PREPARATION OF GUIDELINES FOR MANAGEMENT OF POISONING AT ST.MARTHA’S HOSPITAL , BANGALORE

Amit Sharma's picture

Publication Type:

Thesis

Source:

Al-Ameen college of pharmacy, RGUHS, Volume M.PHARM, BANGALORE, p.210 (Submitted)

Keywords:

poisoning

Full Text:

Introduction: Poison is a substance capable of producing damage or dysfunction in the body by its chemical activity. Poisoning can be accidental or intentional. In many parts of the developing countries pesticide poisoning, insecticidal poisoning, drug over dose, and cosmetics poisoning, causes more deaths than infectious diseases.
Objectives: To study the pattern of poisoning cases admitted in Medical Intensive Care Unit of St. Martha’s Hospital, to list the type of poisons consumed, observe the symptoms, antidotes used in these cases and to prepare guidelines for the management of the same.

Methodology: The study was conducted for a period of 9 months(June’08–Feb’09).The ethical committee clearance was obtained from Institutional Review Board of St.Martha’s Hospital. Data of all patients admitted to MICU for the treatment of poisoning was collected from their case sheets. The data was analyzed for demographic profile of patients, patterns of specific drug and antidote use.
Results and conclusion: During the period of study, 55 patients were enrolled out of whom 29(52.73%) were male and 26(47.27%) were female. The age of patients ranged from 12-84 yrs with a majority of the patients in the age group between 19-30 yrs (41.81%). Most of the patients (97%) were from urban region. 80% of the patients were literates. The patients who consumed poison ranged from businessmen, students to housewives. 68% of the patients were married. 96.4% of the cases were due to intentional poisoning and 3.6% were accidental poisoning. Intentional poisoning was more with alcoholics. Poison was mostly consumed orally.

Organophospohorous compounds constituted 60% of the poison cases followed by overdose of drugs and cosmetics. The symptoms were CNS, GI, CVS, and respiratory related. Specific antidotes were used in 90.9% of the cases. The antidotes used were atropine, PAM, and N-acetyl cystine. General antidote used was charcoal. Out of 55, 54 patients recovered and 1 expired. Duration of hospital stay ranged from 3 to 30 days with a mean of 10-15 days.
Guidelines for the management of poisons that we came across in our study were made for the reference of the clinicians. In conclusion it can be said that identification of pattern of poisoning cases and antidotes used helps in making guidelines for the management of the same.

Key Words: Toxicity, Poison, Drug Overdose, Antidotes, Organophosphrous,
Insecticides, Pesticides.

A poison is any substance that causes harm if it gets into the body. Harm can be mild (for example, headache or nausea) or severe (for example, fits or very high fever), and severely poisoned people may die.
Some chemicals are poisonous in very small amounts (for example, a spoonful by mouth or a tiny amount injected by snakebite); others are only poisonous if a large amount is taken.
Every individual has a risk of exposure to toxic chemicals accidentally or intentionally. Although the global incidence of poisoning is not known, it may be speculated that up to half a million people die each year as a result of various kinds of poisoning, including poisoning by natural toxins. WHO estimates that the incidence of pesticide poisoning, which is high in developing countries, has doubled during the past 10 years; It was estimated in 1982 that, while developing countries accounted for only 15% of the worldwide use of pesticides, over 50% of cases of pesticide poisoning occurred in these countries Around 15%-20% of the workload of medical units and 10% of the workload of accident and emergency departments in the India are due to self poisoning. Episodes of self poisoning in India continue to rise, particularly in young men, and alcohol is often taken with the overdose.
The principal toxic risks that exist in any country may be readily identified by surveys of hospital accident and emergency wards, forensic departments, and rural hospitals in agricultural areas. The growing incidence of poisoning has highlighted the importance of countries having special programmers for poison control and, in particular, the facilities for diagnosis, treatment, and prevention of poisoning.
Some countries have already established poison control programmer in hospitals that provide the framework for both prevention and management of poisoning. The main elements of such

programmers are identification of the toxic hazards existing locally (in order to establish preventive measures), and making guidelines for the treatment.
These guidelines are intended to establish or strengthen facilities for the prevention and management of poisoning.
The specific aim of this study was to evaluate poisoning cases in patient population as they present to St.Martha’s Hospital, severity of symptoms as observed by the physicians, biochemical manifestation of poisoning, the lethality of the suicide attempt, and the outcome.
Objectives of the study
1 To document the cases admitted to Medical Intensive Care unit of St.Martha’s Hospital due to poisoning.
2 To list the poisons consumed and observe the symptoms of poisoning.
3 To list the type of antidotes used.
4 To make guidelines for the management of cases due to the poisons consumed by the patients during the course of our study.

INTRODUCTION

Paracelsus, the father of toxicology, once wrote: "Everything is poison, there is poison in everything. Only the dose makes a thing not a poison."
A Poison is any substance that causes harm if it gets into the body. Harm can be mild (for example, headache or nausea) or severe (for example, fits or very high fever even death) and several poisoned may die. The word poison comes from the Latin word - potare - meaning to drink
Poisoning is the harmful effect that occurs when a toxic substance is swallowed, is inhaled, or comes in contact with the skin, eyes, or mucous membranes, such as those of the mouth or nose.
Poisoning, either accidental or intentional is a common cause of admission at accident and emergency departments.
Almost any chemical can be a poison if there is enough in the body. Some chemicals are poisonous in very small amount. (For example a spoonful by mouth or a tiny amount injected by snakebite.) Others are only poisonous if a large amount is taken.1
The amount of a chemical substance that gets into the body at one time is called the dose. A dose that causes poisoning is a poisonous dose or toxic dose. The smallest amount that causes harm is threshold dose. If the amount of a chemical substance that gets into a body is less than the threshold dose, the chemical will not cause poisoning and may even have good effects. For example, medicines have good effect if people take the right dose, but some can be poisonous if people take too much.1

Poison was discovered in ancient times, and was used by primitive tribes and civilizations as a hunting tool to quicken and ensure the death of their prey or enemies. This use of poison grew more advanced, and many of these ancient peoples began forging weapons designed specifically for poison enhancement. Later in history, particularly at the time of the Roman empire, one of the more prevalent uses for poison was assassination. As early as 331 BC, poisonings executed at the dinner table or in drinks were reported, and the practice became a common occurrence. The use of fatal substances was seen among every social class; even the nobility would often use it to dispose of unwanted political or economic opponents3
Exposure to a poison
When people are in contact with a poison they are said to be exposed to it. The effect of exposure depends partly on how long the contact lasts and how much poison gets into the body, and partly on how much poison the body can get rid of during this time. Exposure may happen only once or many times.

Acute exposure is a single contact that lasts for seconds, minutes or hours, or several exposures over a day or less.

Chronic exposure is contact that lasts for many days, months or years. It may be continuous or broken by periods when there is no contact. Exposure that happens only at work; for example, is not continuous.2

How poison gets into the body The way poison gets into the body is called the route of exposure or the route of absorption. The amount of poison that gets into the blood during a given time depends on the route.
Through the mouth by swallowing (Ingestion)
Most poisoning happens this way. Small children often swallow poison accidentally, and adults who want to poison themselves may swallow poison. If people eat, drink or smoke after they have been handling poisons without first washing their hands, they may accidentally swallow some of the poison. This is a common cause of pesticide poisoning.

When poisons are swallowed they go to the stomach (Fig. 1). Some poisons can pass through the gut walls and into the blood vessels. The longer a poison stays in the gut the more will get into the blood and the worse the poisoning will be.1

If a person vomits soon after swallowing a poison, it may be expelled from the body before a poisonous dose gets into the blood. So, if the person does not vomit straight away, it is sometimes useful to make the person vomit. There are two other ways to stop poisons passing from the gut into the blood: (1) give activated charcoal because this binds some poisons so that they cannot pass through the gut walls; or (2) give laxatives to make the poison move through the gut and out of the body more quickly. The circumstances when it is useful to make a patient vomit or to give activated charcoal or laxatives, and the circumstances when these procedures may be dangerous.2
Poisons that do not pass through the gut walls do not get into the blood and so cannot affect other parts of the body. They move along the gut and leave the body in the faeces. For example, mercury metal cannot pass through the gut walls; if mercury from a thermometer is swallowed, it passes out of the body in the faeces and does not cause poisoning.1

Through the lungs by breathing into the mouth or nose (inhalation)
Poisons in the form of gas, vapours, dust, fumes, smoke or fine spray droplets may be breathed into the mouth and nose and go down the air passages into the lungs (Fig. 2). Only particles that are too small to be seen can pass into the lungs. Larger particles are trapped in

the mouth, throat and nose and may be swallowed. A person may breathe in poison when working with a poisonous substance inside a building without fresh air, or when spraying pesticide without wearing adequate protection. Oil or gas heaters, cookers, and fires give off
poisonous fumes which may reach dangerous concentrations if the smoke cannot get outside or if the room does not have a good supply of fresh air.
Poison that gets into the lungs passes into the blood vessels very quickly because the air passages in the lungs have thin walls and a good blood supply.1

Through the skin by contact with liquids, sprays or mists
People working with chemicals such as pesticides may be poisoned if the chemical is sprayed or splashed onto the skin or if they wear clothes soaked with chemical.
The skin is a barrier that protects the body from poisons. However, some poisons can pass through the skin (Fig. 3). They pass through warm, wet, sweaty skin more quickly than through cold, dry skin, and they pass through skin damaged by scratches or burns more quickly than through undamaged skin. A poison that damages the skin will pass through more quickly than one that does not damage the skin. It may be possible to wash poison off the skin before a poisonous dose gets into the body.1
Poisons can be injected through the skin from a syringe, or a pressure gun, or during tattooing, or by the bite or sting of a poisonous animal, insect, fish or snake. The injection may go directly into the blood vessels or under the skin into muscle or fatty tissues.

By injection through the skin
Poison injected into the blood has a very quick effect. Poison injected under the skin or into

muscle has to pass through several layers of tissue before reaching the blood vessels, so it
acts more slowly. Once a poison gets into the blood it is carried to the whole body as the blood is pumped round the body by the heart (Fig. 4).

How poison is broken down by the body
Some poisons are changed by the body into other chemicals. These are called metabolites, and may be less poisonous or more poisonous than the original substance. The metabolites are more easily passed out of the body than the original chemicals. These changes take place mostly in the liver.1

How poison leaves the body
Unchanged poisons or their metabolites usually leave the body in the urine, faeces or sweat, or in the air that a person breathes out. The movement of poison from the blood into urine takes place in the kidneys, and the movement of poison from blood into breathed-out air

takes place in the lungs. Poison in the faeces may have passed down the gut without being absorbed into the blood or it may have been absorbed into the blood and then passed out into the gut again. Some poisons, like DDT, pass into body tissues and organs where they may stay for a long time.2

The effects of poison
The effects of a chemical substance on the body may be described as either local or systemic.
• A local effect is limited to the part of the body in contact with the chemical: the skin, the eyes, the air passages or the gut. Examples of local effects are skin rashes, skin burns, watery eyes, and irritation of the throat causing coughing. Many poisons cause local effects, but there are also many poisons that do not.2
• A systemic effect is a more general effect that occurs when a poison is absorbed into the body.
Chronic exposure to small amounts of poison may not cause any signs or symptoms of poisoning at first. It may be many days or months before there is enough chemical inside the body to cause poisoning.2

For example, a person may use pesticide every day. Each day the person is exposed to only a small amount of pesticide, but the amount of pesticide in the body gradually builds up, until eventually, after many days, it adds up to a poisonous dose. Only then does the person begin to feel unwell. With the availability of a vast number of chemicals and drugs, acute poisoning is a common medical emergency in any country.

