Toxicology Flashcards
Why should SpO2 levels be regarded with suspicion following exposure to burning materials?
CO exposure causes falsely high SpO2 readings
What are generally considered to be harmful doses of acetaminophen?
- 250mg/kg single dose
- 12g in 24h
What is the SLUDGEM/BBB mnemonic, and what does it describe?
- Salivation
- Lacrimation
- Urination
- Defecation
- GI upset
- Emesis
- Miosis
- Bronchorrhea
- Bronchospasm
-
Bradycardia
- The three “Bs” – bronchorrhea, bronchospasm, and bradycardia – are the most common causes of death in organophosphate and carbamate poisoning.
What is the primary indication of TCAs, and what is a common example?
- treatment refractory depression
- Amitryptiline (Elavil)
Describe the toxidrome of TCA overdose
- Sedation
- may also feature confusion, delirium, and hallucinations.
- Anticholinergic effects
- hyperthermia, flushing, and dilated pupils are common.
- Hypotension
- most ominous finding; the majority of patients who die from TCA overdose do so as a result of refractory, uncorrectable hypotension.
What are important pieces of information to gather about a chemical at scene if organophosphate/carbamate poisoning is suspected?
- name and amount of the substance the patient was exposed to
- the pesticide control number
- WHMIS information
- photo of the label
What is the role of high-flow O2 therapy in CO poisoning
- Displaces CO from Hemoglobin
- Reduces half-life of COHb in body (from 4-5 hrs. to 1-2 hrs.)
- Ensures adequate oxygen of non-poisoned hemoglobin and plasma
Describe pre-hospital management of TCA overdose
- Supportive/ABC care
- Prompt 12-lead ECG
-
Sodium bicarbonate
- 1 mEq/kg IV/IO slow push
- May repeat 0.5 mEq/kg IV/IO slow push every 10-15 minutes as required
- Tricyclic overdoses may require doses as high as 2-3 mEq/kg IV/IO
- assess for QRS narrowing following administration
- Consider push-dose EPINEPHrine for hypotension refractory to fluid bolus
- Magnesium sulfate may be an acceptable antiarrhythmic in the context of cardiac arrest
Briefly describe CO toxicity
- CO competitively binds to hemoglobin 200-250 times more strongly than oxygen
- Causes a left shift in the oxyhemoglobin dissociation curve and widespread tissue hypoxia
Which beta blockers are associated with significant pro-arrhythmic tendencies?
Sotalol and Propranolol
Describe in-hospital management of CO poisoning (single intervention which is not available in pre-hospital setting)
Hyperbaric oxygen therapy
Which beta-blocker is more likely to require treatment with magnesium sulfate?
sotalol!
causes QTc prolongation, increased risk of TdP
The primary goal of most prehospital management of toxic exposures is:
Supportive care and transport
What is a common ECG finding in organophosphate/Carbamate poisoning that is NOT related to bradycardia, and what is the treatment if it is symptomatic?
- QTc prolongation
- May lead to PMVT or TdP
- Tx is Magnesium Sulfate
- 2g IV over 20 minutes
Describe physical properties of Carbon Monoxide
colourless, odourless, tasteless, non-irritating gas produced by the incomplete combustion of carbon-containing material such as gasoline, heating fuels, propane, oil, wood, and coal
Describe full management of organophosphate/carbamate poisoning
- Call Clinicall!
