Preparation of Guidelines for Management of Poisoning at St.Martha's Hospital,Bangalore

Dear Thomas

Fund can be generated from the multi specialty hospitals , even from the pharma industry.
and ya of course we need the permission from the WHO as well as from state pharmacy council permission to open the PIC..

dear thomas

The Drug and Poison Information Center's specially trained staff of pharmacists, pharmacologists and nurses answer questions about poisonings, drug abuse, product contents, substance identification interactions and adverse reactions.

The Drug and Poison Information Center also works to provide you with important poison prevention information.

Emergency Actions for Poisoning numbers can be hang on your refrigerator or near a telephone, where it is available and visible to family members. so that in case of emergency where source of information is not available. because its very difficult to uneducated person who dont have source of information.
and if the doctors is sitting in OPD they dont have time to refer these sources, i mean to say multiple source of information.
General Poisoning Statistics

Seventy-nine percent of all poison control center cases involve children -- 64 percent occur in children under age 5.
An estimated one in five children will be exposed to a potential poison before age 5.
Nationally, during the year 2000, 1.2 million children under age 5 were exposed to potentially poisonous substances.
An estimated 70 percent of accidental poisonings are preventable.
A partial list of products that can be dangerous includes: acetaminophen, antifreeze, carbon monoxide, berries, mushrooms, camphor, fuel, insecticides, iron preparations, pool chemicals, rat poisons, rubbing alcohol.
Where in the Home Do Poisonings Generally Occur?

Generally, poisonings in the home breakdown as follows:

Kitchen -- 41 percent.
Bathroom -- 21 percent.
Bedroom -- 12 percent.
All Other Places -- 26 percent.
When Do Poisonings Occur?

Poisonings occur . . .

When there are changes in the daily routine such as holidays, illnesses, moving, vacations, stressful times and celebrations.
When a product is being used.
When products are carelessly or improperly stored.
When adults fail to follow package directions for products such as herbicides, insecticides, fertilizers and medications.
When visiting a grandparent or friend.
When children are hungry or thirsty.
When teens or adults become angry or depressed.
When someone becomes confused and disoriented.

Reference:- DIC , Karnataka state pharmacy council.

dear Srujana

example of an indirect emetic is indirect, or systemic, emetics, such as apomorphine ...
In poisoning, emetics or the stomach pump are indicated if the poison has not yet been absorbed, and where other less severe means are not effective. In order to produce vomiting warm water may be given, or, if necessary, a tablespoonful of mustard stirred to creamy consistency with water; this to be followed by large draughts of water. Generally this is later followed by demulcent drinks, such as flaxseed, whites of eggs beaten tip in water, slippery elm, etc. No emetics should be given, however, in poisoning by acetic, hydrochloric or muriatic, nitric and sulphuric acid..

