A DISSERTATION ON

PROSPECTIVE STUDY OF CLINICAL PROFILE AND OUTCOME OF CHILDREN PRESENTING WITH POISONING IN GOVT MOHAN KUMARAMANGALAM MEDICAL COLLEGE HOSPITAL, SALEM

Submitted to

THE TAMILNADU DR. M. G. R. MEDICAL UNIVERSITY, CHENNAI

In partial fulfillment of the regulations for the award of

M. D. DEGREE IN PAEDIATRICS BRANCH VII

GOVERNMENT MOHAN KUMARAMANGALAM MEDICAL COLLEGE, SALEM APRIL 2017

Government Mohan Kumaramangalam Medical College Hospital

DECLARATION BY THE CANDIDATE

I hereby declare that this dissertation titled “PROSPECTIVE STUDY

OF CLINICAL PROFILE AND OUTCOME OF CHILDREN

PRESENTING WITH POISONING IN GMKMCH, SALEM” is a bonafide and genuine research work carried out by me under the guidance of

DR.T. S. SUNDARARAJAN, M.D,D.C.H , Professor, Department of

Paediatrics , Government Mohan Kumaramangalam Medical College Hospital,

Salem, Tamil Nadu, India.

Place : Salem Signature of the Candidate

Date : DR.M. S.BALAMURUGAN

Government Mohan Kumaramangalam Medical College Hospital

CERTIFICATE BY THE GUIDE

This is to certify that this dissertation “PROSPECTIVE STUDY OF

CLINICAL PROFILE AND OUTCOME OF CHILDREN PRESENTING WITH

POISONING IN GMKMCH, SALEM” is a bonafide work done by

Dr.M.S.BALAMURUGAN in partial fulfillment of the requirement for the degree of

M. D. in PAEDIATRICS, examination to be held in 2017.

Signature of the Guide

Dr. T.S.SUNDARARAJAN,M.D.,D.C.H., Place: Salem Professor & Head of the Department, . Date : Department of peadiatrics Government Mohan Kumaramangalam \ Medical College Salem,Tamil Nadu,India .

Government Mohan Kumaramangalam Medical

College Hospital

ENDORSEMENT BY THE HEAD OF DEPARTMENT

This is to certify that this dissertation titled “ PROSPECTIVE STUDY OF

CLINICAL PROFILE AND OUTCOME OF CHILDREN PRESENTING

WITH POISONING IN GMKMCH, SALEM” is a bonafide work done by

Dr.M.S.BALAMURUGAN under overall guidance and supervision of

Dr. T.S.SUNDARARAJAN,M.D,D.C.H., Professor and Head, Department of paediatrics, Government Mohan Kumaramangalam Medical College Hospital, in partial fulfillment of the requirement for the degree of M. D. in Paediatrics, examination to be held in 2017.

Seal & Signature of the of the H.O.D

Dr. T.S.SUNDARARAJAN,M.D.,D.C.H., Professor & Head of the Department, Department of Paediatrics, Government Mohan Kumaramangalam Medical College, Salem, Tamil Nadu, India.

Government Mohan Kumaramangalam Medical College Hospital

ENDORSEMENT BY THE DEAN OF THE INSTITUTION

This is to certify that this dissertation titled“PROSPECTIVE STUDY OF

CLINICAL PROFILE AND OUTCOME OF CHILDREN PRESENTING

WITH POISONING IN GMKMCH, SALEM” is a bonafide work done by Dr.M.S.BALAMURUGAN under the guidance and supervision of

Dr.T. S. SUNDARARAJAN, M.D, D.C.H., Professor and Head, Department of

Paediatrics, Government Mohan Kumaramangalam Medical College Hospital, in partial fulfillment of the requirement for the degree of M. D. in Paediatrics, examination to be held in 2017.

Seal & Signature of the of the Dean

Prof. Dr.P.KANAGARAJ, M.D., Dean Government Mohan Kumaramangalam Medical College, Salem, Tamil Nadu, India.

Government Mohan Kumaramangalam Medical College Hospital

COPYRIGHT

I hereby declare that THE TAMILNADU DR. M. G. R. MEDICAL

UNIVERSITY, CHENNAI, TamilNadu, India, shall have the rights to

preserve, use and disseminate this dissertation / thesis in print or electronic

format for academic / research purpose.

Place: Salem Signature of the Candidate

Date : DR.M. S.BALAMURUGAN

© THE TAMILNADU DR. M. G. R. MEDICAL UNIVERSITY, CHENNAI, Tamil Nadu, India

Acknowledgement

I feel greatly indebted to Prof.Dr.P.KANAGARAJ, M.D., Dean, Govt.

Mohan Kumaramangalam Medical College, for permitting me to undertake this study.

I would like to express my humble gratitude and sincere thanks to Prof.

Dr.T.S.SUNDARARAJAN,M.D,D.C.H, Head of the Department of

Pediatrics, Govt. Mohan Kumaramangalam Medical College and Hospital,

Salem for his excellent guidance and encouragement during this study.

I sincerely thank our Associate Professors Dr. D.SAMPATH KUMAR

M.D., D.C.H for their invaluable guidance to complete this dissertation.

I am thankful to Dr. P. SAMPATH KUMAR, M.D., DCH,

Assistant Professor of Paediatrics for his guidance and help for completion of this dissertation in time.

I am grateful to Dr. S.GOPINATHAN, M.D,D.C.H., Asst. Professor of Pediatrics for showing special interest in my work and for his valuable advice.

I am thankful to all my Assistant Professors Dr. P. KANIMOZHI

M.D, D.C.H., Dr.K. SURESH KANNAN, M.D., Dr.P.VASUMATHY,

M.D., Dr. V. NARMADHA, M.D., Dr.M.NIRMALA, M.D. DCH,

Dr.V.ANUREKHA,M.D., Dr.AMUDHADEVI,M.D., Dr.V.BALAJI,M.D.,

Dr. R. SASIVARADHAN,M.D, Dr.A.LOGESH ANAND, M.D,

Dr.P. KUMAR,M.D.,D.C.H., Department of Pediatrics, for their valuable suggestions.

I thank all my PG colleagues, friends and staff members of the department of Pediatrics who helped me a lot in completing this dissertation successfully.

I extend my hearfelt thanks to all my family members for their support rendered during my study.

Last but not the least; I bow my head in reverence to all our patients who formed the back bone of this study without whom this would not have been possible.

LIST OF ABBREVIATIONS

ABG ARTERIAL BLOOD GAS AChE ACETYL CHOLINEESTERASE AgNO3 SILVER NITRATE AgCl2 SILVER CHLORIDE ARDS ACTE RESPIRATORY DISTRESS SYNDROME APTT ACTIVATED PARTIAL THROMBOPLASTIN TIME AST ASPARTATE AMINOTRANSFERASE ALT ALAINE TRANSAMINASE CCL4 CARBON TETRACHLORIDE BT BLEEDING TIME CBC COMPLETE BLOOD HEMOGRAM CUSO4 COPPER SULPHATE CT CLOTTING TIME CO CORBONMONAXIDE CO2 CORBONDIOXIDE CNS CENTARL NERVOUS SYSTEM CVS CARDIOVASCULAR SYSTEM ECG ECLECTRO CARDIOGRAPHY FFP FRESH FROZEN PLASMA ET ENDOTRACHEAL GABA GAMMA AMINO BUTYRIC ACID G6PD GLUCOSE 6 PHOSPHATASE DEFICIENCY HCL HYDROCHLORIC ACID IM INTRAMUSCULAR IMS INTERMEDIATE SYNDROME INR INTERNATIONAL NORMALIZED RATIO IV INTRA VENOUS LFT LIVER FUNCTION TEST MODS MULI ORGAN DYSFUNCTION SYNDROME NAHCO3 SODA BICARBONATE NICU NEWBORN INTENSIVE CARE UNIT

OPC ORGANO PHOPHOROUS COMPOUND OG ROUTE ORO GASTRIC ROUTE PAM PRALIDOXIME PCV PACKED CELL VOLUME PEGLEC POLYETHYLENE GLYCOL PT PROTHROMBIN TIME PICU PAEDIATRIC INTENSIVE CARE UNIT RFT RENAL FUNCTION TEST RS RESPIRATORY SYSTEM SC SUBCUTANEOUS SSU SECONDS SAYBOLT UNIVERSAL WBI WHOLE BOWEL IRRIGATION

TABLE OF CONTENTS

PAGE SI.NO TITLE NUMBER

1 1 INTRODUCTION

3 2 AIM AND OBJECTIVES

4 3 REVIEW OF LITERATURE

58 4 MATERIALS AND METHODS

61 5 OBSERVATION AND RESULTS

88 6 DISCUSSION

95 7 CONCLUSION

96 8 SUMMARY

ANNEXURES

(I)BIBLIOGRAPHY (II)STUDY PROFORMA (III)PARENT CONSENT FORM (IV)MASTER CHART

LIST OF TABLES

S.NO Title Page no 1 Poisons syndromes 18 2 Mini toxidromes 20 Screening laboratory clues in toxicological 3 22 diagnosis 4 Specific antidotes for poison 30 5 Additional antidotes 34 6 Age distribution of poisoning 61 7 Sex wise distribution of poisoning 63 8 Educational status of parents 63 9 Socioeconomic status 64 10 Type of poisoning 65 11 Agent of poisoning 67 12 Mode of poisoning 69 13 Route of poisoning 70 14 Pre referral treatment 72 15 Duration between poisoning and presentation 74 16 Mode of presentation 75 17 Duration of hospital stay 77 18 Duration of ICU stay and antidote used 79 19 Outcome of this study 79 20 Outcome in relation to age 81 21 Outcome according to duration and presentation 81 22 Outcome in relation to clinical features 82 23 Outcome in relation to ICU stay 84 24 Outcome in relation to antidote used 84 25 Outcome in relation to duration of hospital stay 86

LIST OF FIGURE Page S.NO Title No 1 Pie chart showing age distribution 62

2 Pie chart showing sex distribution 62

3 Bar diagram showing type of poisoning 66 Bar diagram showing agent of poison in relation to 4 socio economic status 68 5 Bar diagram showing mode of poisoning 71

6 Bar diagram showing route of poisoning 71

7 Bar diagram showing pre referral treatment 73 Bar diagram showing duration between poisoning and 8 73 presentation 9 Pie chart showing mode of presentation of poisoning 76

10 Bar diagram showing duration of hospital stay 78 Bar diagram showing outcome of poisoning in relation 11 80 to age Bar diagram showing correlation of outcome with 12 83 duration between poisoning and presentation Bar diagram showing correlation of outcome with 13 83 clinical feature Bar diagram showing correlation of outcome with ICU 14 85 stay Bar diagram showing correlation of outcome with 15 antidote used 85 Bar diagram showing correlation of outcome with 16 duration of hospital stay 87

ABSTRACT

ABSTRACT

Background: Child hood poisoning covers the entire gamut from accidental ingestion in toddlers and preschool children to intentional over dosage in adolescents..

Aims and Objectives: Our study is aimed at finding out the clinic- epidemiological profile of poisoning regarding age, sex, type of poison, manner of poisoning, common clinical features, duration between poisoning and presentation to hospital , duration of hospital stay ,to find out the different agents involved , duration of ICU stay, pre referral treatment and treatment given and evaluating the outcome of those children admitted with Poisoning in NICU,PICU and paediatric ward at

GMKMCH, Salem

Materials and methods: All children below 12 years of age admitted during the one year study period with a history of poisoning were included. Animal bites, snake and scorpion envenomation, chronic poisoning, drug allergy were excluded. All children were examined, investigated and treated according to hospital policy .Outcome of poisoning were recorded.

Results: There were 143 cases of children with poisoning admitted.

Accidental poisoning constituted 88.1% cases (n126),7.7% (n11) were suicidal and the remaining 4.2%(n6) were homicidal .In most of the cases poisoning was due to hydrocarbons followed by pesticides. kerosene oil was the most common substance followed by OPC. The higher incidence of poisoning was found in lower middle socio economic class 65.7%(n136) an analysis of the outcome showed that 95.1% were discharged home and death in 4.9% (n7) cases.

Conclusion: The highest incidence of poisoning was observed in children below 5 years of age and from lower middle socio economic group. Most of the poisons were household products and the most common nature of exposure was accidental in most of the cases, recovery was complete.

Key words: Childhood poisoning, Accidental ,hydrocarbons , Outcome.

INTRODUCTION

INTRODUCTION

“POISONS AND MEDICINES ARE OFTEN TIMES SAME SUBSTANCES GIVEN WITH DIFFERENT INTENTS” -Peter mare Latham (1789-1875)

Childhood poisoning is one of the emergencies commonly encountered in paediatric practice. Since the usage of chemicals have been increase in houses acute poisoning cases also increased. Accidental poisoning is more common in childhood and most of the cases are preventable[1].

Among hospital admissions Poisoning is the 12th most common in children. It contributes majority of total cases and fatality. In many poisoning cases in childhood is a result of oral consumption of poisonous agents [2].

The present day household offer toxic substances at every corner including caustics ,insecticides and medicines that provide easy settings for childhood inquisitiveness to end in disaster(3). These agents are often mistaken by children for soft drinks or water.

Average incidence among varies studies range from 0.3% to 7.6%

[2-6]. The poisoning type and incidence of poisoning also differ from hospital to hospital and has a special bearing on the emergency paediatrics care of the area [7,8,9].

Accidental poisoning is common in the preschool or toddler age group(less than 5 years) because the children up to this age have exploratory tendency for the substance by taking it into the mouth while the suicidal poisoning is due to arguments by parents or stress [10].

Male children predominate the poisoning accidents accounted for by their greater degree of activity and more number of cases belong to poor socio economic status because of less space

The present day households offer toxic substances at every corner including caustics, insecticides and medicines that provide all too easy settings for childhood inquisitiveness to end in disaster

So far, the studies on poisoning have not undertaken this hospital, hence there is a definite need for the study to known the definite and detailed epidemiological evidence of poisoning.

My study is intended to known the various epidemiological factors, clinical profile and outcome of children presenting with poisoning cases admitted in our Department at Govt Mohan Kumara mangalam Medical college hospital , Salem.

AIMS And OBJECTIVES

AIMS AND OBJECTIVES OF STUDY:

1. Our study is aimed at finding out the clinic-epidemiological profile

of poisoning regarding age, sex, type of poison, manner of

poisoning, common clinical features, duration between poisoning

and presentation to hospital , duration of hospital stay, duration of

ICU stay, pre referral treatment and treatment given for the

children admitted with Poisoning in NICU,PICU and paediatric

ward at GMKMCH, Salem

2. To find out the different agents involved in childhood poisoning.

3. Evaluating the outcome of those children admitted with poisoning.

REVIEW OF LITERATURE

REVIEW OF LITERATURE

INCIDENCE:

Averagely incidence among various studies range from 0.3% to 7.6% and this contributes significant number of admissions to the hospital wards.

