treatment and management of poisoning

TREATMENT AND MANAGEMENT OF POISONING

TABLE OF CONTENTS

CHAPTER 1………………………………………………………………………………………

1

CHAPTER 2………………………………………………………………………………………

21

CHAPTER 3………………………………………………………………………………………

22

CHAPTER 4……………………………………………………………………………………….

31

CHAPTER 5……………………………………………………………………………………….

32

CHAPTER 6………………………………………………………………………………………..

56

BIBLIOGRAPHY………………………………………………………………………………….

62

ANNEXURE-I………………………………………………………........................................

66

ANNEXURE-II……………………………………………………………………………………..

90

ANNEXURE-III……………………………………………………........................................

91

ANNEXURE-IV……………………………………………………………………………………

94

ANNEXURE-V…………………………………………………………………………………..

100

ANNEXURES-VI…………………………………………………………………………………..

102


CHAPTER 1 INTRODUCTION 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

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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.

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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

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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

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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, faces 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 faces 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.

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

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.

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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, P a g e 7 | 109


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 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 carbonmonoxide, 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 after absorption when they damage internal organs, especially those of excretion. Some examplus 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.

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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 buildup 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 selfpoisoning. 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 P a g e 9 | 109


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 these 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 P a g e 10 | 109


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.

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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 aluminum 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. P a g e 12 | 109


 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. P a g e 13 | 109


 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 center 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 center 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

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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)

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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

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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 toxic vigilance, the center 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 center 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

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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

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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. P a g e 19 | 109


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. 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. P a g e 20 | 109


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.

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CHAPTER 2 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.

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CHAPTER 03 REVIEW OF LITERATURE Gupta SK, Peshin A. et al: (2008) concluded that organophosphates were the main cause of pesticide poisoning and pesticide related death in North India. The majority of subjects (92%) were adults, 36 % were 20 -30 years old and 95 % of events were intentional poisoning. There were seasonal variations of poisoning events with a higher frequency in the spring [39%] and in summer [35%]. Severity was considered mild in 60%, moderate in 27% and severe in 13% of cases. The overall mortality was 7%. The majority of cases [55%] were hospitalized for one day. 95% were intentional poisoning and 5% were accidental poisoning. In all ingestions, gastric lavage was usually preformed as the first procedure in hospital management.10 Vaswani VR, Vaswani RN et al. (2008) conducted a study to analyze the pattern of poisoning, at a district Hospital in North Karnataka, India & to study the epidemiological factors associated with the same. Over two years, the authors analyzed the data of poisoning cases retrospectively to record the incidence, age & sex distribution, religion, location, time to hospital, duration of hospital stay, type of poisoning, intent & outcome. The total number of poisoning cases was 544 (1.95% of all admissions to the hospital). The results revealed that the male to female ratio was 1.6:1. The types of poisons were organophosphates, alcohol, organochlorines, drugs, rodenticides, carbamates, corrosives, aliphatic compounds, pyrethroids & others. The intent for poisoning was suicidal in 508 & accidental in 36 cases. The average time to reach the hospital from time of poison ingestion was 3.59 hours. The urban rural ratio was 1.07:1. The average hospital stay was 2.07 days. Majority of the cases included organophosphates & alcohol. In comparison with others, the study revealed that higher prevalence of OP poisoning11 Hettiarachchi J and Kodithuwakku G C S et al. (2008) conducted an epidemiology study to evaluate the poisoning in a geographically defined area of rural Sri Lanka. The results revealed that the incidence of poisoning was 75 per 100 000 populations and the death rate was very high (22 per 100 000 population). Both were highest in the age group 15– 34 and there were significant ethnic differences in the incidence of poisoning. Agrochemicals were responsible for 59% of all poisonings. Paraquat was the commonest poisoning agent with a high fatality rate of 68%. Use of highly toxic agents may have resulted in deaths where there was no intention to commit suicide. Strict legislation regarding the sale, distribution and storage of agrochemicals could result in the reduction

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of mortality and perhaps the incidence of poisoning, in developing agricultural countries.12 Senanayake N, Peiris H et al. (2007) conducted a study to evaluate the mortality due to poisoning in a developing agricultural country. They concluded that the cause of death as recorded in 37,125 death certificates (DCs) issued in the Kandy District over 20 years at 5-year intervals beginning in 1967 were analysed to determine the trends in mortality caused by poisoning in the community. Poisoning accounted for 718 (19.3 per 1000) deaths, the highest number being in the third decade of life (41.9%). Male:female ratio was 3:1. The agent responsible for 77% of the deaths was pesticides. The authors observed that, this increase paralleled the increase in suicide figures in the country. Other poisons each contributing to less than 1% of the deaths were: plant poisons, food items, drugs, kerosine oil and alcohol.13 De Alwis LB, Salgado MS. Et al. (2007) conducted a study to evaluate the morbidity and mortality rates of the entire country over a 10-year period. The authors observed that, the male/female ratio was 2:1. Seventy-five percent of deaths from agrochemical poisoning were recorded in the 15-39-year age group, while 33% of deaths belonged to the 20-24 age groups. One third of cases of agrochemical poisoning were dead on being brought to hospital, while 50% were dead within 2 h and 60% dead within 24 h. Organophosphates accounted for 57.6% of all cases of agrochemical poisoning, while paraquat accounted for 21.2% of cases. The authors observed that, deaths were also reported from what are called safe chemicals like Carbamates and Pyrethrums due to their lethal additives.14 Singh B, Unnikrishnan B et. al. (2007) conducted a study to evaluate the poisoning cases admitted to the Government Wenlock Hospital (a teaching hospital of Kasturba Medical College) Mangalore, India. The authors observed that, out of total 33,207 patients admitted in the hospital for treatment, 325 patients were of acute poisoning. This was 1% of all emergency admissions. Of these, 70% were male and 30% female. The majority (36%) of the cases were from age group of 21–30 years. Most (72%) poisoning cases were intentional and only 27% were unintentional. The most important agents of acute poisoning were agrochemical pesticides (49%) followed by drugs (17%), and alcohols (13%). In the study forty-eight (15%) patients died. The result of their study significantly demonstrated that the poisons responsible for most of the mortality were organophosphate pesticides (65%) and aluminium phosphide (15%).15 Senanayake N, Karalliedde L. (2007) reported from their study, one hundred and seventy nine cases of acute poisoning constituting 1.1% of all admissions to the medical P a g e 24 | 109