Acids—Acetic, Hydrochloric, Nitric and Tartaric: Use alkalies, oil, stimulants, demulcent drinks; large draughts. of water or milk with whiting, baking soda or magnesia; strong soap suds to neutralize acid; olive oil; these to be followed by demulcent drinks.
Acid Chromic: Chalk, milk, demulcent drinks; emetics if necessary.
Acid Hydrocyanic: Stomach pump if possible. Ammonia, atropine and diluted cardiac stimulants; artificial respiration. Carbonate of ammonia 3 to 5 grains every 15 to 30 minutes. Fresh air is important,
Acid Nitric: Alkalies, soap, demulcents, stimulants.
Acid, Oxalic: Lime, chalk.
Acid, Sulphuric: Chalk, magnesia, soap, demulcent drinks.
Aconite: Emetics, afterwards powerful stimulants, both externally and internally. Nux vomica has been used with success. Animal charcoal followed by emetics is recommended. Carbonate of ammonia 5 grains every 20 minutes to 1/2 hour is very good.
Alcohol: Evacuate stomach; coffee, electricity, amyl nitrite, hot and cold douches.
Alkalies: The caustic alkalies, such as ammonia, potassium, soda, etc. Try and induce vomiting with large quantities of water. Give lemon juice diluted, olive oil or vinegar. The white of eggs beaten up with water or demulcent drinks of slippery elm, linseed or flaxseed.
Ammonium and Its Compounds: Demulcents; vegetable acids.
Antimony and Its Compounds: Tannic acid, demulcent drinks, opium, alcohol, external heat, strong tea or coffee; emetics if necessary.
Antipyrin: Recumbent position, warmth, nux vomica, stimulants, oxygen. Artificial respiration.
Apomorphine: Cardiac and respiratory stimulants.
Arsenic: Persulphate of iron solution. Solution of iron chloride and calcined magnesia, mix in 1/2 cup of water, and when well diluted give to patient. The water should be warm. Ferric hydrate is a good antidote, it combining with arsenic, forming arseniate of iron, which is a harmless salt; 35 parts are needed to neutralize one part of arsenic.
Auri et Sodii Chloridum: Albumen is an antidote.
Belladonna: Emetics, stomach pump, iodine, purgatives, ammonia, cold to head in comatose stage. External stimulants.
Bryonia: Infusion of galls.
Caffeine: Emetics, stimulants, warmth, morphine, atropine.
Camphor: Evacuate stomach, give stimulants. Warmth, hot and cold douches.
Cannabis Indica: Evacuate stomach and give stimulants.
Carbolic Acid: Olive oil until vomiting is produced; if no other remedy is at hand use vinegar or diluted acetic acid. Alcohol is the best in local poisoning from carbolic acid.
Cantharides: Stomach pump, demulcents, opiates and stimulants. Oils are injurious and should not be used.
Chloral Hydrate: First give emetics, then stimulants, such as brandy, digitalis, nux vomica. The heart must be stimulated. Use also local means to stimulate.
Chloroform: Draw out tongue, use faradism. Hot and cold douches. Amyl nitrite or ammonia. Hypodermic injection of strychnine or nitroglycerine. Dilate the sphincter ani by all means as this is the best and quickest way to cause reaction. Slapping the soles of the feet is very good. If taken by mouth evacuate the stomach and give stimulants.
Coal Gas: Fresh air, artificial respiration, ammonia, oxygen, coffee, hot and cold, douches. The first measure should be to put patient in a position the reverse from standing to eliminate gas, and then start respiration by proper means, stimulation being very important.
Conium: Evacuate stomach, then give vinegar.
Croton Oil: Evacuate stomach, demulcent drinks camphor; morphine; stimulants; poultice to abdomen.
Cocaine: 1% solution of glonoine in one or two drop doses is very good. Artificial respiration. Amyl nitrite or other powerful stimulants.
Digitalis: Evacuate the stomach at once by warm water or drinks; sinapisms to wrists and ankles. This should he followed by stimulants. Carbonate of ammonia in 5 grain doses every 1/2 hour or less. Tannic and gallic acid are good. Patient should in all cases maintain the recumbent position.
Gelsemium: Brandy, quinine or aromatic spirits of ammonia. When indicated tincture of opium may be given with above.
Hyoscyamus: Emetics, stomach pump, stimulants, acids, galvanism.
Iodine: Starch water amyl nitrite. Emetics followed by demulcent drinks if necessary.
Iodoform: See iodine.
Jaborandi: 1/60 grain of atropine will counteract the effect of an overdose.
Lead Poisoning: Sulphate of soda, sulphuric acid and sulphate of magnesia.
Lead Acetate: Evacuate stomach, dilute sulphuric acid; Epsom salts; milk; morphine; potassium iodide to eliminate poison.
Lobelia Inflata: Evacuate stomach; tannic or gallic acid; stimulants; strychnia; warmth; recumbent position.
Morphine: Cocaine is the best antidote; caffeine. Permanganate of potash is very good if poison is not absorbed by the system. Keep patient moving.
Mercuric Chloride: Albumen in some form. Raw whites of egg or flour; evacuate stomach; opium; potassium iodide.
Nitroglycerin: Recumbent position; cold to head; atropine.
Nux Vomica: Chloral in large doses is useful. Morphia. Our best antidote, however, is jaborandi in large and often repeated doses, gradually decreasing doses and giving at longer intervals as symptoms subside.
Nitrate of Silver: Solution of salt, say 4 drachms in warm water as an emetic.
Opium: Active cathartic. The patient should be kept in motion and cold water dashed on the head and shoulders. Give tincture of green coffee. Belladonna. Slap the soles of the feet.
Physostigma: Nux vomica or atropine.
Phosphorus: Emetic of sulphate of copper. Give also copious draughts of water with magnesia. Turpentine is a partial antidote.
Resorcin: Induce vomiting; give olive oil; stimulants.
Rhus Tox.: Grindelia robusta internally and locally is our best remedy. Echinacea in large doses internally and locally in 25% solution is good treatment. Rhus tox. 12d in the primary form is useful in rhus tox. poisoning. In recent cases, locally a solution of sodium hyposulphite is recommended by some. Others have used locally a mild solution of carbolic acid and claim success in recent cases.
Santonin: Evacuate stomach; stimulants; chloral.
Savin: Evacuate stomach; castor oil in large doses. Morphine. Poultice to abdomen.
Silver Salts: Salt and water; evacuate stomach; a large amount of milk.
Strophanthus: Coffee and brandy should be given freely to counter-act.
Stramonium Leaves: Evacuation of the stomach,, after which vinegar and water may be administered, followed by mucilaginous drinks, with strong coffee and any stimulating cordial, according to the prostration.
Snake Bites: Rattlesnakes, etc, Echinacea is our best remedy. In these cases it must be given in very large doses. In adults say 20 to 30 drops every 1/2 hour, and this to be continued for some hours, then as the severer symptoms subside gradually decrease dose and give at longer intervals. Also apply the tincture pure or little diluted with water to the wound freely. Locally formaldehyde diluted is a good application. In cases where depression is great muriate or carbonate of ammonia in solution may be alternated with echinacea. Locally chloroform on a flannel applied over swelling is recommended.
Tarantula Bites and other poisonous spiders or insects use echinacea as directed under snake bites, only modify the dose in cases that are not so severe. In other words the dose depends on the severity of the case. In cases where depression is great muriate or carbonate of ammonia in solution may be alternated with echinacea.
Tobacco: Carbonate of ammonia 5 grains as a dose is a good antidote.
Veratrum Viride: Morphine or laudanum with brandy, coffee. Recumbent position.
Appearance of Tongue after some Poisons are taken by the Mouth.
Acid, Carbolic: Mucous membrane is shriveled and puckered into folds. The spots where the acid has touched are, if acid is pure, white. If acid is impure spots will be brownish.
Acid, Chromic: Tongue is shriveled and of a lemon yellow color.
Acid, Hydrochloric: Tongue a lemon yellow color.
Acid, Nitric: Tongue is shriveled and of a lemon yellow color.
Acid Nitrate of Mercury: Color of tongue red.
Acid, Sulphuric: Tongue has a parchment-like color or appearance. At first it is white, then gray or brownish gray, then gets covered with a thick slough which when it separates leaves a swollen excoriated patch.
Ammonia: If swallowed in poisonous doses undiluted will make the tongue white.
Cantharides: Produces large lingual blisters and sores.
Corrosive Sublimate: Tongue appears white and shriveled, and the papillae at the base are unusually large.
Potash Caustic: Softens mucous membrane, making it pulpy and easily detached.
Sodium Caustic: Softens mucous membrane, making it pulpy and easily detached