DEFINITION:

The definition of poison is vague and unsatisfactory for

(a) A substance which is harmless in small quantities may act as poison and cause death when taken in large amount and

(b)Bacterial toxins are not regarded as poisons in ordinary sense of term.

A poison has been defined as a substance (solid, liquid or gaseous) which when introduced into or absorbed by living organisms causes injury or death.

“CLASSIFICATION OF POISON(11)”

Poison may be classified according to the chief symptoms which they produce.

(1) “CORROSIVES:[1]Strong acids”

(a) Mineral or inorganic acids: Sulphuric, nitric, hydrochloric

(b) organic acids: carbolic acid, oxalic, acetic, salicylic

(2) Strong alkalis: Hydrate and carbonates of sodium,potassium

and ammonia

(3) Metallic salts: Zinc chloride, ferric chloride, copper sulphate,

silver nitrate, potassium cyanide, chromates and bichromates

(2) “IRRITANS: [1]Agricultural (2)Inorganic:”

(a) Non metallic:

Phosphorus, iodine,chlorine,bromide,carbontetrachloride

(b) Metallic: arsenic, antimony, copper, lead , mercury, silver,

zinc

(c) Mechanical : powdered glass, diamond dust, hair

(3) Organic:

(a) Vegetable: abrus precatorius, castor, calotropis

(b) Animal: snake and insect venom, canthrides

(3) “SYSTEMIC”:

(1) Cerebral :

(a) CNS Depressants: Alcohols, general anaesthetics, opioid

analgesics, hypnotics, sedatives and etc

(b) CNSStimulants:

(1) cyclicantidepressents, amphetamine, caffeine, hyocyamus,

cannabis, cocaine , etc.

(2) Spinal: Nux vomica , gelsemium

(3) Peripheral: conium, curare.

(4) Cardiovascular: Aconite, quinine, oleander, tobacco, cyanide

(5) Asphyxiants:CO,CO2,Hydrogen sulphide

(6) Miscellaneous: Food poisoning, botulism

Poison may also be classified according to their morbid anatomic manifestations

(1) No morphological changes are present which can be attributed to

direct chemical action by the toxic agent, e.g. acute CNS

depressants (alcohols, sedatives, hypnotics, tranquilisers,

salicylates); chemical asphyxiants (carbon monoxide, hydrogen

cyanides); organophosphates and most alkaloids. The

abnormalities seen at autopsy result from shock and terminal

anoxia.

(2) Systemic lesions are produced without injury at the portal of entry,

e.g. acute haemolytic poisons (arsine, nitrobenzene).

3) Injury is present at portal of entry without systemic injuries, e.g.,

corrosives, chlorine, sulphur dioxide. Death may be caused by

local tissue changes (pulmonary oedema) or acute vasomotor

collapse.

4) Local and systemic injuries are present, e.g., heavy metals.

NATURE OF POISONING :

I) Ideal Homicidal Poison : It should have the following character

1) Cheap and Easily available,

2) Colourless, odourless and tasteless,

3) If mixed with food or drinks should not produce clear change ,so

that suspicious is avoided

4) More toxicity,

5) Signs and symptoms should mimics a natural disease

6) There should not be any antidote

7) There should be no post-mortem changes

8) Unable to detected by routine chemical test s and

9) Destroyed rapidly or made undetectable in the body.

Organic compounds of fluorine (used as rodenticides), and thallium satisfy several of the above criteria. Arsenic and aconite are commonly used.

(II) Ideal Suicidal Poison : It should have the following character

1) Cheap

2) Easily available

3) Highly toxic

4) Pleasant taste

5) Able to mix with drinks or food

6) Producing painless death.

(III) Stupefying : Datura, cannabis indica, chloral hydrate.

(IV) Abortion : Calotropis, oleanders, aconite, croton, semecarpus,

cantharides, ergot, lead arsenic, mercury, potassium permanganate,

etc.

(V) Accidental : Household poison. Abusing children below 21/2

years contribute to non accidental poisoning.

(VI) Rare : Bacteria, insulin.

(VII) Cattle Poisoning : The usual motive is destruction of cattle of an

enemy, or to obtain the hides. The usual poisons are abrus

precatorius, oleanders, calotropis, organophosphorus, arsenic,

aconite, strychnine, zinc phosphide, nitrate, etc.

(VIII) Arrow Poisons : Abrus precatorius, croton oil, calotropis,

aconite, strychnine, curare and snake venom are used as arrow

poisons.

(IX) Aphrodisiacs : Cantharides, cocaine, cannabis, opium, strychnine,

arsenic.

POISONING MAY RESULT FROM :

(1) Criminal purpose

2) The ingestion of poison /toxin mistake

3) Wrong medicinal preparation with a poison

4) Intake of increased dosage of medicine with poison

5) Drug overdose

6) Addiction to drugs.

7) Venomous animal /insect bite

8) Food particle contaminated bacterial with bacterial toxins and

bacterial life forms

ROUTES OF ADMINISTRATION

IN ORDER OF RAPIDITY OF ACTION :

1) Inhalation form. Early vaporisable products like gaseous ,smoke

producing substances aerolized products. Solvents like benzene,

toluene, xylene, acetone, methylene chloride, methyl chloroform,

and CCL4 ,solvent sniffing by young adults/youths or household

accidents. Industrial accidents Eg. Radiation hazards like CO,

methane.

2) Intravenous injection.

3) Intramuscular, subcutaneous and intradermal injection.

4) Application to a wound.

5) Application to a serous surface.

6) Application to a bronchotracheal mucous membrane.

7) Introduction into stomach.

8) Introducing substances like aspirin, phenobarbitone, chlorpromazine,

with rectal, vaginal and urethral orifices to produce effects

systemically.

9) Applying of poisonous substances to the intact skin like Organic

phosphates can penetrate the skin and cause poisoning and people

can die.

FATE OF POISONS IN THE BODY :

The greater part of a poison is thrown out of the body as a result of vomiting and purging. The portion absorbed is mainly deposited in a less soluble form in the liver, which either partially metabolises or completely destroys it. The unaltered portion enters into the general circulation and acts on the body as a whole, or on the particular organs with which it has special affinity, provided the poison is not destroyed or made harmless by the kidneys and muscles.

ROUTES OF ELIMINATION :

The absorbed portion of poison is mainly excreted by the kidneys and to some extent by the skin. Other routes are bile, milk, saliva, mucous and serous secretions. The unabsorbed portion is excreted in the vomit and faeces.

ACTION OF POISONS :

I) LOCAL : The local action by coming in direct contact with part.

(1) Chemical destruction by corrosive.

2) Irritant will produce inflammation and congestion.

3) Effects on motor and sensory nerves, e.g., tingling of skin and tongue by aconite, dilation of pupils by belladonna or datura.

(II) REMOTE : Remote action produced either by corrosives causing severe pain followed by shock(reflex)or by poison being first absorbed into the system through the blood, and excreted through tissue will produce organ damage .e.g., cantharides acting on kidneys produces nephritis, nux vomica .

(III) COMBINED : Drugs like carbolic acid, oxalic acid, phosphorus, etc., have local and remote actions.

CAUSES MODFYING ACTIN OF POISONS

I) QUANTITY : More the quantity, more severe are the toxic effects. A large quantity of poison taken orally may cause excessive vomiting, causing its rapid elimination and decreased toxicity e.g.,alcohol,

CUSO4. Action can be modified by varying the dose significantly more amount of arsenic produce death without causing noticeable symptoms by shock.

(II) FORM : (A) PHYSICAL STATE : Poisons act most rapidly when gaseous and less when liquid. In case of solids, the action depends on their solubility.

(B) BY CHEMICAL MIXATION : Based on the mixing ability of the poisonous substances with one another action of a poison varies. This chemical combination of poisons, HCL &AgNO3 when combined together form ,un dissolvable salts of Agcl2 which is harmless. Some poisons are not soluble in water, they become soluble in H2O and also mixes with acid in the stomach and being dissolved in to the blood like copper arsenite and lead carbonate.

(C) MECHANICAL COMBINATION : when mixing of poison with inactive or inert substance may produce alteration of poisons like using very small amount /increased concentration of acid producing corrosion when same amount mixed with large quantity of water decrease become harmless.

(III) MODES OF ADMINISTRATION OF VARYING POISON:

The fastness of the action is in the order described under routes of administration. As rough guide if the active dose by the mouth is considered as unit, The rectal dose is about one-and half to tow, and the hypodermic dose about one-fourth. A lethal dose is usually ten or more times the maximum medicinal dose.

The rate of absorption from the alimentary canal is variable. The stomach when empty without food it absorbs more quickly than the filled with substances ,also the content of stomach’ nature is in favour of dissolving the poison like when you take phosphorous poison and drink oil following it. This will enhance the action of phosphorous by increasing its absorption. Gastro enterostomy hastens the entry of poisons into the small bowel. Sleep, narcosis and trauma causing gastrointestinal stasis will retard it. Retardation during gastrointestinal absorption, dilution and alteration during digestion. The skin is on the whole a bad absorptive organ.

(IV) CONDITION OF THE BODY (A) AGE : Age has a considerable effect upon the dosage of drugs. Underdeveloped enzyme system in children less than two years , more susceptible to the effect of most drugs. There are some drugs of which children can take more than their proportionate dose, e.g., mercury and belladonna. There are some of which they can not take even a proportionate dose e.g. mercury and belladonna. There are some of which they cannot take even a proportionate dose e.g., morphine.

B) IDIOSYNCRACY : It may be defined as the inherent personal hypersensitivity to the agent in question. Certain people are sensitive for certain drugs and even articles of diet e.g., shellfish, eggs and fruit. The

symptoms usually occur in the skin as an urtricaria, but may be of more general nature with dysponea, rigors, fever, diarrhoea, haemorrhage from the bowel and albuminuria. Fatal cases are comparatively rare, but symptoms may be alarming or dangerous, iodine, bromine, opium, belladonna, cocaine, aspirin, penicillin, and mercury are common examples of drugs to which many people are allergic.

(C) HABIT : Habituation will change the certain drug effects in the body. Tolerance is the organism capability in showing decreased response to a chemical substance in a specified dose when compared to its same action when giving on the same specified dose. Opium preparations frequently taken, lose much of their effect after a time, and require to be administered in increased doses. Addicts can tolerate quantities of the drug which would endanger life if they had been initial does. Tolerance is seldom a natural phenomenon. The same effect of habit occurs from the use of tobacco, alcohol, cocaine, morphine and other alkaloids, It is more usually a feature of natural substances, less of synthetic drugs, such as barbiturates, chloral, etc.

D) STATE OF HEALTH : A unhealthy person not tolerates than healthy. General debility, senility, chronic or disabling disease may cause death of a person to a dose that is ordinarily safe, e.g. CO may kill at a blood saturation of only 25 to 30 % . Some substances can be used in

certain diseases /conditions with no harm. But when these substances are used in other conditions, even smaller quantity can be poisonous.

E) SLEEP AND INTOXICATION :when a person is taking poison along with alcohol or any other substance intoxication or immediately going to sleep after consuming poison ,time of action of the poisoning gets delayed.

F) CUMULATIVE ACTION : Poisons which are eliminated slowly may accumulate in the body when given in repeated doses for a long time and may ultimately produce symptoms of poisoning.

TYPES OF POISONING :

1) Acute or sudden onset of poisoning can be taking single large bulky dose and also by consuming small quantity multiple times within a short duration .

2) Chronic method is consuming minimal quantity for a long time causing progressive worsening of the general condition. The poisons which are commonly used for the purpose of chronic poisoning are arsenic, phosphorus, antimony and opium.

3) Sub acute poisoning shows features of both acute and chronic poisoning.

4) Fulminant poisoning is produced by a massive dose. In this death occurs rapidly, sometimes without preceding symptoms.

IDENIFICATION OF POISON(12)

1) In the Living : There is no single symptom, and o definite group of symptoms, which are absolutely characteristic of poisoning. The closest resemblance to disease, may be produced by thallium poisoning. A detailed clinical history is of great importance.

The following groups of symptoms are suggestive of poisoning.

1) The immediate appearance of pain abdomen, nausea, vomiting,

loose stools.

2) The unexplained coma with miosis.

3) The sudden onset of seizure.

4) Delirium with dilated pupils.

5) Paralysis, especially of lower motor neurone type.

6) Jaundice and hepato cellular failure.

7) Anuria or oliguria with proteinuria and haematuria.

8) Persistent cyanosis.

9) Rapid onset of neurological or gastrointestinal illness in persons

known to be occupationally exposed to chemicals.

A priority of suspicion is needed to recognize poisoning if history

is unavailable.

 Whenever a normally active children suddenly gets sick with

symptoms of chocking, suffocation ,breathlessness,

swollen/puffiness of face ,abnormally cold or warmth in a

surrounding of an empty bottle lying around ,spilling of chemical

substances over the dress & empty cover of tablets or medicine.

 By taking into account of the number of tablets or chemical left in

the bottle we can assume the quantity of ingestion.

TABLE:1:POISONS SYNDROMES (TOXIDROMES) (13) VITAL MENTAL BOWEL TOXIDROME PUPILS SKIN OTHER POSSIBLE TOXINS SIGNS STATUS SOUNDS Sympatho mimetic Hypertension, Agitation, Dilated Diaphoretic Normal to Amphetamines, cocaine, tachycardia, psychosis, increased PCP, bath salts, ADHD Hyperthermia delirium, medication violence Anti cholinergic Hypertension, Agitated, Dilated Dry, hot Diminished Ileus ,urinary Antihistamines, tricyclic tachycardia, delirium, coma, retention antidepressants, atropine, hyperthermia seizures jimson weed Cholinergic Bradycardia BP Confusion, Small Diaphoretic Hyperactive Diarrhea, urination, Organophosphates and temp coma, bronchorrhea, (insecticides, nerve agents) typically normal fasciculations bronchospasm, carbamates (physostigmine, emesis, neostigmine, phridostigmine) lacrimatin, Alzheimer medications, salivation myasthenia treatments Opioids Respiratory Depression, Pinpoint Normal to Normal to Methadone, buprenorphine, depression coma, euphoria decreased decreased morphine, oxycodone, bradycardia, heroin, etc. hypotension, hypothermia Sedative-hypnotics Respiratory Somnolence, Small or Normal Normal Barbiturates, depression, coma normal benzodiazepines, ethanol HR normal to

Serotonin Hyperthermia, Agitation, Dilated Diaphoretic Increased Neuromuscular SSRIs, lithium, MAOIs, syndrome(similar tachycardia, confusion, hyper linezolid, tramadol, findings with hypertension or coma excitability:clonus, meperidine, neuroleptic hypotension hyper reflexia dextromethorphan malignant syndrome) (autonomic (lower extremities instability) > upper extremities) Salicylates Tachypnea, Agitation, Normal Diaphoretic Normal Nausea, vomiting, Aspirin and aspirin- hyperpnea, confusion, tinitus, ABG with containing products, methyl- tachycardia, coma primary respiratory salicylate hyperthermic alkalosis and primary metabolic acidosis; tinitus or difficulty hearing Withdrawal Tachycardia, Agitation, Dilated Diaphoretic Increased Lack of access to ethanol, (sedative-hypnotic) tachypnea, tremor, seizure, benzodiazepines, Hyperthermia hallucinosis, barbiturates, GHB, or delirium excessive use of flumazenil tremens Withdrawal (opioid) Tachycardia Restlessness, Dilated Diaphoretic Hyperactive Nausea, vomiting Lack of access to opioids or anxiety diarrhea excessive use of naloxone

TABLE-2-“MINI-TOXIDROMES(14)”

Based on specific symptoms and signs we can identify a specified

poisoning agent.

