Intro to Emergency Toxicology

Intro to Emergency Toxicology
Author: Cheryl Hunchak MD, CCFP(EM), MPH, Lecturer, University of Toronto Date Created: March 2011

Lecture Outline Bedside approach to the patient with suspected overdose/intoxication Universal antidotes Principles of decontamination Toxidrome recognition and management Cases

Learning Objectives Develop a structured bedside approach to the intoxicated patient in the ED Apply universal antidotes when appropriate Feel comfortable choosing appropriate decontamination strategies Feel confident recognizing and managing patients with classic toxidromes

What constitutes a poisoning?
Whenever an exposure to a substance adversely affects the function of any system within the body

Major Routes of Poisonings
Inhalation Ingestion Injection Cutaneous exposures Ingestion is by far the most common route among patients seen in the ED

Case 1 An 18 year old woman is brought to the ED by her parents. She has been unresponsive for 8 hrs and has the following vital signs: HR 105 RR 10 BP 90/60 Temp 34.5 How should you proceed?

Bedside Approach to Suspected Intoxication
“ABCDDDDD” ABC Oxygen, monitors, IV access Full set of vitals including O2 sat Gather history and collateral information Check glucose* Disability : GCS, pupils Detailed physical exam Drugs: Consider universal antidotes Decontamination Draw Labs Specific antidotes and care *give IV glucose empirically if do not have capacity to check glucose quickly at bedside (see slides on ‘universal antidotes’) Also consider 12 lead ECG and CXR where available/appropriate PSYCH ASSESSMENT – assess possibility of suicidality, and consult appropriate in-patient psychiatric services (if available) once patient is medically cleared. If legislation is in place, consider involuntary admission if patient does not consent to voluntary psychiatric treatment and poisoning was self-induced with suicidal intent. CONTACT POISON CONTROL CENTRE IF AVAILABLE

What history would you like to know?

History Often difficult to obtain COLLATERAL very important
Family, friends Careful body search re bottles, powders, etc Patient’s occupation, hobbies Prior psychiatric history Prescription medications

History Drug(s) or substance taken/exposed to
Number of tablets, dosage per tablet Estimated time since ingestion Type of preparation (sustained release?) Chance of caustic ingestion? Co-ingestions (alcohol, etc)

The plot thickens… The patients’ parents tell you that she has been very stressed at school. They found an empty pill bottle in the house but do not know what was inside. They found her unconscious in her room 8 hours ago. There were no other substances/exposures noted.

Physical Exam….after the ABCs
Completely undress the patient Carefully search belongings General observation Odours, powders, track marks Agitation, confusion, obtundation Protect yourself from exposures, needle stick injuries, etc.

Detailed Physical Exam
Neuro GCS, extremity tone, tremors, fasiculations Detailed exam if possible Eyes Pupil size and reactivity Nystagmus, excessive lacrimation Skin Cyanosis, flushing, diaphoresis, dryness Signs of injury/trauma Extremity tone – assess for myoclonus, rigidity, flaccid paralysis Skin - Bruising can signify trauma, coagulopathy, or approximate duration of time unconscious

Physical Exam CVS Lungs GI Rate, rhythm, peripheral pulses
Bronchorrhea, bronchoconstriction GI Bowel sounds Bladder size Rigidity/tenderness

Drugs: Universal Antidotes
“TONG” Thiamine 100 mg IV/IM/PO Oxygen Nasal / face mask Naloxone 0.4 mg IV/IM/ETT Glucose 1 ampule IV D50W *give the strongest dose of glucose available in your ED if suspect hypoglycemia. In certain settings, D40W may be what is available.