- Thorough decontamination and BSI
- Supportive/ABC care
- Manage seizure/arrhythmia
- Consider Magnesium Sulphate for VT due to QTp
-
ATROPINE
- 1-2mg IM/IV
- Double the dose q.5 minutes until effect is seen
- Goal is to reverse bradycardia/hypotension (fast) and reduce secretions (slow)
BLS-level interventions for CO poisoning include:
- Removal from source
- Decontamination as required
- Keep warm and place in position of comfort
- 100% FiO2 (NRB + HFNC or BVM)
- Airway/ventilation support
- Transport
Describe the toxidrome of organophosphate/carbamate poisoning
- Symptoms can be divided into muscarinic and nicotinic effects
- Muscarinic
- miosis, excessive sweating and bronchial secretions, bradycardia, hypotension
- Nicotinic
- mydriasis, tachycardia, fasciculations, muscle weakness, paralysis
- May use the SLUDGEM/BBB mnemonic
Describe management of opioid overdose pre-hospitally
- Emphasize airway, ventilation, and oxygenation support
- Consider alternative DDx
- Naloxone IM/IV
- 0.4mg-0.4mg-0.8mg-2.0mg
- 4.0mg then 10.0mg (Clinicall consult required) for ACP
- Target return of spontaneous respirations, not increased LOC
Describe ACP-Level management of cyanide poisoning, not including BLS measures
- Fluid + Pressors as needed
- Manage seizures
- Midazolam, 2-5mg IV/IO or 5-10mg IM
Describe how management of CCB overdose is different from standard bradycardia care
- BGl testing is routine to aid in diagnosis
- CaCl2 administration occurs early (prior to epi administration)
- 1-2g IV over 10 minutes
- Atropine less likely to be successful
- TC pacing not included in CPGs (likely still appropriate)
What popoulation will have chronically elevated carboxyhemoglobin levels?
smokers
Describe the pathophysiology and toxidrome of cyanide poisoning
- Cyanide inhibits the activity of cytochrome oxidase A3 in the mitochondria, preventing aerobic respiration
- Poisons the electron transport chain
- For toxidrome: First fast, then slow! (i.e. elevated vitals, followed by depressed)
- Tachycardia, mild transient hypertension progressing to hypotension, bradycardia, and cardiovascular collapse
- Tachypnea is common initially with progression to respiratory depression and respiratory arrest; pulmonary edema may develop
- Headaches, anxiety, dizziness, agitation and confusion are common in early stages; patients may become obtunded or seize
- Nausea and vomiting may develop; ingestion of caustic, alkaline cyanide salts may cause gastrointestinal bleeding
What is the goal of naloxone administration in opioid overdose?
the restoration of adequate respirations – a return of full consciousness is not necessary
Describe physical properties of hydrogen cyanide
- colourless gas with a faint, bitter, almond-like odor
Prior to treating anyone with suspected cyanide poisoning, what must be done first?
DECONTAMINATION!!!!
Decontaminate or die, you ding-dong
Describe pathophysiology of Beta-Blocker overdose
- Bradycardia
- Hypotension
- Myocardial depression and cardiogenic shock can develop in severe cases
- Mental status changes, such as confusion, delirium, seizures, and unconsciousness, can occur at virtually any point.
- Respiratory depression has been reported. Bronchospasm and hypoglycemia, produced by the beta blockade, can complicate management.
- Ventricular dysrhythmias are more common with propranolol and sotalol
Describe ACP-level management of Beta-Blocker Overdose
- Always obtain a 12-lead ECG
- Manage bradycardia
- Atropine (may have limited success)
- Transutaneous Pacing (may have limited success)
- Epinephrine infusion (clinicall consultation, high doses likely required!)
- Manage seizures
- Midazolam
-
Glucagon
- 5mg IV push (that’s a lot!)
- Arrhythmia management
- CaCl2
- NaHCO3
- MgSO4 - especially with sotalol ingestion
Describe the mechanism of action of naloxone in reversal of opioid OD
- Competitive opioid receptor antagonist
Is decontamination required for patients with CO exposure?
No. Not in isolation. But may still be warranted if Cyanide exposure co-exists
Define a “dry decontamination”
removal of clothing prior to placing in ambulance
What are risk factors for unintentional acetaminophen overdose?
- more common among individuals who have low levels of health literacy and who do not recognize its prevalence in multiple products.
