Downloaded 1,236 times
![Resources
Pusat Racun Negara
Emergency First-Aid Databases
Office Hours : 1-800-88-8099 / 04-6570099
Monday to Friday: 8.10am - 4.40pm
Saturday: 8:10am -1.00pm
After office hours : 012-4309499
[including weekends and public holidays]](https://image.slidesharecdn.com/acutepoisoning-100819051204-phpapp02/85/Acute-poisoning-87-320.jpg)
More Related Content
Acute poisoning
- 1. Update on MedicalEmergencies Course, Terengganu Acute Poisoning and Drug Overdose Dr. Rashidi Ahmad MD (USM), MMED (USM), FADUSM, AM Dept. Emergency Medicine School of Medical Sciences USM Health Campus 8th December 2007
- 2. Objectives • Understanding poison •Develop methodical approach to Poisoned Patients • Characterize Toxidromes & its management • Evidence-Based GI Decontamination • Learn Antidotes
- 3. Outline • Definition • Relevantepidemiological data • Risk assessment • Treatment
- 4. Poison “Substance that whenintroduced into, or absorbed by a living organism destroys life or injures health” (Oxford Dictionary) “Poisons and medicines are oftentimes the same substance given with different intents” (Peter Mere Latham; 1789 – 1875)
- 5. “What is itthat is not a poison? All things are poison and nothing is without poison. It is the dose only that makes a thing not a poison.” Paracelsus (1493-1541), the Renaissance “Father of Toxicology,” in his Third Defense.
- 7. 7 Mechanisms ofToxicity 1. Interfere with O2 transport or tissue utilization of oxygen (i.e: cyanide, CO) 2. Affect lungs (paraquat) 3. Affect cardiovascular system (TCA, Ca++ channel blockers) 4. Affect CNS (cocaine, sedatives) 5. Affect ANS (organophosphates) 6. Direct local damage (acids, bases) 7. Delayed effects on liver or kidneys (acetaminophen, metals)
- 8.
- 9. Most lethal humantoxic exposure
- 10. Two Sources ofData • Data from Dr. Rozlan Ishak, Environmental Health, Unit Disease Control Division, MOH (1999) • Data from the Occupational Health Unit of the MOH (1997-2000) • Data from the National Poison Centre, Universiti Sains Malaysia (1995 to 2002)
- 11. Site of Exposure 1997 1998 1999 2000 HOME 357 400 684 767 WORKPLACE 83 115 136 136 OTHERS 15 20 50 68 MISSING 253 11 18 75 TOTAL 708 546 888 1,046
- 12. Age Group 1997 1998 1999 2000 < 10 76 22 161 210 10-19 101 90 179 197 20-29 143 177 221 261 30-39 111 105 134 172 40-49 35 60 72 75 50-59 24 23 42 42 60-69 12 16 22 15 70-79 3 5 7 17 79 5 0 2 14 MISSING 198 48 48 60 TOTAL 708 546 888 1,046
- 13. Poisoning cases inMalaysia, 1999 2000 1798 1794 1800 1600 1427 No. of Cases 1400 1200 10291058 1045 926 1000 778 800 660 566 522 600 355 395 267 400 176 222 200 0 14 -4 -9 75 4 20 9 30 9 4 40 9 4 50 9 4 60 9 65 4 9 4 -2 -1 -2 -3 -3 -4 -4 -5 -5 -6 -6 -7 – > 1 5 15 25 35 45 55 71 10 Age Groups Poisoning cases
- 14. Ethnic Group 1997 1998 1999 2000 MALAY 229 170 393 399 CHINESE 137 106 173 175 INDIAN 254 159 177 290 OTHERS 87 110 136 159 MISSING 1 1 9 23 TOTAL 708 546 888 1,046
- 15. Ethnic difference ofChemical Poisoning in Malaysia in 1999 6000 4843 5000 No. of Cases 3630 4000 3000 2000 984 952 910 1161 1000 34 24 340 283 0 Malays / Chinese Indians Others Missing Data Bumiputra Ethnicity in Malaysia Male Female
- 16. Female Male ak aw Sar ah Sab Gender Difference in Poisoning in Malaysia, 1999 an ant Kel u gan eng Ter ang Pah or States in Malaysia Joh laka bila n Me Sem pur er i um Neg aL ual PK W. or ang Sel ak Per ang Pin au Pul ah Ked lis Per 0 1200 1000 800 No. of Cases 600 400 200
- 17. Nationality 1997 1998 1999 2000 MALAYSIAN 633 512 844 972 INDONESIAN 44 19 31 43 BANGLADESHI 14 3 2 3 PHILIPPINO 3 2 1 2 OTHERS 3 7 5 10 MISSING 11 3 5 16 TOTAL 708 546 888 1,046