Universal Antidotes Thiamine: administer if appear malnourished or known alcohol/drug abuse Glucose: administer if no immediate access to glucometer or confirmed hypoglycemia Order in which glucose & thiamine given no longer felt to be important

Naloxone Competitive opioid antagonist
0.4 mg IV/IM/ETT titrated to effect T ½ = 30 mins Consider for patients with RR < 12 Naloxone has no intrinsic toxicity Anaphylaxis very rare Routes of administration: IV/IM/SC (double dose)/ ETT (same dose) Often completely reverses the hypoventilation and neurologic depression for mins after administration **need protocol in place to ensure patients do not leave the ED once reversed until adequately observed for 2-3 hours

Naloxone Can safely give 6-10 mg over <10 min
Can precipitate acute withdrawal in chronic opiate users Acute opiate withdrawal is not life threatening BUT can cause aspiration Observe patients for 2-3 hrs May require re-dosing or infusion Therefore titrate in small doses to effect rather than indiscriminate large doses Naloxone infusion: 2/3 of initial effective dose over 1 hr

What universal antidotes would you consider giving this patient?
Naloxone for RR < 12 -> no response Glucose because have no glucometer Thiamine not necessarily indicated since lives at home with parents, not malnourished, no known substance abuse issues Oxygen definitely re hypopnea, hypotension

Case 1 An 18 year old woman is brought to the ED by her parents. She has been unresponsive for 8 hrs and has the following vital signs: HR 105 RR 10 BP 90/60 Temp 34.5 How should you proceed?

What labs would you consider drawing for this patient?
Complete blood count, electrolytes, creatinine, liver function tests, serum osmolality, venous blood gas, lactate, urine tox screen, serum acetaminophen level, serum salicylates level, serum ETOH level, septic work up since hypothermic (septic shock is in the DDX), BHCG (pregnancy test).

What next?

Decontamination Principles
Activated charcoal Orogastric lavage Whole bowel irrigation Urine alkalinization Syrup of Ipecac

Activated Charcoal Adsorbs substances from the gut
Establishes concentration gradient that favours movement into the intestinal lumen, enhancing excretion by defecation Can intercept entero-hepatic circulation Binds substances excreted in bile as well Adsorption is the adhesion of atoms, ions, biomolecules or molecules of gas, liquid, or dissolved solids to a surface Can administer with a cathartic (1st dose) to decrease transit time in gut and enhance elimination (osmotic cathartic = sorbitol 70% 1g/kg or Mg citrate 10% solution 250 mL adults or 4mL/kg children) (POOR EVIDENCE FOR THIS)

What makes charcoal “activated”?

Charcoal prepared from vegetable matter
‘‘Activated’’ by heating at high temperature in stream of oxidizing gas (steam, CO2, air) or with activating agent (phosphoric acid, zinc chloride) Creates complex internal pore structure which increases surface area from 2–4 m2/g to >1500 m2/g Vegetable matter = peat, wood, coconut shell, coal

Activated Charcoal Most effective within 1 hr ingestion
1 g/kg OR 10:1 charcoal : dose ingested Administer whichever is larger Given in slurry of water, coke, juice PO/NG

Activated Charcoal Indications: Contraindications:
Ingestion within 1 hr Airway protected Contraindications: Known/suspected GI perforation/obstruction GCS <8 or declining rapidly (risk of aspiration) Known ingestion of substance that charcoal does NOT adsorb

Hydrocarbons = gasoline, parrafin, lighter fluid (naphtha), diesel fuel, methane, butane, propane, terpentine, etc

Multi-dose Activated Charcoal
Repeated use of activated charcoal to enhance elimination ingested toxins Ideal for toxins with long t ½, small volume of distribution, reduced gut motility, bezoar formation Theophylline, phenobarbitol, quinine, carbamazepine Improves clearance rates comparable to hemodialysis Also ideal for toxins that have entero-hepatic and enterohepatic/enterocutaneous circulation or slow release into gut lumen Interrupts entero-enteric circulation (main mechanism) Case reports for specific substances above showing improved outcomes Typical adult regimen = g for first dose then g q 4 h PO Volume of distribution = theoretical volume in which the total amount of drug would need to be uniformly distributed to produce the desired blood concentration of a drug. (increased in kidney/liver failure due to edema/decreased protein binding and decreased in dehydration)