unit over 3 were . The results revealed that Eighty-three per cent of the patients were under 30 years of age and 72% were males. The common agents were: OP insecticides in 51%, kerosene oil in 12%, rat poison in 8% and drugs in 8%. Ingestion with suicidal intent was the common mode of poisoning. The authors also observed that the overall mortality was 16% .16 Khadka SB, (2005). Conducted a study to determine the pattern and severity of poisoning cases in emergency. The authors also studied the poisoning cases due to various agents who attended Emergency from 1st of April 2002 to 30th of March 2003 retrospectively. The author observed that a total of 67 poisoning cases attended emergency Kathmandu Medical College Teaching Hospital over a period of one year. They found that overall female to male ratio was 1.09:1. And most poisoning occurred in the age group 21-30 for adults (38.8%) and 2-5 yrs for the children. Organophosphorous was the most common poisoning for the adults whereas kerosene was common in children. Oral route was the most common route of administration which accounted 86.57%. Students (35.8%) and housewives (23.3%) were commonly involved in self poisoning. Intentional poisoning comprised of 58.2% of all poisonings. In their study, the authors found that the majority of the intentional poisoning occurred in the female housewife & students of younger age group but accidental poisoning was found common in children less than five years mostly with kerosene ingestion.17 Ramisetty-Mikler S, Mains D, Rene A et al. (2005) conducted a systematic review, Using hospital discharge data for the year 2004. This study examines age and gender differences in the pattern of poisoning hospitalizations of Texas youngsters (N = 1246) aged between 10 to 17 years and investigates self-inflicted poisoning as a function of age and gender. The author found that nearly three quarters of poisoning admissions are girls and two thirds of admissions are older children (aged 15 through 17 years). Analgesics and psychotropic drugs are the two most common agents used. Nearly 1 in 3 admissions among younger children aged 10 through 14 years and 1 in 2 among older children are due to analgesics, with a higher proportion of female admissions. The authors stated that accidental and intentional poisoning is a public health concern requiring intervention. Residents in family practice and pediatrics need increased training to become proactive in educating adolescents and their parents about the dangers of drug overdosing.18 Dieserud G, Loeb M, Ekeberg O. (2006) in their study author reported that approximately 33% reported one or more previous parasuicidal acts, and 21% repeated the parasuicide during the observation period. In their study 94 % used self-poisoning as P a g e 25 | 109


parasuicide method. A total of 2.4% of the parasuiciders committed suicide during the observation period. The author concluded that the parasuicide rates were lower than those in several comparable studies. Rates were higher for divorced female and separated male compared to married and other marital states, and the pattern of relative risk of parasuicide with respect to marital status was stable. Unemployment and substance abuse were positively correlated with parasuicidal behavior for both male and females.19 Guloglu C, Kara IH (2005) studied the hospital records of all admissions to the Emergency Department (ED) of Dicle University Hospital following acute poisoning were revised and all data from January to December 2005 were analyzed. Their study included 44 (25.9%) male (M) and 126 (74.1%) female (F), a total of 170 patients. The M/F ratio was 1.0/3.5. The author found that most intoxication cases occurred during the summer season (93 of 170 patients). 62 % (36.5%) cases involved accidental poisoning while 108 (63.5%) involved deliberate poisoning. In suicide attempts, intoxications were more common in females (77 cases, 71.3%, P < 0.05), and in unmarried persons (74 cases, 68.5%, P < 0.05)20 Tagwireyi D, Ball DE, Nhachi CF (2002) conducted a retrospective study to evaluate and described the pattern of poisoning cases admitted to eight major urban referral hospitals in Zimbabwe over a 2-year period (1998-1999 inclusive). There were a total of 2494 hospital admissions due to poisoning, involving a total of 2346 toxic agents. Accidental poisoning (AP) and deliberate self-poisoning (DSP) accounted for 54.21% (1352 cases) and 45.79% (1142 cases), respectively. The highest number of cases (45.9%) occurred in children below the age of 5 years, with half of these due to chemicals, mainly paraffin. In the DSP group, however, more than 60% of all cases occurred in the 16-25-year age group. Compared with the last major survey of poisoning in Zimbabwe (1996), the pattern of poisoning at referral hospitals has changed over the last decade, with an increase in pesticide and pharmaceutical cases and a marked fall in cases of traditional medicine poisoning. Educational and legislative interventions may be required to address these changes. The author found that there is the need also to investigate further the high mortality rates associated with traditional medicine poisoning.21 Goksu S, Yildirim C, Kocoglu H (2005) conducted a study to evaluate the rate and characteristics of acute human poisoning in their province. All cases of acute human poisoning admitted to the emergency department were included in the study. The authors found that there were 179 (0.7%) poisoning cases among 25,605 patients who admitted to the emergency department. The authors observed that 64.3% were female and 35.6% P a g e 26 | 109


were male patients. The poisoning made a peak between the ages of 16 and 25 years. The majority of poisoning cases resulted from oral ingestion with deliberate intake accounting for 78.7% of the cases. Most of the suicide attempt cases were also females. Analgesics were the most common agents (42.4%) among the drugs incriminated in poisoning. 24 patients were admitted to intensive care unit, of whom 42% were female and 58% were male patients. Drugs for suicide attempts were the main cause of poisoning in the patients who admitted to intensive care unit. Five patients (2.8% of all cases) died in the intensive care unit.22 Jane M. Burns, George C. Patton (2005) explain to identify the areas of ‘research need’ and to provide an evidence base to identify ‘best buy’ preventive interventions for youth suicide. They studied the design, development, implementation and evaluation of the prevention strategies ranging from clinical interventions to population-based universal approaches, are considered within five risk factor domains: individual, family, community, school and peer. The author found that there is a paucity of evidence on the effects of interventions targeting depression and suicidal behavior. Youth suicide prevention strategies in Australia have generally employed traditional approaches that focus on clinical interventions for self-harmers, restricting access to lethal means, providing services to high risk groups and enhancing general practitioner responses. Both program development and research evaluation of interventions for many important risk and protective factors for suicide have been neglected.23 Kelly CB, Weir J, Rafferty T, et al. (2005) monitored deliberate self-poisoning in a rural area of Northern Ireland over a 20-year period and compared with reports from large urban centers. In addition, a local prescribing database allows assessment of any association between psychotropic drug prescription and use for deliberate self-poisoning. The author found that in rural area the pattern of deliberate self-poisoning has changed, as in urban centers, with a rise in frequency and the male/female ratio approaching unity. The pattern of drug use has altered, with paracetamol overtaking benzodiazepines as the most commonly used agent. More recently, antidepressants have become the second most frequently used drug class for this purpose. The author also found that care should be taken to prescribe the least toxic agent available as this is associated with likely frequency of self-poisoning for most classes of psychotropic drug.24 Turkey Ozkose Z, Ayoglu F. (2006) Carried out retrospective study to evaluate etiological and demographical characteristics of acute adult poisoning patients during 1 year at a university hospital in Ankara. 228 adults (180 were suicidal poisoning cases) P a g e 27 | 109