- 18. Circumstances 1997 1998 1999 2000 TOTAL OCCUPATIONAL 74 94 105 92 365 (11.5%) SUICIDE 257 220 273 327 1077(33.8%) HOMICIDE 9 6 8 6 29 (0.9%) OTHERS 226 226 430 417 MISSING 14 20 72 204 TOTAL 708 546 888 1,046 3188
- 19. Chemical Poisoning inMalaysia in 1999 Venomous animals 44.07 Pesticides 8.76 Diuretic and others 8.03 Analgesic 7.73 Organic solvents 6.19 Other noxious food 5.56 Topical agents 4.91 Corrosive substances 2.98 Other and unspecified 2.37 Antiepileptic 1.55 Other psychotropic drugs 1.11 Other gases, fumes and vapors 1 Type of Chemical Poisoning Haematological agents 0.96 Antibiotic 0.69 Carbon Dioxide 0.52 Soaps and detergents 0.49 Agents affecting Muscular system 0.46 Noxious substances eaten as seafood 0.4 Alcohol 0.34 Drugs affecting ANS 0.26 Hormones 0.26 Anaesthetic 0.22 Metals 0.21 Narcotic 0.2 Agents affecting CVS 0.19 Agents affecting GIS 0.17 Halogen and aromatic hydrocarbon 0.17 Other inorganic substances 0.09 Other antibiotic 0.07 Alfatoxin and other mycotoxin 0 0 5 10 15 20 25 30 35 40 45 50 Percentag N: 13133 Chemical Poisoning
- 20. Type of Chemicals 1997 1998 1999 2000 Total Pesticides 256 183 288 406 1133 (35%) Agrochemicals 29 32 17 18 96 (3%) Therapeutic Drugs 86 135 246 237 704 (22%) Chemicals 182 176 290 357 1005 (32%) Metals 6 1 1 2 10 (0.3%) Unknown 149 29 36 26 240 (7.7%) TOTAL 708 556 878 1046 3188
- 21. Data on PesticidesAvailability (1996-1998) Total number of pesticides marketed/used: 1,983 Breakdown: Insecticides/Nematicides: 539 (27.2%) Fungicides: 229 (11.6%) Herbicides: 692 (34.9%) Household, veterinary & public health pesticides 373 (18.8%) Rodenticides 50 ( 2.5%) Others 100 ( 5.0%)
- 22. Type of Pesticides 1997 1998 1999 2000 Paraquat 171 92 113 187 Glyphosate 6 11 19 18 Organophosphate 46 43 70 69 Organochlorine 0 5 8 2 Pyrethroids 4 0 1 12 Carbamate 0 6 7 6 Others 29 26 48 45 Non Pesticides 452 363 600 640 Unknown/missing - - 22 67 TOTAL 708 546 888 1,046
- 23. • Review ofdata from the National Poison Centre, USM • Data extracted from inquiry records for the years 1995 to 2002
- 24. Enquiries on specificpoisoning (1995 – 2002) Pesticides Chemicals/Heavy Metals 45.3 % 8.6 % Household Products 18.0 % Natural Toxins 3.2 % Unknown 1.2 % Others 0.4 % Pharmaceuticals (n=1666) 22.3 % Gases 0.8 %
- 25. Route of exposure Ingestion 643 Inhalation 79 Cutaneous 20 Ocular 2 Race Malay 142 Chinese 106 Indian 280 Type of Incidents Intentional 385 Unintentional 241
- 26. Types of PoisonsInvolved Drugs • Paracetamol Animal • Calamine Lotion • Snake bite Pesticides • Traditional Products • Spider bite • Haloperidol • Glyphosate • Jellyfish sting • Paraquat • Bees sting • Malathion Plants • Endosulfan • Datura • Carbofuran • Natural rubber latex
- 27. Types of PoisonsInvolved Chemicals/Heavy Metals • Lead • Mercury Household Products • Formic acid • Household insecticides • Thinner • Mosquito Aerosol Spray • Ammonia • Vape Mat • Mosquito Coil • Dettol • Silica gel • Mothballs
- 28. Type of pesticides Glyphosate 269 Paraquat 67 Malathion 15 Endosulfan 19 Carbofuran 42 Glufosinate Ammonium 12 Chlorpyrifos 14 2,4-D 16 Lindane 8
- 29. Conclusions • Home >Workplace • Ingestion • Suicidal attempt • Male • Malay • Children • Pesticides > Pharmaceuticals > Chemicals
- 30. Phases Of Poisoning •Preclinical phase • Toxic phase • Resolution phase
- 31. Preclinical phase • Followsexposure before s/sx • History guides management • Aim: to reduce or prevent toxicity • Decontamination is a priority