Orogastric Lavage Intubate patient
Place in left lateral decubitus position Head tilted 20 degrees downward Insert 40F orogastric tube (24F peds) Ideal length measured from chin to xiphoid Instill 200 cc body-temp fluids repeatedly until fluid clear Instill 10 mL/kg fluid in kids Ensure that amount returned is equal to amount instilled (approximately) Instill activated charcoal at end if indicated (re substance ingested) before pulling OG tube

Orogastric Lavage Indications Contraindications
Life-threatening ingestions Pills able to fit through orogastric tube holes Ingestion within 1 hr Contraindications Non-life threatening ingestions Pills known to be too big for holes of tube Caustic ingestions No ability to intubate patient Ingestions where lung toxicity>>GI toxicity

Whole Bowel Irrigation
Instillation of large volumes of polyethylene glycol in osmotically balanced electrolyte solutions Promotes rapid, mechanical elimination of ingested toxins

Intubate patient Infuse polyethylene glycol through NG tube at: 2L/hr adults 1 L/hr children > 6 years 0.5 L/hr children < 6 years Infuse until rectal fluid clear

Indications Ingestion of sustained release drugs Ingestion of substances that charcoal cannot adsorb (HAILL) Drugs ingested by body packers/stuffers Contraindications Known or suspected bowel obstruction Inability to intubate patient Ingested toxin known to cause diarrhea

Syrup of Ipecac Induces short-lived vomiting
Peripherally and centrally acting 90% patients vomit within 20 mins Typical vomiting < 5X and < 2 hrs 30 mL PO (adults) 15 mL PO (peds 1-12 years) 97% vomit after second dose – do not give more than 2 doses Plant derived compound; acts on stomach receptors and also centrally at chemotactic trigger zone to induce vomiting

Syrup of Ipecac Indications Contraindications
Very recent ingestion (<1hr) Toxin known not to cause decreased LOC Toxin known not to fit through OG tube Contraindications Ingestion > 1 hr ago Toxin known to cause decreased LOC/seizure Caustics, hydrocarbons, TCAs Contraindicated in anticholinergic OD Indications: toxin known not to cause decreased LOC or hemo instability or seizures (re airway protection) Complications include (rarely): aspiration, Boerhaave’s, MW tears, intractable vomiting

Urinary Alkalinization
Infusion of sodium bicarbonate to raise urinary pH to enhance clearance of toxins excreted by kidneys 1-2 mEq/kg NaHCO3 IV push 3 ampules of NaHCO3 in 850 cc of D5W at 1.5X maintenance fluid rate Monitoring during sodium bicarbonate infusion: electrolytes and venous blood gas q 2 hrs Urinary pH q 30 min Correct hypokalemia as indicated Risks = volume overload/CHF, hypokalemia, pH shifts For TCA overdoses and ASA toxicity when indicated

Urinary Alkalinization
Target urinary pH Monitor electrolytes q2-4hrs (re hypokalemia) For ASA, phenobarbitol, INH, quinolone OD Watch for volume overload, hypokalemia, hyponatremia,

What decontamination strategy would you choose for this patient?
a) Orogastric lavage b) Syrup of Ipecac c) Urinary decontamination d) Activated charcoal e) None of the above

What decontamination strategy would you choose for this patient?
a) Orogastric lavage b) Syrup of Ipecac c) Urinary decontamination d) Activated charcoal e) None of the above MDAC would be a potential option but do not know dose taken - ?benefit. No airway protection. Remember that decontamination strategies are only appropriate in a select few ED patients based on time since ingestion and a balance of risk vs benefit. This lecture is meant to provide an overview of all available options, including syrup of ipecac, which is not routinely used in North America currently, but may still have a (small) role to play in resource limited patients in the right (narrow) clinical setting.