References :- http://www.henriettesherbal.com/eclectic/petersen/poisons.html

Dear Roshan the references are given below.. i hope it will be useful for u.

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

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

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

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

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

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

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

Dear Murthy sir.

i have made the guidelines. which i cant give in the PPT . coz the matter is lot . and ya surely i have made the guidelines for all the poison which are included in my study

here is some examples......

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

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

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

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

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

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

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

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

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

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

Preparations containing NSAIDs

Product Contents

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

References:- own research work

dear himangi

i have used this book as an reference for making guidelines...

Henry JA, Wiseman HM. General information on poisons and poisoning. In: Management of poisoning: A handbook for health care workers. New Delhi: AITBS publishers; 2004: 3-11.

Dear Himangi

Sample size in my studies was N number of patients. and during 9 month i got 59 poisoning cases in one hospital

hello sakshi

duration of my research work was 9 month i.e. that is last year. now presently the work is going on .
- maximum number of business men are suffering from intentional poisoning as they have financial problems , and related to emotional disturbance.
most of the businessmen have used the oral route of poisoning . and poison consumed was OP or insecticides.

- ya one patient dies out of 59 because he didnt reach on time from the suitable treatment

Regards

Dear Sujata

ya poisoning cases are increasing not even in India but globally

because Acute poisoning is an important medical emergency and one of the causes of death. A thorough
knowledge of the profile of the victim is essential for management and prevention of poisoning. The
present paper evaluates pattern of poisoning cases including deaths over a period of two years from
1999 to 2001 in Berhampur, Orissa. 53.3% of the cases were male with male to female ratio 1.14:1. Peak
incidence was observed in the age group 21-30 years(124 cases). More than four-fifth of the cases
belonged to medium socioeconomic status and 58.1% cases were from rural areas. Majority of the victims
were literate and married outnumbered the unmarried cases. Occurrence of poisoning was more common
in day time and during Summer season. Organophosphate compounds was the most commonly (22.9%)
abused substance. Based on these findings preventive measures like restriction of sale and strengthening
the legislature on availability of poison, promoting poison information center etc have been put forward.

