This document provides an outline and overview of acute poisoning and antidotes. It discusses classification of poisons, common causes of poisoning, routes of exposure, how poisoning manifests and can lead to death, and principles of management. Specific poisons like kerosene, organophosphates, iron, salicylates, acetaminophen, and their treatments are explained. The roles of supportive care, preventing absorption, enhanced elimination, and antidotes in management are described.

1. ACUTE POISONING AND ANTIDOTES
Dr. Rebecca OMOZUAPO
2018

2. OUTLINE
 Introduction
 Classification
 Causes of poisoning
 Routes of acquisition and circumstances
 Manifestation
 How does the poisoned patient die
 Approach to the poisoned patient
 Principles of management
 Common poisons and mgt
 Antidotes
 Prevention
 Conclusion
 References
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3. INTRODUCTION
 Acute poisoning refers to the development of dose-related
adverse effects following exposure to chemicals, drugs, toxins
or venoms.
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4.  Poisoning may be local (skin, eyes or lungs) or systemic
depending on the chemical and physical properties of the
poison, its mechanism of action and the route of exposure.
 Acute poisoning is a medical emergency
 Effective management could save life.
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5. EPIDEMIOLOGY
 USA:
 ~ 3 million reported cases/year = 1% of the population
 ~ 600 fatal poisonings/year
 = 2 death per 10 000 reported poisonings
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6. CLASSIFICATION OF POISONS
Based on the chief symptoms they produce
1. Corrosives- strong acids, strong alkalis, metallic salts.
2. Irritants- organic, inorganic.
3. Systemic- cerebral, spinal, peripheral, CVS, asphyxiants.
4. Miscellaneous- food poisoning & botulism.
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7. CAUSES OF ACUTE POISONING
 Drug overdosage e.g digoxin, TCA, analgesic,
anticoagulants
 Exposure to chemicals like hydrocarbon, carbon-monoxide
 Ingestion of contaminated food; food poisoning
 Venom e.g snake bite , scorpion sting
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8. ROUTES OF ACQUISITION OF POISON
 Oral
 Inhalation
 Ocular
 Injection
 Bites
 Stings
 Body stuffing or packing; ingestion or concealing of illicit drugs
in a body cavity
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9. CIRCUMSTANCES OF POISONING
 Accidental Poisoning
improper use of chemicals at work
product mislabelling
label misreading
mistake of identity of unlabelled chemicals
dosing error/uninformed self medication
 Deliberate self-harm
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10. MANIFESTATIONS
 Effects of Poisoning could be local and or systemic.
 Manifestations depends on substance in question
 Fatality may be high if prompt medical intervention not
instituted.
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11.  How does the poisoned patient die?
 Many toxins depress the Central Nervous System(CNS),
resulting in coma.
 Patients under the influence of hallucinogens may die in
flights or falls from high places.
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12. HOW DOES THE POISONED PATIENT DIE?
 Comatose patients frequently lose their airway protective
reflexes and their respiratory drive. Thus they may die as a
result of airway obstruction by the flaccid tongue, aspiration of
gastric contents into the tracheobronchial tree, or respiratory
arrest .
 These are the most common causes of death due to overdose
of narcotics and sedative-hypnotic drugs.
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13. HOW DOES THE POISONED PATIENT DIE?
 Cardiovascular toxicity is also frequently encountered in
poisoning. Hypotension may be due to depression of cardiac
contractility; peripheral vascular collaps due to blockade of
alpha adrenoceptor-mediated vascular tone or cardiac
arrhythmias.
 Lethal arrhythmias such as ventricular tachycardia and
fibrillation can occur with overdoses of many cardioactive
drugs such as epinephrine, amphetamines, cocainee, digitalis
and theophylline.
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14. HOW DOES THE POISONED PATIENT DIE?
 Hypothermia or hyperthermia
 Due to exposure as well as the temperature dysregulating
effects of many drugs, they can produce hypothermia.
 Hyperthermia may result from sustained muscular
hyperreactivity and can lead to muscle breakdown and
myoglobinuria, renal failure, lactic acidosis, and hyperkalemia.
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15. HOW DOES THE POISONED PATIENT DIE?