The exact incidence of this problem in our country remains uncertain but it is estimated that about 10-15 million cases of poisoning are reported every year, of which, more than 50,000 die.2
Poisoning is as old as our society. Of-late, the incidence of poisoning cases is increasing steadily with each passing year. By definition, anything which when used internally or on the body surface in a dose or in repeated doses, if acts chemically and physiologically,

causing disturbances of body functions and leads to disease or death is a poison. Poisoning, either intentional or accidental, significantly contributes to mortality and morbidity throughout the world. According to WHO, 3 million acute poisoning cases with 2, 20,000 deaths occur annually. Out of these, 90% of fatal poisoning occurs in developing countries, particularly amongst the agricultural workers. Developing countries such as India and Sri Lanka have reported alarming rates of toxicity and deaths due to poisons. In United States, deaths due to poisoning number more than 775 per year. Most of the people who die from poisoning are adults and deaths often results from intentional rather than accidental exposure.2
Terminology
Some poisons are also toxins, usually referring to naturally produced substances, such as the bacterial proteins that cause tetanus and botulism. A distinction between the two terms is not always observed, even among scientists.
The derivative forms "toxic" and "poisonous" are synonymous.
CLASSIFICATION OF POISONS
Gaseous Poisons
These poisons are present in the gaseous state and if inhaled, destroy the capability of the blood as a carrier of oxygen and irritate or destroy the tissues of the air passages and lungs. When in contact with the skin and mucous membranes, gaseous poisons produce

lacrimation, vesication, inflammation, and congestion.Examples are carbon-monoxide, carbon-dioxide, hydrogen sulfide, sulfur dioxide, ammonia gas, chlorine gas, and chemical warfare agents.3
Inorganic Poisons
Inorganic poisons fall into two classes: (a) Corrosives, which are substances that rapidly destroy or decompose the body tissues at point of contact. Some examples are hydrochloric, nitric, and sulfuric acids, phenol, sodium hydroxide and iodine. (b) Metals and their salts, which are corrosive and irritate locally, but whose chief action occurs afterabsorption when they damage internal organs, especially those of excretion. Some exam-ples are arsenic, antimony, copper, iron, lead, mercury, radioactive substances, and tin.
Alkaloidal Poisons
These poisons are nitrogenous plant principles that produce their chief effect on some part of the central nervous system. Some examples are atropine, cocaine, morphine, and strychnine.
Non-alkaloidal Poisons
These poisons include various chemical compounds, some obtained from plants, having hypnotic, neurotic, and systemic effects. Some examples are barbiturates, salicylates, digoxin, and turpentine.

Pesticide poisoning
Pesticides are chemicals made to poison insects, weeds or other pests. Most pesticides are also poisonous or harmful to humans if they get on the skin, or if they are breathed into the lungs in the form of gases, fumes, dust or fine spray droplets, or if they are swallowed.

Insecticide poisoning
Insecticide is a chemical that kills bugs. Insecticide poisoning occurs when someone swallows or breathes in this substance. Most household bug sprays contain chemicals called pyrethrins. These chemicals are generally not harmful, but can cause life-threatening breathing problems if breathed- in. The properties that make insecticides deadly to insects can sometimes make them poisonous to humans. Most serious insecticide poisonings result from the organophosphate and carbamate types of insecticides, particularly when used in suicide attempts.
Industrial insecticides, often found in household garages and greenhouses, contain many dangerous substances, including:
• Carbamates
• Organophosphates
• Paradichlorobenzenes (mothballs)
Organophosphates and carbamates cause eye tearing, blurred vision, salivation, sweating, coughing, vomiting, and frequent bowel movements and urination. All OP/Carbamate insecticides are fat soluble and therefore are easily absorbed through the skin and then

transported throughout the body. These chemicals kill insects and cause poisoning in animals by inhibiting the enzyme, acetylcholinesterase (AChE) which normally functions to degrade acetylcholine in nerve synapses. Inhibition of AChE in the nerves results in a build-up of acetylcholine (ACh) and overstimulation of ACh receptors.
Poisoning at work
Many chemicals that are made, used, or stored in workplaces are poisonous. People who work with these chemicals need to know how to handle them safely to avoid being poisoned.Sometimes workers may not know that they are handling a poisonous chemical, or they may know that the chemical is poisonous but not have been told or shown how to handle it safely. They may not have read the label or the safety information. Sometimes they may know the dangers but be too lazy or careless to use safe methods.3

Self-poisoning
People may try to harm themselves by deliberately taking poison this is called self-poisoning. In some countries people take medicines to poison themselves, but people living in rural communities are more likely to take pesticides. People suffering from depression, serious illness, or alcohol dependence may try to kill themselves by taking poison. They may swallow large amounts of medicine, pesticide or other poisons. If they recover they might try to poison themselves again unless they receive appropriate treatment. Many young people who try to poison themselves are unhappy because of problems they do not know how to deal with, such as unhappy love affairs.4

Poisoning in childhood
Many poisoning accidents in the home happen to small children aged between 1 and 4 years. At this age children want to explore. They can crawl or walk round the house on their own and by the age of 2 they can probably climb onto a chair to reach a high shelf. They can open drawers and cupboards, and they may be able to open screw-top bottles.7
The damage caused by poisoning depends on the poison, the amount taken, and the age and underlying health of the person who takes it. Some poisons are not very potent and cause problems only with prolonged exposure or repeated ingestion of large amounts. Other poisons are so potent that just a drop on the skin can cause severe damage.7
Some poisons produce symptoms within seconds, whereas others produce symptoms only after hours or even days. Some poisons produce few obvious symptoms until they have damaged vital organs such as the kidneys or liver sometimes permanently

Poisoning in old age
Old people may poison themselves accidentally. If they cannot see very well, they may pick up the wrong bottle and swallow a household cleaner, for example, instead of a drink or a medicine. Old people tend to be forgetful and confused. They may forget to take their medicine, or they may take too much and poison themselves because they cannot remember how much to take or when they took the last dose.4

Medical poisoning:
Sometimes people are poisoned by medicines given to them by the doctor or another health care worker. They may be given the wrong medicine or be given the wrong dose of the right medicine. There are many reasons why this can happen. The doctor may not know the patient is allergic to a medicine, or may give the wrong dose because of a mistake in measuring it.
Abuse of drugs, chemicals or plants
People may take drugs to change their mood or behavior, to feel relaxed, or to get more energy. This is called drug abuse, because it is not a medical use of the drug. Some people abuse drugs such as heroin, cocaine or barbiturates. Drinking too much alcohol is an important kind of drug abuse. Other substances may produce some of the same effects. Some people breathe in chemicals such as glue, paint, nail varnish remover, cigarette lighter, gas, petrol or dry-cleaning fluid. This is sometimes called solvent sniffing or solvent abuse. People may breathe fumes from a cloth soaked in liquid or put chemicals or glue into a plastic bag and breathe deeply from the bag.4
In many societies people use plants or fungi for their hallucinogenic, stimulant or relaxing effects. Some plants may be eaten raw, others are cooked, made into drinks, or smoked. Two plants commonly used in this way are tobacco and cannabis.
Many of the drugs, chemicals and plants that are abused are poisonous if people take too much at one time or use them for many months or years. For example, alcohol causes liver damage, smoking causes lung cancer and cannabis can affect people's memory.

Drugs
Drugs that are helpful in therapeutic doses may be deadly when taken in excess.
Examples include:
• Beta blockers: Beta blockers are a class of drugs used to treat heart conditions (for example, angina, abnormal heart rhythms) and other conditions, for example, high blood pressure, migraine headache prevention, social phobia, and certain types of tremors. In excess, they can cause difficulty breathing, coma, and heart failure.
• Warfarin (Coumadin): Coumadin is a blood thinner used to prevent blood clots. It is the active ingredient in many rat poisons and may cause heavy bleeding and death if too much is taken.
• Vitamins: Vitamins, especially A and D, if taken in large amounts can cause liver problems and death.

Chemical poisons
There are many ways chemical poisons can get into food and drink, for example:
• When people working with chemicals eat in the workplace or do not wash their hands before eating.
• When chemicals spill onto food as it is being moved from place to place, or when it is in a storeroom.

Poisonous plants, mushrooms, animals and sea-creatures
Some plants, mushrooms, animals and sea-creatures contain toxins. Sometimes it is very hard to tell the difference between plants or fish that are good to eat and those that are poisonous.
Every individual is exposed to toxic chemicals, usually in minute, sub toxic doses, through environmental and food contamination. In some instances people may be subjected to

massive or even fatal exposure through a chemical disaster or in a single accidental or intentional poisoning. Between these two extremes there exists a wide range of intensity of exposure which may result in various acute and chronic toxic effects. Such effects clearly lie in the public health domain particularly in cases of chemical contamination of the environment that may result in exposure of an unsuspecting public. The situation is similar to but subtler than exposure to infectious diseases. Although chemicals may be absorbed in small quantities they do not induce pathological signs until toxic concentrations are reached in the tissues of exposed individuals.4
Both homicidal and suicidal cases of poisoning are more common in India than in western countries, owing to easy availability of poison in the Indian markets. Insecticides and pesticides account for majority of these poisoning cases. More recently, Aluminum phosphide, because it is cheap, easily available, highly toxic, and has no antidote, has emerged as the most common suicidal agent. The toxic effects of Aluminium phosphide are due to deadly phosphine gas liberated when it reacts with water or hydrochloric acid in the

stomach. Organophosphorus compounds are other more common cause of insecticide poisoning in India4.
Foods
• Some mushrooms are poisonous
• Drinking water contaminated by agricultural or industrial chemicals
• Food that has not been properly prepared or handled
Poisoning Symptoms
The signs and symptoms seen in poisoning are so wide and variable that there is no easy way to classify them.
• Some poisons enlarge the pupils, while others shrink them.
• Some result in excessive drooling, while others dry the mouth and skin.
• Some speed the heart, while others slow the heart.
• Some increase the breathing rate, while others slow it.
• Some cause pain, while others are painless.
• Some cause hyperactivity, while others cause drowsiness. Confusion is often seen with these symptoms.

When the cause of the poisoning is unknown
A big part of figuring out what type of poisoning has occurred is connecting the signs and symptoms to each other, and to additional available information.Two different poisons, for example, may make the heart beat quickly. However, only one of them may cause the skin and mouth to be very dry. This simple distinction may help narrow the possibilities.
• If more than one person has the same signs and symptoms, and they have a common exposure source, such as contaminated food, water, or workplace environment, then poisoning would be suspected.
• When two or more poisons act together, they may cause signs and symptoms not typical of any single poison.