It can help us in diagnosing the particular agent of toxin.

MANAGEMENT:

GENERAL PRINCIPLES OF MANAGEMENT INCLUDE

 Stabilization of Airway ,Breathing, Circulation ,Dextrose and emergency

management

 Focused history and problem oriented examination

 Decontamination, elimination or removal of absorbed toxin

 Laboratory and supportive management

 Antidote

 Monitoring and supportive management

 Preventive education and environmental change

LABORATORY INVESTIGATIONS

In lab testing of the serum or urine sample based on consumption

of the substance and its proportion of toxicity by the measuring the level

of poison. This is less need for toxic screening in children as the

substance is known clearly.

TABLE-3- Screening Laboratory Clues in Toxicologic

Diagnosis

PREVENTION OR REDUCTION OF ABSORPTION

The term ‘gastrointestinal decontamination’ includes interventions

that are used to prevent the absorption of an ingested toxin.

SYRUP IPECAC(15)

Ipecac has no role in the routine management of acutely poisoned

patients.

GASTRIC LAVAGE.(16,17,18)

 Unless intubated, gastric lavage is contraindicated. If children whose

airway protective reflexes are lost.

 Gastric lavage is not indicated in case of hydrocarbon with high

aspiration potential has been ingested.

 Gastric lavage is also not indicated, in case of corrosive ingestion

 Advantage from effective GI Contamination method(19)

 Cases with immediately reaching the hospital

 Consuming life endangering or massive quantity

 Ingestion of sustained release tablets

 Drugs that could delay gastric emptying

METHOD

1. Intactness of gag reflex tested and confirmed.

2. After making the baby restrained place him or her in trendelenburg

posture to avoid or reducing the bowel movement and decreasing the risk

of aspiration.

3. Place large bore single lumen tube in OG Route

4. Ryles tube is placed properly

5. NS in aliquots of 10-15 mL/kg of body weight administered into the ryles

tube and aspirated by continuous suction until all the toxic substances has

been removed. procedure repeated several times to bring a clear

secretion.

After one hour of swallowing poison only 30% of the toxin

substance is removed . Hence its use beyond the 1st hour is questionable.

Increasing the likelihood of a absorption can occur by improper

method.(20)

Nasogastric aspiration is performed by placing a nasogastric tube

(smaller than a orogatric tube) and aspirating gastric contents without

instilling water.

“NG aspiration also effective in cases of liquid poison consumption(21”).

ACTIVATED CHARCOAL:

It can be administrated less than 1 hour consumption of poison(22)

Activated charcoal ‘adsorbs’ poisons dissolved in the intestine such that

the poison remains in the gut rather than being absorbed into circulation.

It reduce the systemic absorption of many drugs and may reduce the

need for antidote therapy for children who present within 2 hours of

acetaminophen ingestion(23).

However, activated charcoal has not been shown to improve the

outcomes of non-selected poisoning patients.

Currently super activated charcoal products with increased surface

area are available. These products decreased systemic absorption of the

ingested toxins when compared with standard activated charcoal(24,25).

They are also more palatable than standard charcoal products.

‘If given less than one hour after taking poison this will decrease

the absorption of poisoning around 70-75%.If gives in the ratio of 10:1

maximum toxins are absorbed(26)’.

Recommended dose is 1 g/kg body weight.

Method of Administration

Normal mental status :

 Mix activated charcoal in fruit juice or bottled drinks for children.

 Charcoal is more edible when gives along with juice by not reducing its

effect.

 Young one may protest or fight or resist for drinking this surflly for

effective action.

 Introduces a Naso gastric Tube in young children to ensure prompt

administration.

Depressed mental status or respiratory failure :

 Intubate (for airway protection ) and use nasogastric tube for

administration.

 Elevate head end by 450

Complications

Though as an inert substance it can cause vomiting and results in

aspiration(27,28,29,30),there by entering lungs and cause lung injury. when

given through misplaced NG tube into the trachea can cause life

threatening complications, ARDS and death. The Bowel sounds should

be monitored, since constipation and rarely intestinal obstruction have

been reported.

Indications for Activated Charcoal

Medications that are well bound by charcoal are drugs that undergo

enterohepatic or enteroenteric circulation such as :

 Salicylates, Phenobarbital , Carbamazepine, Digoxin, Theophyline

Substances which are not adsorbed by activated charcoal are

remembered by the mnemonic PHAILS :

 P : Pesticides

 H : Hydrocarbons

 A : Acids, alkalis, alcohols

 I : Iron

 L : Lithium

 S : Solvents.

CATHARSIS

Cathartic agents have been advocated in poisoned victims to

increase GI movement and favour fast removal of toxic substances

expulsion from the GI tract(31).

Commonly used osmotic agents are magnesium citrate and

sorbitol. These substances increase the retaining time of colonic fluid in

the colon .

“WHOLE BOWEL IRRIGATION (WBI)(32,33,34)”

Large quantity of solution are introduced through the rectum till

the excretion of the fluid content become clear .PEGLEC solution has

been made in such away to avoid the maximum absorption or secretion in

the GI mucosa.

 Elevate head end of bed to at least 45 to prevent aspiration.

 Discontinue the infusion for 30 minutes, if emesis occurs and restart at

half the previous rate.

 Increase the rate as tolerated.

 Administer Metoclopramide (antiemetic), since it increase GI motility.

 Provide a bedside commode for patients who are awake.

It is safer even in 44 litre can be given without side effects. Rates

of administration are 500-1,000 mL/h.

Major side effect of this method is abdominal distention cramps

,vomiting.

Advantage of gastric decontamination has to be weighted

against its harm and also taken into account of the toxins effect .It can be

judiciously used in life threatening poison .so that we can make use of

this method of decontamination effectively rather than thinking if the

patient had substances by using forceful administration of charcoal ,

stomach wash etc,..

Enhancement of Excretion : Ion Trapping

URINE ALKALINIZATION

Alkalinisation(35) of urine by giving I.V NaHCO3 to make PH 7.5

rather than a diuresis as the prime objective of treatment.

 It can be used in moderately severe paracetamol poisoning who do not

need hemodialysis.

 Urine alkalinization cannot be recommended as first line treatment in

cases of phenobarbital poisoning as multiple-dose activated charcoal is

superior.

FORCED NEUTRAL DIURESIS

This is a method of flushing the toxin out of the system by increasing the administration of fluids.

Increase urinary flow by infusion of large volume of intravenous crystalloid.

Indications : Lithium, bromide ingestion.

Contraindications : Pulmonary edema, cerebral edema and renal failure.

HEMODIALYSIS

An invasive procedure, hemodialysis is reserved for specific life- threatening toxins in the intensive care setting.

Indications

 Methanol , ethylene glycol

 Salicylate, phenobarbital,

 Theophylline, lithium.

ANTIDOTES(36)

For Opioid toxicity rarely naloxone can be used as a emergency antidote

Despite the vast number of toxins/poisons and drugs that are ingested only few antidote only available.

Following table contain specific antidote dosage and their side effects.

TABLE:4: SPECIFIC ANTIDOTE FOR POISON

ADVERSE EFFECTS, POISON ANTIDOTE DOSAGE ROUTE WARNINGS, COMMENTS Acetaminophen N. Acetyl cysteine 140 mg/kg loading, followed PO Vomiting (patient-tailored regimens (Mucomyst) by 70 mg.kg q4h are the norm) N. Acetyl cysteine 150 mg/kg over 1 hr, IV Anaphylactoid reactions (most (Acetadote) followed by commonly seen with loading dose) 50mg/kg over 4 hr, followed (Higher doses of the infusion are by often recommended depending upon 100mg/kg over 16 hr the acetaminophen level and the degree of injury) Anticholinergic Physostigmine 0.02 mg/kg over 5 min; may IV/IM Bradycardia, seizures, bronchospasm repeat q5- 10min to 2 mg max Note: Do not use if conduction delays on ECG Benzodiazepines Flumazenil 0.2 mg/kg over 30 sec; if IV Agitation, seizures; do not use for response is inadequate, repeat unknown ingestions q1 min to 1 mg max Blockers Glucagon 0.15 mg/kg bolus followed by IV Hyperglycemia, vomiting infusion of 0.05-0.15 mg/kg/hr Calcium channel Insulin 1 unit/ kg bolus followed by IV Hypoglycemia blockers infusion of 0.5-1 unit/kg/hr Follow serum potassium and glucose closely

Calcium salts Dose depends on the specific IV calcium salt

Carbon Oxygen 100 % FIO2, via non-re Some patients may benefit from Monoxide breather mask (or ET if hyperbaric oxygen (see text)

intubated) Inhalation

Cyanide Cyanide kit: 1 crushable ampule; inhale 30 Methemoglobinemia

Amyl nitrate sec of each min Inhalation Sodium nitrate 0.33 mL/kg of 3% solution if IV Methemoglobinemia Hypotension hemoglobin level is not known; otherwise, based on tables with product Sodium thiosulfate 1.6 mL/kg of 25% solution; IV If inducing methemoglobinemia is may be repeated q30-60min contraindicated; consider only using to max of 50 Ml the thiosulfate component of the kit Hydroxocobalamin 70 mg/kg (adults: 5 g) given IV Flushing/ erythema, nausea, rash, (Cyanokit) over 15 min heamaturia, hypertension, headache

Digitalis Digoxin-specific 1 vial binds 0.6 mg of IV Allergic reactions (rate), return of Fab antibodies digitalis glycoside; condition being treated with digitalis (Digibind; # vials = digitalis level x glycoside DigiFab) weight in kg/100

Ethylene glycol, Fomepizole 15mg/kg load; 10mg/kg IV Infuse slowly over 30 min; methanol q12hx 4 doses; 15mg/kg q12h If fomepizole is not available, can until EG level is <20 mg/dL treat with oral ethanol (80 proof) Iron Desferoxamine Infusion of 5-15 mg/kg/hr IV Hypotension (minimized by avoiding (max: 6 g/24hr) rapid infusion rates) Isoniazid (INH) Pyridoxine Empirical dosing : 70 mg/kg IV May also be used for mushroom (max dose = 5g) ingestions

Lead and other, BAL (dimercaprol) 3.5 mg/kg/dose q4hr, for the Local injection site pain and sterile st heavy metals 1 day; subsequent dosing abscess, vomiting, fever, salivation,

(e.g., arsenic, depends on the toxin IM nephro toxicity inorganic Caution: prepared in peanut oil;

mercury) Deep contraindicated in patients with peanut allergy Calcium disodium 35-50 mg/kg/day x 5 days; IV Vomiting, fever, hypertension, EDTA may be given as a continuous arthralgia, allergic reactions, local infusion or 2 divided inflammation, nephro toxicity doses/day (maintain adequate hydration, follow UA and renal function)

Dimercaptosuccini 10 mg/kg/dose q8h x 5 days, PO Vomiting, hepatic transaminase c acid (succimer, then 10mg/kg q12hx 14 days elevation, rash DMSA, Chemet)

Methemoglobine Methylene blue, 0.1-0.2 mL/kg (1-2 mg/kg) IV Vomiting, headache, dizziness, blue mia 1% solution over 5-10 min; may be discoloration of urine repeated q30-60min

Opioids Naloxone 0.01-0.1 mg/kg; IV Acute withdrawal symptoms if given adolescents/adults: 0.04-2 mg, to addicted patients repeated as needed; may give May also be useful for clonidine continuous infusion ingestions (inconsistent response)

Organophosphate Atropine 0.05-0.1 mg/kg repeated q5- IV/ET Tachycardia, dry mouth, blurred s 10min as needed vision, urinary retention

Pralidoxime (2- 25-50 mg/kg over 5-10 IV/ Nausea, dizziness, headache, PAM) min(max: 200mg/min); can be IM tachycardia, muscle rigidity, repeated after 1-2hr, then q10- bronchospasm (rapid administration) 12hr as needed Salicylates Sodium Bolus 1-2 mEq/kg followed IV Follow potassium closely and replete bicarbonate by a continuous infusion as necessary Goal urine pH 7.5-8.0 Sulfonylureas Octreotide and 1-2 g/kg/dose (adults 50-100 IV/SC dextrose g) q6-8hr Tricyclic Sodium Bolus 1-2 mEq/kg; repeated IV Indications: QRS widening antidepressants bicarbonate bolus dosing as needed to (>110ms), hemodynamic instability; keep QRS <110 msec follow potassium

TABLE-5-ADDITIONAL ANTIDOTES

COMMON CHILDHOOD POISONING

OPC’S AND CARBAMYL POISONING

Epidemiology

Incidence is <1% of total cases. The incidence of this poisoning is more common in children from lower socio economic group of family.

Inexperience, immaturity, uneducated and not knowing the risk potential plays a major role for accidental intake of poison.The most affected are agricultural workers and their childrens.(37)

Pathophysiology

OPC group binds to one of the ester sites of AChE(38) where as carbamates bind to the anionic site of AChE .So that pralidoxime Which acts on the anionic site and causing cleavage of OPC’S from AChE

Cannot be given in Carbamate poisoning and also ageing occurs in OPCS by the loss of alkyl group .So P2AM will not act after 48 hours after poisoning .

Since AChE is phosphorylated it cannot breakdown acetylcholine

.So the action of Ach increases causing symptoms and signs related to stimulation of muscarinic and nicotinic receptors.

Regeneration of phosphorylated AChE will take days to month time.

Dosing

It can vary from one compound to another(39) .Household formulation are less potent than agricultural. Children should be watched over for 2-3 days to detect delayed effect of poison.

Symptoms

 CNS Depression ,hypotonia are more common

 Muscarinic symptoms are uncommon(40)

Pesticides are absorbed through mucosal surface ,skin and inhalation.

PICTURE:1:- Showing salivation in OPC Poisoning

PICTURE:2: Showing mydriasis after atropine

Respiratory failure(41,42)

Due to both depression of centrally located respiratory centres or by peripheral suppression.

Intermediate Syndrome

No relation to the type or forms of compounds.Its develops 2-4 days after poisoning when the cholinergic symptoms settle down.