 Cellular hypoxia may occur in spite of adequate ventilation
and oxygen administration when poisoning is due to carbon
monoxide, cyanide, hydrogen sulfide, and other poisons that
interfere with transport or utilization of oxygen.
 In such patients, cellular hypoxia is evident by the
development of tachycardia, hypotension, severe lactic
acidosis, and ischemia
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16. HOW DOES THE POISONED PATIENT DIE?
 Convulsion, muscular hyperactivity, and rigidity may result in
death.
 They may cause hypoxia, and brain damage.
 Drugs and poisons that often cause seizures include
antidepressants, isoniazid, diphenhydramine, cocaine, and
amphetamines.
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17. HOW DOES THE POISONED PATIENT DIE?
 Some organ system damage may occur after poisoning and is
sometimes delayed in onset.
 Massive hepatic necrosis due to poisoning by acetaminophen
or certain mushrooms result in hepatic encephalopathy and
death 48-72 hours or longer after ingestion.
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18. APPROACH TO THE POISONED PATIENT
ASSESSMENT / MANAGEMENT
 A health care facility’s systematic approach to the assessment of the
poisoned or overdosed patient includes but not limited to:
 A) Obtaining the patient’s history,
 B) Performing a physical examination, and
 C) Conducting laboratory studies.
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19. INITIAL MANAGEMENT OF THE POISONED PATIENT.
 History ; the poison-identity, time, route, quantity, intent &
circumstances
Features -time of onset, nature, severity of symptoms.
 Laboratory evaluation; assay, E&U, RBS , ECG
 Treatment
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20. PRINCIPLE OF TREATMENT OF THE POISONED PATIENT
R A R E
 Resuscitation and supportive care
 Prevention/Reduction of poison absorption
 Enhancement of elimination/excretion of poison
 Administration of antidotes
 Prevent re-exposure
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21. I. RESUSCITATION
 Includes Airway- proper positioning head tilt and chin lift,
suction of secretions from oropharynx, falling back of tongue
is prevented by suitable airway tube.
 Breathing- oxygen via a mask, when gag/cough reflects is
absent- ET tube inserted. if necessary positive pressure
ventilation with ABG monitoring.
 Circulation- proper IV access, maintenance of fluid &
electrolyte balance, IV drugs for treatment.
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22. I. SUPPORTIVE CARE
 Vital signs, general and systemic exam, and pupil size
 cardiac monitoring
 cervical immobilization if suspect trauma
 Rule out hypoglycaemia
 Catheterize
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23. II. PREVENTING ABSORPTION
a) Gut decontamination
• Single-dose activated charcoal
• Gastric lavage
• Catharsis
• Total bowel irrigation
• Syrup of ipecac
• Surgical or endoscopic evacuation of poison.
b) Ocular or dermal- N/S
c) Inhaled – removal from the site
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24. III. ENHANCED ELIMINATION OF THE DRUG OR TOXIN
 The absorption rate, body distribution, metabolism, and
elimination must be considered when choosing methods to
eliminate the drug or toxin from the body.
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25. METHODS OF ENHANCED ELIMINATION:
 Multiple dose activated charcoal --carbamazepine,
phenobarbitone, quinine, theophylline
 Urine alkalinisation/ Alteration of urine pH/forced diuresis ---
aspirin, certain herbicides or acidification
 Haemodialysis/Peritoneal dialysis/Haemoperfusion--ethanol,
ethylene glycol, salicylate, methanol
 Chelation
 Hyperbaric oxygen- carbon monoxide poisoning
 Exchange blood transfusion
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26. IV. ADMINISTRATION OF ANTIDOTES
 V. PREVENT RE-EXPOSURE
 Counselling... Train and retrain workers
 Psychiatric evaluation and treatment
 Child proof containers
 Proper labelling etc
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27. COMMON POISONS AND THEIR MANAGEMENT
 Kerosene
 Clinical features:
 Fever, cyanosis, restlessness
 Breathlessness, cough
 Vomiting, diarrhoea
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28. INVESTIGATIONS
 E ,U,Cr
 Chest xray (right basal infiltrates, emphysema, pleural
effusion)
MANAGEMENT
 Avoid emetics
 Avoid gastric lavage
 Oxygen may be useful
 Assisted ventilation
 Antibiotics –Penicillin G 50000/kg/24hrs IV dly
 Kanamycin:10-15mg/kg/24hrs IM bd
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Complications Pneumothorax Pleural effusion Bronchopneumonia Coma