What toxin did your patient take?
Next issue: What toxin did your patient take?

Common Toxidromes Sedative-hypnotic Anticholinergic Cholinergic
Sympathomimetic Opioid

Sedative-Hypnotic Toxidrome
CNS depression Slurred speech Ataxia Coma/stupor Respiratory depression apnea Hypotension Hypothermia Severe overdose is manifested by a cold, apneic, hypotensive patient. Pupils, nystagmus, and pulse rate are variable. Delayed gastric emptying, ileus common Early deaths are from CVS collapse and resp arrest. Lethal dose is 10 X that of hypnotic dose (exact toxic dose unknown) Toxicity enhanced with co-ingestions ETOH, benzos Can follow barbituate serum levels if available – to confirm diagnosis and determine disposition (admit vs discharge) Levels not reliable indicators of clinical course Levels invalid in chronic users Respiratory depression and hypothermia are centrally mediated Hypotension is from decreased vascular tone Mortality ranges from 1-3% Cause of death usually MODS (multi-organ dysfunction) Serum drug levels do not predict clinical outcome and do not reflect blood-brain concentrations MDAC has been shown to decrease serum levels of barbituates but NOT to alter/improve clinical outcomes

Common Sedative-Hypnotics
Benzodiazepines Diazepam, lorazepam, etc Barbituates Phenobarbitol

Case closed…. The patient’s sister shows up to the hospital very worried. The patient had admitted yesterday that she felt suicidal and today the sister could not find her bottle of phenobarbitol tablets that she takes for her seizure disorder. Management priorities??

Sedative-hypnotic OD management
Airway management IV fluids ++ (warm) Warming as needed Pressors as needed Manage airway re protection, oxygenation, ventilation Pressors – likely dopamine

Case 2 34 yo male found at home by wife Combative, agitated, confused
Vitals: HR 108, BP 146/92, T 38.6, RR 20 Pupils round, 5mm bilat Skin dry, flushed Distended bladder palpable below umbilicus

Anticholinergic Toxidrome
Blind as a bat (mydriasis) Mad as a hatter (confused, decr. LOC) Red as a beet (flushed, vasodilation) Dry as a bone (dry skin/membranes) Hot as a hare (hyperthermia) Stuffed as a pipe (urinary/bowel retention) Seizures, rhabdomyolysis, dysrhythmias Tachycardia is early, sensitive sign Can also think of toxidrome as ‘fast as a hare’ to remind learners about importance of tachycardia

Common Anticholinergics
Atropine, scopolamine Antidepressants (TCAs, SSRIs) Antihistamines Antipsychotics Antiparkinsonians Antispasmodics Amanita mushroom species Also anti-emetics, jimson weed SSRIs = fluoxetine, paroxetine, sertraline Atropine and the others are belladonna alkaloids Muscle relaxants are another class of drugs with anticholinergic effects

Anticholinergic Management
IV fluids Cooling (fluids, mist, fans) Sedation Diazepam IV Prevents trauma, hyperthermia, rhabdomyolysis Physostigmine 0.5 – 2 mg slow IV over 5 min **Not for TCA overdoses Due to Na channel blockade with TCA overdose, combination of physostigmine and TCAs can cause life-threatening/fatal bradyarrythmias and asystole, via AV node blockade (synergistic). Physostigmine can also cause seizures, as do TCAs. Relative contraindications of physostigmine: intestinal obstruction, reactive airway disease, epilepsy, conduction abnormalities Relative indication (UpToDate) : peripheral AND central manifestations of antimuscarinic activity Physostigmine is a carbamate acetylcholinesterase inhibitor that binds reversibly to inhibit acetylcholinesterase in both the peripheral and central nervous system (CNS). Once physostigmine blocks acetylcholinesterase, the concentration of acetylcholine at muscarinic receptors increases, and usually overcomes any anticholinergic blockade. If physostigmine given in too high doses or patient did NOT have anticholinergic toxidrome can develop cholinergic toxicity – can give atropine (1/2 dose of physostigmine given) to correct