- Individuals with pre-existing liver disease are at increased risk of acetaminophen toxicity and can experience significant liver dysfunction, even with doses of acetaminophen that are generally considered safe
Describe normal and abnormal COHb levels in adults
- 0-3% normal or sub-normal (no treatment required)
- 3-10%
- Potentially pathological
- If symptomatic, treat and transport
- If asymptomatic, non-conveyance appropriate if patient is otehrwise healthy, non-pregant, is a responsible adult, and has no risk factors
- >10%
- Always requires tratment and transport
Describe the pathophysiology of organophosphate and carbamate poisoning
- Acetylcholinesterase inhibitors
- Cause accumulation of ACh at nicotinic and muscarinic receptor synapses
- Combination of parasympathetic signs AND muscle paralysis
- Death is usually due to diaphragmatic paralysis and respiratory failure
A patient was found with CO poisoning from automobile exhaust in an apparent suicide attempt. Will they likely require decontamination?
No!
CO exposure in isolation does not require decontamination.
Describe common changes in BGl with BB and CCB overdose
- BB overdose associated with hypoglycemia
- should be treated in field
- CCB overdose associated with hyperglycemia
- aids in DDx, but does not require in-field management
What are the dihydropyridines and non-dihydropyridines, and how are they different?
- Calcium channel blockers
- dihydropyridines (vasodilation)
- amlodipine, nifedipine, felodipine
- block L-type calcium channels in the vasculature
- non-dihydropyridines (negative inotropy)
- verapamil, diltizaem
- act on calcium channels in the myocardium
- more likely to directly cause decreased cardiac output
Why is cyanide poisoning suspected in patients exposed to structure or vehicle fires?
Fires involving modern building materials, plastics, and furnishings can produce large amounts of cyanide
Desribe the mechanism of acute pulmonary edema in CCB overdose and identify the class of CCB more closely associated with this presentation
- non-dihydropyridines (Diltizaem and Verapamil) cause negative inotropy
- leads to acute heart failure, resulting in pulmonary congestion
Describe pre-hospital and definitive management for acetaminophen overdose
- Pre-hospital
- prompt recognition and documentation
- Supportive care
- Rapid transport or meet with CCP
- Definitive
- NAC (N-acetyl-cysteine)
- Generally most effective within 8 hours
- Pre-notify hospital, consult with clinicall
A patient was found with CO poisoning from a house fire. Will they likely require decontamination?
Yes!
If the source of contamination is a fire, CN exposure should be suspected
What are common ECG findings in TCA overdose?
- Wide QRS
- >100 ms
- Deep S waves in leads I, aVL
- Likely associated right axis deviation
- Tall R waves in lead aVR
- Dominant R wave often demonstrates Brugada-esque morphology
- Tachycardias, including sinus tachycardia
Describe BLS management of Beta-Blocker overdose
- Supportive (ABC) care
- Correct hypoglycemia
- Transport
Describe ways in which management of Beta-blocker poisoning is different from normal management of bradycardia
- atropine and TC pacing are less likely to be effective
- but should still be attempted!
- Epinephrine infusion may require unusually high dosing to be effective
- consult clinicall!
- High-dose IV glucagon may be indicated
- 5mg IV push!
- Hypoglycemia may also be present
Describe the Mechanism of Action of sodium bicarbonate in management of TCA overdose
- Serum alkalinization
- Favors neutral, non-ionized form of the drug, preventing sodium-channel binding
- Promotes renal clearance/diuresis
- Increased extracellular sodium
- Increases the electrochemical gradient across cardiac cell membranes, potentially attenuating the TCA-induced blockade of rapid sodium channels
Describe the toxidrome for actetaminophen overdose
- Early
- no specific signs or symptoms
- Late
- nausea and vomiting
- malaise
- lethargy
- pallor and diaphoresis
- right upper quadrant abdominal pain
What are the three primary mechanisms by which TCAs exert cardiotoxic effects in OD?