were admitted to the emergency center with acute poisonings. The female-to-male ratio was 3:1, and the majority of patients (63.6%) were below the age of 25 years. The author found that the drugs were the major cause in 75.9% of the cases, followed by inhalation of gases (17.6%), food (2. 6%), corrosives (2.2%), pesticides (0.9%), and alcohol (0.9%). Analgesics were the most common cause of drug poisoning (29.7% of all substances). There were no fatalities. It is important to realize that this study was a hospital-based study, and hence it may be considered difficult to draw conclusions for the whole population of Turkey. However, they considered that the reason for such a high ratio of analgesic poisoning is probably due to the habit of extensive analgesic prescribing in Ankara. 25 Tufekci IB, Curgunlu A, et al. (2004) conducted a retrospective study to analyse the characteristics of acute adult poisoning cases admitted to a university hospital in Istanbul, Turkey. They analysed the clinical charts for aetiological and demographical characteristics of the acutely poisoned patients. In their study, the authors found that there were 284(2.4%) poisoning cases (207 females and 77 males) among 11834 patients admitted to the Emergency Unit. The female-to-male ratio was 3:1. The mean age was 27+/-12 years (age range 15-87) and the majority of the patients (73.94%) were below the age of 30 years. whereas the route of administration was as follows: 84.51% orally, 14.44% by inhalation and 1.06% by intravenous injection. In 32.04% of cases, there was more than one medicinal drug responsible for the poisoning.26 McLoone P, Crombie IK. (2006) conducted a study to evaluate the self-poisoning cases with paracetamol (increased most rapidly) in contrast to aspirin which showed little change. Opiate analgesics, antirheumatics, antidepressants and antipsychotics have also shown some increase in their use in both genders. The author found that there has been a substantial fall in the use of benzodiazepines in women, but little change among men. They also found that there was a rapid increase in self-poisoning particularly among young adults present. Controlling this epidemic is made difficult because the principal drug involved, paracetamol, is readily available.27 Dhattarwal.S.K et al. (2006) evaluated the pattern of poisoning cases deaths in Rohtak during the year 2005. All the cases of self-poisoning were in variably suicidal in manner. The incidence of self-poisoning was maximum in second and third decades of life. Males outnumbered the females due to their relatively more active and energetic lifestyle. The incidence f poisoning was maximum among individuals of rural backgrounds belonging

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to agricultural and middle class families. Aluminum phosphate and insecticides being commonly abused for self-poisoning.28 Langley R, Sumner D. (2002) in their study on pesticide mortality in the United States 1979-1998 have highlighted the fact that the Pesticide mortality in the US is usually reported on a case-by-case basis. The Vital Statistics of the US and the publications of the American Association of Poison Control Centers publish yearly statistics on pesticide mortality. They evaluate the incidence of pesticide mortality in regard to intent, geography, sex, race, age and trends from the years 1979-1998. In this fashion, it appeared easier to identify likely areas of exposures and to develop steps to reduce mortality. They found in their studies that pesticide mortality has decreased substantially over the last 20 yrs. Intentional poisonings, primarily suicides, represent the greatest fraction and are decreasing more slowly than accidental poisonings. Mortality is thus following intentional exposure rather than accidental exposure.29 Tandon S.K. et.al. (2004) studied 322 poisoning cases admitted in emergency department of S.N.Hospital, Agra during the period October 2002 to September 2003. It was revealed that majority [70%] of cases was male and 63 % people were from urban areas. Most of them [61%] were in age group of 15 to 30 yrs. 240 cases of known poison and rest of unknown poison. Majority of the patients took cephos, followed by copper sulphate, insecticide and alcohol. Only 37 patients expired out of 322 cases and 65.5 % were discharged satisfactorily.30 Kalkan S, Erdogan A et al. (2003) conducted a study to analyze the poisonings caused by pesticides that were reported to Drug and Poison Information Center (DPIC), in Izmir from 1993 to 2001. Patient demographics, type of the pesticide, distribution according to month and year, route and reason for exposure, clinical effects and outcome were analyzed from 25,572 poisoning calls. Pesticide intoxications accounted for 8.8% of the poisonings, with 80.3% insecticides and 19.7% rodenticides. The authors analyzed that the majority of poisonings aged from 0 to 6 y (28.2%) and 19-29 y (23.2%). Most were intoxicated with organophosphates (47.6%), 54.1% did not develop signs and symptoms of toxicity. Fatality due to pesticide poisoning was 0.4%. The authors also observed that the preventive education against pesticide poisoning is needed.31 Mohanty MK, Patnaik M et al. (2007) carried out a study to analyze the Suicide incidents in India: a four-year retrospective study. The purpose of the study was to identify the risk groups. In the four-year period from January 2000 to December 2003, 588 suicide victims were identified. Information was obtained by interviewing the acquaintances of the P a g e 29 | 109