Physostigmine Reversible acetylcholinesterase inhibitor
Crosses blood-brain barrier Reverses anticholinergic effects Shorter t ½ than most anticholinergic drugs Re shorter t ½ than drugs of overdose: admit and closely observe patients where physostigmine used

Physostigmine Major side effects: Indications Contraindications
Profound bradycardias, dysrhythmias Seizures Indications Severe agitation and delirium not responsive to benzodiazepines Contraindications TCA overdose or Na channel blockade Asthma or known cardiac conduction abnormalities Profound bradycardias can include asystole Severe agitation and delirium not responsive to benzos = central muscarinic effects

TCA Overdose IV fluids NaHCO3 IF:
QRS > 100 msecs R axis deviation terminal 40 msecs QRS Hypotension refractory to IV fluids Ventricular dysrhythmias NaHCO3 1-2 mEq/kg IV push then infusion: Mix 3 amps of NaHCO3 into 850 cc D5W Run at 1.5X maintenance Monitor serum lytes, pH (max 7.55) Expect hypokalemia! Activated charcoal +/- orogastric lavage for decontamination MDAC not warranted Bicarb improves cardiac conduction, contractility, and suppresses ventricular ectopy If cardiac toxicity is going to manifest, it will do so within 6 hours

TCA Overdose A later lecture will cover TCA overdose in more detail – this is intended as an introduction and subset of anticholinergic toxidrome management

Case 3 15 yo girl from rural area brought to ED by family on bus
Found behind barn 6 hours prior Decreased LOC, drooling, tears streaming Covered in vomit and urine, feces HR 101, RR 16, BP 90/60, T 36.5

Cholinergic Toxidrome
Salivation Lacrimation Urination Defecation GI pain Emesis Muscarinic Effects SLUDGE = muscarinic effects Also, miosis and muscle weakness

Cholinergic Toxidrome
Bradycardia Bronchorrhea Bronchospasm Muscle fasiculations, miosis Seizures, resp failure, paralysis “The Killer Bees” Miosis and muscle fasciculations are reliable signs of organophosphate toxicitiy Muscle fasciculations, miosis and killer BBB’s are all muscarinic effects as well

Common Cholinergics Organophosphate insecticides
Diazinon, acephate, malathion, parathion Carbamate insecticides Systemic absorption by inhalation, ingestion, transdermal and transcorneal exposure Chemical insecticides are neuro toxins Must give antidotes before permanent binding of organophosphates to acetylcholinesterase, otherwise must wait for new enzymes to be regenerated within 4-10 WEEKS (this process is called ‘ageing’ – give antidotes before aging occurs to reverse effects quickly) **miosis and muscle fasciculations are reliable signs of organophosphate toxicity

Organophosphate Poisoning
Bind irreversibly to acetylcholinesterase Allows accumulation of Ach at NMJ Cholinergic crisis causes central and peripheral toxidrome Must give antidotes before permanent binding of organophosphates to acetylcholinesterase (“ageing”)