Delayed onset of symptoms
A person can be poisoned and not show symptoms for hours, days, or months. Cases of poisoning with a prolonged onset of symptoms are particularly dangerous because there may be a dangerous delay in obtaining medical attention.
• Acetaminophen is considered one of the safest drugs but is toxic to the liver when taken in large quantities. Because it acts so slowly, 7-12 hours may pass before the first symptoms begin (no appetite when normally hungry, nausea, and vomiting).

• The classic example of a very slow poison is lead. Before 1970, most paints contained lead. Young children would eat paint chips and after several months, develop abnormalities of the nervous system.
Some signs and symptoms of poisoning can imitate signs and symptoms of common illnesses.
• For example, nausea and vomiting are a sign (vomiting) and symptom (nausea) of poisoning. However, nausea and vomiting can also be found in many illnesses that have nothing to do with poisoning. Examples include: stroke, heart attack, stomach ulcers, gallbladder problems, hepatitis, appendicitis, head injuries, and many others.
• Almost every possible sign or symptom of a poisoning can also be caused by a non–poison-related medical problem
• Over the counter medications are not safe even if taken in excess.
• With many pills, it may take several hours or longer for symptoms to develop. Do not wait for symptoms to develop, rush the patient to the nearest hospital.
• If someone looks ill after a poisoning or possible poisoning. Take the person to the nearest emergency department of a hospital.
• An infant or toddler who may have ingested a poison, even if the child looks and feels fine.
• Anyone who has taken something in an attempt to harm him or herself, even if the substance used is not known to be harmful.

• When you go to the hospital's emergency department, take all the medicine bottles, containers (household cleaners, paint cans, vitamin bottles), or samples of the substance (such as a plant leaf) with you.
Toxicovigilance
It is the active process of identifying and evaluating the toxic risks existing in a community, and evaluating the measures taken to reduce or eliminate them. Analysis of enquiries received by poison information centers permits the identification of those circumstances, populations, and possible toxic agents most likely to be involved, as well as the detection of hidden dangers. The role of a centre in toxicovigilance is to alert the appropriate health and other authorities so that the necessary preventive and regulatory measures may be taken. For

example, the centre may record a large number of cases of poisoning by a specific product newly introduced to the local market; cases occurring in a particular population group (e.g. analgesic poisoning in children); or cases occurring in particular circumstances (e.g. carbon monoxide poisoning from faulty heating stoves) or at particular times of the year (e.g. mushroom poisoning in the autumn or snake bites in the summer). Only now is the unique role of poison information centers in toxicovigilance being widely recognized. This role enables them to make a major contribution to the prevention of poisoning through their collaboration with the health and other appropriate authorities. 5

Analytical toxicology is the detection, identification and often also the measurement of drugs and other foreign compounds (xenobiotics) in biological and related specimens to help in the diagnosis, treatment, prognosis, and prevention of poisoning. Analytical toxicology is important since it is the only means by which objective evidence of the nature and magnitude of exposure to a particular compound or group of compounds can be obtained. Most obviously such objective evidence is needed in a court of law and most if not all countries have established analytical toxicology facilities as part of governmental forensic science laboratories.
Acute poisoning is a common reason for presentation to hospital and most poisoned patients Make a full recovery without specific treatment. However, with some common poisons analytical toxicology data can be important in establishing a diagnosis of poisoning and guiding treatment. Examples include iron, lithium, and paracetamol (acetaminophen). The availability of reliable analytical facilities can also assist in other clinical areas such as assessing illicit drug use and the diagnosis and treatment of poisoning with environmental

toxins such as lead, as well as in the management of incidents related to the accidental or deliberate release of chemicals into the environment (chemical incidents) and other aspects of chemical safety. An essential preliminary to the task of establishing an analytical toxicology service is to undertake a detailed survey of the perceived toxicological problems encountered in the region or country.5
A combination of history, physical examination, and laboratory studies will help reveal the cause of most poisonings. Frequently, treatment must begin before all information is available.

History: As a family member or friend of a poisoned person, you can greatly assist the doctor and provide valuable clues by telling the doctor about these details:
• Everything the person ate or drank recently
• Names of all prescription and over-the-counter medications the person is taking
• Exposure to chemicals at home or at work
• Whether others in the family or at work have been similarly ill or exposed
• Whether the person has any psychiatric history to suggest an intentional ingestion (suicide attempt)
Testing: Many poisons can be detected in the blood or urine. However, a physician cannot order "every test in the book" when the diagnosis is unclear. The tests ordered will be based on information revealed in the history and physical exam.
A toxicology screen or "tox" screen looks for common drugs of abuse. Most toxicology screens will detect acetaminophen, aspirin, marijuana, opioids (heroin, codeine), benzodiazepines (Valium, Librium), amphetamines (uppers), cocaine, and alcohol.
• A specific blood test will give serum levels of some drugs, including phenytoin, theophylline, digoxin , lithium, and acetaminophen.
• Some drugs affect the electrical activity of the heart. An electrocardiogram (ECG) may reveal toxicity.

• Sometimes a person is unconscious for no obvious reason. A CT scan of the brain will help tell if there has been a structural change in the brain, such as a stroke.
Poison information centers: their role in the prevention and management of poisoning.
Recognition of the problem of poisoning and of the need for specialized facilities to deal with it, as well as the existence of a number of health care professionals concerned with human toxicology, has invariably been the primary pre-requisite for the establishment of poison information centre. The first centre was instituted in North America and Europe during 1950s. Since then, many others have been created, principally in the industrialized countries. The early poison information centre originated in a wide variety of fields including pediatrics, intensive care, forensic medicine, occupational health, pharmacy, and pharmacology. To some extent, the original character of many poison information centers has been maintained, and there is thus considerable heterogeneity in their structure and organization.
A global study undertaken during the period 1984-1986 indicated that, while most developed countries had well established facilities for poison control, this was rarely the case in developing countries. Furthermore, in industrialized countries, there may be a number of institutions that provide different types of information on toxic chemicals. It must be remembered however that each ministry or agency in a developed country may have its own information services for its specialized needs, but that, in a developing country, the poison information center where it exists may be the only source of information on toxic

chemicals available 24 hours a day. Centers in developing countries may therefore have to provide a much broader toxicological information service than their counterparts in some developed countries.
Poisoning of animals may have important economic consequences, and special veterinary poison information centre have been established in some countries including Australia, France, and USA. In most countries, however, many poison information centers may deal with toxicological problems that affect both animals and humans.8
Poison information centre may operate effectively with various types of organizational structure. The majority depends on a hospital administration and are, to some extent, connected with a university and with the country's public health service at national or regional level.
The poison information centre is a specialized unit providing information on poisoning, in principle to the whole community. Its main functions are provision of toxicological information and advice, management of poisoning cases, provision of laboratory analytical services, toxicovigilance activities, research, and education and training in the prevention and treatment of poisoning. As a part of its role in toxicovigilance, the centre advises on and is actively involved in the development, implementation, and evaluation of measures for the prevention of poisoning. In association with other responsible bodies, it also plays an important role in developing contingency plans for, and responding to, chemical disasters, in monitoring the adverse effects of drugs, and in handling problems of substance abuse. In fulfilling its role and functions, each centre needs to co-operate not only with similar

organizations, but also with other institutions concerned with prevention of and response to poisoning8
Diagnosis and Treatment
Identifying the poison is crucial to successful treatment. Labels on bottles and other information from the person, family members, or coworker’s best enable the doctor or the poison center to identify poisons. Urine and blood tests may help in identification as well. Sometimes, blood tests can reveal how serious the poisoning is.
Many people who have been poisoned must be hospitalized. The principles for the treatment of all poisoning are the same: prevent additional absorption, increase elimination of the poison, give specific antidotes (substances that eliminate, inactivate, or counteract the effects of the poison), if available; and prevent exposure. With prompt medical care, most people recover fully. The usual goal of hospital treatment is to keep the person alive until the poison disappears or is inactivated. Eventually, most poisons are inactivated by the liver or are passed into the urine.8
Stomach emptying may be attempted if an unusually dangerous poison is involved or if the person appears very sick. In this procedure, a tube is inserted through the mouth or nose into the stomach. Water is poured into the stomach through the tube and is then drained out (gastric lavage). This procedure is repeated several times.
For many swallowed poisons, hospital emergency departments usually give activated charcoal. Activated charcoal binds to the poison that is still in the digestive tract, preventing its absorption into the blood. Charcoal is usually taken by mouth but may have to be given

through a tube that is inserted through the nose into the stomach. Sometimes doctors give charcoal every several hours to help cleanse the body of the poison.
A medical practitioner is likely to come across a variety of cases of poisoning during his professional career. Most of these cases are suicidal or accidental in nature. When a patient is brought to the hospital with a history of poisoning or with a suspicion of poisoning, the attending physician must bear in mind his duties and responsibilities. It need not be emphasized that the first and foremost of his duties is to save the life of the patient by exercising reasonable skill and care in the management, failing which charges of negligence may be framed against the doctor. The following are the basic principles of management.
First - Removal of the patient from the source of exposure.
Second - Emergency aids to stabilize the patient.
Third - Proper clinical evaluation.
Fourth - Removal of unabsorbed part of poison from G.I. Tract/ Skin/ Eyes.
Fifth - Removal of absorbed part of poison by forced diuresis, dialyses etc.
Sixth - Administration of specific antidote (A list of antidotes for common poisoning
cases is appended).
Seventh - Symptomatic treatment and assessment of clinical improvement.
A doctor working in a government hospital should never refuse to treat a case brought to the hospital. A private practitioner on the other hand has the right to choose his patient but it is unethical to refuse to provide proper management in emergency situations. When a patient, in full possession of his senses, reports to the hospital, the doctor has the right to treat the patient by virtue of implied consent. But when he is brought in an unconscious state, the

consent of legal guardian is necessary. It may also be remembered that whatever a doctor does in good faith during an emergency situation, will be protected by ethical principles. In order to avoid legal complications it is always advisable to consult a senior colleague and seek his advice in the matter. Observation of patients brought with history of poisoning, At least for 24 hours, even in the absence of tell-tale signs and symptoms may go a long way in preventing malpractice suits being advanced against the doctor. It should not be forgotten that certain agents can produce delayed onset of signs and symptoms of poisoning.9
If a poisoning remains life threatening despite the use of charcoal and antidotes, more complicated treatments may be needed. The most common involve filtering poisons directly from the bloodstream—hemodialysis (which uses an artificial kidney [dialyzer] to filter the poisons—see Dialysis: Hemodialysis) or charcoal hemoperfusion (which uses charcoal to
help eliminate the poisons). For either of these methods, small tubes (catheters) are inserted into blood vessels, one to drain blood from an artery and another to return blood to a vein.
The blood is passed through special filters that remove the toxic substance before being returned to the body9
Poisoning often requires additional treatment. For example, a person who becomes very drowsy or comatose may need a breathing tube inserted into the windpipe. The tube is then attached to a ventilator, which mechanically supports the person's breathing. The tube prevents vomit from entering the lungs, and the ventilator ensures adequate breathing. Treatment also may be needed to control seizures, abnormal heart rhythms, low blood pressure, high blood pressure, fever, or vomiting. If the kidneys stop working, hemodialysis
is necessary. If liver damage is extensive, treatment for liver failure may be necessary. If the liver or kidneys sustain permanent, severe damage, organ transplantation may be needed. People who attempt suicide by poisoning need mental health evaluation and appropriate treatment.9
Poison Management Systems
Poison management systems refer to the whole series of processes that begin from the time a drug or chemical is produced, to its ingestion as a poison, and all the steps required for a complete patient management.
Such a system may have various components, some of which are: -
1. Formulation and manufacture.
2. Distribution and control of access.
3. Measures to ensure prophylaxis against wrongful ingestion in the home, workplace or
general environment.
4. Community measures for handling one or more episodes of poisoning.
5. Poisons information.
6. Emergency patient management and after-care.
7. Toxicological analysis.
8. Education of patient and relatives.