Three hundred and six cases were admitted
to the Hospital with diagnosis of acute poisoning.
Total male affected are 163 (53.3%) dominating
the female. (Table - 1) The incidence of poisoning
according to age and sex shown in Table - 2 reveals
that there is an increasing trend of poisoning with
increase in age up to 30 years and then declines
with a peak incidence in the age group 21 - 30
years which represented 124 (40.5%) cases in this
study.
It is evident that 256 (83.7%) of victims were
of medium socio-economic status (Table-3). The
domicile pattern of the victims shows 178 (58.2%)
cases were from rural area. (Table - 4)
Literacy status of the victims reveals that at the
time of incidence 257 (83.9%) cases were
literate(Table- 5). Among the 306 cases admitted
to the hospital with diagnosis of acute poisoning
156 (50.9%) cases were married. (Table-6)
Maximum incidences of cases 97 (31.7%)
were recorded in Summer season. (Table - 7)
Considering the time of poisoning, this shows that
the majority of cases (55.9%) were observed during
the daytime, between 6 AM to 6 PM. (Table - 8)
Organophosphrous is the most commonly abused
poison.

TABLE - 3
Showing the socio-economic status of the
patients
Socio-economic No. of cases Percentage
Status n=306
Low 49 16
Medium 256 83.7
High 1 0.3
TABLE - 4
Showing domicile pattern of the victims
Domicile No. of cases Percentage
N= 306
Rural 178 58.2
Urban 128 41.8
TABLE - 5
Showing literacy status of the victims
Sex Literate Illiterate
Male 131(51%) 32 (65.3%)
Female 126 (49%) 17 (34.7%)
Total 257 (83.9%) 49 (16 %)
TABLE - 6
Marital status of the victims
Marital status No. of cases Percentage
N= 306
Married 156 51
Unmarried 150 49
TABLE - 7
Showing seasonal incidence of poisoning
Seasons of the year Total Percentage
Summer (Mar, Apr., May) 97 31.7
Rainy (Jun, Jul, Aug) 85 27.8
Spring (Sept, Oct, Nov) 70 22.9
Winter (Dec, Jan, Feb) 54 17.6
Reference:- SOCIODEMOGRAPHIC PROFILE OF POISONING CASES JIAFM, 2005 ; 27 (3). ISSN 0971 -0973

Dear Mahalaxmi

Age group 19-30 are mostly Students and if they are failed in the examination , because of emotional disturbance they will do the suicide attempts.. even the love failure will occur in this age mostly....

1. can you give some examples of materials which are likely to produce toxicity though they were not administred for the purpouse of poison .
2. Give some examples of pharmaceuticals excipients whose decomposed products are toxic.

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

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

Supportive therapy
This may be all that is required in some poisoned patients. During this phase, frequent monitoring of vital signs, fluid and electrolyte balance, cardiorespiratory support as indicated, and aggressive nursing care to preserve integrity of body systems, should all be carried out.

Observation and disposition - Observation may be necessary to evaluate delayed effects of certain poisonings, to manage an underlying disease that has been exacerbated because of the overdose and to evaluate and treat complications. Final disposition would depend on the results of this further observation.

After care -
Management of the poisoned victim is not only the relief of the physical effects of the toxic agent on the human body. Many victims of poisoning have lead acutely stressful lives that lead them to overdose themselves with various medicaments and chemicals. They require emotional support through all phases of emergency management and very early intervention of the medical social worker and perhaps even a psychiatrist. Follow-up by both may be required even after discharge from the hospital. Victims of accidental exposure to toxic agents have undergone an acutely stressful situation. Rather than only providing psychological support to those with over symptoms of post-traumatic stress disorder, one has to presume that all have potential for stress disorders. Therefore stress counseling for all has to be planned for. Such counseling must continue in the post-hospital phase of management.46

1 Dhattarwal SK, Dalal SS. Profile of deaths due to poisoning in Rohtak, Haryana in the year 1995. Journal of Forensic Medicine & Toxicology. 1996; 19: 9-10.
2 Dutta AK. Poisoning in children: Indian scenario. Indian J Pediatr 1998; 65(3): 365-70
3 Louis A, Marchil S, Renier G, Messil, Barbone F. A Population Study in Trieste, Italy from 1975-1994. BMJ 1998: 24-30.
4 Moghadamia AA, Abdollahi M. An epidemiological study of poisoning in Northern Islamic Republic Of Iran. East Mediterr Health J 2002; 8(1): 88-94.

hi Mr Dixon Thomas

common route for pesticide poisoning is inhalation for accidental poisoning and oral route for intentional poisoning...