victim, perusal of hospital records and the autopsy findings. The author absorbed that the largest number of victims were found in the age group of 21-30 years. Hanging and poisoning constituted the two major modes of suicides (63%). Majority of the victims were mentally sound, married and were from rural background. Victims were mostly drawn from low socioeconomic status (48%). Less educated or illiterates were usually the victims. Suicidal note was detected in 5% of cases. Suicidal tendency and alcohol intake could not be encountered in most of the cases. Authors observed that the financial burden (37%) and marital disharmony (35%) were the principal reasons for the suicide.32 Willis GA., (2005) discussed the general principles of management for poisoning that includes the use of oral dilution, emetics, activated charcoal and cathartics. Over 50,000 Canadians were poisoned yearly; large number of poisoning incidence is not reported: 58% of the cases involve drugs. There were specific antidotes for every poison. Therefore, initial therapy was directed at preventing or minimizing the absorption of poisons. The immediate admiration of milk or water to dilute the poison is the first aid measure of choice ingestion or topical exposures. Emesis should be carried out in alert patients if a hydrocarbon contains pesticides, camphor, toluene, benzene, heavy metals of chlorinated hydrocarbons. If the patient were extremely drowsy, gastric lavage with a cuffed end tracheal tube should be used. In all hydrocarbons ingestions, a saline cathartic was recommended.33 Tagwireyi D, Ball DE, et al (2006) conducted a study to know the morbidity and mortality in acute pesticide poisoning. The author observed that acute pesticide poisoning (APP) is a well-recognized cause of morbidity and mortality but is not well described in developing countries. We describe the toxicoepidemiology of APP in Zimbabwe. All cases of APP admitted to eight major referral hospitals in Zimbabwe from January 1998 to December 1999 (inclusive) were identified using ICD-9 codes and ward registers and relevant information recorded on a standard data collection sheet. In their study, the authors observed there were a total of 914 single pesticide exposures. Almost half (49.1%) resulted from oral exposure to rodenticides, 42.2% from anticholinesterase-type pesticides (AChTP), mostly organophosphates (OP) that were responsible for over 90% of admissions from AChTP. Accidental and deliberate self-poisoning (27.1% and 58.6%, respectively) accounted for most cases with only eight homicides. The authors finally observed that Greater control in the sale and use of these products could help prevent significant morbidity and mortality.34

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Kanchan T, Menezes RG. et al. (2008) carried out a study to assess the leading causes of morbidity and mortality worldwide due to poisoning. A five-year retrospective study from January 2000 to December 2004 was conducted. The author observed that during this period, a total of 137 cases of suicidal poisoning related deaths were autopsied. Males were predominantly affected (male: female 2.8:1). Maximum victims of suicidal poisoning mortalities were in their 3rd decade. Mean age for males and females was 40.5 years and 34.4 years, respectively. 27.8% of females and 10.9% males were suffering from depression. Preference for organophosphates was relatively more in males when compared to females, who preferred zinc phosphide, carbamates and medicinal agents. In this study, the authors observed that difference in pattern of suicidal poisoning among males and females to identify population at risk, and understand the problem status among both genders.35

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CHAPTER 4 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].

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CHAPTER 5 RESULTS AGE DISTRIBUTION OF PATIENTS The age of patients ranged from 12 to 84 yrs. Majority of the patients belonged to the age

group of 19-30 years.

Table – 1: Age of patients Age group of patients

Number

Percentage

0-11

0

0

12-18

1

1.81

19-30

23

41.81

30-40

12

21.81

40-50

9

16.36

50-60

6

10.90

Above 60

4

7.27

in years

Fig- 5: Age group of patients

PERCENTAGE

Series1, 1930, 41.81

Series1, 12Series1, 0-11, 18., 1.81 0

Series1, 3040, 21.81 Series1, 40Series1, 50, 16.36 Series1, 50Above 60, 60, 10.9 7.27

AGE GROUP

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GENDER DISTRIBUTION OF PATIENTS Among the 55 patients who got admitted due to poisoning, male (29) were slightly more than female (26) patients. Table -2: Gender distribution of patients

Gender

Number

Percentage

Male

29

52.73

Female

26

47.27

Fig -6- Gender distribution of patients

PERCENTAGE

52.73 %

47.27 %

GENDER

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REGION OF PATIENTS Majority of the patients were from urban region (53) followed by rural region (2) Table -3: Region of patients

Region

Number

Percentage

Urban

53

97

Rural

2

3

Fig -7: Region of patients

PERCENTAGE

97 %

3% ,,0 REGION

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LITERACY OF PATIENTS Number of patients with primary education and more (Literates) constituted 80 % whereas

20 % were illiterates.

Table-4: Literacy of patients

Literacy of patients

Number

Percentage

LITERATE

44

80

ILLITERATE

11

20

Fig- 8: Literacy of patients.

PERCENTAGE

80 %

20 %

LITERACY

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OCCUPATION OF PATIENTS Maximum number of the patients were businessmen (27) followed by students (16), and housewives (10). Table-5: Occupation of patients.

Occupation

Number

Percentage

Businessmen

27

49.00

Housewives

10

18.2

Laborer

1

1.81

Students

16

29.1

Unemployed

1

1.81

Fig -9: Occupation of patients.

PERCENTAGE

49 %

29.3 % 18.1 % 1.8 %

1.8 %

OCCUPATION

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MARITAL STATUS OF PATIENTS Majority of the patients were married followed by single and widowed patients Table -6: Marital Status of patients Marital Status

Number

Percentage

Married

37

67.3

16

29.1

2

3.6

Single Widow

Fig – 10: Marital Status of patients

PERCENTAGE

68 %

29 %

3%

MARITAL STATUS

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HABITS OF 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. 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.19 [34.54%] patients were both smokers and alcoholic out of whom 17(89.47%) were male and 2(10.52%) were female. Table – 7: Habits of patients Number

Habits of Patients

Percentage

Male

Female

Male

Female

Alcoholics

27

2

93.1

6.89

Smokers

17

2

89.47

10.52

Nil

2

5

28.57

71.42

Fig – 11: Habits of patients

PERCENTAGE

Male, Alcoholics, 93.1

Females, Alcoholics, 6.89

Male, Smokers, 89.47

Females, Nil, 71.42

Male, Nil, Females, 28.57 Smokers, 10.52

Male Females

HABITS

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PAST HISTORY OF PATIENTS Although 73 % of the patients were admitted due to intentional poisoning for the 1st time, 19% of the cases were due to 2nd attempt and 5.5 % cases due to 3rd attempt. Accidental poisoning was in 2.5% of cases. Table -8: Past history of patients Past history

Number

Percentage

1st Time

40

72.72

2nd Time

10

18.18

3rd Time

3

5.45

Accidental poisoning

2

3.63

( Intentional poisoning )

Fig – 12: Past history of patients

PERCENTAGE

72.72 %

18.18 % 5.45 %

3.63 %

PAST HISTORY

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MONTH OF EXPOSURE Maximum numbers of admissions were in the month of December followed by January, October and November. Table – 9: Month of exposure

Month of Exposure

Number

Percentage

Jun-08

1

1.80

Jul-08

4

7.30

Aug-08

5

9.1

Sep-08

5

9.1

Oct-08

8

14.5

Nov-08

8

14.5

Dec-08

13

23.6

Jan-09

9

16.4

Feb-09

2

3.6

Fig -13: Month of Exposure

PERCENTAGE

23.6 %

14.5 % 14.5 % 7.3 %

16.4 %

9.1 % 9.1 % 3.6 %

1.8 %

MONTH OF EXPOSURE

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TIME OF POISONING Majority of the patients [55 %] were admitted in the night time, followed by 45 % during the day. Table -10: Time of poisoning