METHODOLOGY

The present study was carried out in the in-patient Medicine Department of St.Martha’s Hospital after obtaining the ethical committee clearance from the Institutional Ethical Review Board of the hospital.
Informed consent was obtained from the conscious patients or from their relatives if the patients were unconscious.
The study was conducted for a period of 9 months.

STUDY CRITERIA
Inclusion Criteria
• All in-patients admitted due to poisoning in Medicine Intensive Care Unit and who were willing to participate in the study.

Exclusion Criteria
• All out-patients.
• Patients who were not willing to participate in the study.
• Poisoning due to long-term ingestion of drug.

Source of Data
Data was collected from case sheets, lab reports and prescriptions of poisoned patients admitted in MICU.

Method
The clinical pharmacist participated in the ward rounds, identified the poisoning cases and collected the data. A visit to emergency ward was given each day to check for any new cases.
Details of each poisoning case was recorded in the data collection form which included details of age, gender, region, literacy levels, occupation, marital status, habits, past history, month & time of exposure to poison, nature of poisoning, route of exposure, reasons for intentional poisoning, type of poison consumed, signs & symptoms, form of poison, treatment given before admission, current treatment including antidotes, lab reports, length of hospital stay and patient status after treatment.[Copy of the data collection form enclosed in annexure-III]
Based on the type of poisoning cases seen in the hospital, a set of guidelines were made for the management of cases due to the poisons consumed by the patients during the course of our study. [Guidelines enclosed in Annexure – I].

DISSCUSION

Ethical committee clearance was obtained from the Institutional Review Board of St. Martha’s Hospital, Bangalore, before the start of the study.
During the study period of 9 months [June 08 – Feb. 09], number of individuals who got admitted to Medical Intensive Care Unit due to poisoning were 55 patients.
The age of patients ranged from 12 to 84 years. Majority of the patient’s age ranged from 12-60 years followed by geriatric [above 60 years] and there was just one case [1.8%] in pediatrics. The maximum number of cases [41.81 %] were in the age group between 19-30 years as this age group is more prone to stress and challenges in life.
Among 55 patients who got admitted due to poisoning, 29(52.7%) were male and 26(47.3%) were female.
Majority of the cases i.e. 97% were from the urban area and 3% were from the rural area. This represents the increased stress of rapid urbanization.
The number of patients with primary education and more constituted 80% where as 20% of the patients were illiterate.
The nature of work of the individuals who consumed poison varied from a simple laborer [1.8 %] to businessmen [49 %], students [29.8%] and housewives [18.28 %]. Unemployed youth constituted 1.8 %.

Businessman topped the list followed by students and housewives which correlates well with the reasons submitted by the patients for consuming poison. 68% of the people were married, 29% were single followed by 3.6% widows.
The number of patients who were alcoholic was 29 [52.72%], out of which 27(93.1%) were male and 2(6.89%) were female. Smokers were 19 [34.54%] patients, out of whom 17(89.47%) were male and 2(10.52%) were female. 7 [12.74%] patients were neither smokers nor alcoholic, out of which 2(28.57%) were male and 5(71.42%) were female. Intentional poisoning was more with alcoholic male patients
Although majority of cases [73%] were first time poisoning ,19% of the cases was found to be second time and for 5.5%, it was third time which might indicate an underlying psychiatric illness in those patients with suicidal tendencies.
Number of admissions month wise indicates many admissions due to poisoning in December followed by January, October & November. However, significance of this in our study is unclear.
About 55 % cases were admitted in the night and 45 % during the day.
Out of 55 cases, 53 [96.4 %] were intentional poisoning and 2 [3.6%] were accidental poisoning. This finding is similar to the report by S.K. gupta et al.10
In 54 cases the poison was consumed orally and one case taken intravenously.

The poisons consumed were Organophosphrous compounds {Pesticide and Insecticide} 60%, overdose of drugs 34.5 % and cosmetics 1.8 %. Unidentified poison amounted to 3.60 %. Among OP compounds, Insecticides constituted 76.4%.
The reasons for intentional poisoning were found to be financial [52.7 %] followed by emotional disturbance [29 %], and family problems [18.2%].
The amount of poison consumed was known in 75% of cases whereas in 27% it was not known as patients were unconscious and not in a position to tell.
The high incidence of poisoning due to pesticides and Insecticide is [60%], [34.5%] cases were due to overdose of drugs consumed namely Diazepam, Acetaminophen, Diclofenac, Asprin, and Dicycloverine HCL. Out of these drugs CNS Depressants were 48% followed by Analgesic and Antipyretics 31.5 % and Antispasmodics drugs 10.52 %.
Out of 55 cases, neuromuscular symptoms involving CNS such as headache, dizziness, confusion, depression, irritability were seen in 52.2 %, GI symptoms such as nausea, vomiting, stomach cramps and stomach ache was seen in 61.81 %, CVS symptoms such as hypertension and hypotension were seen in 71 % of cases, respiratory symptoms such as breathlessness amounted to 78.18 % and 7.27 % patients presented with no symptoms, however there was considerable overlap of symptoms in patients.
The specific antidotes were used in 81.82% % of the cases. The specific antidotes that were used most frequently are Atropine [47.27 %], followed by PAM [29.09 %], N-Acetyl cystine [5.45 %]. General antidote such as charcoal was used in [18.18%] of the cases.

The concurrent medication prescribed were analgesics [83.63%] followed by antibiotic s [63.63%]. All the patient were given supportive management such as antacids and antiulcer medication, IV fluids, and oxygen therapy
In case OP poisons, strength of the antidote administered was adjusted on the basis of clinical condition of the patients.
Whereas in drug poisoning drug specific antidote was given [e.g. Flumazenil was administered in case of benzodiazepine poisoning, N-acetyl cystine was administered in acetaminophen poisoning etc].
In case of low dose drug poisoning e.g. Aspirin, it did not require alkali treatment and was managed by the supportive therapy.
Out of 55 cases, 54 patients were recovered and one patient expired because he was not able to reach on time for treatment.
The duration of stay in the hospital varied from three to thirty days depending on the type of poison. In case of Organophosphrous poisoning, hospitalization days ranged from 7 to 20 days with a mean of 10-15 days. Those who develop respiratory failure were put on ventilators. The mean stay was 15 days.
Most of the patients showed increase in blood count [23.6%] followed by decrease in Pseudocholinesterase [21.8%] in the cases of OP poisoning, whereas 40% of the patients showed the normal laboratory reports. Toxicology screen showed increase in blood count positive for benzodiazepine in case of benzodiazepine overdose.

All cases were admitted to MICU for observation and after recovery were discharged after psychiatric counseling.
Guidelines were prepared for the management of poisons that were consumed in our present study for the quick reference of the physicians.

CONCLUSION

Intentional poisoning is a major problem in urban setting leading to hospitalization and even death of individuals.
• Maximum incidence of poisoning was seen in patients from urban region in the age group of 19-30 yrs.
• Majority of the patients were literates with businessmen, followed by students and housewives.
• Most of the patients were alcoholics.
• Majority of the cases were due to intentional poisoning by oral route.
• OP compounds are the most common cause of poisoning (60 %) of cases with longest duration of stay of 10-15 days or more.
• Atropine was the antidote used in most of the cases (47.27%) followed by PAM (29.10 %)
• Although most of the patients were recovered, there was one death.

Having information about the commonly consumed poisons and guidelines for the management of the same would be helpful to the clinicians as a quick reference before treating the patients.

SUMMARY

By definition, anything which when used internally or on the body surface in a dose or in repeated doses, if acts chemically and physiologically, causing disturbances of body functions and leads to disease or death is a poison.
The growing incidence of poisoning has highlighted the importance of having special programs for poison control, and in particular the facilities for diagnosis, treatment, prevention of poisoning and ultimately making guidelines for the treatment.
The objectives of the present study are to study the pattern of poisoning cases at St. Martha’s Hospital, Bangalore and to make guidelines for the management of the same.
At the outset, ethical committee clearance was obtained from the Institutional Review Board of St. Martha’s Hospital, Bangalore.
Informed consent was obtained from the patients/their relatives before enrolling them in the study. Patients were enrolled in the study as per inclusion and exclusion criteria.
The clinical pharmacist participated in the ward rounds, identified the poisoning cases and collected the data from the case sheets, lab reports and prescriptions of the poisoned patients admitted to MICU.
During the 9 months study period, 55 patients were enrolled.
The age of the patients ranged from 12-84 yrs. Majority of the patients’ age ranged from 12 to 60 yrs followed by geriatrics (>60yrs) and there was just one case of pediatrics (1.81%). Out of 55 patients, 29(52.7%) were male and 26(47.3%) were female. 97% of the enrolled patients

were from the urban area whereas 3% were from rural area. The number of patients with primary education and more constituted 80% whereas the other 20% patients were illiterate.
Majority of the patients belonged to the category of businessmen (49%) followed by students (29.8%), and housewives (18.28%). Labourer and unemployed youth constituted 1.81%.
In the present study, 68% of the patients were married, 29% were single and 3% were widows.
Among 55 patients, the number of patients who were alcoholic was 29 [52.72%], out of which 27(93.1%) were male and 2(6.89%) were female. 19[34.54%] patients were smokers, out of whom 17(89.47%) were male and 2(10.52%) were female. 7 [12.74%] patients were neither smokers nor alcoholic, out of which 2(28.57%) were male and 5(71.42%) were female. Intentional poisoning was more with alcoholic male patients.
It was observed that 72.72% cases were first time poisoning; second time poisoning constituted 18.18% followed by 5.45% of the cases as third time poisoning.
Out of 55 cases, 53(96.4%) were intentional poisoning and 2(3.6%) were accidental poisoning.
In 54 cases, the poison was consumed orally and in one case the poison was taken intravenously.
From the data collected, it was observed that the poisons consumed were OP compounds (60%) followed by drug overdose (34.5%), cosmetics (1.8%) and unidentified poison amounted to 3.6%. In majority of the cases (52.7%), financial problems was found to be the main reason for intentional poisoning followed by emotional disturbances(29.10%) and family

problem (18.18%). The amount of the poison consumed was known in 75% of the cases, whereas in 25% of cases it was not known.
Among the 55 patients enrolled, the observed signs & symptoms were respiratory symptoms (78.18%), CVS symptoms (71%), GI symptoms (61%) CNS symptoms (52.2%) followed by no symptoms in 77.27% of patients.
Specific antidotes like atropine, PAM, N-Acetyl Cystine were used in 90% of the cases and the general antidotes like charcoal used in 10% of the cases.
In majority of the cases, analgesics (86.63%) were found to be used as concurrent medication followed by antibiotics (63.63%). Other concurrent medication constituted antiemetics, CNS depressants, diuretics, antiulcer.
In the OP poisoning, strength of antidote administered was adjusted on the basis of clinical condition of the patients, whereas in drug poisoning, drug specific antidote was given.
Out of 55 cases, 54 patients recovered and one patient expired as he was unable to reach on time for treatment.
The duration of the stay in hospital ranged from 3-30 days with the mean of 10-15 days depending on the type of poison. All cases were admitted to MICU for observation and upon recovery they were discharged after psychiatric counseling.
Guidelines were prepared for the management of poisons that were consumed by the patients in our present study for the quick reference of the clinicians.