Main symptoms of IMS are weakness of respiratory muscle ,limb muscles and weakness of muscles supplied by cranial nerves.More common with OPC’S like diazinon, dimethoate, methlparathion, methamidaphos, monocrotophos, fenthion and e thylparathion.(41,43)

Most of the symptoms are increased secretion ,GI motility

,bronchospasm and bradycardia.(44)

Treatment(45-51)

 We have to maintain the airway ,breathing and circulation initially

for all poisoning

 Gastric decontamination by stomach wash through activated

charcoal plays little role since its absorbed rapidly being lipid

soluble .Decontamination(46,50,51) determines the outcome of varies

intoxication .

 Atropine neutralizes the muscarinic effects of acetylcholine by

competitive antagonism at postsynaptic muscarinic receptors.

Dose :

 Children < 12 years with signs of moderate of severe toxicity :

 Administer 0.05 to 0.1 mg/kg of atropine.

 In children > 12 years and adults with signs of moderate to severe

toxicity: Administer 2 to 4 milligram

 Every 5 minutes interval Increases the dosage twice till secretions

resolve (dry mouth), crepitations disappear, oxygenation improves

and tachycardia >140/minute occurs.

 Repeat doses, based on recurrence of symptoms for 2-12 hours.

 Atropine should be used for at least 24 hours to reverse the

cholinergic sign, while the organophosphate is metabolized.

 Dosing can be decreased when symptoms do not recur for 6 hours.

 The Cochrane group recommends incremental dose administration

of atropine as the standard of care.

 P2AM(protopan) is a reactivater of AChE.

 Dose : 25-50 mg/kg (5% solution) in isotonic saline over 5- 10

minutes as early as possible followed by a continuous infusion of 8

mg/hour.

 The drug is probably not useful 36 hours after exposure.

RODENTICIDE POISONING (47,48,50,51)

 Rodenticides are not leading agents for severe poisoning .

 Two types: one dose and multiple dose types.

PICTURE:3: Shows rat killer paste

Contents:

 They are commonly The components of rodenticide are

usually aluminum and zinc phosphide, As, thallium,Ba

compounds, warfarins and super warfarins group.

 Warfarins are commonly used group of poison.

Pathophysiology

Warfarin act by inhibiting enzymes producing activation of Vit K thereby depleting VitK dependent clotting factors and resulting in

PT/INR prolongation after 11/2-2days.Phosphides release lethal potent phosgene gas.

Clinical presentation

 Chestpain, hypertension,unconsciousness can occur

 Liver and renal failure eventually occur

 Cardiac injury also been reported

 Bleeding diathesis occurs from petechial hemorrhage to

intracranial bleed.

 Thalium may cause seizure and renal failure

Toxic dose varies from one compound to another .Toxicity rarely occurs since concentration is low in rat killer compounds.

Lab tests

PT,INR , aPTT , BT ,CT ,LFT ,RFT ,ECG, CBC can be done to asses the organ Dysfunction and bleeding manifestation at the time and two days after admissions .X-Ray abdomen shows radio opaque metals used in poisoning,AgNO3 detected from gastric content analysis

Treatment

 We have to maintain the Airway,breathing and circulation first.

 Stomach wash ,cleaning the skin is a must to remove dermal

absorption

 Vit-K Can be given if bleeding tendencies present

 FFP Can be given to save life of children with this poisoning.

 Monitor in case of asymptomatic or accidental case for 3 days

 For thalium poisoning –Prussian blue is the specific antidote

given250mg/day in QID till the urinary concentration of thalium

less than 0.5mg.

Specific antidote not available for Aluminum phosphide intoxication. (48).

HYDROCARBON AND RELATED COMPOUNDS POISONING

Hydrocarbon is the most common poison in our country(52,53)

Hydrocarbon have low viscosity causing aspiration to be earlier..Further with reduced surface tension in the lungs makes it to spread in the lung tissue early and with high volatile nature displaces alveolar air and disrupts ventilation on aspiration.

Kerosene viscosity is <60SSU where as mineral seal oil is <47

SSU viscosity causes more severe complication lipoid pneumonia with chemical pneumonitis .Mineral oil, lubricating oil, fuel oil has >100 SSU

,So low aspiration effect.

Because of the lipid soluble nature of hydrocarbons they go into airway cause pneumonitis(54), within hours of aspiration

.Polymorphonuclear leukocytes are found in the secretion of bronchioles resulting in cough, crepitations ,bronchospasm and x ray changes.Patients become symptomatic within few hours and recover with in 48hours -8 days.

GI symptoms are common resulting in aspiration

May produce CNS depression due to anesthetic property followed by hypoxia.(55)

Hypoxia causing other CNS problems like dis inhibition, depression,euphoria like in alcohol intoxication.

Clinical features

Locally cause burning sensation in mouth ,gastric symptoms like belching, abdominal pain, diarrhoea,nausea these don’t require any treatment . Increased leukocyte count and fever in kerosene ingestion does not correlate with an infection.(56,57)’’

Imaging

A chest radiography will show features of chemical pneumonitis.

PICTURE-:4: Shows aspiration Pneumonitis

Treatment

Airway stabilization is the foremost important in treatment

Oxygen supplementation should be given to everyone with prongs or mask

Complications

(a)Aspiration pneumonia

(b) Pneumothorax

(c)Barotrauma in meachanically ventilated child

( d)Cardiovascular collapse.

“Sudden cardiac death due to vasospasm of coronaries can occur (58)’’

ACETAMINOPHEN

 Most commonly used in children as analgesic and antipyretics.

 Therapeutic dose range from 10-15 mg/kilogram every 4-6 hourly.

Maximum amount of 4g/day can be given. Adults are more prone

for toxicity than adolescents because of increased sulfation among

the adolescents.(59)

 For liver toxicity to develop 250 mg/kg in a single consumption

would sufficient.

 Higher plasma concentration occurs within 30 minutes to 2 hours

Four stages of toxicity(60)

1. Stage I :Within 24 hours-patient may be asymptomatic or with GI

upset. sweating. fatigability and pallor.

2. Stage II :Within 24-48 hours-GI symptoms go away and right hypo

chondrial tenderness with jaundice and elevation of liver enzymes

with PT prolongation.

3. Stage III :Within72-96 hours-acute liver failure going for hepatic

encephalopathy , coagulopathy and MODS.

4. Stage IV days to week-Resolution or progression of liver failure or

death.

Laboratory Investigations

 AST ,ALT, Bilirubin,PT levels

 Blood concentration of acetaminophen done within 24 hours to

assess the amount ingested and peak plasma concentration

attaining time in case of extended release tablets.

 Rumack - Mathew nomogram helps in interpretation

Management

(A) Maintaining airway ,breathing and circulation and gastric lavage

(B) N-acetyl cysteine (NAC) is the antidote should be given within 24 hours after ingestion. It is given through NG tube or orally.

Dose-140 mg/kg loading dose followed by 70mg/kg QID up to 18 total doses. In case of severe vomiting not controlled with anti emetics ,IV use can be given. It can be mixed with water, juice, drinks to avoid

emesis.10%-20% NAC diluted to 5% solution. IV Use also be given in late presentation.(61,62,63) .

ANTICONVULSANTS

Phenytoin,sodium valproate,barbiturates are the most commonly used antiepiletics in children.

“Core facts (64,65,66,)”

Phenytoin follows zero order kinetics and hepatic metabolism.

T ½ is >8 hours .Metabolising site is liver

Valproaic acid increases GABA ergic neurons and also follows hepatic metabolism. The t½ is 6-16hrs .

Toxic effects are

1. CNS Effects- Nystagmus, ataxia, dystonia, lethargy, dyskinesia,

Seizure and coma

2. Respiratory depression, cardiac arrhythmias as well as heart blocks

can occur

3. Hypersensitivity reaction like erythema multiforme and stevens-

Johnson syndrome, hepatic failure, bone marrow suppression also

occurs

4. Carbamazepine cause fever ,flushing ,depression and delirium

5. Rashes and hypothermia with barbiburate poisoning.

CORROSIVE POISONING

PHENOL (CARBOLIC ACID)

Phenolicompoundslikecresol,hydroxyquinine,resorcinol,hexachlor ophene been used as antiseptics, caustics, germ killer Phenol or its related compounds .children drinks it accidentally.

Denaturation of protein occurs and kills cells causes capillary damage locally and thrombus formation in superficial vessels, respiratory depression occurs. Cardiac and renal failure also occur.

Symptoms like excruciating pain. dysentary, hypertension, difficulty in breathing ,coma, seizures and pulmonary edema occurs after few days.

Death is by respiratory or cardiac centre depression.

Lab test--Add ferric chloride to urine and the colour of urine changes to violet or blue if phenolic compounds present.

Treatment-

 Intubation if necessary

 Stomach wash using plain water glycerine till the secretion are

clear.

 Albumin egg also used .Renal failure corrected by peritoneal

dialysis or hemodialysis.

 Caster oil application used for skin burns.

HOUSE HOLD MATERIAL POISONING

NAPHTHALENE

It is a produce of coal tar. Been used as moth balls,bathroom perfumes ,cupboard , antifungals treatment for scabies and pediculosis.

Lethal dose

Average lethal dose is 5-15 gms.2gms ingestion becomes fatal. In

G6PD deficiency, small dose can be fatal. Newborn are more prone.

Absorption of naphthalene from skin is favoured by thinner and oil application. Newborns chew naphthalene balls and cause toxicity on them. Trans placentally also it can cross and cause toxicity. Hemolysis caused by epoxide metabolite. Occur effects are due to lipid peroxidation and oxidative stress. Newborns are more susceptible because they cannot conjugate naphthalene and bilirubin causing kernictrus.

Immediate toxicity due to intravascular hemolysis,fever ,anemia, renal &hepatic failure, lelevated total count, hemoglobinuria,GI

Symptoms also occur. Methemoglobinemia, optic neuritis and pulmonary edema occurs in children with poisoning.

Lab test: Hemoglobin, retic count , PCV, peripheral smear study, RBC count ,S.Billirubin, methemoglobin level.

Urine analysis for haemoglobin. RBC’s have heinz bodies with aniso poikilocytes. Reticount increases for short duration.

Treatment:

 Cleaning of external surfaces with warm water

 Person should be removed from poisonous surrounding when

inhaling it

 Stomach with activated charcoal ,maximum 50 gram can be used

 Fatty meals should be avoided

 Supportive care

 Blood transfusion till the hemogobin reaches eight grams

 Steroids, hemodialysis and exchange tranfusion

 “In cases of methemoglobinemia of >30%, intravenous methylene

blue is indicated(67)”

CAMPHOR POISON

It is produce of produced of Cinnamonum camphora wood.

Camphor is used as counter irritant, preservative, antipruritic, rubefacient(68).

Lethal dose is 0.5-1 gm, for infans-70mg/kg

Clinical features:

Camphor is absorbed early through mucosal surfaces. Smell of it comes in breathing

Uses

Camphor is used as rubefacient, counterirritant and antipruritic, as moth repellant, preservation, in dentistry with para chlorophenol for antibacterial activity, as carminative to relieve griping and as mild expectorant.

Toxicity

Lethal dose for children is 0.5 – 1 gm and for infants 70mg/kg(69).

Clinical effects

Camphor is readily absorbed from skin, GIT and respiratory tract.

Odour of camphor can be observed in breathe. Onset of symptoms is seen within 11/2 hours after ingestion. Burning sensation of stomach, GI

Symptoms, dilation of pupils, visual impairment occur. CNS Symptoms like headache, vertigo, delirium, myotonia, hallucination and seizure activity can occur

COWDUNG POWDER POISONING:

Cowdung powder is locally called as sanipowder and used to smear the floor mixed with water on festival season in rural areas .The clinical features of cowdung powder poisoning are due to heavy metals namely copper.

PICTURE :5 Showing cow dung powder

Clinical features start 15 to 30 minutes after ingestion and include metallic taste, increased salivation, burning in stomach, thirst,nausea vomiting, diarrhoea rarely mixed with blood, hematuria, oliguria, and renal failure. The neurological features include nonspecific muscle cramps, spasms, convulsions, focal deficits, coma and death.

Management : Since emesis is a feature of all case, there is no need to induce vomiting but gastric lavage with 1% ferrocyanide solution is very useful. This forms insoluble cupric ferrocyanide complexes.

Benzodiazepines is very effective for sedation and neurological findings and to allay anxiety.

PREVENTION EDUCATION AND ENVIRONMENTAL CHANGE

 Poisoning in young children is mostly accidental.

 It is the duty of parents and care givers to keep the home

environment safer for the curious toddler.

 Practice of storing toxic material in familiar containers like

mineral water bottles and cough syrup bottles should be stopped.

 Adult on chronic medication should not take the medicines in

front of the children.

 After consuming the medicine, container should be closed and kept

in a safe place beyond the reach of the children.

 Medicines should not be administered to the child in dark

environment as the toxic medications will be mistaken as routine

medicines.

 Parents must be educated about verifying the name, strength and

volume of the measure before giving the medicine.

 In case of intentional poisoning, child must be counselled by the

child guidance team along with the family paediatrician. It should

be done when the child is still hospitalized as it will be difficult to

call them for follow up.

 Manufacturers should dispense the possible toxic drugs in child

proof containers and external appearance of the containers of these

oral medications must be different from medications meant for

external application.

 It is essential to be familiar with specific antidotes that must be

readily available in both the emergency department and ICU.

REMOVING HOUSEHOLD ENDANGERMENTS:

Through incidence of house hold injuries are decreasing every year child belonging to 1-3 years of age group are more prone for injuries due to high activity and curiosity. Since they cannot reason out between harms and good thing become endangered easily.They will try to take and put things in their mouth for exploration which is very common among these age group.

How to prevent?

 Remove all reachable or touchable objects,harmful products by

carefully obscuring at children’s point of view.

 They can move chairs or little stools to climb up .so it can be

avoided by removing them from their reach

 Keep all the cupboards closed

 Label all the products into clear name and store in the original

bottle

 Give or store the poison centre /nearby hospital number in the

family member telephone.

STUDIES ON POISONING

1. NARAYAN PRASAD MODI et al (70) in 2013 studied 288 children who where <15 years of age in utkal .Majority(43%) were under 5 years. Male accounting 70% cases. Median duration between poisoning and presentation being 17 hours. 65.7% received pre-referral treatment in the form of decontamination(gastric lavage), atropine etc.

27.7% Snake bite followed by 17.3% kerosene and insecticide(12.4%) are the commonest agents involved in poisoning children. Accidental exposure being 85.8%. Suicidal cases being more common in >11 years age children(68%)(F:M 1.7:1). Most common presentation being respiratory distress(32.5%), cellulitis of limb(24.5%) and altered sensorium (18.3%).During treatment, 46.4% received antidote and

46.37% received antibiotics.Overall Mortality was 7%, the outcome is good with 92% survival.