- Sodium channel blockade (QRS prolongation, tall R wave in aVR)
- inhibition of potassium channels (QTc prolongation)
- direct myocardial depression
Describe the mechanism of action of Glucagon in Beta-Blocker OD management
- Glucagon increases heart rate and myocardial contractility, and improves atrioventricular conduction.
- These effects are unchanged by the presence of beta-receptor blocking drugs.
- This suggests that glucagon’s mechanism of action may bypass the beta-adrenergic receptor site.
i.e. glucagon acts on an independent receptor to stimulat chronotropic, inotropic, and dromotropic effects.
Factors which determine the severity of CO exposure are:
- Concentration of atmospheric CO
- Duration of exposure
- Individual physiology
- Toxic levels vary widely between individuals
Describe Prehospital managment of CCB overdose
- Supportive care (ABCs)
- Obtain BGl
- may assist in DDx, hyperglycemia is often seen in CCB OD
- Atropine
- may not be successful
-
CaCl2
- 1-2g IV slow IVP over 10 MINUTES
- Epinephrine
- IV push dose or infusion
- only if bradycardia is refractory to CaCl2
Describe the toxidrome and supportive findings of carbon monoxide poisoning
- Follows exposure to combustion
- headache, weakness, dizziness, and nausea along with tachycardia and tachypnea
- “Cherry Red” skin
- Paradoxically high SpO2 readings
- High COHb readings
- 3-10% may be normal for Pt or pathological. Always transport if high risk or symptomatic
- >10% is always pathological
Describe BLS Tx of cyanide poisoning
- Decontaminate thoroughly
- Remove clothing
- Flush exposed skin and mucosal membranes with soap and water
- If eyes are involved, flush with a gentle stream of water for at least 15 minutes
- Supportive care (ABCs)
- Mandatory Clinicall consultation
- Arrange prompt access to Hydroxocobalamin
Describe ACP-level interventions for CO exposure (Not including BLS interventions)
- Prophylactic glucose administration
- Alkalosis avoidance (do not hyperventilate!)
- Obtain COHb (rainbow probe)
- IV Fluids and vasopressors to manage hypotension
- Manage sizures with benzodiazepenes
Describe common ECG changes in Beta-Blocker overdose
- PR prlongation
- QRS prolongation
- any bradydysrhythmia
Briefly list drugs which have unique applications in the following toxicological emergencies:
- Cyanide
- Calcium Channel Blockers
- Beta Blockers
- Acetaminophen
- TriCyclic Antidepressants
- Organophosphates/carbamates
- Cyanide
- Hydroxocobalamin
- Calcium Channel Blockers
- CaCl2 (1-2g IV over 10 minutes)
- Given PRIOR to IV epinephrine
- Beta Blockers
- Glucagon (5mg IV push)
- Acetaminophen
- N-acetyl cysteine
- TriCyclic Antidepressants
- Sodium Bicarbonate
- 1mEq/kg IV slow push (consult clinicall, may require up to 2-3 mEq/kg), repeat 1/2 dose q. 10-15 minutes
- Organophosphates/carbamates
- Atropine (1-2mg, double dose every 5 minutes to effect)
Describe pathophysiology of beta-blocker overdose
- The primary mechanism for beta blocker toxicity is through the adrenergic blocking action of these medications.
What is the importance of an organosphosphate being labelled “contact” or “systemic” to human physiology?
None!
refers to MOA in pests and plants
What are priorities of care in CO poisoning?
- Removal from source
- High flow O2 administration
- Transport
Why is glucose administration indicated in CO exposure?
- intracellular glucose may be decreased even in presence of normal or elevated blood glucose
- Inadequate intracellular oxygen supply leads to globally inefficient anerobic respiration and rapid depletion of intracellular glucose stores
Which toxidrome is suggested by the following ECG?
TCA overdose, as evidenced by
- Wide QRS
- tall R wave in aVR
- deep S waves in I and aVL
- Tachycardia