GUIDELINES

Annexure -I
GUIDELINES FOR THE MANAGEMENT OF POISONING.
The primary goals of the guideline were to:
(1) Establish principles to aid in identifying a minimally toxic substance.
(2) To provide examples of substances that met the principles.
(3) To provide an approach to adding additional substances to the list.
General practitioners or family doctors are often the first medically qualified persons consulted during poisoning. Most patients with serious poisoning, if they survive, will sooner or later reach a hospital, ideally one with a wide range of medical facilities.
Emergency Patient Management
The care given to victims of poisoning is usually determined by the symptomatology produced. Generally speaking, aggressive treatment measures are not necessary if the patient is asymptomatic. Eight stages have been identified in the approach to the poisoned patient.44
Emergency management
This refers to the resuscitation and stabilization of the patient by paying attention to attaining a conscious state, maintenance of an open airway, adequate ventilation and oxygenation and ensuring adequacy of the hemodynamic state. This may sometimes require the use of specific antidotes in the very initial stages of management.
Clinical evaluation
This includes obtaining the history, performing a physical examination and laboratory evaluation and an assessment of major toxic signs such as coma, cardiac arrhythmias, metabolic acidosis, gastrointestinal disturbances and seizures. Completion of

clinical evaluation would allow the patient to be triaged into one of three categories, viz. mild, moderate or severe. The overall management of each of these categories of patients is as described in Annexure I.
Decontamination of the patient –
This can be gastrointestinal, topical or respiratory. Many methods of decontamination are available. The method used would depend on the route of poisoning and known responses of the toxic agent to the effect of the decontaminants. Whatever procedure used should be carried out aggressively so as to limit the toxic effects of the poison.
Antidote
Though specific antidotes are relatively uncommon, administering these should be done as early as possible not only to reverse pharmacological effects of the poison, but also to displace poisons from target organ receptor sites or to deactivate the poison by binding irreversibly to the molecule.
Enhanced elimination of absorbed poison
This is usually resorted to when antidotes are not available. Methods of enhanced elimination include forced diuresis, alkalinisation or acidification of the urine, dialysis, hemoperfusion and hyperbaric oxygen.
Supportive therapy
This may be all that is required in some poisoned patients. During this phase, frequent monitoring of vital signs, fluid and electrolyte balance, cardiorespiratory support as indicated, and aggressive nursing care to preserve integrity of body systems, should all be carried out.

Observation and disposition - Observation may be necessary to evaluate delayed effects of certain poisonings, to manage an underlying disease that has been exacerbated because of the overdose and to evaluate and treat complications. Final disposition would depend on the results of this further observation.45
After care - Management of the poisoned victim is not only the relief of the physical effects of the toxic agent on the human body. Many victims of poisoning have lead acutely stressful lives that lead them to overdose themselves with various medicaments and chemicals. They require emotional support through all phases of emergency management and very early intervention of the medical social worker and perhaps even a psychiatrist. Follow-up by both may be required even after discharge from the hospital. Victims of accidental exposure to toxic agents have undergone an acutely stressful situation. Rather than only providing psychological support to those with over symptoms of post-traumatic stress disorder, one has to presume that all have potential for stress disorders. Therefore stress counseling for all has to be planned for. Such counseling must continue in the post-hospital phase of management.46
Antidotes and their availability
Antidotes may play an important role in the treatment of poisoning. While good supportive care and elimination techniques may, in many cases, restore a poisoned patient to good health and stabilize his or her body functions, the appropriate use of antidotes and other agents may greatly enhance elimination and counteract the toxic actions of the poison. In certain circumstances they may significantly reduce the medical resources otherwise needed to treat a patient, shorten the period of therapy, and, in some cases, save a patient from death. Thus, antidotes may sometimes reduce the overall burden on the health service of managing cases

of poisoning. In areas remote from good hospital services, and particularly in developing countries that lack adequate facilities for supportive care, antidotes may be even more essential in the treatment of poisoning.48
Antidotes needed immediately must be stocked at all hospitals, as well as in health centers or doctors' surgeries if the nearest hospital is some distance away. It may also be necessary to have certain antidotes available at places of work for use under medical supervision (e.g. in factories using cyanide). Antidotes needed within 2 hours can be stocked at certain main hospitals; patients can be taken to these hospitals for treatment or the antidotes can be transported within the time limit to the health facilities at which treatment is provided. Antidotes needed within 6 hours may be stocked at central regional depots, provided that there are adequate facilities for transporting them within the time limit. For all categories of antidotes, there is the further option of keeping a small amount, sufficient to start treatment, in stock locally, further supplies being obtained from a central source as required.49
The economic management of the supply of antidotes could be improved by a central, preferably computerized, record system, regularly updated. The need to hold contingency stocks of antidotes for response to chemical disasters should be considered, especially in areas where large amounts of potentially hazardous chemicals are being manufactured, used, transported or stored.

GUIDELINES FOR THE MANAGEMENT
OF POISONING

GUIDELINES FOR THE MANAGEMENT OF
ORGANOPHOSPHROUS COMPOUNDS
Organophosphrous compounds range from slightly to highly hazardous.
Clinical Features
Anorexia, nausea, headache, anxiety and restlessness, mental confusion followed by bradycardia, respiratory distress, vomiting, abdominal cramps, excessive cold sweating, salivation and finally muscular twitching, urinary incontinence, ‘pin-point’ pupils and coma. Death is normally due to respiratory failure.
Management of Toxicity
• Maintain airway, treat coma, seizures and hydrocarbon pneumonitis if they occur.
• Perform gastric lavage; administer activated charcoal and a cathartic. Do not induce emesis.
• If skin is contaminated, it should be washed with alkaline soap which will not only remove but also help to hydrolyze the phosphate ester.
Antidote:
• Administer IV atropine 2-4mg; repeat every 15mins until the pupils start to dilate. Then give IV pralidoxime 1-2g (25-50mg per kg body weight for children) over 2 mins. Another 1-2 dose can be given if necessary. Max. dose 12g/24hrs. See pg 134.
• Maintain atropinization.
• Give the following supportive treatment if necessary:
- Administer slow IV diazepam 5-10mg (0.2-0.5mg for children) for convulsions, extreme restlessness and excitement.
- Give IV saline drips continuously.

- Remove bronchial hypersecretion by repeated bronchial aspiration and postural drainage.
- Give oxygen if breathless.
- Sample blood for cholinesterase activity.
- Monitor for at least 24 hours.
Caution:
- Ensure cyanosis or severe hypoxia is corrected before atropinization.
- Do not give morphine, aminophylline and phenothiazines such as promazine and chlorpromazine.
Laboratory tests:
Cholinesterase level, electrolytes, glucose, BUN, creatinine, hepatic transaminases, prothrombin time (PT), ECG monitoring.
List of Organophosphrous insecticides are given in Annexure II

GUIDELINES FOR THE MANAGEMENT OF (PESTICIDE) CARBAMATE POISONING
Carbamate insecticides are moderately hazardous.
Clinical Features
As for Organophosphorus compounds but of lesser intensity.
Management of Toxicity
• Maintain airway, treat coma and seizures if they occur.
• Perform gastric lavage for large ingestions.
• Wash contaminated skin with soap and water.
• Irrigate eyes with water or saline.
• Give IV saline to correct dehydration and electrolyte imbalances.
• Keep patient under constant observation for at least 24 hours.
Caution:
• Ensure cyanosis and severe hypoxias are corrected before atropinization.
• Pralidoxime is generally not recommended for carbamates poisoning.
• Avoid CNS depressants such as reserpine, chlordiazepoxide and phenobarbitone which may potentiate Carbamate poisoning.
Antidote: Administer IV atropine 2-5 mg and repeat every 15 mins until mydriasis occurs.
Laboratory tests: Red blood cell cholinesterase, electrolytes, glucose, BUN,
creatinine, arterial blood gasses

GUIDELINES FOR THE MANAGEMENT OF DRUG POISONING
Analgesics, Antipyretics and Anti-inflammatory Agents
Analgesics and Antipyretics
PARACETAMOL (ACETAMINOPHEN)
Paracetamol is widely used as an OTC analgesic, antipyretic, and in cold remedies. It may also be combined with other analgesics such as codeine.
Preparations containing paracetamol
Dhamol , Dolo , Tempra, Disprol , Panadol, Tylenol, Crocin, Calpol , Metacin
Toxicity
Hepatotoxicity is caused by the reactive metabolite N-acetyl-pbenzoquinoneimine (NABQI) produced by the cytochrome P450 enzyme. Normally the NABQI is conjugated with glutathione. In overdose, the excess NABQI reacts with hepatocytes causing necrosis.
Acute toxicity: Acute ingestion of 140 mg/kg in children and 6 g in adult is potentially toxic. Children <10 years are less susceptible to hepatotoxicity. It has been suggested that conjugation of NABQI with glutathione is more efficient in children than in adults. Chronic
alcoholics and patients with induced cytochrome P450 are more susceptible to hepatotoxicity since there will be an increase production of NABQI.
Chronic toxicity: Children are more susceptible to chronic toxicity presumably because they are less able to clear paracetamol by the other main conjugation pathways due to saturation. In alcoholics, chronic toxicity has been reported with daily consumption.

Clinical Features
Early signs: anorexia, nausea, vomiting. After 24 hours: Increase in prothrombin time (PT) and transaminases indicating hepatic necrosis, encephalopathy, metabolic acidosis, renal failure may occur with or without liver failure, myocardial damage, coma.
Management of Toxicity
• Supportive treatment
• Treat spontaneous vomiting so that activated charcoal may be administered orally.
• Support hepatic and renal failure, coma if they occur
• Obtain 4-hour post-ingestion serum sample for paracetamol concentration to assess severity of toxicity
• If paracetamol concentration falls above the treatment line .Treatment line is lower for chronic alcoholics, or if serum concentration is not immediately available, start treatment with antidote N-acetylcysteine. Early treatment is imperative as antidote is most efficacious within 8 hours of ingestion. However, in view of recent clinical trials where late N-acetylcysteine was found to be beneficial, the recommendation is that it should be given even when patient is already in liver failure. Nomogram is for acute toxicity and not chronic toxicity.51
• Gastric decontamination. Administer activated charcoal and cathartic. Since activated charcoal may adsorb antidote N-acetylcysteine, it is considered prudent to administer N-acetylcysteine by the intravenous route, as opposed to the oral route. Gastric lavage is not necessary if charcoal is given promptly.