- 32. Toxic phase • Periodfrom onset to peak of manifestation of toxicity clinical or laboratory • PE guides treatment • Aim: to shorten or lessen the severity of toxicity • Priority: stabilize airways, breathing and circulation and consider antidote
- 33. Resolution phase • Frompeak toxicity to recovery • Clinical status guides management • Major goal: shorten the duration of toxicity & supportive care
- 34. Suspect intoxication Cumbridge &Murray. CHEST 2003; 123:577-592
- 35. Approach to thePoisoned Patient • ABC’s are always first ! • Most Patients Do Fine - Majority of poisoned patients require only supportive Rx • But, those who don’t … often present with undifferentiated AMS
- 36. Approach to thePoisoned Patient • Approach to AMS • Toxicologic History • Toxicologic Physical Exam • Toxicologic Labs Think Toxins in any patient with AMS !
- 37. Approach to AMS •A – Airway (mental status, suicidal trauma) • B – Breathing (resp depression, pulm oedema, ARDS) • C – Circulation (dysrhythmias, CV depression) • D – Dysfunction CNS (hypoglycemia, alcohol, opiate & benzodiazepine overdose, seizure control) • E – Exposure (hyperthermia)
- 38. “Coma Cocktail” intoxin induce AMS • Use of D50%, thiamine, nalaxone, flumazenil • Toxin-induced LOC is generally well-tolerated and achieving "arousal" of the patient does not necessarily improve outcome. • ? cost-effectiveness and risks of the coma cocktail
- 39. • D50% &thiamine should probably be given to patients with AMS from unknown causes. • Strongly suspected opiate overdose: Naloxone is indicated. Lack of response to 10 mg of naloxone generally excludes opioid toxicity • Flumazenil should be used mainly for reversal of therapeutic conscious sedation. Hoffman RS, et al. The poisoned patient with altered consciousness. Controversies in the use of a "coma cocktail." JAMA 1995;274:562-9
- 40. • Reversal ofBZD intoxication with flumazenil is a/w significant toxicity in patients with benzodiazepine dependence or coingestion of proconvulsant medications (TCA) • May be useful to reverse excessive sedation when BZDs are used for procedural sedation. Toxicology in ECC. Circulation. 2005;112:IV-126-IV-132
- 41. Toxicology history • Riskassessment - to predict the likely clinical course and potential complications - To allow the clinician to make specific decisions about all subsequent management steps (appropriate supportive care and monitoring; screening and specialized testing; decontamination; enhanced elimination; antidotes and disposition)
- 42. Toxicology History • Goalis Identification of Etiologic Agent(s) • Use all Available Resources - Pill bottles - Pre-hospital personnel - Family and Friends - Medical Records - Past medication and medical history • Assess for Suicidal Behavior - Must assume suicidal until proven otherwise - Low threshold for Psychiatric consultation
- 43. Evaluation of Toxicity •Evaluate the SATSC – Substance – Amount – Time since ingestion – Symptoms – Co-morbid • Regional Poison Control Center
- 44. Toxicology PE • Vitals,Vitals, Vitals ! - Measure accurately - Measure often - Temp, HR, BP, RR, Pulse Ox • Assess for Signs of Trauma • “Skin” exam is critical - Diaphoresis ? - Trauma (scalp, elsewhere) ? • Odor!! • Pupil examination
- 46. Odor Poison Sweet/fruity Ketone, alcohol Almond Cyanide Gasoline Hydrocarbon Garlic Organophospate Wintergreen Methylsalicylate Pear Chloral hydrate John J. Marini, Arthur P. Wheeler. Critical care Medicine. The essentials – Textbook 2006