2. NOWNEET KUMAR BHAT et al(71) in 2008 studied 117

Patients presented with acute poisoning during the study period. Median age was 4 years (range from 0.75-17.75 years). The majority of our patients (60.68%) were in the 1-6 year age group. Male to female ratio was 1.4:1. The majority of the patients resided in rural areas. In this study showed 37.61% Insecticides followed by 25%drugs and 19% kerosene were the commonest agents involved. Accidental Poisoning was

more(97.2%) in 1-6 years of age group and suicidal poisoning were common in the 12-18 year group.30.7% of children received with no symptoms,the rest developed symptoms related to toxic ingestion and required symptomatic or definitive treatment. Gastric lavage was done in

34% patients and specific antidote was given to 28(23.9%) patients with mortality of four patient .

3.BASAVARAJ et al(72) in 2 013 studied a total of 50 patient patients presented with acute poisoning. Majority of the resided in urban areas. Drugs (40%),kerosene oil(24%) and insecticides(20%) were the agents most frequently implicates.52%cases were suicidal and the above children belongs to age group of 12-18 years. Almost all cases in 1-6 years age group were accidental in nature. One case died in kerosene ingestion .

4.VASANTHAN et al.(73) In 2015 studied 75 cases of poisoning out of the total 4074 admissions. Accidental poisoning constituted 73.3% cases and 26.7% were suicidal. Fuel (28%) or drugs (21.3%), and kerosene was the most common substance (28.0%) followed by camphor

(14.7%). The higher incidence of poisoning was found in lower middle socio-economic class (56.0%). The outcome showed that 92.0% were discharged home, 4.0% and death in 4.0% cases.

5. DR ARCHINTA MANDAL et al(74)-In this prospective cross sectional study(n-89) ,71 patients came from rural areas,39(43.8%) cases were OPC poisoing,22(24.7%) cases were hydrocarbons. In this sudy 6 cases were died. Total no of death was 6(6.67%) and that of survival was

83(93.25%) giving a p-value of <0.0001 which is statistically significant.

6.HAMID MH et al(75) in 2005 studied 344 cases in Lahore over 5 years and concluded that 59% cases were less than 2 years with median age of

18 months ,80 % belonged to urban areas and presented during summer and monsoon seasons(57%).Drugs were the leading cause(51%) followed by petroleum(23%),chemicals (8.4%) and household products(7.6%).the most common symptom seen was gastrointestinal(40%) and overall mortality was 11%.

7.PRADHUM RAM et al(76) in 2010 studied 81 cases in Mangalore over one year among which 50.6% were male while 49.4% girls.

Kerosene (28.4%) and OPC (19.8%) were the most common agents causes for poisoing and overall mortality was 7.4%.84% of patients were discharged.

8. RATHORE et al(77) in 2011 studied 100 cases prospectively in lucknow over one year period and observed 62% were below 5 years of age and70% male.55% belong to urban while 45% belongs to rural areas.

kerosene and snake bite were the most common agents ,both accounting for 31%cases each. Overall mortality was 4%.

9. GANGAL RAVI et al(78) in 2015 studied and observed the median duration of the patient was 5.5 with female predominates.

Insecticides and pesticides (55.04%), house hold agents (21.48%) and drugs (11.41%) were the most common agents causing poison among children. Most common presenting symptoms was vomiting (63.75%) followed by altered consciousness (38.92).63% were accidental were as

32% were suicidal and median duration of hospital stay was 2 days. Over all mortality was 4.71%.

10. DR.HALAK VASAVADA et al(79) in 2012 studied over three years period and observed the mean age of poisoning was 4.5 years out of

176 cases .male and female ratio was 1.17:1,Most common poisoning among the studied population was kerosene. Insecticides poisoning frequency was low. Most of the patients belongs to urban population.

Accidental poisoning found in 98.59% and rest being suicidal. Mean duration of hospital stay 3.3days. Vomiting is the commonest clinical presentation. Mortality was 5.1%.

11. UTKARSH KOHLI et al(80) in 2004 studied over 2 years period among 111 children and observed mean age was 3.12 years, Among them 1-3 years was 63.9%.majorities belonging to urban areas. Incidence

of kerosene 27.9%,Drug19.8%,insecticides 11.7%.. 96.9% accidental, remaining being suicidal. 32.4% were asymptomatic, 66.7% symptomatic. No mortality was found.

12. SBUDHATHOKI et al(81) in 2005-2008 studied in Nepal among 122 children and observed 43.4% children received pre referral treatment .45.1% was Organophosphorus poisoning followed by hydrocarbons 19.8%,mushroom 8.2% and organochlorine 8.2%.50% received antidote during treatment. Overall survival rate was 87.4% and mortality was 12.6%.

MATERIALS AND METHODS

MATERIALS AND METHODS

PLACE OF STUDY

Govt Mohan kumaramangalam Medical College Hospital ,Salem-

636001

STUDY DESIGN

Prospective study

PERIOD OF STUDY

July,2015-June ,2016

SOURCE OF DATA

All children less than 12 years of age admitted in our NICU ,PICU

,and paediatric ward with history of poisoning or intoxication during the study period of July , 2015 to June ,2016 at Govt Mohan Kumara mangalam Medical College Hospital , Salem.

SAMPLE SIZE AND DESIGN

This is a hospital based prospective study where children less than

12 years of age ,admitted with history of poisoning during study period of 12 months from July 2015 to June 2016 were included in the study group.

INCLUSION CRITERIA:

1. All children less than 12 years of age who come with history of poison consumption/intoxication, irrespective of signs and symptoms, accompanied or unaccompanied by poison or container.

2.Children with doubtful history of ingestion of poison but with definite symptoms and signs of poisoning.

EXCLUSION CRITERIA

1. Chronic poisoning

2. Snake bite , scorpion sting and other poisonous bite

3. Idiosyncratic reactions to drug

4 .Food poisoning

METHOD OF COLLECTION OF DATA:

Children admitted with history of poisoning in NICU,PICU and paediatric ward during study period will be studied regarding age ,sex

,social demographic data. Ethical committee clearance was obtained in our hospital to conduct our study. Informed consent obtained from parents and care givers of the children before including them in the study

.Details of the poison will be noted as, name, type of agent, route of exposure, time of arrival to hospital after poison exposure, manner of poisoning .Clinical examination will be done by seeing vital signs, systemic examination of CVS, RS, Abdomen, CNS. Necessary

investigations will be done according to the type of poisoning by investigations like complete blood hemogram, renal function test and liver function test, chest-x ray, electrocardiography ,echo, urine routine, ultrasound abdomen, cholinesterase level, ABG analysis, serum calcium, serum electrolytes and treatment given according to standard protocol including psychiatry counselling and outcome noted.

RESULTS AND OBSERVATIONS

OBSERVATION AND RESULTS

During the period of 12 months from July, 2015to June, 2016,

6305 cases got admitted in the paediatric department at Govt Mohan kumara Mangalam, salem.Out of this 143 cases were childhood poisoning

AGE DISTRIBUTION (figure:1)

Table-6.Age Distribution of poisoning

Age Frequency Percent

<1 YEAR 6 4.2 1-3 YEARS 87 60.8 3-6 YEARS 25 17.5 6-12 YEARS 25 17.5 Total 143 100.0

The mean age of case was 3.80 years.In this study maximum number of cases 60.8 % was seen in the 1-3 years age group(n-87) followed 17.5% in the age group 3-6 years(n-25) .Similarly 17.5 % in the age group 6-12 years(n25) and less commonly 4.2% in the less than one year age group.

FIGURE:1:Pie Chart Showing Age Distribution

Age distribution of poisoning

6-12 YEARS <1 YEAR 17% 4%

3-6 YEARS 18% 1-3 YEARS 61%

FIGURE:2:Pie Chart Showing Sex Distribution

Sex Distribution

FEMALE 38%

MALE 62%

SEX WISE DISTRIBUTION (figure:2)

Table:7:-Sex wise distribution of poisoning

Sex Frequency Percent

Male 88 61.5

Female 55 38.5

Total 143 100.0

In our study out of 143 cases 61.5% were male children (n-88) and

38.5% were female children(n-55).MALE TO FEMALE RATIO 1.6:1

EDUCATIONAL STATUS OF PARENTS

Table:8:-Educational status of parents

. Educational status of parents Frequency Percent Illiterate 4 2.8 Primary 16 11.2 Middle school 87 60.8 High school 31 21.7 Graduate 2 1.4 Secondary 2 1.4

Intermediate 1 0.7 Total 143 100.0

Most of the parents belong to the middle school level (n87)60.8% followed by 21.7% (n31)in high school level.Then 11.2%(n16) in primary level.Then 2.8%(n-4) in the illiterate level, 1.4%(n-2) in both graduate and secondary level and 0.7%(n-1) in intermediate level.

SOCIOECNOMIC STATUS

Table-9- Socioeconomic status

Socioeconomic status Frequency Percent Lower 21 14.7 lower middle 94 65.7 Upper lower 10 7.0 Upper middle 18 12.6 Total 143 100.0

In this study maximum 65.7%(n94) belong to lower middle socioeconomic status followed by 14.7% in lower class and 12.6% in upper middle class. Least in the upper lower (n10)7%.

TYPE OF POISONING (figure-3)

Table-10 -Type of poisoning

(a) Type of poisoning Frequency Percent Corrosive 8 5.6 Drugs 10 7.0 Household 16 11.2 Hydrocarbon 54 37.8 Insecticide 31 21.7 Pesticide 7 4.9 Plant 16 11.2 Unknown 1 0.7 Total 143 100.0

Type of poisoning Chi Age Corrosive Drugs Household Hydrocarbon Insecticide Pesticide Plant Unknown Total p square N % N % N % N % N % N % N % N % <1 2 33 1 17 2 33 1 17 6 YEAR 1-3 2 2 5 6 11 13 48 55 16 18 2 2 3 3 87 < YEARS 62.12 0.001 3-6 5 20 1 4 1 4 5 20 6 24 2 8 5 20 25 ** YEARS 6-12 1 4 4 16 2 8 7 28 3 12 7 28 1 4 25 YEARS Total 8 5.6 10 7 16 11.2 54 37.8 31 21.7 7 4.9 16 11 11.2 0.7 143

In this study 37.8% (n54) belong to hydrocarbon group,

21.7%(n31) in the insecticide group ,11.2% (n16) in both household and plant group .7% (n-10)belongs to drugs ,5.6%(n-8)belong to corrosive

,4.9%(n7) belongs to pesticides and 0.7%(n1) in unknown group.

Chi square for type of poisoning according to age group from 0-12 year-

X2 is 62.12-p <0.001-which is significant

FIGURE-3-Bar diagram Showing Type of poisoning in relation to

Age

60 Type of poisoning

50 Corr osive

Drug s 40 Household

30 Hydr ocarbon

Insecticide 20 Pesti cide

10 Plant

Count 0 Unknown <1 YEAR 3-6 YEARS 1-3 YEARS 6-12 YEARS

Age

AGENTS OF POISONING (figure-4)

Table-11- Agents of poisoning

Agent of poison Frequency Percent 1%GBHC 1 0.7 Aluminium phosphide 2 1.4 Amytrptaline 3 2.1 Ant killer 2 1.4 Bleaching powder solution 1 0.7 Camphor 3 2.1 Carbamates 5 3.5 Cowdung powder 10 7.0 Dhatura 1 0.7 Diesel 1 0.7 Kerosene 43 30.1 Mineral spirit 11 7.7 Mushroom 2 1.4 Napthalene ball 1 0.7 Oduvan leaf 4 2.8 Oleander seed 9 6.3 Oraganophosphorous 14 9.8 Organochloride 1 0.7 Paracetamol 2 1.4 Phenol 7 4.9 Phenytoin 2 1.4 Phorate powder 4 2.8 Progestin 1 0.7 Pyrethrins 10 7.0 Ratkillerpaste/yellow 2 1.4 phosphorus Sodiumvalproate 1 0.7 Total 143 100.0

In this study kerosene(30.1%) , organophosphorous (9.8%), mineral spirit(7.7%), pyrethrins(7%) and oleander seed(6.3%) poisoning being the common poisoning agents .

FIGURE-4- Bar diagram showing Agent of poison in relation to socio economic status

Sodiumvalproate Ratkillerpaste/yellow phosphorus Pyrethrins Progestin Phorate powder phenytoin Phenol Paracetamol Organochloride OPC

Oleander seed

Oduvan leaf Napthalene ball Mushroom

Mineral spirit Agent ofpoison Agent kerosene Diesel Dhatura Cowdung powder Carbamate Camphor Bleaching powder solution Ant killer Amytrptline Aluminium phosphide 1%GBHC

0 5 10 15 20 25 30 35 40 45 50

lower lower middle Upper lower Upper middle

MODE OF POISONING(figure-5)

Table -12-Mode of poisoning

(a)

Mode of poison Frequency Percent Accidental 126 88.1 Homicidal 6 4.2 Suicidal 11 7.7 Total 143 100.0 (b)

Mode of poison Chi Age Accidental Homicide Suicidal Total p square N % N % N % <1 YEAR 5 83 1 17 6

1-3 87 100 87 YEARS < 3-6 69.26 23 92 2 8 25 0.001** YEARS 6-12 11 44 3 12 11 44 25 YEARS Total 126 88.1 6 4.2 11 7.7 143

In this study accidental poisoning being the most common 88.1%(n-

126).Least mode of poisoning is homicide(4.2%).Among the accidental poisoning 1-3 years(61%) being the commonest age group with male predominance(41%).the incidence of homicidal poisoning is equal in both male and female sex(2%).suicidal poisoning is more common in 6-12 years and more common in male sex.

Chi square of p- value in mode of poison with relation to age group is

<0.001-significant.

ROUTE OF POISONING(figure-6)

Table-13-Route of poisoning

(a)

Route of poison Frequency Percent Dermal absorption 1 0.7 Injection 1 0.7 Oral 141 98.6 Total 143 100.0 (b)

Route of poison Dermal Chi Age Injection Oral Total p absorption square N % N % N % <1 YEAR - - - - 6 100 6 1-3 YEARS 1 1 1 1 85 98 87 3-6 YEARS - - - - 25 100 25 1.31 0.971 6-12 ------25 100 25 YEARS Total 1 0.7 0.7 1 141 98.6 143

In this study oral ingestion is the most common route

98.6%(n141),least common shared by parenteral and dermal absorption(0.7%) with chi square of p- value 0.971 is not significant.