Antidotes & Therapeutic drugs for management of Acetaminophen (Paracetamol) Poisoning.
ANTIDOTE: - Acetylcysteine (N-Acetylcysteine, NAC)
General Treatment
Intravenous: 150 mg/kg IV in 200 mL 5% dextrose over 15-30 min followed by 50 mg/kg in 500 mL over 4 h then 100 mg/kg in 1000 mL over 16 hr or Methionine Oral: 2.5g initially, followed by 2.5g every 4 hours for another 3 doses.
Note: Methionine is NOT the antidote of choice as its efficacy has not been established.
Laboratory tests: Serum paracetamol concentration with respect to time of ingestion is used to assess severity of toxicity. These levels must be determined immediately. Liver function panel (AST, ALT, bilirubin and PT) should be done daily and for 3 days until they return to normal. Other tests: FBC, creatinine, glucose, electrolytes and BUN.
Continue acetylcysteine therapy when acetaminophen concentration is on or above dashed line. Plasma or Serum Acetaminophen Concentration (μg/mL) (4h, 200 μg/mL)
If acetaminophen concentration falls above solid line, hepatotoxicity is PROBABLE
If acetaminophen concentration falls between dashed and solid lines, hepatotoxicity is POSSIBLE (12h, 50 μg/mL)

Specification of Acetaminophen poisoning
Indications - Paracetamol overdose
Dosage -IV to be given in glucose 5% w/v intravenous infusion, initially 150 mg / kg in 200 ml over 15 minutes, followed by 50 mg / kg in 500 ml over 4 hours, then 100 mg / kg in 1000 ml over 16 hours
Method of Use / Administration - IV infusion
Contraindications - Known hypersensitivity to the drug
Adverse Reactions - Rash, pruritus, nausea, vomiting, wheezing, angioedema, tachycardia, bronchospasm, hypertension, flushing and hypotension, especially with IV administration.
Drug Interactions - Not know
Note:
1) This antidote is most efficacious within 8 hours of ingestion and should be given as soon as possible. Re-assess when serum concentration result is available.
2) Late administration of NAC has been found to be beneficial. Therefore, NAC is still recommended in patients who are already in liver failure.
In case of overdose:
Minimum Toxic - Not known
Maximum Tolerated Dose - 5 g/day for 3 months
Sign & Symptoms of toxicity – Anaphylactic reactions - urticaria, hypotension
Management of Toxicity - Aimed at reversing anaphylactic reactions and controlling nausea & vomiting. Supportive treatment such as airway support, maintaining vital signs and reversal of bronchospasms, may be required. Emesis, gastric lavage and/or activated charcoal may be applied if the overdose is detected soon after ingestion.52

ASPIRIN POISONING
Salicylates and their usual contents in dosage forms
Aspirin, salicylic acid, methyl salicylate, glycol salicylates (2-30% for external use)
Preparations containing salicylate
Product Contents:- Aspirin Aspro Acetylsalicylic acid , Counterpain Methyl salicylate, Disprin 500mg , Ecospirin 75 mg, 150 mg, 325 mg, Monospirin 150 mg.
Toxicity
Toxic oral dose: 300 - 500 mg/kg (salicylates)
Toxic effects appear at varying plasma levels depending on the duration of poisoning but are uncommon below 300mg/L.
Toxic blood levels: >500 mg/L in adults , >300 mg/L in children
Severe poisoning blood levels: >1000 mg/L in adults ,>600 mg/L in children.
Chronic poisoning: Not well correlated with serum concentrations. Chronic users of salicylates showing confusion and lethargy and levels >600 mg/L require haemodialysis.
Clinical Features
Hyperpnoea, acid-base imbalance, mild pain in throat and stomach, vomiting particularly in infants and children, sweatiness, hypoprothrombinaemia, tinnitus (which may sometimes lead to deafness), delirium, convulsions, oliguria, uraemia, cyanosis, pulmonary oedema, respiratory failure. Coma is not uncommon and indicates very severe poisoning.
Management of Toxicity
• Maintain airway,
• Treat seizures, coma, metabolic acidosis and dehydration if they occur.

• Gastric lavage is not necessary after small ingestions (i.e. <200 – 300 mg/kg) if activated charcoal can be given promptly.
• Administer activated charcoal. Multiple doses of activated charcoal would be reasonably likely to enhance elimination of a significant amount of absorbed salicylate.
• In severe poisoning, begin hydration in the first hour with intravenous fluids 400mL/m2. Maintain acid/base balance.
• Treat metabolic acidosis with IV sodium bicarbonate.
• Forced alkaline diuresis can be considered if plasma- salicylate concentration reaches toxic levels (>500 mg/L). Difficult to achieve in critically ill patients. There are currently other more efficient methods of enhancing elimination, such as multi-dose activated charcoal and hemodialysis.
Antidotes: No specific antidotes. Sodium bicarbonate is given to prevent acidaemia and to promote salicylate elimination by the kidneys.
Laboratory tests: Plasma salicylate levels (obtain stat and serial serum levels), acid-base status (pH of arterial blood), arterial blood gases, urinalysis, FBC, liver function tests, prothrombin time.

GUIDELINES FOR THE MANAGEMENT OF {NSAIDS} POISONING
NONSTEROIDAL ANTI-INFLAMMATORY AGENTS
NSAIDs fall into several subgroups based on chemical structure:
• Acetic acid: diclofenac,
• Anthranilic acids (fenamates): meclofenamate, mefenamic acid
• Indole(indene acetic acid): etodolac, indomethacin, sulindac
• Propionic acids: fenbufen, flurbiprofen, ibuprofen, ketoprofen, naproxen
• Oxicams: piroxicam
• Pyrazolones: phenylbutazone

Preparations containing NSAIDs

Product Contents

Diclofenac Na (voveron) (50 mg, 100 mg)
Diclofenac Na (25 mg)
Indomethacin (Macrocid) (75 mg)
Piroxicam (20 mg)
Ibuprofen (200-600 mg)
Ketoprofen (100mg)

Pericam Piroxicam (10 mg)
Ponstan Mefenamic acid (250-500 mg)
Spasmo Proxivon (400 mg)

Toxicity
Generally, significant symptoms occur after ingestion of more than 5 – 10 times the usual therapeutic dose.

Clinical Features
• With most NSAIDs: Anorexia, nausea, vomiting, abdominal pain, haematemesis, drowsiness, lethargy, ataxia, tinnitus, disorientation.
• With more toxic agents e.g. Phenylbutazone and oxyphenbutazone ,mefenamic acid, piroxicam, and massive ibuprofen overdose:- acidosis, hepatic dysfunction, hypoprothrombinaemia, convulsions, cardiopulmonary arrest, renal failure, coma
Management of Toxicity
• Supportive management.
• Administer activated charcoal. Gastric emptying is not necessary for most ingestions if activated charcoal can be given promptly. Perform gastric lavage for massive overdoses.
• Antacids may be used for mild GI upset.
• Management is mainly symptomatic.
Clinical Aspects of NSAID Poisoning
Organ Manifestation Management
Gastrointestinal: - Anorexia, nausea, Non absorbable antacids vomiting abdominal e.g. aluminium and pain, gastric mucosal magnesium antacids irritation H2-receptor antagonists,
proton pump inhibitors, misoprostol .Hepatobiliary hepatic dysfunction, hyperamylasemia
Respiratory Hyperventilation: - Respiratory depression Mechanical ventilation
Cardiovascular :- Sinus tachycardia,Hypotension IV fluids, vasopressors, cardiovascular
Antidotes: no specific antidotes. Vitamin K may be used for patients with elevated prothrombin time caused by hypoprothrombinaemia.
Laboratory tests: renal and liver function tests, FBC, electrolytes, blood glucose, PT, urinalysis

GUIDELINES FOR THE MANAGEMENT OF BENZODIAZEPINES POISONING
ANTICONVULSANTS / SEDATIVES, CENTRAL NERVOUS SYSTEM DRUGS
Preparations containing benzodiazepines
Chlorazepate, chlordiazepoxide, clonazepam, diazepam, flurazepam, lorazepam, nitrazepam, oxazepam, temazepam, triazolam, midazolam
Product Content
Alzolam Alprazolam, Valium Diazepam, Ativan Lorazepam, Benpine, Librium, Chlordiazepoxide, Domar Pinazepam, Dormicum Midazolam,
Indications: Anxiety or agitation due to intoxication by sympathomimetic or hallucinogenic drugs. Acute seizure activity or status epilepticus due to convulsant drug overdose or idiopathic epilepsy. Excessive muscle rigidity or contractions, caused by black widow envenomation or strychnine poisoning. Cardiotoxicity due to chloroquine overdose .
Alcohol or sedative-hypnotic withdrawal
Dosage - Anxiety / Agitation: - 0.1 - 0.2 mg/kg, intravenous. Repeat as needed every 1-4 hours.
Convulsions: 0.1 - 0.2 mg/kg intravenous, every 10-15 minutes to a total dose of:
- Adults, 30 mg intravenous.
- Older children, 10 mg intravenous.
- Young children, 5 mg intravenous.
Muscle Relaxation - 0.1 - 0.2 mg/kg, intravenous. Repeat as needed every 1-4 hours.
Chloroquine Intoxication - 1 mg/kg, intravenous.
Alcohol Withdrawal - Initial 5-10mg, intravenous. May be repeated with 5mg every 10 minutes.

Method of Use / Administration: - Administer by slow intravenous injection; do not use intramuscular route. Rectal administration (5 mg) can be used to control status epilepticus in young children. Patients on high-doses of diazepam (eg. 1 mg/kg for cardiotoxicty) are likely to experience apnoea; they should be incubated and have their ventilation controlled.
Contraindications - Known sensitivity to benzodiazepines.
Adverse Reactions - Respiratory arrest due to rapid and/or high-dose IV administration.
- Cardiorespiratory depression caused by the diluents.
Drug Interactions - Potentiates other CNS depressant drugs. Causes false-negative reaction for some urine glucose test strips. Response reduced by flumazenil
Toxicity
Toxic effects are minimal. In general, large quantities can be taken without causing serious illness and uncomplicated recovery has been reported after ingestion of massive doses. In contrast, respiratory arrest has been reported after ingestion of 5 mg of triazolam. Rapid intravenous injection of benzodiazepines may cause respiratory depression.
Clinical Features
All benzodiazepines produce similar effects. Coma seldom deeper than grade 2 and lasting less than 24 hours may follow. Hypothermia may occur. Mild hypotension and respiratory depression may occur.
Management of Toxicity
• Maintain airway, treat coma hypotension, hypothermia if they occur.
• Administer activated charcoal. Gastric decontamination is probably valueless unless more than 30 tablets or capsules have been taken within 4 hours.
• Correct dehydration

• Toxic effects of benzodiazepines taken alone are so minimal that little treatment is necessary.
Antidotes: Flumazenil, a benzodiazepine antagonist. It reverses the CNS depression, and can be used to confirm suspected diagnosis of benzodiazepine overdose or exclude benzodiazepine intoxication as a cause of CNS depression in an undiagnosed patient. However, flumazenil administration may precipitate seizures in poisoning with combinations of benzodiazepines and tricyclic antidepressants.
Laboratory tests: Poor correlation between plasma levels and severity of intoxication; FBC, electrolytes, blood glucose, BUN, creatinine, arterial blood gases.
Note: Since benzodiazepine overdose is rarely fatal, the role of flumazenil in routine management has yet to be established.