- 47. Toxicology laboratory • Mainlyto assess the severity • Asymptomatic Patients - Acetaminophen Level – the “Silent” killer • Toxin Identified/Strongly Suspected - Testing based on suspected toxin - Consider acetaminophen level as well • In any patient with Undifferentiated AMS - Blood: CBC, Chem 7, LFT’s, CPK, Serum osm - Urine: U/A, UPT, UTox - Tox-Specific: Acet, ASA,
- 48. Toxicology laboratory • Mostpoisonings can be managed appropriately without extensive laboratory studies. • “Tox screens" rarely helpful. - Undetected: bromide, carbon monoxide, chloral hydrate, clonidine, cyanide, organophosphates, tetrahydrozoline, beta-blockers, calcium-channel blockers, clonidine, colchicine, digitalis, and iron. • PCM screening helps especially in multiple medications in intentional overdose.
- 49. Importance of ancillarytesting • Wide anion gap metabolic acidosis – MUDPILES • Low anion gap metabolic acidosis – bromides, lithium, abnormal cationic proteins • Wide anion gap, ketone & glucose negative, osmolar gap > 10mOsm/L – methanol, ethylene glycol • Wide anion gap, ketone & glucose negative, osmolar gap < 10mOsm/L – iron, paraldehyde, CO, cyanide • Respiratory alkalosis – salicylate • Plain abdominal films: CHIPES (chloral hydrate, heavy metals, iron, iodides, phenothiazines, enteric coated pills, sustained-release preparations and solvents
- 50.
- 51.
- 52. Level-guided treatment Substance Level Rx Carboxyhaemoglobin > 25% Hyperbaric Oxygen Ethylene glycol > 20mcg/dL Ethanol +/- haemodialysis Lithium > 2.5mEq/L Haemodialysis Iron > 350mcg/dL Desferrioxamine Methaemoglobin > 30% Methylene blue Salicylate > 100mcg/dL Haemodialysis Lead > 45mcg/dL Chelation
- 53. Urine toxicology Drug Durationsin the urine Drug Duration Amphetamines 48 hours Alcohol 12 hours Barbiturates 10-30 days Valium 4-5 days Cocaine 24-72 hours Heroin 24 hours Marijuana 3-30 days Methaqualone 4-24 days Phencyclidine 3-10 days Methadone 3 days
- 54. Toxidromes • Constellation ofPhysical Findings - Provides Clues - Narrows Differential Diagnosis • Beware: Many Exceptions Exist! - Poly-drug Overdoses - Overlapping and confusing mixed syndromes
- 55. Autonomic Nervous System •Parasympathetic (PNS) - “Rest and Digest” - Mediated by Acetylcholine - Muscarinic and Nicotinic Receptors • Sympathetic (SNS) - “Fight or Flight” response - Mediated by Catecholamines - Sympathetic Cholinergic: Sweating
- 56. Toxidrome review • Physiologicstimulants - Anticholinergics - Sympathomimetics (ex. cocaine) - Hallucinogens - Drug withdrawal - Miscellaneous (thyroid hormones) • Physiologic depressants - Cholinergics - Narcotics - Symphatholytics (cyclic antidepressants) - Sedative-hypnotics - Miscellaneous (carbon monoxide) • Serotonin Syndrome (mixed)
- 57. Serotonin Syndrome • Hyperthermia •Mental status changes • Autonomic instability • Neuromuscular abnormalities • Examples: Antidepressants (SSRIs), Meperidine, Dextromethorphan, Ecstasy
- 62. Toxidrome Summary • ANTI-CHOLINERGIC - Decreased Parasympathetic - Hot…Mad…Dry…etc… • (PRO) CHOLINERGIC - Increased Parasympathetic - SLUDGE/DUMBELS • SYMPATHOLYTIC - Decreased Sympathetic - AMS, Decreased Respiratory, Miosis • SYMPATHOMIMETIC - Increased Sympathetic • SEROTONIN SYNDROME - Altered Parasympathetic and Sympathetic - Fever, AMS, Dysautonomia, NM
- 63. Points to ponder •Anticholinergic • Think TCA toxicity • Procholinergic • Think Terrorism/OP • Sympatholytic • Think Intubation • Sympathomimetic • Think Withdrawal • Serotonin Syndrome • Fever and AMS
- 64. “CLUB DRUGS” • Raveparties increasing in popularity • Drugs meant to intensify sensory experience of lights/music, facilitate prolonged dancing