Female 6 2 3

12 YEARS 12 Male

- 5 1 8

6

Female 13 10

6 YEARS 6 -

Male 10 10

3

Age

Female 29 0 3 YEARS 3

- Male 58 0

1

Female 10

<1 YEAR <1 Male 4 10

0 10 20 30 40 50 60 70 Frequency

Accidental Homicide Suicidal

FIGURE:5: Bar diagram showing Mode of poisoning

100

80

60

40 Route of poison

Dermal absorption 20 Injection

Count 0 Oral <1 YEAR 3-6 YEARS 1-3 YEARS 6-12 YEARS

Age

FIGURE:6: Bar diagram showing Route of poisoning

PREREFERRAL TREATMENT(figure-7)

Table-14-Prereferral treatment

(a)

Prereferral treatment Frequency Percent No 95 66.4 Yes 48 33.6 Total 143 100.0 (b)

Pre referral treatment Age No Yes Total Chi square p N % N % <1 YEAR 4 67 2 33 6 1-3 YEARS 65 75 22 25 87 8.78 0.032* 3-6 YEARS 15 60 10 40 25 6-12 YEARS 11 44 14 56 25 Total 95 66.4 48 33.6 143

In this study 33.6% (n48) was given pre refferal treatment in the form of gastric lavage, atropine,oxygen and etc.66.4% were not given pre referral treatment with chi -square of p- value 0.032 is significant.

FIGURE-7-Bar diagram showing Prereferral treatment

70

60

50

40

30

20 Prereferral treatmen

10 No

Count 0 Yes <1 YEAR 3-6 YEARS 1-3 YEARS 6-12 YEARS Age

FIGURE-8-Bar diagram showing Duration between poisoning and presentation

80

60

40 Duration between poi

<1 H OUR

20 1-6 H OURS

7-24 HOURS

Count 0 >24 H OURS <1 YEAR 3-6 YEARS 1-3 YEARS 6-12 YEARS

Age

DURATION BETWEEN POISONING AND PRESENTATION

(Figure-8)

Table-15-Duration between poisoning and presentation

(a)

Duration between poisoning and Frequency Percent presentation <1 HOUR 13 9.1 1-6 HOURS 114 79.7 7-24 HOURS 12 8.4 >24 HOURS 4 2.8 Total 143 100.0

(b)

Duration between poisoning and presentation Chi Age <1 1-6 7-24 >24 Total p Hour hours hours hours square N % N % N % N % <1 1 17 3 50 2 33 6 YEAR 1-3 8 9 75 86 2 2 2 2 87 YEARS 15.17 0.086 3-6 3 12 17 68 4 16 1 4 25 YEARS 6-12 1 4 19 76 4 16 1 4 25 YEARS Total 13 9.1 114 79.7 12 8.4 4 2.8 143

The mean duration between poisoning and presentation was 4.31 hours. In this study most of the children 79.7% reached the hospital within

1-6 hours.9.1% Reached the hospital within one hour and 8.4% reached the

hospital with in 7-24 hours. Only 2.8% reached the hospital more than 24 hours with Chi- square of p- value 0.086 is not significant

MODE OF PRESENTATION(figure-9)

Table-16-Mode of presentation

Clinical feature/ Frequency Percent Mode of presentation NO 10 7.0 Abdominal pain 13 9.1 Altered sensorium 12 8.4 Cough 20 14.0 Fasciculation 1 0.7 Giddiness 10 7.0 Nasal bleed 1 0.7 Seizure 5 3.5 Tachypnea 17 11.9 Vomiting 54 37.8 Total 143 100.0

In this study 37.8% (n54) presented with vomiting commonly followed by cough14%(n20%),tachypnea11.9%(n17),abdominal pain

9.1%(n13),altered sensorium 8.4%(n12) .7% in asymptomatic and children presenting with giddiness .Least being seizure, nasal bleed and fasciculation respectively.

FIGURE-9- Pie diagram showing mode of presentation of poisoning

Mode of presentation

Asymptomatic 7%

Abdominal pain 9% Vomiting 38% Altered sensorium 8%

Cough 14%

Tachypnea 12% Seizure Giddiness Fasciculation 3% 7% 1% Nasalbleed 1%

DURATION OF HOSPITAL STAY

Table -17-Duration of hospital stay(figure-10)

(a)

Duration of hospital stay Frequency Percent <3 DAYS 18 12.6 3-5 DAYS 87 60.8 6-10 DAYS 37 25.9 >10 DAYS 1 0.7 Total 143 100.0 (b)

Duration of hospital stay 3-5 6-10 >10 Chi Age <3 days Total p days days days square N % N % N % N % <1 YEAR 6 100 6

1-3 14 16 48 55 24 28 1 1 87 YEARS 3-6 10.20 0.335 4 16 16 64 5 20 25 YEARS 6-12 17 68 8 32 25 YEARS Total 18 12.6 87 60.8 37 26 1 0.7 143

The mean duration of hospital stay was 4.5 days. In this study 60.8

% of the children was being discharged with in 3-5 days and 25.9% in 6-

10 days,12.6% in less than 3 days only 0.7% in more than 10 days

FIGURE-10-Bar diagram showing Duration of hospital stay

60

50

40

30 Duration of hostital

<3 D AYS 20

3-5 D AYS 10 6-10 DAYS

Count 0 >10 D AYS <1 YEAR 3-6 YEARS 1-3 YEARS 6-12 YEARS

Age

DURATION OF ICU STAY AND ANTIDOTE USED

Table-18-Duration of ICU stay and antidote used

No Yes Total N % N % ICU STAY 85 59 58 41 143 Specific antidote used 115 80 28 20 143

In this study 59% (n-41%) of children were admitted in ICU and 41

%(n-41) were not admitted in ICU. Out of 143 cases only 20%(n-28) were received specific antidote and 80% were received supportive treatment.

OUTCOME (figure-11)

Table -19-Out come of this study

Outcome Chi Sex Dead Discharged Total P square N % N %

Male 4 5 84 95 88 0.060 0.806 Female 3 5 52 95 55

Total 7 4.9 136 95.1 143

In this study 95.1%(n136) were discharged where as 4.9%(n7) died.

Fatality is more(n4) in male children than female(n3).

FIGURE-11-Bar Diagram showing Out come of poisoning in relation to age and sex

70

60

50

40

Frequency 30 56

20

29

10 13 13 10 10

5 0 2 0 0 1 0 1 1 1 1 Male Female Male Female Male Female Male Female <1 YEAR 1-3 YEARS 3-6 YEARS 6-12 YEARS Age

Dead Discharged

Table-20- Outcome in relation to age

Outcome Age Dead Discharged Total Chi square p N % N % <1 Year 1 17 5 83 6 1-3 Years 2 2 85 98 87 4.08 0.253 3-6 Years 2 8 23 92 25 6-12 Years 2 8 23 92 25 Total 7 5 136 95 143

In present study,mortality rate in <1 year is 17% and least belonging to 1-3 years(2%)

Outcome of death in relation to the age group according to the chi squre –X2-P-0.253 which is not significant.

Table-21- Outcome in relation to duration and presentation(figure-12)

Duration between Outcome Chi poisoning Dead Discharged Total p square and presentation N % N % <1 HOUR 1 8 12 92 13 1-6 HOURS 114 100 114 < 58.73 7-24 HOURS 3 25 9 75 12 0.001** >24 HOURS 3 75 1 25 4 Total 7 5 136 95 143

In this study mortality is 75% when duration between poisoning and presentation >24 hours and 8% in duration of presentation less than one hour.

According to chi-square-X2-58.73-p<0.001 value-which is clinically significant.

Table-22-Out come in relation to clinical features(figure-13)

Outcome Clinical feature/ Chi Mode of Dead Discharged Total p square presentation N % N % NO 10 100 10

Abdominal pain 13 100 13

Altered sensorium 7 58 5 42 12

Cough 20 100 20

Fasciculation 1 100 1 < 80.35 Giddiness 10 100 10 0.001**

Nasalbleed 1 100 1

Seizure 5 100 5

Tachypnea 17 100 17

Vomiting 54 100 54

Total 7 5 136 95 143

120

100

80

60

40 Outcome

20 Dead

Count 0 Discharged <1 H OUR 7-24 HOURS 1-6 H OURS >24 H OURS

Duration between poisoning and presentation

FIGURE-12-Correlation of outcome with duration between poisoning and presentation

60

50

40

30

20 Outcome

10 Dead Alterted sensorium Abdominal pain Fasciculation Nasalbleed Tachypnea Giddiness Vomiting Count 0 Cough Seizure Discharged NO

Clinical feature/Mode of presentation FIGURE-13-Correlation of outcome with clinical feature

In present study mortality is 58% when child presented with altered sensorium.

According to chi square of p-value <0.001in death related to clinical features is significant.

Table-23- Outcome in relation to ICU Stay (figure-14)

Outcome Chi ICU STAY Dead Discharged Total p square N % N % No 85 100 85 10.79 0.001** Yes 7 12 51 88 58 Total 7 5 136 95 143

In this study ,death in ICU stay is 12%(n7),88%(n51) were discharged from ICU.Death in ICU stay with chi square of p -value

<0.001 is clinically significant.

Table -24-Out come in relation to antidote used(figure-15)

Outcome Specific Chi antidote Dead Discharged Total p square used N % N %

No 2 2 113 98 115 < 12.57 Yes 5 18 23 82 28 0.001** Total 7 5 136 95 143

FIGURE-14- Correlation of outcome with ICU Stay

100

80

60

40

Outcome 20 Dead

Count 0 Discharged No Yes

ICU STAY

120

100

80

60

40 Outcome 20 Dead

Count 0 Discharged No Yes

Specific antidote used

FIGURE-15-Bar diagram showing Correlation of outcome with antidote used

In present study showed death is 18% (n5) in the specific antidote used group and 2% death in the other group were antidote not used.

Which is also significant according to p-value 0.001.

Table-25-Outcome in relation to duration of hospital stay(figure-16)

Outcome Duration of hospital Dead Discharged Total Chi square p stay (DAYS) N % N % <3 Days 3 17 15 83 18 3-5 Days 4 5 83 95 87 7.33 0.062 6-10 Days 37 100 37

>10 Days 1 100 1

Total 7 5 136 95 143

In this study death is 17% in < 3days of hospital day and 5% in 3-5 days duration, with chi square of p-value 0.062-which is not significant.

FIGURE-16-Bar diagram showing Correlation of outcome with Duration of hospital stay

100

80

60

40

Outcome 20 Dead

Count 0 Discharged <3 D AYS 3-5 D AYS 6-10 DAYS >10 D AYS

Duration of hospi tal stay (DAYS)

DISCUSSION

DISCUSSION

In our study we are trying to give the data in poisoning cases admitted to our hospital over the period of 12 months.

In the present study 143 children’s with poisoning were admitted during the study period

AGE DISTRIBUTION

In this study highest number of cases occur in the 1-3 years of age group(60.8%) followed by 3-6 years of age group(17.5%).In our study 6 cases were admitted less than one year of age group .youngest case is nineteen days old. In 3-6 years age group female predominant is more than male. Incidence of the poisoning highest in the 1-3 years age group in vasanthan et al study (73) and Dr Achinta Mandal et al study(74)

Children with age group of less than than 5 years have been affected more in concordance with many literature reports.(82,83,84).The high incidence less than 5 years because of inherent inquisitiveness and higher oral exploratory activity aide by their newly acquired mobility and hand skills.

SEX DISTRIBUTION

Highest incidence of poisoning occurred in male children(61.5%) than female children(38.5%).and male to female ratio 1.6:1.This is similar to many studies found a male preponderance.(70,74,78,80,81).

EDUCATIONAL STATUS OF PARENTS:

Most of the cases parents studied upto middle school level (60.8%)

Number of cases more in less educated parents group.

SOCIOECONOMIC STATUS

Most of the case parents belongs to lower middle class group(65.7%) according to modified kuppusamy scale. probably due to less educational status, more number of family members ,less storage spaces and overcrowding in these families. A similar study pattern was observed in a study done by vasanthan et al(73),ahamed et al (85),Pyarelal kajala(86)

TYPE OF POISONING

Among the type of poisoning most common is hydrocarbons

,kerosene oil(30.1%) is commonest agent involved .Is shows kerosene being the commonest household fuels used in lower middle class group families ,since it being kept in bottles on the floor in kitchen, children’s easily drink those bottles as water or playing due to curiosity. Similar results found in rathore et al,(77),vasanthan et al (73)studies, although other

studies from Moradabad conducted by ravi gangal found(78), Insecticides

&Pesticides to be the most commonly consumed substance and another study conducted in Pakistan(87) found drugs as the common poisoning agent. In our study the second common agent involved in poisoning is

OPC. Attributed to the agriculture based rural population. Similar result also found in narayana Prasad Modi et al study.(70)

The third commonest agents involved is mineral spirit or thinner, usually mixed with paints for painting the houses. It also comes under hydrocarbons group. Children accidently were drinking it as water. This type of poisoning found in the children’s families involved in the building construction work.

The next commonest poisoning agents is cowdung powder

(7%)shared with pyrethrins . Cowdung powder commonly used in rural areas for mopping the floor in festival seasons. pyrethrins are found in mosquitoes repellents and liquids .Oleander seed and oduvan leaf poisoning though common in adult group, significant number of cases also occured in adolescent age group. Households poisoning (11.2%) commonly encountered are naphthalene, camphor and rat killer paste and etc,. Drug constitutes (7%) of cases. The drugs Are

1%GBHC,Amytrptaline,paracetamol,phenytoin,sodium valproate and progestin. One cases of accidental diesel ingestion seen in our study.

Most of the cases admitted in our hospital belongs to rural population and lower socio economic status .Hydrocarbons and organophosphorus compounds being commonest to compare to developed areas where drug poisoning where more common.

MODE OF POISON:

In our study most common mode is accidental followed by suicidal.

Accidental poisoning is more common in 1-3 years age group with male predominance because most of the male child is more active and poor care given to the children by parents since they are going to works. Most of the caregivers are grandparents and difficult to manage the children in home.

Suicidal is the next common mode due to immaturity, Fear of parents scolding them for poor school performance and family dispute. Agents used for suicidal poisoning is OPC,oduvan leaf, cowdung powder and alumium posphide. Male Child affected more than female involved in suicidal poisoning in other studies suicidal poisoning by drug ingestion being most common (88).

Both male and female are equally involved in homicidal poisoning it does not show any disparity.

ROUTE OF POISON:

Oral ingestion is the most commonest route. A peculiar case of injection of mosquito repellent noted. Dermal absorption of OPC poisoning is common like other study groups.

PREREFERRAL TREATMENT:

In our study majority of the child received, without pre referral treatment and 33.6 % of children received pre referral treatment in the form of atropine, gastric decontamination and Oxygen etc, at surrounding referral hospitals.

DURATION BETWEEN POISOING AND PRESENTATION:

The mean duration of poisoning and presentation was 4.31 hours.

The duration was shorter in urban population compare to rural population

.This could be explained by the longer distance that these rural patients travelled to reach our hospital and also received initial treatment at a nearby hospital .This was similar in study done by kohli et al(1).