29. ORGANOPHOSPHORUS POISONING
 Organic phosphate insecticides cause irreversible inhibition of
the enzyme cholinesterase.
 As result acetycholine accumulates in various tissues.
 Excessive parasympathetic activity occurs.
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30. Clinical presentations include:
 Weakness, blurred vision, headache
 Nausea, vomiting
 Chest pain
 Excessive secretion in the lungs
 Salivation is marked
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31. CONTD
 Pupils are constricted
 Papilledema
 Muscle twitching
 Convulsion
 Reflexes are absent
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32. MANAGEMENT
 Atropine sulphate:0.03-0.04mg/kg IV.
 Repeat half the dose in 15minutes and if necessary every
hour until signs of toxicity disappear.
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33. IRON
 Ingestion of a number of tablets of ferrous sulphate may
cause acute poisoning
 Lethal dose is 300mg/kg of iron.
Clinical presentations
 Severe vomiting
 Diarrhoea (bloody)
 Severe shock
 Hepatic and renal failure within a few hours or after a latent
period of 1 to 2 days
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34. CONTD
 Lavage, whole bowel irrigation,

 Iron salts are chelated with desferroxamine IV at 15mg/kg/hr
until the serum iron is <300mg/dl or till 24 hours

 The dose may be repeated after an hour if acidosis is
persisting.
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Activated charcoal does not bind iron

35. SALICYLATE
 Ingestion of 150mg/kg of salicylates causes intoxication.
 Salicylate level of 50-80mg/dl causes moderate symptoms.
 Severe symptoms are associated with blood levels above
80mg/dl
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36. CONTD
 Clinical presentations:
 Nausea,abdominal pain
 Tininitus
 Respiratory acidosis
 Metabolic acidosis
MANAGEMENT
 Urine is alkalinized by administering 1-2mmol/l/kg of sodium
bicarbonate at 30mins for 4hours to promote excretion in
urine.
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Potassium correction

37. ACETAMINOPHEN
 It is safe in pharmacological doses.
 Overdosage may cause hepatic damage
 Clinical presentation include:
 Weakness, abdominal pain, nausea
 Complications include kidney failure, pancreatitis, lactic
acidosis
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38. ACETOMINOPHEN
 Max dose:
 4g/day adults
 90 mg/kg day kids
 Peak serum levels: 4 hours after overdose
 What are the three methods of PCM metabolism?
 Glucuronidation (90% normal thru pathway)
 Sulfonation
 P450 mixed oxidase enzymes (5% nl thru pathway)
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NAC inihibits toxic metabolites in gluthathione pathway

39. ACETOMINOPHEN (PCM)
 Toxicity
 140mg/kg acute ingestion
 Direct hepatocellular toxicity with centrolobular
distribution (hepatic vein)
 Can also have renal damage and pancreatitis
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40. STAGES OF PCM TOXICITY
 I (0-24hrs): nausea/vomiting, but most asymptomatic
 II latent stage (24-48hrs): subclinical increase in ast/alt/bili
 III hepatic stage (3-4dys): liver failure, RUQ pain, vomiting,
jaundice, coagulopathy, hypoglycemia, oliguria, metabolic
acidosis
 IV recovery stage (4dys-3wks): resolution of hepatic
dysfunction
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Therapy is most effective when initiated within 8hrs of ingestion