- 65. MDMA “Ectasy” • Structurallyresembles amphetamine (stimulant) and mescaline (hallucinogen) • SX: trismus, bruxism, tachycardia, mydriasis, diaphoresis, hyperthermia, hyponatremia, hepatic failure, CV toxicity (tachycardia, HTN) • Treatment – Mainly supportive – Benzodiazepines – Calm environment – Avoid beta-blockers Can result in unopposed alpha effect If essential consider labetolol
- 66. GHB: Date rapedrug “Georgia homeboy, liquid ectasy, or grievous bodily harm” • Developed as anesthetic agent. GABA analog • Symptoms: bradycardia, hypothermia, hypoventilation, somnolence, vomiting, myoclonic jerking • Treatment – Conservative mx – Intubation – Careful exam for sexual assault
- 67. Ketamine: “K”, “specialK” • Developed as an anesthetic, structurally resemble PCP • Acts on all six neurotransmitter systems – Anticholinergic: dry skin, miosis – Dopamine/norepinephrine: agitation, delusions – Opioid: pain perception alterations – Serotonin: perceptual changes – GABA receptor inhibition: excitation • Treatment – Benzodiazepines/haloperidol – Supportive care – Can consider urine alkalinization
- 68. Treatment of acutepoisoning • Primary goal - keep concentration of poison as low as possible by preventing absorption and increasing elimination • Secondary goal - counteract toxicological effects at effectors site, if possible
- 69. Management principles • GIdecontamination • Antidote • Resources
- 70. Principle of GIdecontamination • Toxins poorly absorbed in stomach, toxins well absorbed in SI • Decrease amount in stomach, therefore less presenting to SI for absorption • Maximum benefit: present soon after the ingestion. • Delayed presentation + without symptoms - probably does not contribute to the outcome • Drugs with delayed absorption/reduce GI motility, activated charcoal may reduce the final amount absorbed. ?? Prehospital GI decontamination of toxic ingestions
- 71. Methods of GIdecontamination • Gastric - Ipecac - Activated Charcoal - Single dose vs multi-dose - Gastric Lavage • Gastro-Intestinal - Cathartics - Whole Bowel Irrigation
- 72. You make thechoice…
- 73. Ipecac • Little evidencethat ipecac prevents drug absorption or systemic toxicity • No convincing data that it significantly alters the clinical outcome of patients who are awake and alert on presentation to the ED. • Considered only in fully alert patients • Never indicated after hospital admission • CI: corrosives, petroleum products, or antiemetics, high risk of seizures or altered consciousness. Vale JA, Meredith TJ, Proudfoot AT. Syrup of ipecacuanha: is it really useful? BMJ 1986; 293:1321–1322
- 74. Ipecac • No evidencefrom clinical studies that ipecac improves the outcome of poisoned patients and its routine administration in the emergency department should be abandoned. • Insufficient data to support or exclude ipecac administration soon after poison ingestion. • Ipecac may delay the administration or reduce the effectiveness of activated charcoal, oral antidotes, and whole bowel irrigation. Krenzelok AP et al. J Toxicol Clin Toxicol. 2004;42(2):133-43.
- 75. Single-dose activated charcoal •Should not be administered routinely • The effectiveness of activated charcoal decreases with time; the greatest benefit is within 1 hour of ingestion. • Consider if a patient has ingested a potentially toxic amount of a poison: insufficient data to support or exclude its use after 1 hour of ingestion. • There is no evidence that the administration of activated charcoal improves clinical outcome. Chyka PA et al. J Toxicol Clin Toxicol. 1997;35(7):721-41.