GUIDELINES FOR THE MANAGEMENT OF CARBAMAZEPINE POISONING
Preparations containing Carbamazepine
Product Contents
Tegretol Carbamazepine 200 mg tab, 200 mg CR tab, 100 mg/5 mL syrup, 125mg .Neurotop Carbamazepine 200 mg cap, 300 mg retard tab Carzepin Carbamazepine 200 mg tab
CENTRAL NERVOUS SYSTEM DRUGS
Toxicity
Patients have survived ingestion of 80 g but death has also been reported after ingestion of 6-60 g. Other toxic manifestations occur at higher doses. Peak serum levels have ranged from 23 to 93 mcg/mL in obtunded or comatose patients.
LD50 (oral) mouse : >500 mg/kg
Clinical Features
• Ingestion of large amounts produces an unpredictable clinical course. Seizures, slurred speech, myoclonus, coma, respiratory depression, apnoea, abnormal deep tendon reflexes, nystagmus, ataxia, encephalopathy, hypertension or hypotension, prolonged PR, QRS and QT intervals, dystonia and ballistic and athetoid posturing have been reported.
• A waxing and waning sensorium, seemingly corresponding to plasma levels may occur a few days following carbamazepine overdose. Cyclic CNS depression and a protracted clinical course should be expected57
Management of Toxicity
• Maintain airway, treat coma, hypertension or hypotension if they occur
• Perform gastric lavage for large and recent ingestions.
• Administer multiple doses of activated charcoal.

•Charcoal hemoperfusion may be indicated if there is a worsening of clinical condition in a patient treated with multiple doses of charcoal.
• Hemodialysis and peritoneal dialysis are ineffective due to the high degree of protein binding
•Forced diuresis is of no benefit as only 2% of Carbamazepine and 1% of the epoxide metabolite are excreted in the urine.
Antidotes: There are no specific antidotes for over dosage. Physostigmine which has been used to diminish dystonic posturing, has little or no effect on other signs or symptoms of poisoning. The dystonic effects are not in any case life threatening and generally resolve spontaneously. Excessive physostigmine may lead to cholinergic toxicity (e.g. bronchospasm). Anticholinergic side effects are not a serious problem in poisoning and there is, therefore, little rationale for use of physostigmine.58
Laboratory tests: FBC, vital signs, electrolytes, renal function, liver enzymes, arterial blood gases and ECG should be monitored periodically in the chronically treated patient and for at least 24 hours after admission in the overdose patient.

GUIDELINES FOR THE MANAGEMENT OF COSMETIC POISONING
{LIFEBOY SOAP POISONING}
Detergents are synthetic surface active agents classified as:
-Anionic/nonionic type (used in soap powders, shampoo, bar soap and liquid detergents).
- Cationic type (used in antiseptic and disinfectant products, fabric softeners).
Many such products may contain bleaching agents, anti-bacterial or enzymatic agents.
ANIONIC/NONIONIC DETERGENTS
Toxicity
- Anionic/nonionic detergents are only mildly irritating.
- Cationic detergents may be caustic and more hazardous.
- Fatal dose: No information available.
- Mortality and morbidity are rare.
Clinical Features
• Nausea, vomiting, diarrhoea, intestinal distension
• Rarely, dehydration and electrolyte abnormalities.
Management of Toxicity
• Give oral fluids in small amounts, allow vomiting to occur.
• Administer IV fluids to correct dehydration and electrolyte imbalance if necessary.
• If corrosive injury is suspected, consult a gastroenterologist for possible endoscopy.
• If symptomatic hypocalcaemia occurs administer IV calcium
• Activated charcoal is ineffective.
Antidotes: None.

Laboratory tests:
• There are no specific blood or urine levels.
• It is useful to perform FBC and test for electrolytes, glucose, calcium & phosphate (after ingestion of phosphate-containing products).
CATIONIC DETERGENTS
Common cationic detergents
Pyridinium compounds Cetalkonium chloride,Cetrimide,Cetrimonium bromide,Cetylpyridi-nium chloride,Stearalkonium chloride ,Quaternary ammonium,Benzalkoniumchloridecompo-unds, Benzethonium chloride, Quinolinium compounds, Dequalinium chloride
Toxicity
Deaths have been reported with doses of between 30mg/kg to 400mg/kg depending on which cationic detergent was ingested.
Clinical Features
• Corrosive burns of mouth, pharnyx and oesophagus.
• Nausea, vomiting, diarrhoea, pulmonary oedema, hypotension, metabolic acidosis, CNS depression, convulsions
Management of Toxicity
• Maintain airway
• Administer milk or water to dilute
• Administer activated charcoal followed by cathartic.
• Do not perform gastric lavage or emesis because of corrosive effects.

• If methaemoglobin occurs, administer methylene blue.
• Monitor and treat seizures, hypotension, pulmonary oedema
• If corrosive injury is suspected, consult a gastroenterologist for endoscopy
• Dialysis and diuresis are not effective
Antidote: None
Laboratory test:
• There are no specific blood or urine levels.
• It is useful to perform FBC and test for electrolytes, glucose, calcium & phosphate (after ingestion of phosphate-containing products).

LIST OF ANTIDOTES
ATROPINE
Indications: Organophosphate / Carbamate / insecticide poisoning. Drug-induced atrioventri-cular conduction impairment (e.g.digitalis, beta-blockers,organophosphates, carbamates, physostigmine)
Dosage: Drug-induced bradycardia. 0.5 to 1 mg, intravenously. Children 0.01 -0.05 mg/kg up to a maximum dose of 0.5 mg IV Dose repeated as necessary, up to a maximum of 3 mg in adults (additional doses not expected to be effective)
Brand available: ATP, Tropine 0.6mg/ml
Method of Use / Administration: Administer by IV injection. Treatment aimed at achieving satisfactory relief of clinical symptoms
Contraindications: Close-angle glaucoma, Hypertension, tachyarrhythmias, congestive heart failure, coronary artery disease, Obstructive uropathy, Myasthenia gravis
Adverse Reactions: Dry mouth, blurred vision, cycloplegia, mydriasis, urinary retention, tachycardia, (aggravation of) angina, constipation,
Drug Interactions: Increased atropinisation when used concurrently with pralidoxime, Additive effects with other antimuscarinics and antihistamines, Delayed gastric motility reduces drug absorption from the GI tract
In case of overdose:
Minimum & Maximum Doses: Variable & unpredictable. Judgment on toxicity should be
based on clinical signs & symptoms, rather than on quantitative values.

Sign & Symptoms: CNS effects - delirium, hallucinations, coma, seizures of Toxicity, disordered body temperature levels, hyperthermia/ hypothermia, mydriasis, peripheral vasodilatation, dry mouth, urinary retention, dilated pupils, diminished bowel signs, CVS effects - tachycardia, hypertension, arrhythmias, shock, cardio respiratory arrest59

PRALIDOXIME (2-PAM, PYRIDINE ALDOXIME)
Indications: Organophosphate poisoning, usually insecticides
Dosage: 1 - 2 g (children 25 - 50 mg / kg), intravenously. Repeat dose in 1 hour if muscle weakness is not relieved. Repeat dose every 4 to 12 hours as needed, to control nicotinic symptoms, especially for long acting organophosphates. Max. dose is 12 g/24 hours.
Method of Use / Bolus
Administration: Administer over 5 - 10 minutes at a rate not exceeding 200 mg/min. (4 mg / kg / min in children) Infusion. Give in 100 mL of normal saline, over 15 - 30 minutes. Maintain therapy with careful observation of clinical response
Contraindications - Patients with myasthenia gravis. Use with caution in patients with renal impairment
Adverse Reactions - Nausea, headache, dizziness, diplopia, hyperventilation. Rapid administration may result in tachycardia, laryngospasm, muscle rigidity and transient
neuromuscular blockade.
Drug Interactions - Enhanced atropinisation when used with atropine and related drugs.
In case of overdose:
Minimum Toxic Dose: Not known.
Maximum Tolerated Dose: Not known.
Sign & Symptoms - Neuromuscular blockade of Toxicity - Visual disturbances, Asystole. CVS effects - transient hypertension, ECG changes.
Management: Supportive treatment, only for critical symptoms.

CHARCOAL (ACTIVATED)
Indications: Ingestion of drug overdoses or poisons, High serum levels of drugs & toxins with long halflives useful in cases where rapid elimination would be beneficial.
Dosage:
Initial dose: (Amount of ingested drug / toxin unknown) 1 g/kg body weight. (Amount of ingested drug / toxin known) 10 times the amount of ingested toxin by weight, in divided doses if necessary.
Repeat dose: 15-20 g, every 4-8 hours.
Method of Use / Administration: Administer orally or through a nasogastric tube. First dose of activated charcoal is preferably given together with sorbitol as a cathartic.Subsequent doses should be pure activated charcoal, and the cathartic is given only when no bowel movement occurs.
Note: a cathartic should NOT be given with every dose. In young children, usually only one dose of cathartic is needed.
Contraindications: Gastrointestinal obstruction, Ingestion of strong acids or alkalis (charcoal makes endoscopic evaluation more difficult)
Adverse Reactions: Constipation; diarrhoea, dehydration and hypernatraemia due to the concurrent use of cathartics. Distention of the stomach; risk of aspiration. Intestinal bezoar / particulate concretion with obstruction.
Drug Interactions: Reduces, prevents and/or delays absorption of orally administered drugs, including antidotes.

In case of overdose: This substance is not believed to cause any adverse effects if an overdose is ingested.
Note: Activated charcoal is available commercially in 2 forms : those formulated in sorbitol (cathartic) and plain. Do not administer another cathartic when using sorbitol type

ACETYLCYSTEINE (N-ACETYLCYSTEINE, NAC)
General Treatment: Intravenous: 150 mg/kg IV in 200 mL 5% dextrose over 15-30 min followed by 50 mg/kg in 500 mL over 4 h then 100 mg/kg in 1000 mL over 16 hr OR Methionine Oral: 2.5g initially, followed by 2.5g every 4 hours for another 3 doses.
Note: Methionine is NOT the antidote of choice as its efficacy has not been established.
Brand available :- Cilol-200mg/ml, Mucare 200mg/ml, Mucomex 6 mg tab, Nacfil 600 mg.
Specification of Acetaminophen poisoning:
Indications: - Paracetamol overdose
Dosage -IV to be given in glucose 5% w/v intravenous infusion, initially 150 mg / kg in 200 ml over 15 minutes, followed by 50 mg / kg in 500 ml over 4 hours, then 100 mg / kg in 1000 ml over 16 hours
Method of Use / Administration - IV infusion
Contraindications - Known hypersensitivity to the drug
Adverse Reactions - Rash, pruritus, nausea, vomiting, wheezing, angioedema, tachycardia, bronchospasm, hypertension, flushing and hypotension, especially with IV administration
Drug Interactions - Not known
Note:
1) This antidote is most efficacious within 8 hours of ingestion and should be given as soon as possible. Re-assess when serum concentration result is available.
2) Late administration of NAC has been found to be beneficial. Therefore, NAC is still recommended in patients who are already in liver failure.