MODE OF PRESENTATION:

In this study the most common mode of presentation is vomiting

(37.8%) followed by cough (14%).11.9% of children presented with respiratory distress. Other common manifestations were altered sensorium, abdominal pain,giddiness,seizure,fasciculation.kerosene and mineralspirit

poisoning usually presented with cough and respiratory distress. Only 7% of children were asymptomatic.

In our study children received various form of treatment. In most of the cases(80%) treatment was supportive including gastric lavage ,oxygen, intravenous fluid and other supportive therapy.

Among the 143 children, only 20 %(n-28) them were received specific antidote like atropine,P2AM,Physiostigmine,NAC,VIit K. When indicated and this observation was similar to previously done study by kohli et al(1).

The majority of the patient required only shorter duration ICU stay compare to insecticide and pesticide poisoning cases.

DURATION OF HOSPITAL STAY

The mean duration of hospitalization was 4.5 days and lesser in expired cases. This might due to poor general condition at presentation.

Supportive measures and antidotes are less effective if there is much delay in presentation and poisoning.

The mean duration of hospital day was as low as 0.66 days in a

Nigeria study to 3.8 days and 3.78 days in buthathoki et al study (81)

In our study, 95.1 %(n-136) of children with poisoning were survived and discharged . Death occurred in 4.9% (n-7) cases .The mortality of this study was similar to that seen in previous studies

(73,89,90,91,92).

The maximum number (n-5) of death occurred with insecticide group especially OPC followed by cowdung powder and kerosene oil with male predominance.

Outcome was poor in children admitted to hospital more than 6 hours of poison ingestion. According to chi square p –value is 58.73-is significant.

If the child presented with altered sensorium ,the outcome will be guarded. The p value of chi-square is 80.35-<0.001-which is significant.

More number of deaths occurs in children with ICU stay. Which is also significant (p-0.001) according to chi square.

CONCLUSION

CONCLUSION

 Childhood poisoning is one of the paediatric medical emergencies like

other emergencies and causes significant mortality and morbidity in

children

 Most of the accidental poisoning seen in less than five years age group

due to their innovative character ,curiosity, mouthing tendencies and

exploratory nature

 Majority of the accidental poisonings are preventable by means of simple

preventive measures and reduce the significant mortality among child

hood poisoning.

 Despite of rapid socio economic changes, still kerosene is the commonest

agents involved in paediatric poisoning followed by insecticides due to

location of our centre surrounded by many rural areas.

 Main cause of paediatric poisonings due to negligence and ignorance and

this could be prevented by giving more attention at home.

 At present lack of community based childhood poisoning prevention

programme ,simple preventive measures like education to the parents,

proper storage ,child proof container ,proper placement of drugs could be

preventing mortality and morbidity in children with poisoning.

SUMMARY

SUMMARY

143 cases with poisoning were studied over a period of one year with the following results

 In this study the mean age of childhood poisoning is 3.8 years

 The majority of the poisoning in children is accidental with 88.1%

 Childhood poisoning occur most commonly in male child, with male

to female ratio of 1.6:1

 Most of the poisoning occurs in lower middle class socio economic

class families (65.7%)

 Hydrocarbons is the commonest agent involved in childhood

followed by insecticides

 Oral ingestion were the predominant route of poisoning

 The mean duration of hospital stay is 4.5 days

 In our study 20% cases were treated with specific antidote

 Overall survival rate is 95.1% and mortality is 4.9%

ANNEXURES

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PROFORMA

Name :

Age and sex :

Address :

D.O.A :

D.O.D :

IP NO :

Educational status & :

Profession of parents

Occupation & income : of the parents

Socioeconomic status :

Type of poison :

Insecticides & pesticides/hydrocarbons/Plant and plant products Corrosive/Alcohol/household products/tablet/Unknown poison

Mode of poison : accidental/suicidal/Homicide

Route of poisoning : oral/inhalation/injection/Dermal absorption

Place&Time of consumption :

Pre referral treatment :

Duration between poisoning and presentation:

Chief complaints and clinical features : :

Vomiting/Salivation/Seizure/Miosis/Mydriasis /Coma/ hyperthermia / Crepitations in Lungs / Tachypnea /Diarrhoea / weakness/paralysis/ hemorrhage / Respiratory failure/ Fever/ Shock/ drowsiness/ sweating/ cyanosis/ oliguria/ auria/ hematuria / tachycardia/flushing/urination/defecation/ abdominal pain/discoloured urine

General physical examination:

1. Cry/activity/alertness : 2. Nourishment : Good/ Poor 3. Anemia : Present/ Absent 4. Jaundice/ Cyanosis/ : Clubbing/ Edema 5. GCS :

Vitals:

PR :

BP :

RR :

Temperature :

Weight : ( ) kg

SYSTEMIC EXAMINATION:

Inspection/ Palpation/ Percussion/ Auscultation.

1.cardiovascular system :

S1S2: Murmur : Added sounds

2.Respiratory system :

Bilateral air entry:

Added sounds :

3. per abdomen: Soft/distension, tenderness –present/absent

BS-present/absent

Organomegaly-

4.Central Nervous System: GCS-

Consciousness

Power

RIGHT UL LEFT UL

LL LL

Tone

RIGHT UL LEFT UL

LL LL

Deep tendon reflexes

RIGHT UL LEFT UL

LL LL

Superficial reflexes

Plantar reflexes RIGHT LEFT

Flexor/extensor flexor/extensor

Pupil size - right: left:

Reacting/not reacting to light

FOLLOWING INVESTIGATIONS VARY ACCORDIND TO POISON

1. Complete blood examination 2. Urine examination 3. Bleeding time, Clotting time 4. ECG 5. Blood sugar 6. Serum sodium ,potassium 7. Blood urea,s. creatinine 8. Serum calcium 9. ABG 10. Pseudocholinesterase level 11. LFT 12. CXR 13. USG abdomen 14. CECT abdomen

TREATMENT;

1. O2 through nasal canula/NRM/hood/mechanical ventilator/JR circuit

2. Shock correction {NS-10-20ml/kg}—done/not done

3. Inotropes infusion-given /not given

Dopamine/dobutamine/adrenaline

4 .Hypoglcemia correction-done/not done

[5ml/kg of 10%detrose]

5. Gsastric lavage -done/not done

6. Activated charcoal –given/not given

7. WBI - done/not done

8. Urine alkalization-done/not done

9. Hemodialysis-done/not done

10. IV Fulid

11. IV Antibiotics

12. Anticovulsant used:

13. SPECIFIC ANTIT0DE USED:

i. Physostigmine0.5 mg iv

ii. Dimercprol

iii. Glucogon

iv. Flumazenil

v. Calcium

vi. Pure oxygen vii. Penicillamine viii. Sodium nitrite 3%solution 0.2ml/kg+sodium thiosulphate 25%solution 1ml/kg iv

ix. Digoxin specific FAB fragments

x. Fomepizole

xi. Protamine xii. Desferrioxmine

xiii. Pyridoxine

xiv. Sodium calcium edetete

xv. Naloxone-0.1ml/kg iv

xvi. Methylene blue xvii. Atropine xviii. PAM

xix. N-acetylcysteine

xx. Benadry

xxi. Octreotide xxii. Vitamine k

14. Supportive measures:

15. Duration of hospital stay:

15. Out come :

PARENT CONSENT FORM

STUDY TITLE: PROSPECTIVE STUDY OF CLINICAL PROFILE AND OUTCOME OF CHILDREN PRESENTING WITH POISONING

Department of PAEDIATRICS, GMKMCH, SALEM

PARTICIPANT NAME : AGE : SEX:

I.P. NO :

I confirm that I have understood the purpose of investigatory procedure for the above study. I have the opportunity to ask the question and all my questions and doubts have been answered to my satisfaction.

I have been explained about the possible complications that may occur during and after medical procedure. I understand that my son/daughter participation in the study is voluntary and that I am free to withdraw my son/daughter at any time without giving any reason.

I understand that investigator, regulatory authorities and the ethics committee will not need my permission to look at my son/daughter health records both in respect to the current study and any further research that may be conducted in relation to it, even if I withdraw my son/daughter from the study. I understand that my son/daughter identity will not be revealed in any information released to third parties or published, unless as required under the law. I agree not to restrict the use of any data or results that arise from the study.

I hereby consent to participate my son/daughter to this study for various investigatory procedures and their outcomes.

Time :

Date : Signature / Thumb Impression Of Parent

Place :

Parents’s name:

Signature of the investigator: ______

Name of the investigator : ______

MASTER CHART

S.

al

of

S)

on on

Sex

mic

and

Age

ICU ICU

used status

No. Name

ode of ode of

STAY

poison poison poison

parents

Type of Type of

Specific Specific

Clinical

between between

Address antidote

Mode of

Agent of Agent of Route of

Educatio

Duration Duration Outcome

presentai

Prereferr

nal status

poisoning poisoning

Socioecno treatment stay(DAY

of hostital

presentati feature/M 1 Devishree 5Y FCH RURAL MS LM Plant Oduvan leaf HL O YES 12 hr Vomiting NO NO 4 DIS 2 Devadharshini 1Y6M FCH RURAL PR LM Insecticide Pyrethrins AL O YES 2hr Vomiting NO NO 3 DIS Abdominal 3 Naveenkumar 7Y MCH RURAL MS LM Plant Oduvan leaf HL O YES 12hr NO NO 4 DIS pain Oleander 4 Sabarinathan 1ymch MCH RURAL HS LM Plant AL O NO 3hr No NO NO 3 DIS seed 5 Rohith 2y MCH URBAN MS LM Household Camphor AL O NO 1hour Seizure NO NO 7 DIS 6 Stephy 3y FCH RURAL IL L Insecticide Pyrethrins AL I NO 5hr Vomiting NO NO 10 DIS Mineral 50minu 7 Guna 3Y MCH URBAN MS LM Hydrocarbon AL O NO Tachypnea YES NO 9 DIS spirit tes Oleander 8 Yogesh 6M12 MCH RURAL IL L Plant HL O NO 6 hr Seizure NO NO 5 DIS seed 9 Sarvesh 1Y6M MCH URBAN IL UL Hydrocarbon Kerosene AL O NO 1hour Tachypnea YES NO 6 DIS Aluminium 10 Keerthana 10Y FCH RURAL MS LM Pesticide SL O YES 7hr Vomiting YES NO 8 DIS phosphide 2hour1 11 Dharsan 2y MCH RURAL MS LM Hydrocarbon Kerosene AL O NO Vomiting NO NO 4 DIS 5min 50minu 12 Vanajaya 2y FCH RURAL MS LM Hydrocarbon Kerosene AL O NO Vomiting NO NO 3 DIS tes Alterted 13 Vetrivel 4y6M MCH URBAN MS L Insecticide OPC AL O YES 27hr YES YES 1 D sensorium Ibrahim 14 1Y6M MCH URBAN MS LM Hydrocarbon Kerosene AL O NO 4hr Tachypnea YES NO 7 DIS bhadhusa Bleaching Abdominal 15 Nishanth 4y MCH URBAN HS LM Corrosive powder AL O NO 3hr NO NO 5 DIS pain solution Alterted 16 Akash 7Y MCH URBAN MS LM Insecticide OPC SL O YES 6hr YES YES 9 DIS sensorium 17 Nandhan 1y6m MCH URBAN MS LM Household Camphor AL O NO 1hourr Vomiting NO NO 3 DIS

Alterted 18 Karthick 10Y FCH URBAN MS LM Insecticide OPC HL O NO 2hr YES YES 10 DIS sensorium Mineral 1hour1 19 Moulika 3y FCH RURAL MS LM Hydrocarbon AL O NO Cough NO NO 2 DIS spirit 5min 1hour3 20 Thishik 2Y MCH RURAL GR UM Hydrocarbon Kerosene AL O NO Cough NO NO 3 DIS 0min 21 Thanishka 1Y6M MCH URBAN IL UL Hydrocarbon Kerosene AL O NO 1hour Cough NO NO 3 DIS Oleander 4hour3 22 Kishore 2Y MCH RURAL PR UL Plant AL O NO Vomiting NO NO 6 DIS seed 0min 2hour 23 Mythili 3y FCH RURAL HS LM Hydrocarbon Kerosene AL O NO Tachypnea YES NO 9 DIS 30min Cowdung Abdominal 24 Naveenkumar 11y MCH RURAL HS LM Household SL O NO 4hr NO NO 4 DIS powder pain 25 Dhineshkumar 3y MCH URBAN MS LM Hydrocarbon Kerosene AL O NO 2hr Vomiting NO NO 3 DIS 26 Myvizhi 3Y FCH URBAN MS LM Insecticide Pyrethrins AL O NO 1hour Vomiting NO NO 3 DIS 27 Dhinesh 2Y MCH URBAN MS UM Insecticide Pyrethrins AL O NO 2hr No NO NO 2 DIS Abdominal 28 Poovarasan 10Y MCH RURAL MS UM Plant Mushroom AL O NO 3hr NO NO 3 DIS pain 29 Srimathi 8Y FCH RURAL MS LM Plant Mushroom AL O NO 3hr Vomiting NO NO 3 DIS 30 Ashwin 11m MCH URBAN MS LM Insecticide Pyrethrins AL O NO 4hr No NO NO 3 DIS 31 Dhanyasri 2y FCH RURAL HS LM Hydrocarbon Kerosene AL O NO 2hr Tachypnea YES NO 5 DIS 32 Srikavi 1y6m MCH RURAL MS LM Hydrocarbon Kerosene AL O YES 2hr Tachypnea YES NO 5 DIS Cowdung 33 Kavin 3Y MCH URBAN MS LM Household AL O NO 2hr Vomiting NO NO 3 DIS powder Cowdung 2hr15m Abdominal 34 Manisha 1Y6M FCH RURAL PR L Household AL O NO NO NO 3 DIS powder in pain Aluminium 35 Siddarth 2y6M MCH RURAL HS LM Pesticide AL O NO 7hr Vomiting YES NO 8 DIS phosphide 36 Haripriyan 3Y MCH RURAL MS LM Insecticide Carbamate AL O NO 2hr Giddiness NO YES 5 DIS 37 Nithyasri 5Y FCH RURAL MS LM Insecticide Carbamate AL O NO 2hr Giddiness NO YES 5 DIS 38 Mohanapriyan 3Y MCH RURAL MS LM Insecticide Carbamate AL O NO 2hr Giddiness NO YES 5 DIS 39 Priyadharshan 5y MCH RURAL MS LM Insecticide Carbamate AL O NO 2hr Vomiting NO YES 5 DIS 40 Sadhana 2y FCH RURAL MS LM Hydrocarbon Kerosene AL O NO 30min Vomiting YES NO 7 DIS Cowdung 41 Viroshan 3Y MCH RURAL HS UM Household AL O NO 1hour Vomiting NO NO 3 DIS powder