Cholinergic Management
Decontamination and staff protection! 1:9 bleach : water Airway management Atropine sulphate 2 mg IV/IM Every 5-20 mins until tracheobronchial secretions dry up Treats muscarinic symptoms Pralidoxime 2 g IV/IM infused over 5 min Treats nicotinic symptoms Continue for 48 hrs if used Wear neoprine, not latex gloves All healthcare workers need to wear protective clothing Put patient’s clothes in plastic bags and dispose of as hazardous waste Wash patient with dish soap and water or bleach and water Can decontaminate instruments used to treat the patient with bleach afterwards Airway – gentle suctioning of airway secretions and as much O2 as can give Do not intubate with succinylcholine if need to intubate as it is also metabolized by plasma acetylcholinesterase and will result in prolonged paralysis Choose a non-depolarizing agent like rocruonium/vec Gastric lavage and activated charcoal are often used (in Asia, etc) but evidence lacks re outcome PUPIL DILATION IS NOT A THERAPEUTIC ENDPOINT! mg/kg (never <0.1mg) atropine for peds Can give 6mg IM if no IV access available Absence of anticholinergic symptoms after a dose of atropine this large is indicative of organophosphate OD Atropine does NOT reverse muscle weakness Atropine is a competitive antagonist of acetylcholine at central and peripheral muscarinic receptors Used to reverse muscarinic effects Pralidoxime restores acetylcholinesterase activity by regenerating phosphorylated acetylcholinesterase and also displaces OGP molecules from the Ach receptors Treats the muscarinic, nicotinic, and central symptoms More effective in acute poisonings but even > 48 hrs after poisoning is recommended to use Can reverse muscle weakness if given before aging occurs Dose in children: 40-60mg/kg IV (max 1 g) Run infusion of 500 mg/hr if paralysis not reversed or recurs (preferable to repeat bolus dosing) Evidence to show effectiveness lacking in acute OGP OD but still used worldwide. Not necessary to use pralidoxime for carbamate poisonings Hemodialysis is not of proven value Can substitute diphenhydramine if atropine not available

Fatal Pesticide Poisonings
258,000 deaths from pesticide self-poisonings worldwide each year Accounts for 30% suicides worldwide Suicides in developing countries >> developed countries likely explained by very high case fatality rates in developing countries

Case 4 26 yo male found on street by police No family present
Eyes bloodshot, agitated, sweaty Uncooperative HR 126, BP 178/104, RR 20, T 38.5

Sympathomimetic Toxidrome
Mydriasis Diaphoresis Tachycardia Hypertension Hyperthermia Seizures, rhabdomyolysis, MI, SAH If lethargic or comatose suggests patient is post-ictal or intracranial hemorrhage

Common Sympathomimetics
Cocaine Amphetamines Khat (cathinone and cathine)

Sympathomimetic Management
IV fluids Cooling (fans, mist, fluids) Sedation: benzodiazepines Seizures: benzodiazepines, phenobarbitol HTN: benzodiazepines, nitroprusside Chest pain: ASA, nitroglycerin Avoid beta-blockers! Monitor for rhabdomyolysis HTN Emergencies: phentolamine (alpha blocker), nitroprusside (alpha blocker), benzos ++++ Cocaine promotes coronary vasospasm and also chronic use leads to atherosclerosis, direct myocardial toxicity and platelet aggregation MI common in concurrent smokers and chronic cocaine use Benzo of choice: Diazepam 5 mg IV titrated to effect (repeated doses) or Lorazepam 2 mg IV After benzos for seizures, phenobarbitol load is often necessary CT scan of head advised if seizures occur because intracranial hemorrhage is common Manage chest pain with ASA, benzodiazepines, and nitroglycerin AVOID BB’s because unopposed alpha receptor stimulation can worsen coronary and peripheral vasoconstriction, hypertension, and possibly ischemia as well. If wide complex tachycardias, alkalinize the urine with bicarb push/infusion. (first line). If not responsive, consider lidocaine. AVOID HALOPERIDOL or CHLORPROMAZINE as they can decrease seizure threshold and increase chance of dysrhythmias (long QT) For severe HTN not responsive to benzos/sedation: Nitroprusside infusion is 0.3 mcg/kg/min IV Phentolamine mg IV push

Case 5 42 yo female Found at home by daughter unresponsive in bed
HR 90, RR 6, GCS 6, T 36.3, BP 92/60 Pupils pinpoint

Opioid Toxidrome Respiratory depression CNS depression/coma Miosis
Not all agents cause miosis – RR<12 is most sensitive indicator of opioid toxicity