In case of overdose:
Minimum Toxic - Not known
Maximum tolerated dose - 5 g/day for 3 months
Sign & Symptoms of toxicity - Anaphylactic reactions - urticaria, hypotension
Management of Toxicity - Aimed at reversing Anaphylactic reactions and controlling nausea & vomiting
Supportive treatment such as airway support, maintaining vital signs and reversal of bronchospasms, may be required. Emesis, gastric lavage and/or activated charcoal may be applied if the overdose is detected soon after ingestion.60

REFERENCES

1. Henry JA, Wiseman HM. General information on poisons and poisoning. In: Management of poisoning: A handbook for health care workers. New Delhi: AITBS publishers; 2004: 3-11.
2. Henry JA, Wiseman HM. How poisoning happens. In: Management of poisoning: A handbook for health care workers. New Delhi: AITBS publishers; 2004: 13-18.
3. Chatterjee B, Banerjee DB. Accidental poisoning in children. Indian Journal of Pediatric 1981; 18: 157-62.
4. Reddi YR, Rajeswaramma V. Accidental kerosene poisoning in infants and children. Indian Journal of Pediatric 2004; 4: 141-44.
5. Singh D, Tyagi S. Changing trends in acute poisoning in Chandigarh zone: A 25 years autopsy experience from a tertiary care hospital in northern India. Am J Forens Med Pathol. 1999; 20: 203-10.
6. Roberts DM, Karunarathna A, Buckley NA, Manuweera G, Sheriff MH, Eddleston M. Influence of pesticide regulation on acute poisoning deaths in Sri Lanka. Bull World Health Organ. 2003; 81(11): 789-98.
7. Singer CM. Child & Adolescent Psychiatry. In: Goldman HH, editor. Review of General Psychiatry. California: Lange Medical Publication; 1984: 642-48.
8. Gupta SK. National Poison Information Center, All India Institute of Medical Sciences [AIMS]. 2001 Dec; 1(1).

9. Tandon GU, Qureshi, Panday DN, Agarwal Ajay A. Profile of poisoning cases admitted in S.N. Medical college hospital, Agra. Journal of Forensic Medicine & Toxicology. 1996; 8: 10-12.
10. Gupta SK, Peshin SS, Srivastava A, Kaleekal T, Pandian TV. Epidemiological patterns of poisoning in India. Pharmacoepidemiology & Drug safety 2002; 11: 73-74.
11 Vaswani VR, Vaswani RN. Pattern of acute poisoning in a medical unit in central Srilanka. Int. J. Epidemiol 2008; 18(2): 228-32.
12 Hettiarachchi J, Kodithuwakku GCS. Pattern of poisoning in rural Sri Lanka. Int. J. Epidemiol 1989; 18: 418–422.
13 Senanayake N, Peiris H. Mortality due to poisoning in a developing agricultural country: trends over 20 years. Hum Exp Toxicol. 2007 Oct; 14(10): 808-11.
14 De Alwis LB, Salgado MS. Agrochemical poisoning in Sri Lanka. Forensic Sci Int. 2007 Jan; 36(1-2): 81-9.
15 Singh B, Unnikrishnan B. A profile of acute poisoning at Mangalore (South India). Journal of Clinical Forensic Medicine 2007; 13(3): 112 – 16.
16 Senanayake N, Karalliedde L. Pattern of acute poisoning in a medical unit in central Sri Lanka. Forensic Sci Int. 2007 Jan; 36(1-2):101-04.
17 Khadka SB, Khadka SB. A study of poisoning cases in emergency. Kathmandu Univ. Med. J. 2005 Dec; 3(4): 388-91.

18 Ramisetty Mikler S, Mains D, René A. Poisoning hospitalizations among Texas adolescents. Tex Med. 2005 May; 101(5): 64-71.
19 Dieserud G, Loeb M, Ekeberg O. Suicidal behavior in the municipality of Baerum, Norway: a 12-year prospective study of parasuicide and suicide. Suicide Life Threat Behav. 2006; 30(1): 61-73.
20 Guloglu C, Kara IH. Acute poisoning cases admitted to a university hospital emergency department in Diyarbakir, Turkey. Hum Exp Toxicol 2005 Feb; 24(2): 49-54.
21 Tagwireyi D, Ball DE, Nhachi CF. Drug and toxicology information service, poisoning in Zimbabwe: a survey of eight major referral hospitals. J Appl Toxicol. 2002 Apr; 22(2): 99-105.
22 Goksu S, Yildirim C, Kocoglu H. Characteristics of acute adult poisoning in Gaziantep, Turkey. J Toxicol Clin Toxicol. 2005; 40(7): 833-37.
23 Burns Jane M, Patton George C. Preventive interventions for youth suicide: a risk factor-based approach. Australian and New Zealand Journal of Psychiatry 2005 June; 34(3): 388-407.
24 Kelly CB, Weir J, Rafferty T, Galloway R. Deliberate self-poisoning presenting at a rural hospital in Northern Ireland 1976-1996: relationship to prescribing. Eur Psychiatry 2000 Sep; 15(6): 348-53.

25 Turkey, Ozkose Z, Ayoglu F. Etiological and demographical characteristics of acute adult poisoning in Ankara. Hum Exp Toxicol. 2006 Oct; 18(10): 614-18.
26 Tufekçi IB, Curgunlu A. Characteristics of acute adult poisoning cases admitted to a university hospital in Istanbul. Hum Exp Toxicol. 2004 Jul; 23(7): 347-51.
27 McLoone P, Crombie IK. Hospitalization for deliberate self-poisoning in Scotland from 1981 to 1993: trends in rates and types of drugs used. Br J Psychiatry. 2006 July; 169(1): 81-85.
28 Dhattawal.SK.,Pattern of suicides in Ile-Ife, Nigeria. West Afr J Med. 2004 Sep; 20(3): 259-62.
29 Langley R, Sumner D. Pesticide mortality in the United States from 1979-1998. Vet Hum Toxicol. 2002 Apr; 44(2): 101-5.
30 Tandon S.K.,Suicidal and homicidal deaths: a comparative and circumstantial approach. J Forensic Leg Med 2007 July; 14(5): 253-60.
31 Kalkan S, Erdogan A, Aygoren O, Capar S, Tuncok Y. Pesticide poisonings reported to the drug and poison information center in Izmir, Turkey. Vet Hum Toxicol. 2003 Feb; 45(1): 50-52.
32 Mohanty MK, Patnaik M. Suicide in India: a four year retrospective study. J Forensic Leg Med 2007 May; 14(4): 185-89.
33 Willis GA, Gupta M, Sharma. Suicides in Northern India: comparison of trends and review of literature. J Forensic Leg Med 2007 Aug; 14(6): 318-26.

34 Tagwireyi D, Ball DE, Nhachi CF. Toxicoepidemiology in Zimbabwe: pesticide poisoning admissions to major hospitals. Clinical Toxicol 2006; 44(1): 59-66.
35 Kanchan T, Menezes RG. Suicidal poisoning in southern India: gender differences. J Forensic Leg Med. 2008 Jan; 15(1): 7-14.
36 Haddad LM, Winchester JF. Principles of management of acute poisoning. In: Management of drug overdose and poisoning. 2nd edn. Singapore: W.B Saunders Co; 2000: 14-32.
37 Martindale Extra Pharmacopoeia. 31st Edition.p g.231-234.
38 POISINDEX® System, MICROMEDEX, Inc., Englewood, Colorado.
39 The Medical Letter on Drugs and Therapeutics. Handbook of Antimicrobial Therapy. Revised Edition 1992
40 Olson KR, editor. Poisoning and Drug overdose. 2nd edn. Connecticut: Appleton & Lange; 1994: 312-31.
41 Kucers A, Bennett N, Kemp RJ, editors. The Use of Antibiotics. 4th edn. London: William Heinemann Medical Books; 1988: 167-72.
42 Micromedex, Inc. Volume 102 Poisindex® System Expiration date: 31/03/99.
43 Olson KR, Becker CE, Benowitz NL, Buchanan JF, Mycroft FJ, Osterloh J, Woo OF, editors. Poisoning and Drug Overdose. 1st edn. Connecticut: Appleton and Lange; 1990: 50-52.
44 POISINDEX® System, MICROMEDEX, Inc., Englewood, Colorado.

45 Proudfoot AT, editor. Acute Poisoning - Diagnosis and Management. 2nd edn. Butterworth-Heinemann Ltd; 1993: 72-78.
46 Gilman AG, Rall TW, Nies AS, Taylor P, editors. Goodman and Gilman’s The Pharmacological Basis of Therapeutics. 8th edn. Chicago: Pergamon Press; 1991: 675-84.
47 Janes J, Routledge PA. Recent developments in the management of paracetamol poisoning. Drug Safety 1992; 7: 170-77.
48 Nightingale SL. Warning issued on non-sedating antihistamines terfenadine and astemizole. JAMA 1992; 268: 705
49 Krenzelok EP, Anderson GM, Mirick M: Massive diphenhydramine overdose resulting in death. Ann Emerg Med 1982; 11: 212.
50 Proudfoot AT. Antidotes: benefits and risks. Toxicol-Lett 1995; 82-83: 779-83
51 Ellenhorn MJ, Barceloux DG, editors. Medical Toxicology: Diagnosis and treatment of Human Poisoning. New York: Elsevier; 1988: 326-30.
52 Willis GA. General Principles of Management. Pharmaceutical Journal 1978; 111: 379-82.
53 Proudfoot AT. Acute poisonings with chemicals used in agriculture and horticulture. Prescribes Journal. 1979; 19: 183-89.
54 Wyss PA, Lorent JP. The STIZ (Swiss Toxicofogic Information Center) and the epidemiology of poisoning, Switzerland. Ther Umsch. 1992; 49(2): 74-83.
55 Wig Naveet, Biswas A, Aggarwal P, Handa R, Wali JP. Aluminium phosphide poisoning: Prognostic indicators. Journal of Forensic Medicine & Toxicology 1996; 13: 3-4.

56 Dhattarwal SK, Dalal SS. Profile of deaths due to poisoning in Rohtak, Haryana in the year 1995. Journal of Forensic Medicine & Toxicology. 1996; 19: 9-10.
57 Dutta AK. Poisoning in children: Indian scenario. Indian J Pediatr 1998; 65(3): 365-70
58 Louis A, Marchil S, Renier G, Messil, Barbone F. A Population Study in Trieste, Italy from 1975-1994. BMJ 1998: 24-30.
59 Moghadamia AA, Abdollahi M. An epidemiological study of poisoning in Northern Islamic Republic Of Iran. East Mediterr Health J 2002; 8(1): 88-94.
60 Guigan Me. Common culprits in childhood poisoning: Epidemiology, treatment and parental advice for prevention. Paed Drug 1999; 14: 313-24.
61 Saeed Ahmad, Bashir Zahid M, Khan Delawar, Iqbal Javed, Sohail Raja Khurram, Rehman Anayatur. Epidemiology of suicide in Faisalabad. Crisis 2000; 21(1): 31-35.