batangas Regional Hospital Philippine General Hospital
Poison Control Center 524-2990
Batangas City 554-8400 local 3072
Contact Person: Dr. Rhodora
Madrid-Reyes
Telephone number: (043)-
7233578
Eastern Visayas Regional Medical

Center Poison Control Center
Tacloban City
Contact Person: Dr. Lourdes Agosto
Telephone number: (053)-3213131
Fax number: (053)-3213129
Northern NCR Hospital Poison

Control Center
East Avenue Medical Center
Quezon City
Contact Person: Dr. Visitacion
Antonio
Telephone number: (062) 928-0611 - 23 loc(379)
235

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Please do not photocopy.

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First published 1991

Copyright © 2011, 1998, 1991

Book design by Maria Lurenda S. Westergaard, M.D.

All rights reserved. No part of this publication may be reproduced,

Printed in the Philippines.

Lynn Crisanta R. Panganiban, MD, DPAFP, FPSCOT

Joselito C. Pascual, MD, MSc, FRSAP, FPSCOT

Carissa Paz C. Dioquino, MD, MPH, FPNA, FPSCOT

Maria Lurenda S. Westergaard, MD, MMed

Irma R. Makalinao, MD, FPPS, FPSCOT

Nerissa M. Dando, MD, FPPS, DPSCOT

Erle S. Castillo, MD, FPSCOT

Kenneth Y. Hartigan-Go, MD, MD (UK), FPCP, FPSECP,

Aeesha Yahcob-Pingli, MD, DPAFP

ACRONYMS AND ABBREVIATIONS xii

GENERAL MEASURES IN THE MANAGEMENT OF POISONING 9

OVERDOSE OF COMMON PHARMACEUTICALS 49

HOUSEHOLD AND WORKPLACE CHEMICALS 121

SUBSTANCE ABUSE 173

ANIMAL TOXINS 191

PLANT TOXINS 207

ANNEX A. Properties of Common Drugs Involved in Poisoning 225

IMPORTANT CONTACT NUMBERS 235

The beginning of wisdom is to acquire wisdom; and with all your

In 1975, the science of toxicology was introduced in the Philippines with

The leading causes of poisoning managed at the NPMCC are exposures

Strategies in poisoning prevention and control

The NPMCC engages in various strategies to minimize the risks and

Throughout the years, the NPMCC has realized the importance of

POISON: any agent that is capable of producing deleterious or harmful

POISONING: an event where a living organism is exposed to drugs,

SELF-POISONING AND PARASUICIDE: refers to the deliberate ingestion

ACCIDENTAL POISONING: non-intentional ingestion, overdose or

SUBSTANCE ABUSE: (DSM-IV-TR criteria)

SUBSTANCE DEPENDENCE: (DSM-IV-TR criteria)

Note: The definitions for substance dependence and substance abuse

SUBSTANCE WITHDRAWAL: (DSM-IV-TR criteria)

SUBSTANCE INTOXICATION: (DSM-IV-TR criteria)

ABCs of Life Support for Poisoned Patients

A. Maintain adequate airway

If the airway is obstructed, place the patient in supine position. Perform

B. Provide adequate oxygenation / mechanical ventilation

Inadequate oxygen delivery to the lungs may be due to ventilatory failure,

Common Toxicants that Can Cause Hypoxia

Modes of Oxygen Delivery with Equivalent FiO2

IMPORTANT: Oxygen may be contraindicated in the initial management of

C. Maintain adequate circulation

Secure venous access and initiate intravenous infusion of the

D. Treat CNS disturbances - convulsions and coma

Convulsions in poisoned patients may be due to:

Hypokalemia is usually seen in Causes of Hypokalemia

Hyperkalemia occurs in overdose of Causes of Hyperkalemia

Hypocalcemia is commonly seen in “watusi” and jatropha seed

Adult: 2.25 to 4.5 mmol calcium by slow IV push

Hypothermia, with a rectal temperature < 30º C, is a complication of an

Hyperthermia, with a rectal temperature > 40ºC, is a toxic effect of

Toxicants Associated with Hypothermia

Toxicants Associated with Hyperthermia

Acid-base abnormalities can also be complications of acute poisoning.

Salicylate and xanthine poisoning may lead to mixed respiratory alkalosis