Dear Komal

1st let me know that u have seen the presentation carefully. m making guidelines. not doing the work on nano particles... anyhow if OP poisonous substances are in nano particles, and inhaled accidental than surely it can leads to poisoning.

regards
AMIT

dear varsha ,

i have selected patients which are in OPD dept of the hospital, and all the poisoning cases what ever oral , through skin and inhalation. but i didnt get the snake bite case so i have not mentioned in PPT . but we have made the guidelines too for that...
which is in under evaluation by WHO.

References :Amit S, Biswas A, Aggarwal P, Handa R, Wali JP. General poisoning: Prognostic indicators. Journal of Forensic Medicine & Toxicology 1996; 13: 3-4.

Dear Bhasker

ya OP poisoning is the commonest in my study. ya there is possibilities that farmers can inhale the poison while spreading them in the crops .. and here is the treatment :-

No dear there is still no official guidelines for management of poisoning presently. each poison information centers will use there own guidelines...

GUIDELINES FOR THE MANAGEMENT OF
ORGANOPHOSPHROUS COMPOUNDS

Organophosphrous compounds range from slightly to highly hazardous.
Clinical Features
Anorexia, nausea, headache, anxiety and restlessness, mental confusion followed by bradycardia, respiratory distress, vomiting, abdominal cramps, excessive cold sweating, salivation and finally muscular twitching, urinary incontinence, ‘pin-point’ pupils and coma. Death is normally due to respiratory failure.
Management of Toxicity
• Maintain airway, treat coma, seizures and hydrocarbon pneumonitis if they occur.
• Perform gastric lavage; administer activated charcoal and a cathartic. Do not induce emesis.
• If skin is contaminated, it should be washed with alkaline soap which will not only remove but also help to hydrolyze the phosphate ester.
Antidote:
• Administer IV atropine 2-4mg; repeat every 15mins until the pupils start to dilate. Then give IV pralidoxime 1-2g (25-50mg per kg body weight for children) over 2 mins. Another 1-2 dose can be given if necessary. Max. dose 12g/24hrs. See pg 134.
• Maintain atropinization.
• Give the following supportive treatment if necessary:
- Administer slow IV diazepam 5-10mg (0.2-0.5mg for children) for convulsions, extreme restlessness and excitement.
- Give IV saline drips continuously.
- Remove bronchial hypersecretion by repeated bronchial aspiration and postural drainage.
- Give oxygen if breathless.
- Sample blood for cholinesterase activity.
- Monitor for at least 24 hours.
Caution:
- Ensure cyanosis or severe hypoxia is corrected before atropinization.
- Do not give morphine, aminophylline and phenothiazines such as promazine and chlorpromazine.
Laboratory tests:
Cholinesterase level, electrolytes, glucose, BUN, creatinine, hepatic transaminases, prothrombin time (PT), ECG monitoring.
List of Organophosphrous insecticides are given in Annexure II
references :-1. Tagwireyi D, Ball DE, Nhachi CF. Drug and toxicology information service, poisoning in Zimbabwe: a survey of eight major referral hospitals. J Appl Toxicol. 2002 Apr; 22(2): 99-105.
2. Goksu S, Yildirim C, Kocoglu H. Characteristics of acute adult poisoning in Gaziantep, Turkey. J Toxicol Clin Toxicol. 2005; 40(7): 833-37.
3. Burns Jane M, Patton George C. Preventive interventions for youth suicide: a risk factor-based approach. Australian and New Zealand Journal of Psychiatry 2005 June; 34(3): 388-407.
4. Kelly CB, Weir J, Rafferty T, Galloway R. Deliberate self-poisoning presenting at a rural hospital in Northern Ireland 1976-1996: relationship to prescribing. Eur Psychiatry 2000 Sep; 15(6): 348-53.
Amit Sharma

self poisoning means suicidal attempts by various drugs and insecticides. like phosphorous.... is called self poisoning. and accidental poisoning is by animals like snakebite or scropian bite, self poisoning mainly seen in illiterate due to depression.

hi Sirisha Pingali
see Majority of the cases i.e. 97% were from the urban area and 3% were from the rural area. This represents the increased stress of rapid urbanization.in rural area you will find more illiterate people and have more tendency to do suicidal attempts and The number of patients with primary education and more constituted 80% where as 20% of the patients were illiterate....