2hr30m 42 Pushpa ambika 4y FCH RURAL MS LM Drugs Paracetamol AL O NO Vomiting YES YES 8 DIS in Cowdung 43 Poovarasan 6y MCH RURAL MS LM Household AL O NO 3hr Vomiting NO NO 4 DIS powder Abdominal 44 Srinivasan 2Y MCH RURAL HS LM Drugs Paracetamol AL O NO 2hr YES YES 8 DIS pain 45 Tamilselvan 2Y MCH RURAL MS UM Hydrocarbon Kerosene AL O NO 6hr Cough YES NO 8 DIS 46 Eswari 5Y FCH URBAN MS LM Plant Oleander AL O NO 2hr Vomiting YES NO 10 DIS 47 Kanishka 4y FCH RURAL HS UM Corrosive Phenol AL O NO 1hr30m Vomiting NO NO 5 DIS 48 Kowshik 2Y MCH RURAL HS UM Insecticide Pyrethrins AL O NO 2hr Cough YES NO 4 DIS Ratkillerpast 49 Cheliyan 1y8m MCH URBAN GR UM Insecticide AL O YES 6days Nasalbleed YES YES 6 DIS e 50 Thirumugilan 1Y6M MCH URBAN MS LM Hydrocarbon Kerosene AL O NO 2hr Tachypnea YES NO 3 DIS Alterted 51 B/O pavishna 19D FCH URBAN MS LM Insecticide OPC AL O YES 7hr YES YES 4 D sensorium 52 Siddarth 2y MCH URBAN MS LM Insecticide Pyrethrins AL O NO 2hr No NO NO 3 DIS 53 Anisha 5y FCH RURAL MS LM Insecticide OPC AL O YES 7hr Vomiting YES YES 7 DIS 54 Kavipriyan 2y MCH RURAL HS UM Insecticide OPC AL O YES 6hr Vomiting YES YES 5 DIS 55 Krishnan 2y MCH RURAL MS UM Hydrocarbon Kerosene AL O NO 2hr Vomiting YES NO 6 DIS 56 Manikandan 1y MCH RURAL PR LM Hydrocarbon Kerosene AL O NO 1hour Tachypnea YES NO 7 DIS Organochlor 57 Yugandiran 11y MCH RURAL MS LM Insecticide SL O YES 12hr Vomiting YES YES 7 DIS ide 11hour 58 Nishanth 10M MCH RURAL MS LM Household Ant killer AL O YES No NO NO 3 DIS 30min 59 Sanjai 1y MCH URBAN MS UM Insecticide Pyrethrins AL O NO 2hr Vomiting NO NO 3 DIS 60 Gokul 2y MCH RURAL PR L Insecticide OPC AL O NO 5hr Vomiting YES YES 7 DIS Oleander 61 Dharsan 6Y MCH RURAL MS UL Plant HL O YES 15hr Vomiting YES NO 5 DIS seed Oleander 62 Priyadharshini 8Y FCH RURAL MS UL Plant HL O YES 15hr Vomiting NO NO 5 DIS seed Oleander Abdominal 63 Priyadharshini 8Y FCH RURAL PR UL Plant AL O NO 2hr NO NO 5 DIS seed pain Oleander Abdominal 64 Dharsan 6y MCH RURAL MS L Plant AL O NO 2hr NO NO 3 DIS seed pain 65 Sudharsan 3Y MCH URBAN MS LM Hydrocarbon Kerosene AL O NO 6hr Cough YES NO 5 DIS

Abdominal 66 Yashini 1Y FCH RURAL MS LM Drugs Progestin AL O YES 4hr YES NO 3 DIS pain Phorate 67 Venkatish 5Y MCH RURAL MS LM Pesticide AL O YES 5hr Giddiness NO YES 4 DIS powder Phorate 68 Keerthana 6Y FCH RURAL MS LM Pesticide AL O YES 5hr Vomiting NO YES 4 DIS powder Phorate 69 Rathidevi 10Y FCH RURAL MS LM Pesticide AL O YES 5hr Giddiness YES YES 6 DIS powder Phorate 70 Pooja 11y FCH RURAL MS LM Pesticide AL O YES 5hr Vomiting NO NO 4 DIS powder Cowdung 71 Mohinth 8mon MCH URBAN PR L Household AL O NO 1hour Vomiting NO NO 3 DIS powder Mohamad 72 1Y6M MCH RURAL MS LM Hydrocarbon Kerosene AL O YES 4hr Cough NO NO 5 DIS aadhil 73 Kathirvel 1y 6m MCH RURAL MS LM Hydrocarbon Kerosene AL O NO 1hr30m Vomiting NO NO 2 DIS Cowdung Abdominal 74 Selvakumar 1y MCH RURAL MS UL Household AL O NO 3hr NO NO 3 DIS powder pain 75 Srisarvan 2Y MCH URBAN MS LM Hydrocarbon Kerosene AL O NO 2hr Cough NO NO 3 DIS 76 Shreepriya 12y FCH URBAN MS LM Drugs Amytrptline AL O NO 1hour No NO NO 3 DIS 77 Shankar 8y MCH URBAN MS LM Drugs Amytrptline AL O NO 1hour Giddiness NO NO 3 DIS 78 Ajaykumar 7Y MCH URBAN MS LM Drugs Amytrptline AL O NO 1hour Giddiness NO NO 3 DIS 79 Sanjana 3y FCH RURAL MS LM Insecticide Pyrethrins AL O YES 2hr Vomiting NO NO 3 DIS 80 Karthick raja 1y MCH URBAN MS LM Hydrocarbon Kerosene AL O NO 1hour Tachypnea YES NO 5 DIS 81 Vijith 2y MCH RURAL PR L Hydrocarbon Kerosene AL O YES 1hour Cough NO NO 2 DIS 82 Kannan 2Y MCH URBAN MS LM Hydrocarbon Kerosene AL O NO 1hour Tachypnea YES NO 5 DIS 83 Prema 2y FCH RURAL SE LM Insecticide OPC AL O YES 5hr Tachypnea YES YES 6 DIS 84 Heera 2y FCH URBAN PR LM Hydrocarbon Kerosene AL O NO 30min Vomiting NO NO 3 DIS 85 Sneha 2y FCH URBAN MS UL Hydrocarbon Kerosene AL O NO 1hour Cough NO NO 3 DIS Mineral 86 Rohith 3Y MCH RURAL PR L Hydrocarbon AL O YES 2hr Tachypnea YES NO 4 DIS spirit Cowdung 87 Dhanusree 2y FCH RURAL SE UL Household AL O NO 2hr Vomiting NO NO 3 DIS powder Altered 88 Anbarasan 3Y MCH RURAL MS L Hydrocarbon Kerosene AL O NO 25hr YES NO 2 D sensorium 89 Sabari 5y MCH URBAN MS LM Hydrocarbon Mineral AL O NO 30min Cough NO NO 3 DIS

spirit 90 Sarath 2y MCH RURAL PR L Hydrocarbon Kerosene AL O YES 3hr Vomiting NO NO 3 DIS 91 Mohamedtofi 1y MCH URBAN PR L Hydrocarbon Kerosene AL O NO 1hour Cough NO NO 3 DIS 1hour3 92 Praveenkumar 12y MCH URBAN MS L Unknown SL O NO Giddiness NO NO 4 DIS 0min 1hour3 93 Jasmitha 12y FCH RURAL MS LM Insecticide OPC SL O YES Giddiness YES YES 5 DIS 0min 94 Kirena 2y FCH RURAL MS LM Hydrocarbon Kerosene AL O YES 1hour Cough NO NO 3 DIS Altered 95 Neethidevan 3Y MCH RURAL HS LM Drugs Phenytoin AL O YES 2hr YES NO 10 DIS sensorium Alterted 96 Ramya 4y FCH RURAL HS LM Insecticide OPC AL O YES 13hr YES YES 1 D sensorium 97 Vinoth 3Y MCH RURAL PR L Hydrocarbon Kerosene AL O NO 1hour Cough YES NO 7 DIS 98 Deepak 4mon MCH RURAL MS UM Hydrocarbon Kerosene AL O NO 30min Cough NO NO 3 DIS 99 Selvamani 2Y MCH RURAL IM UM Corrosive Phenol AL O NO 1hr15m Vomiting NO NO 4 DIS Alterted 100 Dhinesh 3y MCH RURAL MS LM Insecticide OPC AL O YES 8hr YES YES 3 D sensorium 101 Sabari 2Y MCH RURAL MS UM Hydrocarbon Kerosene AL O NO 1hour Tachypnea NO NO 3 DIS Mineral 102 Dhanshika 4y FCH URBAN MS LM Hydrocarbon AL O NO 45min Vomiting NO NO 2 DIS spirit 1y6mo Mineral 103 Girija FCH RURAL MS LM Hydrocarbon AL O NO 1hour No NO NO 2 DIS n spirit Abdominal 104 Subha 4y FCH RURAL MS L Corrosive Phenol AL O NO 1hour NO NO 3 DIS pain 1hour2 105 Sudha 4y FCH RURAL HS L Corrosive Phenol AL O NO No NO NO 2 DIS 0min 1y6mo Mineral 50minu 106 Girija FCH RURAL HS LM Hydrocarbon AL O NO Vomiting NO NO 2 DIS n spirit tes Mineral 4huors 107 Ashath 4y MCH RURAL MS L Hydrocarbon AL O YES Cough NO NO 4 DIS spirit 15min 108 Srimathi 3y FCH URBAN PR LM Hydrocarbon Kerosene AL O NO 30min Vomiting NO NO 2 DIS 1hour1 109 Meenmozhi 5y FCH RURAL MS LM Hydrocarbon Kerosene AL O NO Vomiting YES NO 6 DIS 5min 110 Samaradha 1Y FCH URBAN HS LM Household Camphor AL O NO 30 min Tachypnea YES NO 6 DIS 111 Dharan 2Y MCH URBAN HS LM Hydrocarbon Kerosene AL O YES 3hr Tachypnea YES NO 8 DIS

112 Gokulnath 12y MCH RURAL MS LM Insecticide OPC SL O YES 2hr Tachypnea YES YES 6 DIS 2hr15m 113 Dhanusri 2y FCH URBAN HS L Hydrocarbon Kerosene AL O YES Vomiting YES NO 5 DIS in Mineral 114 Samitha 2y6M MCH URBAN HS UM Hydrocarbon AL O NO 40min No NO NO 2 DIS spirit 2hr15m 115 Leemarose 7y FCH URBAN HS UM Insecticide OPC AL O YES Vomiting YES YES 4 DIS in Oleander 1hour4 116 Nanthakumar 4y MCH RURAL MS LM Plant AL O YES Vomiting NO NO 5 DIS seed 0min Cowdung Alterted 117 Gowtharani 10Y FCH RURAL MS LM Household SL O YES 26hr YES NO 3 D powder sensorium Sodiumvalpr Alterted 118 Manikandan 10Y MCH RURAL MS LM Drugs AL O YES 1hour YES NO 5 DIS oate sensorium Napthalene 119 Samandha 3y FCH RURAL HS LM Household AL O YES 2hr Seizure NO NO 11 DIS ball Mineral 120 Rohini 3y FCH URBAN HS L Hydrocarbon AL O YES 40min Vomiting NO NO 2 DIS spirit Alterted 121 Kapil 3y MCH RURAL HS LM Plant Dhatura AL O NO 2hr YES YES 7 DIS sensorium Soundarapandiy 122 4y MCH RURAL MS LM Hydrocarbon Kerosene AL O NO 2hr Cough YES NO 7 DIS an 1hour1 123 Kasiarasan 3y MCH RURAL HS LM Household Ant killer AL O NO Vomiting NO NO 4 DIS 5min 50minu 124 Agalya 3y FCH RURAL HS LM Drugs Pheytoin AL O NO No NO NO 1 DIS tes Alterted 125 Jegan 10Y MCH URBAN MS LM Insecticide OPC SL O YES 30hr YES YES 3 D sensorium 1hour2 126 Bharathi 1y MCH RURAL HS L Hydrocarbon Kerosene AL O NO Vomiting YES NO 5 DIS 0minu 127 Guhan 2Y MCH URBAN HS UM Hydrocarbon Kerosene AL O NO 1hour Vomiting NO NO 3 DIS 1hour4 128 Logeshwari 2y FCH RURAL MS LM Hydrocarbon Kerosene AL O YES Vomiting NO NO 2 DIS 5min 2hour5 129 Sanjai 2y MCH RURAL PR LM Hydrocarbon Kerosene AL O NO Cough NO NO 2 DIS omin 130 Davidprasath 1y MCH URBAN MS L Hydrocarbon Kerosene AL O NO 1hr20m Tachypnea YES NO 6 DIS

131 Manoja 5y FCH RURAL HS LM Corrosive Phenol AL O YES 1hour Vomiting NO NO 3 DIS Abdominal 132 Gowtham 7Y MCH RURAL MS LM Corrosive Phenol AL O YES 1hour NO NO 3 DIS pain Abdominal 133 Kavya 1Y6M FCH RURAL MS LM Corrosive Phenol AL O YES 1hour NO NO 3 DIS pain 134 Sabari 11y MCH RURAL MS LM Plant Oduvan leaf SL O NO 3hr Vomiting YES NO 7 DIS 135 Manikandan 11y MCH RURAL MS LM Plant Oduvan leaf SL O NO 3hr Giddiness YES NO 7 DIS Cowdung 1hour1 136 Priya 3y FCH RURAL PR UL Household AL O NO Seizure YES NO 7 DIS powder 0minu 137 Roshini 2y FCH RURAL MS LM Hydrocarbon Kerosene AL O NO 1hour Cough YES NO 6 DIS Fasciculati 138 Dhivyadharshini 3y FCH RURAL HS LM Pesticide Pyrethrins AL DA NO 2hr NO NO 5 DIS on 139 Hemalatha 2y MCH URBAN HS LM Hydrocarbon Kerosene AL O NO 30min Vomiting NO NO 3 DIS 140 Naveen 2Y MCH URBAN MS LM Hydrocarbon Diesel AL O NO 30 min Cough NO NO 2 DIS 141 Pavan 3y MCH URBAN HS UM Insecticide Carbamate AL O YES 3hr Vomiting YES YES 5 DIS 142 Pradeep 1y MCH URBAN MS LM Drugs 1%GBHC AL O YES 4hr Seizure NO NO 5 DIS Ratkillerpast 143 Anushka 4y FCH URBAN MS LM Insecticide AL O NO 40min Vomiting NO YES 3 DIS e

KEY TO MASTER CHART

AL ACCIDENTAL D DEATH DA DERMAL ABSORPTION DIS DISCHARGED FCH FEMALE CHILD HL HOMICIDAL HS HIGHER SECONDARY GR GRADUATE IL ILLITERATE I INJECTION IM INTERMEDIATE L LOWER LM LOWER MIDDLE MS MIDDLE SCHOOL MCH MALE CHILD O ORAL PR PRIMARY SE SECONDARY SL SUICIDAL UL UPPER LOWER UM UPPER MIDDLE