Opioid Management Naloxone IV/IM/SC/ETT/IN Airway management

Take Home Points

Approach to Tox Patient at Bedside
ABC Oxygen, monitors, IV access Full set of vitals including O2 sat Gather history and collateral information Check glucose (if possible) Disability : GCS, pupils Detailed physical exam Drugs: Consider universal antidotes Decontamination Draw Labs Specific antidotes and supportive care “ABCDDDDD”

4 Universal Antidotes Thiamine Oxygen Naloxone Glucose “TONG”

5 Decontamination Options
Activated charcoal Syrup of Ipecac Orogastric Lavage Whole Bowel Irrigation Urinary alkalinization

5 Decontamination Options
Activated charcoal Syrup of Ipecac Orogastric Lavage Whole Bowel Irrigation Urinary alkalinization These 3 methods of decontamination are only appropriate for acute ingestions within ~1 hr

5 substances charcoal cannot adsorb
Hydrocarbons Alcohols Iron Lithium Lead “HAILL”

5 Toxidromes Sedative-Hypnotic Anticholinergic Cholinergic
Sympathomimetic Opioid

Quiz Question 1 Which of the following is NOT considered a universal antidote? A) Dextrose B) Atropine C) Naloxone D) Thiamine E) Oxygen Answer = B. Atropine is indicated for the acute management of organophosphate poisonings but is not considered a UNIVERSAL antidote for the general management of the intoxicated patient.

Quiz Question 2 Why is it crucial to observe opiate-intoxicated patients who have been given naloxone for 2-3 hours in the ED? A) Naloxone can induce tachycardia B) Naloxone has a high incidence of anaphylaxis C) Naloxone can cause depressed level of consciousness D) The half-life of naloxone is shorter than that of the opiates it is reversing E) Naloxone can precipitate urinary retention Answer = D. The half-life of naloxone is 30 minutes. Patients who improve after naloxone administration are likely to resume a state of depressed level of consciousness, hypotension and respiratory depression when the naloxone wears off. The consequences of this happening in an unsupervised environment are dire and potentially fatal. Many patients require a naloxone infusion or repeated bolus doses until the specific opioid they ingested wears off.

Quiz Question 3 A 50 kg female ingested 30 tablets of 500 mg of acetaminophen 45 minutes ago. What is the appropriate dose of activated charcoal that should be given? A) 50 g B) 100g C) 150g D) Charcoal is contraindicated E) Charcoal will not be effective Answer = C. Charcoal is indicated in this patient, who is within 1 hr of ingestion of an agent that is likely to be toxic and is known to adsorb to activated charcoal. The correct dose is 1g/kg OR 10:1 ratio of charcoal : ingested substance - choose whichever is larger. The patient took 15,000mg of acetaminophen, which is 15g. 1g/kg would be 50g if weight-dosing is used. 10:1 ratio dosing would be 150g (dose taken = 15g, multiplied by 10) Since 150g is the larger dose of the two options, this is the dose that should be given.

Quiz Question 4 Which drug overdoses are not likely to be improved by the use of urinary alkalinization as a decontamination strategy? A) Salicylates B) Phenobarbitol C) Isoniazid (INH) D) Quinolone E) Carbamates Answer = E. Carbamate insecticide overdose is best treated with atropine. Sodium bicarbonate treatment has not been shown to be effective.

Quiz Question 5 Which of the following symptoms are muscarinic manifestations of organophosphate overdose? A) Lacrimation B) Vomiting C) Miosis D) Muscle fasciculations E) All of the above Answer = E.

General References Gunnell D, Eddleston M, Phillips MR, Konradsen F. The global distribution of fatal pesticide self-poisoning: Systematic review. BMC Public Health 2007; 7:357. Tintinalli’s Emergency Medicine. 7th Ed. Tintinalli JE et al McGraw-Hill Companies, Inc. American Academy of Clinical Toxicology Position Statement and Practice Guidelines on the Use of Multi-Dose Activated Charcoal in the Treatment of Acute Poisoning. Clinical Toxicology.1999;37(6): 731–751.

Intro to Emergency Toxicology

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