41. NEED 4 HOUR LEVEL AND
N-ACETYLCYSTEINE (NAC)
 Dx: 4 hour level compared
to the Rumack and
Matthews nomogram
 150ug/ml at 4 hours
 Rx: NAC 140mg/kg then
70mg/kg every 4 hours for
17 doses
 We Have PO and IV dosing
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42. ACETOMINOPHEN (PCM)
 If time of ingestion unknown, draw level immediately and again
at 2-4 hours.
 Labs: LFTs, coags, lytes, aspirin, ETOH, tox screen
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43. NAC INDICATIONS
 Ingestions with potential toxicity
 Late presentations with potential or ongoing toxicity
 Chronic overdose with evidence of hepatic damage
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44. PCM OVERDOSE DISPOSITION
 Admit if…..
 Known toxicity / potential toxic levels
 Lab evidence of hepatic damage
 Unknown time of ingestion and signs consistent with
toxicity
 Unknown ingestion time with measurable
acetaminophen levels.
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45. SALICYLATES (ASA)
 Weak acid, rapidly absorbed
 Enteric coated has delayed absorption
 Toxic dose: 160 mg/kg
 Lethal dose 480 mg/kg
 Mixed respiratory alkalosis-metabolic acidosis
 Stimulates respiratory drive causing hyperventilation, but
limits ATP production metabolic acidosis
 Oil of wintergreen, 1ml = 1400mg
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46. SALICYLATES SYMPTOMS
 Tachypnea, tachycardia,
hyperthermia
 Resp alkalosis-metabolic
acidosis
 Altered serum glucose
 metabolic acidosis
 Dehydration (vomiting,
tachypnea, sweating)
 Abd pain/n/v
 Tinnitus, hearing loss
 lethargy, seizures, altered
mental status
 Noncardiogenic pulmonary
edema
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47. EVALUATION OF ASA OVERDOSE
 Lytes, ABG, LFTs, CBC, urine PH
 Serum salicylate levels (toxicity at 25mg/dl)
 Evaluation with DONE nomogram based on single ingestion of
regular ASA at levels drawn 6 hrs after ingestion
 Underestimates toxicity in cases of severe acidemia or chronic
ingestion
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48. THERAPY FOR ASA OVERDOSE
 ABC’s
 Activated charcoal
 Urinary alkalinization (start if serum level is greater than
35mg/dl)
 3 amps bicarbinate in 1 L D5W at 150
ml/hr(3600L/day)
 By increasing urinary pH to greater than 8, ASA gets
trapped in tubes and cannot be reabsorbed
 Dialysis for severe acidemia, volume overload,
pulmonary edema, cardiac or renal failure, seizures,
coma, levels > 100mg/dl in acute ingestion, or > 60-80
mg/dl in chronic ingestion
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49. DISPOSITION FOR ASA OVERDOSE
 Pt gets charcoal and remain asymptomatic after 6-8
hours = Possible D/C
 Sustained release requires longer observation period
 Pts with toxic levels, symptomatic, or develop symptoms
= Admission
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50. SOME SPECIFIC POISONS AND ANTIDOTES
POISONS ANTIDOTES
Organophosphates Atropine sulphate &pralidoxime
lron Desferroxamine
Lead poisoning Dimercaprol
Cyanide Sodium thiosulfate, Oxygen , hydroxocobalamin
Carbonmonoxide High flow oxygen
Benzodiazepines Flumazenil
Digoxin digibind
Opioid Naloxone
Anticholinergics Physostigime
Ca channel blockers Calcium gluconate
Alcohol Thiamine, formepizole, bicarbonate
Heparin Proteamine sulphate
Warfarin Vit. K
PCM N-acetycysteine or methionine
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51. CONTINUOUS PATIENT MONITORING
 Seriously poisoned or overdosed patients may require
continued monitoring for hours or days after exposure.
 Physical examination, the use of diagnostic tools, and careful
assessment of clinical signs and symptoms provide
information about the patient.
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52. PREVENTION OF POISONING
 Indiscriminate use of drugs should be discouraged.
 Proper dosing should be known before ingestion of any drug
 The label should be read before using the drug. In cases
where labels are worn out, drugs should not be ingested on
assumption.
 No drug should be given or taken in the dark. Drugs after their
expiry date should be disposed in a safe manner.
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53.  The poisonous substances should be kept in secure places
and well labelled out of reach of the child.
 The poisonous substances should be replaced in their
proper place.
 Potential household poisons should not be transferred to
empty containers otherwise used for innocuous food or
beverages.
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54.  Safety regulations by the State should be enforced.
 Establishment of poison control centers to collect, compile
and disseminate information on poisons and their
management. These should promote research on prevention
and treatment.
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55. CONCLUSION
 Acute poisoning is a medical emergency and effective
management could save life.
 Poisons can be ingested through any route accidentally or by
deliberate self harm.
 Manifestations depends on the substance in question.
 Seriously poisoned or overdosed patients may require
continued monitoring for hours or days after exposure.
 Indiscriminate use of drugs should be discouraged and
psychiatric evaluation of the poisoned patient after treatment
may be necessary.
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56. REFERENCES
 Poisoning & Drug Overdose, California Poison Control
System. KR Olson, 3rd edition, Appleton & Lange, 1999.
 Emergency Medicine Board Review Series. L Stead,
Lippincott Williams & Wilkins, 2000.
 Emergency Medicine, A comprehensive study guide.
Tintinalli, 6th edition, McGraw Hill, 2004.
 Harrisons principle of internal medicine 19th Ed.
 Kumar & Clarks clinical medicine 7th Ed.
 Davidson's principles and practice of medicine 22nd Ed.
 Medscape
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57.  Thank you for listening
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