Time of poisoning

Number

Percentage

Day time

25

45

Night time

30

55

Fig- 14: Time of poisoning 55 %

PERCENTAGE

45 %

Series1, , 0

TIME OF POISONING

P a g e 42 | 109


NATURE OF POISONING Out of 55 cases, 53 cases amounted to intentional poisoning and 2 cases were due to accidental poisoning. Table – 11: Nature of poisoning

Nature of poisoning

Number of patients

Percentage

Accidental

2

3.6

Intentional

53

96.4

Fig- 15: Nature of poisoning

PERCENTAGE

96.4 %

3.6 %

NATURE OF POISONING

P a g e 43 | 109


ROUTE OF EXPOSURE In majority of the cases (54), the route of exposure was oral, whereas in one case the poison was injected intravenously Table-12: Route of exposure Route of

Number

Percentage

Oral

54

98.8

Intravenous

1

1.2

administration

Fig -16- Route of exposure

PERCENTAGE

98.8 %

1.2 %

ROUTE OF EXPOSURE

P a g e 44 | 109


REASONS FOR INTENTIONAL POISONING The reasons for intentional poisoning were found to be financial [52.72 %] followed by emotional disturbance [29.10 %], and family problems [18.8%] . Table-13: Reasons for Intentional Poisoning

Reasons

Number

Percentage

Emotional

16

29. 10

Family Problems

10

18.18

Financial Problems

29

52.72

Disturbance

Fig -

17Reasons for Intentional Poisoning

29.1 % 52.72 %

Emotional Disturbance Family Problems

18.18 %

Financial Problems

REASONS FOR INTENTIONAL POISONING

P a g e 45 | 109


POISON CONSUMED Maximum cases (33) were due to consumption of OP compounds (Pesticides/Insecticides) followed by over dose of drugs in 19 cases, cosmetics in 1 case, and in 2 cases the poison consumed was not known. Table- 14: Poison consumed

Poison consumed

Number

Percentage

33

60

Cosmetics

1

1.8

Drugs

19

34.6

Unidentified

2

3.6

OP poisoning (Pesticides and insecticides)

Fig – 18: Poison consumed 60 %

PERCENTAGE

34.6 %

1.8 %

3.6 %

POISON CONSUMED

P a g e 46 | 109


ORGANOPHOSPHOROUS COMPOUNDS CONSUMED Among the OP compounds consumed, 39.39 % were pesticides and 60.61 were insecticides Table-15 Organophosphorous compound consumed Trade

Generic

Class &

Number

Percentage

name

name

category

Chlorpyrifos

Pesticide

13

39.39

Cycothate

Dimethoate

Insecticide

3

9.09

Acet

Acephate

Insecticide

4

12.12

Tic -20

Fenithrothin

Insecticide

6

18.18

Demcos

Demeton

Insecticide

2

6.06

Cyfos Cybil Contaf Cyfos

Acetaf Torpedo

Methyl Decis

Diazinon

Insecticide

1

3.04

Cythion

Malathion

Insecticide

4

12.12

P a g e 47 | 109


In poisoning cases due to over dosage of drugs, 47.37 % cases were due to CNS depressants, 42.12 % cases due to analgesics and antipyretics, and 10.54% of cases due to antispasmodics. Table – 16: Drugs consumed TRADE

GENERIC NAME

NAME Calmpose Larpose

Alprex

Nitrazepam

CNS depressant

Alprazolam

CNS depressant

Imol

Ibuprofen

Proxivon

PERCENTAGE

6

31.56

3

15.79

3

15.79

3

15.79

2

10.54

2

10.54

Lorazepam

Acetamenophen

Spasmo

NUMBER

CATEGORY

Dolo

Disprin

CLASS &

Aspirin

Analgesic and Antipyretic Analgesic AntiInflammatory

Dicycloverine HCL

Antispasmodic

P a g e 48 | 109


SIGNS AND SYMPTOMS OF PATIENTS Out of 55 cases, CNS symptoms were seen in 52.2 % cases, GI symptoms were seen in 61.81 % cases, CVS symptoms were seen in 71 % of cases, respiratory symptoms were seen in 78.18 % cases and 7.27 % cases presented with no symptoms. Table-17- Signs and Symptoms of patients Signs and Symptoms

Number of patients

Percentage*

Gastrointestinal (GI )

34

61.81

CNS

32

58.18

CVS

39

71.00

Respiratory

43

78.18

No symptoms

4

7.27

*There was overlap of signs and symptoms in few cases Fig-19- Signs and Symptoms of patients

71 % 58.18 %

PERCENTAGE

61.81 %

78.18 %

7.27 %

SIGNS AND SYMPTOMS

P a g e 49 | 109


TREATMENT BEFORE ADMISSION 71 % of patients received first aid before admission to MICU, whereas 29 % of patients didn’t get treatment before admission in the hospital. Table- 18: First aid given before admission in MICU Treatment

Number of Patient

Percentage

39

71

16

29

Treatment Previously given Treatment Previously not given

Fig-20: First aid given before admission in MICU

PERCENTAGE

71 %

29 %

FIRST AID GIVEN BEFORE ADMISSION IN MICU

P a g e 50 | 109


FORM OF POISON In majority of the cases, form of poison consumed was liquid (52.72%) followed by solid (32.93%), powder (9.0%) and semisolid (5.45%). Table – 19: Form of poison Form of Poison

Number

Percentage

Liquid

29

52.72

Solid

18

32.73

Semisolid

3

5.45

Powder

5

9.1

Fig 21: Form of poison

PERCENTAGE

52.72 %

32.93 %

9% 5.45 %

FORM OF POISON

P a g e 51 | 109


ANTIDOTES USED The specific antidotes that were used were Atropine (47.27%), followed by Pralidoxime (2-PAM, Pyridine Aldoxime) (29.09%) and N-Acetyl cystine (5.45 %). General antidote such as charcoal was used in 18.18% of the cases. Table- 20: Antidotes used Antidote used

Number

Percentage

Atropine

26

47.27

16

29.10

N-acetyl cystine

3

5.45

Charcoal

10

18.18

Pralidoxime (2-PAM, Pyridine Aldoxime)