- 77. Substances that arenot absorb by charcoal Mnemonic: CHARCOAL Caustics & corrosive Heavy metals Alcohol & glycols Rapidly absorbed substances Cyanide Other insoluble drugs Aliphatic hydrocarbobs Laxatives
- 78. Multiple-dose activated charcoal •Consider only if a patient has ingested a life- threatening amount of: - carbamazepine - dapsone - phenobarbital - quinine - theophylline • Insufficient clinical data: salicylate, amitriptyline, dextropropoxyphene, digitoxin, digoxin, disopyramide, nadolol, phenylbutazone, phenytoin, piroxicam, and sotalol
- 79. • The needfor concurrent administration of cathartics remains unproven and is not recommended. • Cathartics should not be administered to young children because of the propensity of laxatives to cause fluid and electrolyte imbalance. Jefrey B, et al. Clinical Toxicology, 37(6), 731–751 (1999)
- 80. Gastric lavage • Reportedcomplication: – Aspiration pneumonia - most common – Laryngospasm with cyanosis – Kinking of lavage tube in eosphagus – Esophageal perforation Reid et al Arch Dis Child 1970 Mattew et al Br Med J 1966
- 81. “Gastric lavage shouldnot be employed routinely, if ever, in the management of poisoned patients.” J Toxicol Clin Toxicol 2004;42:7:933.
- 82. Evidence based protocols •Ipecac - is effectively obsolete • Charcoal - agent of choice for most poisons - Best if used within one hour • Lavage - Narrow indications - principally for potentially serious amounts of agents not adsorbed by charcoal within half hour ingestion Bateman DN. Gastric decontamination--a view for the millennium. J Accid Emerg Med. 1999 Mar;16(2):84-6
- 83. Cathartics • Use alone- not recommended as a method of gut decontamination. • Conflicting data: combine with activated charcoal: • No clinical studies have been published to investigate the ability of a cathartic, with or without activated charcoal, to reduce the bioavailability of drugs or to improve the outcome of poisoned patients. Donna Seger, et al. CLINICAL TOXICOLOGY. Vol. 42, No. 3, pp. 243–253, 2004
- 84. Whole bowel irrigation(WBI) • No conclusive evidence WBI improves outcome • Consider: potentially toxic ingestions of sustained- release or enteric-coated drugs. • Insufficient/theoretical data for iron, lead, zinc, or packets of illicit drugs • CI: bowel obstruction, perforation, ileus, hemodynamic instability or unprotected airways. • A single dose of charcoal prior to WBI does not decrease the binding capacity of charcoal Hoffman RS. J Toxicol Clin Toxicol. 2000;38(7):689-90
- 85.
- 86. Criteria for ICUadmission
- 87. Resources Pusat Racun Negara Emergency First-Aid Databases Office Hours : 1-800-88-8099 / 04-6570099 Monday to Friday: 8.10am - 4.40pm Saturday: 8:10am -1.00pm After office hours : 012-4309499 [including weekends and public holidays]
- 88. Summary • Resuscitation – Airway – Breathing – Circulation – Seizure control – Correct hypoglycaemia – Correct hyperthermia – Resuscitation antidotes • Risk assessment
- 89. Risk assessment • Distinctcognitive step (predict the likely clinical course and potential complications for the individual patient at that particular presentation) • Quantitative • Takes into account: – Agent(s) – Dose(s) – Time since ingestion – Current clinical status – Patient factors
- 90. Summary • Supportive careand monitoring • Investigations – Screening (ECG, paracetamol) – Specific • Decontamination • Enhanced elimination • Antidotes • Disposition
- 91. Conclusion • Intoxication manifestationis very challenging (non specific, AMS, no hx of intoxication, masked by other conditions) • Methodical approach/toxidrome helps • Decontamination methods are vital – indications determined by type of poisons, conscious level, risk of aspiration, hemodynamic stability, time factor • Antidote: gold standard
- 92. Build me newermolecules, O my Soul - As the swift seasons roll Let each new compound Safer than the last Avoid the reactions observed in the past ……………….. The Pharmacologic Principles of Medical Practice (1954)