Fig-22: Antidotes used 47.27 %

29.1 %

PERCENTAGE

18.18 % 5.45 %

ANTIDOTE USED

P a g e 52 | 109


CONCURRENT MEDICATIONS PRESCRIBED FOR TREATMENT Table -21: Concurrent Medications Prescribed for Treatment Concurrent

Number

Percentage

Analgesics

46

83.63

Antibiotics

35

63.63

Antiemetics

48

87.27

Antiulcers

36

65.45

CNS depressants

10

18.18

Diuretics

48

87.27

50

90.90

52

94.54

Medication

Nutritional supplements Supportive therapy

Fig-23: Concurrent Medications Prescribed for Treatment

Analgesics

94.54 % 90.9 %

83.63 %

Antibiotics Antiemetics

63.63 %Antiulcers

CNS depressants 87.27 %

18.18 %

Diuretics 87.27 % 65.45 % CONCURRENT MEDICATIONS

Nutritional supplements

P a g e 53 | 109


LAB REPORTS DURING TREATMENT Table -22- Lab reports of patients Lab parameter

Number of patients

Percentage

Increase in Blood count

7

12 .73

Increase in blood count

12

21.82

13

23.64

Normal lab reports

22

40

Lab report not

1

1.81

& Pseudocholinesterase Increase in ESR & blood count

available* *Patient expired Fig -24: Lab reports of patients

1.8% 12.5% 40.3% 21.8%

Increase in Blood count Increase in blood count & Pseudocholinesteras e Increase in ESR & blood count

23.4%

P a g e 54 | 109


LENGTH OF STAY IN HOSPITAL DURING TREATMENT The duration of stay in the hospital varied from three to thirty days depending on the type of poison consumed. In case of Organophosphorous poisoning, hospitalization days ranged from 7 to 20 days with a mean of 10-15 days. Table -23: Length of stay in hospital during treatment Number of patients

Type of poisoning

No. of days

1

Cosmetics

3

21

Drug Poisoning

7- 10

OP poisoning

21

8-15

(Pesticide) OP poisoning

12

Above 15 Days

(Insecticide)

Fig- 25: Length of stay in hospital during treatment

LENGHT OF STAY / DAYS

Above 15

7-10

8-15

Series1, Cosmetics, 3

TYPE OF POISONING

P a g e 55 | 109


PATIENT STATUS AFTER TREATMENT Out of 55 cases, 54 patients recovered totally and one patient expired. Table -24: Patient status after treatment

Patient status

Number of patients

Percentage

Recovered

54

98.18

Expired

1

1.82

Fig – 26: Patient status after poisoning treatment

PERCENTAGE

98.18 %

1.82 %

PATIENT STATUS

P a g e 56 | 109


CHAPTER 06 DISCUSSION 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 1930 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. P a g e 57 | 109


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 was 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. P a g e 58 | 109


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. 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.

P a g e 59 | 109


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%). Laborer 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.

P a g e 60 | 109


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 were 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.

P a g e 61 | 109


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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): 36570 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): 3135. P a g e 65 | 109


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

P a g e 66 | 109


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 posthospital 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 P a g e 67 | 109


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.

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GUIDELINES FOR THE MANAGEMENT OF POISONING GUIDELINES FOR THE MANAGEMENT OFORGANOPHOSPHROUS 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: P a g e 69 | 109


Cholinesterase level, electrolytes, glucose, BUN, creatinine, hepatic transaminases, prothrombin time (PT), ECG monitoring. List of Organophosphrous insecticides are given in Annexure II

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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

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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 500 mg/L in adults, >300 mg/L in children Severe poisoning blood levels: >1000 mg/L in adult,>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. 500 mg/L). Difficult to achieve in critically ill patients. There are currently

P a g e 75 | 109


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.

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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

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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.

P a g e 78 | 109


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

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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 P a g e 80 | 109

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.

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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 P a g e 82 | 109


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.

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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 P a g e 84 | 109

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).

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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

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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.

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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

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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 Maximum tolerated dose

- Not known - 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 P a g e 89 | 109


ANNEXURE - II INFORMED CONSENT FORM Name of the Patient:

Date:

Age:

Date of Admission:

Gender:

Hospital IP No:

I ____________________________ hereby give my consent to take part in the project “Preparation of Guidelines for Management of Poisoning at St. Martha’s Hospital, Bangalore” carried out in the Medicine MICU of St. Martha’s Hospital, Bangalore. I have been clearly explained about the objectives of the study. I know about my right to withdraw from the study at any point of time. Signature of the Patient/ Relative:

Signature of Clinical Pharmacist:

Signature of the Clinician:

Signature of the Guide:

P a g e 90 | 109


ANNEXURE - III DATA COLLECTION FORM

Date:

DEMOGRAPHIC DETAILS Name of Patient Age Gender I.P No Date of Admission Literacy status Occupation Location

City

Rural

Religion Marital status Past Medication History (ADR, If any) Alcoholic/Smoker/Drug Abuse Time of Poisoning

Day Time

Night Time

Nature of Poison Agriculture Cosmetics

Drugs Insecticidal

Sting bite

Toxic plants

Food

Others P a g e 91 | 109


Amount Consumed Reported

Not Reported

Unknown

Mode of Poisoning Accidental

Intentional

Suicidal Type of Poison

Liquid

Solid

Gas

Powder

Others

Route of Poisoning Skin

Oral

IV

Gas

Others

Signs & Symptoms GI

CNS

CVS

Respiratory

Others

Diagnosis Treatment already given:-

DRUG & ANTIDOTES

DOSE

DATE OF

DATE OF

START

STOP

1. 2. 3. 4.

P a g e 92 | 109


5. 6. 7. 8. Medication chart LABORATORY RESULTS CLINICAL RESPONSE: Date

Patient Recovered

CLINICAL RESPONSE & CONSEQUENCES

Recovered Totally



Length of stay in Hospital :



Date of discharge :

MICU

Recovered

Death(Reason

Partly

)

General Ward

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ANNEXURE –IV Organophosphrous insecticides TYPE

BRAND NAMES

DESCRIPTION

DOSE IN LD

Oral LD50

Dermal LD50

Systemic insecticide with stomach Acephate

Acephate

action.

Orthene

Cholinesterase

Acephatom

inhibitor. Controls a

>945mg/kg

2000mg/kg

wide range of chewing and sucking insects. Used for control of flies and other insect pests in stables, mosquitoes, Azamethiphos

SNIP

tsetse flies, cockroaches and

1010mg/kg >2150mg/kg

other public hygiene pests.Cholinesterase inhibitor. Non-systemic insecticide for control of soil Chlorpyrifos

Chlorpyrifos

insects and some

Chlorpycin

foliar insect pests

135mg/kg

2000mg/kg

on a wide P a g e 94 | 109


range of crops. Cholinesterase inhibitor. Insecticide and

Diazinon

Diazinon

acaricide with

Basudin

contact, stomach

Fezudin

and respiratory

Trisudin

action.

300mg/kg

540600mg/kg

Cholinesterase inhibitor. Insecticide and acaricide which Dichlorvos

DDVP

gives rapid knock down. Used for control of household and public health insect pests, stored product pests, sucking and chewing insects,

56mg/kg

107mg/kg

15-

255-

30mg/kg

300mg/kg

and spider mites in a wide range of crops. Cholinesterase inhibitor. Systemic insecticide and acaricide. Remains active for 2 to 3 weeks. For control of a wide Dimethoate

Dimethoate

P a g e 95 | 109


Roxion

range of insects and

Dimet

mites on many

Chemathoate

crops. Also used for control of flies in animal house. Cholinesterase inhibitor. Systemic insecticide with contact, stomach, and respiratory action, for control of sucking

Heptenophos

Hostaquick

insects (aphids) and certain Diptera. Also

96mg/kg

2925mg/kg

250mg/kg

890-1300mg

used for control of animal ectoparasites. Cholinesterase inhibitor. Non-systemic insecticide for Dust control of chewing, Fentrothion

Fenitrothion

sucking and boring

Folithion

insects on a range of crops. Also used as a public health insecticide. Cholinesterase inhibitor.

P a g e 96 | 109


Systemic insecticide with contact and stomach action. Absorbed by the Methamidophos Methamidophos roots and leaves. Used for control of chewing and

30mg/kg

118mg/kg

25mg/kg

200mg/kg

sucking insects, and spider mites on a wide range of crops. Contact and stomach action insecticide and acaricide for control Methidathion

Methidathion

of a wide range of

Tamaron SL600 sucking and Tamaron

chewing insects and spider mites in many crops. Cholinesterase inhibitor. Systemic insecticide and acaricide with residual activity. Used for control of

Mevinphos

Phosdrin 24EC

chewing and sucking insects, and spider mites on a wide

4mg/kg

short 16 33mg/kg

range of crops. Cholinesterase inhibitor. P a g e 97 | 109


Systemic stomach and contact action insecticide and acaricide. Used for Monocrotophos

Monocrotophos control of a Azodrin 60

broad spectrum of pests including chewing and boring insects

8-23mg/kg

130250mg/kg

and spider mites on a wide range of crops. Cholinesterase inhibitor. Insecticide and acaricide with contact and Quinalphos

Bayrusil

stomach action. Used for control of a wide

62mg/kg

1750mg/kg

range of insects. Cholinesterase inhibitor Insecticide and acaricide with Triazophos

Hostathion

contact and stomach action. Cholinesterase

57-59

1100mg/kg

mg/kg

inhibitor.

P a g e 98 | 109


Non-systemic insecticide with contact and stomach action. Used for control of pests in Trichlorfon

Trichlorfon Triden

agriculture, forestry, food

250mg/kg

2000mg/kg

storage, household, and animal husbandry. Also controls a wide range of insects. Cholinesterase inhibitor

P a g e 99 | 109


ANNEXURE –V Carbamate Insecticides Type/ Brand Names /Description/ Toxicity Type

Brand Names

Description

Toxicity Oral

Dermal

LD50

LD50

Systemic insecticide and aphicide with contact Bendiocarb

Garvox

and

55mg/kg

800mg

566-

0.04mg/kg

stomach

55mg/kg

566-800mg

action.

Cholinesterase inhibitor. BPMC Insecticide with controlling BPMC

sucking

BPMC

insects,bugs 350 mg/kg

Hopcin

>5000mg Hopcin

and

weevils.

350 mg/kg

350 mg/kg

Cholinesterase inhibitor. /kg(rat) Carbaryl Carbaryl

85WP Servin Avin Sevtox Sevin

Carbofuran

Furadan Carbofuran

Insecticide with contact and stomach action. Also acts as

a

plant

growth

300mg/kg >2000mg/kg

regulator.Cholinesterase inhibitor. Systemic

insecticide,

acaricide

and

8mg/kg

2550mg/kg

nematicide with

P a g e 100 | 109


stomach action.

and

contact

Cholinesterase

inhibitor. Insecticide with contact and

stomach

action.

Control of chewing and Dioxacarb

Elocron

sucking

foliar

insect

pests on a range /kg

90mg/kg

1950mg

(rabbit) of crops. Cholinesterase inhibitor. Non-systemic insecticide with strong contact rapid Propoxur Propoxur

Shelltox Super Raid

action

giving

knock-down.

Cholinesterase inhibitor. Control of insect pests in food

storage

areas,

95mg/kg

>1000mg/kg

houses, animal houses. Control of sucking and chewing insects on a range of crops.

P a g e 101 | 109


ANNEXURE –VI Classified lists of antidotes and other agents Group 1 - List of antidotes Group 2 - Agents used to prevent the absorption of poisons, to enhance their elimination, or to treat symptomatically their effects on body functions Group 3 - Other useful therapeutic agents for the treatment of poisoning Group 4 - List of antidotes and related agents considered obsolete The antidotes listed in Groups 1 and 2 are considered useful in the treatment of acute human poisoning, and their availability in terms of urgency of use may be classified as follows: A

Required to be immediately available (within 30 minutes).

B

Required to be available within 2 hours.

C

Required to be available within 6 hours.

Their effectiveness in practice may be classified as follows: 1 Effectiveness well documented, e.g. reduction of lethality in animal experiments and reduction of lethality or of severe complications in human poisoning. 2

Widely used but not yet universally accepted as effective, owing to lack of research

data

P a g e 102 | 109


and requiring further investigation concerning effectiveness or indications for use.

3 Questionable usefulness; as many data as possible regarding effectiveness should be collected. The classification in terms of urgency of availability (A, B, C) proven effectiveness (1, 2, 3) is given next to the main indication for the antidote. The classification is also given in the right-hand column of the Group 1 list when an antidote has other possible applications. If there is doubt as to the classification of an antidote, the lower score is always given, e.g. B2 instead of A1. Group 1. Antidotes (Type of Poisoning) Antidote

Main indication or pathological condition

Acetylcysteine

Paracetamol (B1)

N-acetyl penicillamine

Mercury (inorganic and vapour) (C3)

Amyl nitrite

Cyanide (A2)

Atropine Benzylpenicillin

Organophosphorus compounds and carbamates (A1) Amanitins (B3)

ß-blockers (ß1 and ß2 preferably

ß-adrenergic agonists (A1)

short-acting)

Theophylline (B1) Fluorides, oxalates (A1)

Calcium gluconate

Calcium antagonists (B3) soluble calcium salts Drug-induced hyperthermia (A2)

Dantrolene

malignant neuroleptic Syndrome (A2) P a g e 103 | 109


Deferoxamine Diazepam Dicobalt edetate Digoxin-specific antibodies Dimercaprol 4-dimethylaminophenol (4-DMAP) Edetate calcium disodium (CaNa2EDTA) Ethanol Flumazenil Folinic acid

Iron(B1) (C2) Organophosphates (A2) Chloroquine (A2) Cyanide (A1)

Digoxin/digitoxin, other digitalis glycosides Arsenic (B3) gold (C3), mercury (inorganic) (C3) Cyanide (A1)

Lead (C2) Methanol, ethylene glycol (A1) Benzodiazepines (B1) Folinic acid antagonists (B1) Methanol (B3)

Glucagon

ß-blockers (A1)

Glucose (hypertonic)

Insulin (A1)

Hydroxocobalamin

Cyanide (A1)

Isoprenaline

ß-blockers (A1)

Methionine

Paracetamol (B1)

Methanol, Coprin,

Aluminium

Disulfiram (B2)

P a g e 104 | 109


Methaemoglobinaemia (A1) Methylthioninium chloride

(Methylene blue poisoning) Arsenic (B3) Gold (C3), Mercury

Dimercaprol

(inorganic) (C3)

Naloxone

opiates (A1) Neuromuscular block (curare type),

Neostigmine

Peripheral anticholinergic efects (B2) Organophosphorus insecticides (B2)

Obidoxime Oxygen, hyperbaric

Cyanide, carbon monoxide, hydrogen sulfide(A1) Cyanide,hydrogen

Carbon monoxide (C2)

Sulfide, Carbon tetrachloride Copper (Wilson disease) (C1)

Penicillamine

Lead, Mercury (inorganic) (C2)

Pentetic acid (DTPA)

Cobalt (C3) Radioactive metals Alpha-adrenergic poisoning (A1)

Phentolamine

Central anticholinergic syndrome from

Physostigmine

Atropine and derivatives (A1)

Phytomenadione (vitamin K1) Potassium ferric, Hexacyanoferrate

Pralidoxime Prenalterol

PAM

Coumarin derivatives (C1)

Thallium (B2) Organophosphorus compounds ß-blockers (A1)

P a g e 105 | 109


Silibinin

Amanitin (B2)

Sodium nitrite

Cyanide (A1)

Sodium nitroprusside

Ergotism (A1)

Sodium thiosulfate

Cyanide (A1)

Group 2.

Agents used to prevent the absorption of poisons, to enhance their

elimination, or to treat symptomatically their effects on body functions Emetics: Apomorphine Ipecacuanha Cathartics and solutions for whole gut lavage: Magnesium citrate/sulfate/hydroxide (B3) Mannitol/sorbitol/lactulose (B3) Sodium sulfate/phosphate/bicarbonate (B3) Polyethylene glycol electrolyte lavage solution (B2) Agents to alkalinize urine or blood: Sodium bicarbonate (A1) Agents to prevent absorption of toxic substances in the gastrointestinal tract: Activated charcoal (A1) Starch (A3)

-- for adsorbable poisons -- for iodine

Agents to prevent skin absorption and/or damage: Calcium gluconate gel (A1)

-- for hydrofluoric acid

Polyethylene glycol (Macrogol 400)

-- for phenol

Anti-foaming agent: Dimethicone

-- for soaps, shampoos

P a g e 106 | 109


Group 3. Other therapeutic agents useful for the treatment of poisoning. Listed below are certain therapeutic agents that are not antidotes according to the accepted definition; however, because of their established value and sometimes specific role in the management of poisoning, they border on the concept of antidotes. In practice, these agents are used frequently in cases of poisoning and in other medical circumstances. Most of them are considered to be essential drugs and should therefore be available for immediate use.

Agent

Indications/symptoms arising from poisoning

Benztropine

Dystonia

Chlorpromazine

Psychotic states with severe agitation Acute allergic reactions, laryngeal oedema,

Corticosteroids (systemic/topical)

bronchoconstriction, mucosal oedema (inhaled)

Diphenhydramine Diazepam

Dystonia Convulsions, excitation, anxiety, muscular hypertonia

Dobutamine

Myocardial depression

Dopamine

Myocardial depression, Vascular relaxation

Epinephrine (adrenaline)

Anaphylactic shock, cardiac arrest

Furosemide

Fluid retention, left ventricular failure

Glucose

Hypoglycaemia

Haloperidol

Hallucinatory and psychotic states

Heparin

Hypercoagulability states

Magnesium sulfate

Cardiac arrhythmias

Mannitol

Cerebral oedema, fluid retention

Oxygen

Hypoxia

Glucose

Hypoglycaemia P a g e 107 | 109


Group 4. List of antidotes and related agents now considered obsolete

Antidote Acetazolamide Ascorbic acid Aurintricarboxylic acid (ATA) ß-aminopropionitrile Castor oil Copper sulfate Cyclophosphamide Cysteamine Diethyldithiocarbamate Fructose Guanidine precursors Levallorphan Nalorphine Potassium permanganate Sodium chloride Sodium salicylate Strychnine Sulfadimidine Potassium permanganate Sodium chloride Tannins Thioctic acid Tocopherol (vitamin E) Tolonium Universal antidote Tannins

Indicated for Modification of urinary ph Methaemoglobinaemia Beryllium Caustics As cathartic As emetic Gold-paraquat Paracetamol Thallium Ethanol Botulism Opiates Opiates Fluorides As emetic Beryllium Central nervous system depressants Amanitine Fluorides Fluorides Alkaloids Amanitine Paraquat Chloride methaemogiobinaemia Ingested poisons Alkaloids

P a g e 108 | 109

treatment and management of poisoning

treatment and management of poisoning

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