Poisoning: MCCQE1 Emergency Medicine Review

Introduction

Poisoning and overdose are frequent presentations in Canadian Emergency Departments. For the MCCQE1, candidates must demonstrate the ability to rapidly assess, stabilize, and manage a poisoned patient. This requires a solid understanding of toxidromes, specific antidotes, and the unique aspects of the Canadian healthcare system, such as collaboration with Poison Control Centres.

This guide is structured to align with the CanMEDS roles, particularly Medical Expert (clinical management) and Collaborator (consulting toxicology resources).

General Approach to the Poisoned Patient

The initial management of any poisoned patient follows the standard resuscitation algorithms. Do not focus on the specific toxin until the patient is stabilized.

Step 1: Resuscitation (ABCDE)

Airway: Assess patency. Early intubation may be required for patients with a GCS <8 or those unable to protect their airway due to secretions (e.g., organophosphates).
Breathing: Assess respiratory rate and oxygen saturation. Administer supplemental oxygen. Be wary of aspiration pneumonia.
Circulation: Establish IV access. Treat hypotension with crystalloids. If refractory, consider vasopressors.
- Note: In suspected Calcium Channel Blocker or Beta-Blocker overdose, high-dose insulin euglycemia therapy is a specific consideration after initial stabilization.
Disability: Check GCS and pupillary response. Check capillary glucose (Dextrose) immediately.
Exposure: Fully undress the patient to check for transdermal patches (e.g., Fentanyl, Nitroglycerin) or signs of trauma. Measure core temperature.

Step 2: The “Coma Cocktail” (Diagnostic/Therapeutic Trial)

In a patient with altered mental status (AMS) of unclear etiology, consider the following reversible causes:

Dextrose: For hypoglycemia.
Oxygen: For hypoxia.
Naloxone: For suspected opioid toxicity (respiratory depression, pinpoint pupils).
Thiamine: Precede glucose in patients with suspected alcohol use disorder to prevent Wernicke’s encephalopathy.

Step 3: Secondary Survey and Toxidrome Recognition

Perform a focused history (SAMPLE) and physical exam looking for specific toxic syndromes.

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MCCQE1 Tip: Always consider Acetaminophen (APAP) and Salicylate (ASA) co-ingestion in any intentional overdose. These are ubiquitous in Canada, and early levels are mandatory.

Toxidromes (Toxic Syndromes)

Recognizing toxidromes is high-yield for the MCCQE1. It allows for empiric management before confirmatory testing.

Toxidrome	Vital Signs	Pupils	Skin/Mucosa	Other Signs	Common Agents
Anticholinergic	HR ↑, BP ↑, Temp ↑	Dilated (Mydriasis)	Dry, Flushed, Hot	Urinary retention, delirium, decreased bowel sounds	Atropine, Antihistamines, TCAs, Antipsychotics
Cholinergic	HR ↓, BP ↓/↑	Constricted (Miosis)	Diaphoretic (Wet)	DUMBELS: Diarrhea, Urination, Miosis, Bronchorrhea, Emesis, Lacrimation, Salivation	Organophosphates, Carbamates, Nerve agents
Sympathomimetic	HR ↑, BP ↑, Temp ↑	Dilated	Diaphoretic	Agitation, seizures, tremors	Cocaine, Amphetamines, MDMA
Opioid	HR ↓, BP ↓, RR ↓↓	Constricted (Pinpoint)	Cool	Hyporeflexia, CNS depression, pulmonary edema	Heroin, Fentanyl, Oxycodone, Morphine
Sedative-Hypnotic	HR ↓, BP ↓, RR ↓	Normal/Variable	Normal	Ataxia, slurred speech, stupor (resembles ETOH)	Benzodiazepines, Barbiturates, Alcohol
Serotonin Syndrome	HR ↑, BP ↑, Temp ↑↑	Dilated	Diaphoretic	Hyperreflexia, clonus (lower > upper), rigidity	SSRIs, MAOIs, Lithium, Linezolid

Canadian Context: Mnemonics

Anticholinergic: “Mad as a hatter (confusion), Blind as a bat (mydriasis), Red as a beet (flushed), Hot as a hare (hyperthermia), Dry as a bone (anhidrosis).”

Diagnostic Investigations

The “Rainbow Draw”

In an undifferentiated overdose, order:

Serum Acetaminophen and Salicylate levels (Mandatory).
Electrocardiogram (ECG): Look for QRS widening (TCAs), QT prolongation (Antipsychotics), or ischemia.
Beta-hCG: In all females of childbearing age.
Blood Gas (VBG/ABG): Assess acid-base status.
Basic Metabolic Panel: Electrolytes, BUN, Creatinine, Glucose.
Serum Osmolality & Ethanol: If toxic alcohols are suspected.

Gap Calculations (Essential for MCCQE1)

Anion Gap

High Anion Gap Metabolic Acidosis (HAGMA)

Formula:

Anion Gap = [Na^+] - ([Cl^-] + [HCO_3^-])

Normal: 8–12 mmol/L (Canadian Reference Range)

Mnemonic: MUDPILES

Methanol
Uremia
Diabetic Ketoacidosis
Paraldehyde / Propylene Glycol
Iron / Isoniazid
Lactic Acidosis
Ethylene Glycol / Ethanol (ketoacidosis)
Salicylates

Decontamination and Elimination

Interventions to limit absorption or increase excretion.

1. Decontamination

Activated Charcoal (AC):
- Dose: 1 g/kg (max 50-100g).
- Indication: Presentation within 1-2 hours of ingestion of an agent that adsorbs to charcoal.
- Contraindications: Unprotected airway (risk of aspiration), bowel obstruction, ingestion of agents NOT bound by AC.
- Agents NOT bound by AC (Mnemonic: PHAILS):
  - Pesticides / Potassium
  - Hydrocarbons
  - Acids/Alkalis (Caustics)
  - Iron / Heavy Metals
  - Lithium
  - Solvents / Alcohols
Whole Bowel Irrigation (PEG solution):
- Consider for “body packers” or sustained-release preparations (e.g., Verapamil SR, Lithium).

2. Enhanced Elimination

Urinary Alkalinization:
- Sodium bicarbonate IV to target urine pH 7.5–8.0.
- Used for Salicylates, Phenobarbital, Methotrexate.
Hemodialysis:
- Used for severe toxicity with dialyzable toxins.
- Mnemonic: I STUMBLE
  - Isopropyl alcohol (rarely needed)
  - Salicylates
  - Theophylline
  - Uremia
  - Methanol
  - Barbiturates
  - Lithium
  - Ethylene Glycol

Specific High-Yield Poisons for MCCQE1

Acetaminophen (Paracetamol)

Mechanism: Depletion of glutathione leads to accumulation of toxic metabolite NAPQI, causing centrilobular hepatic necrosis.
Clinical Stages:
1. (<24h): Nausea, vomiting, malaise.
2. (24-72h): RUQ pain, rising LFTs/INR.
3. (72-96h): Peak hepatotoxicity, fulminant failure, encephalopathy.
4. (4d-2w): Recovery or death.
Management:
- Plot 4-hour level on Rumack-Matthew Nomogram.
- Antidote: N-acetylcysteine (NAC).
- Canadian Practice: Both IV (21-hour protocol) and Oral (72-hour protocol) are used, but IV is preferred for vomiting or fulminant failure.

Salicylates (Aspirin)

Pathophysiology: Uncoupling of oxidative phosphorylation.
Presentation: Tinnitus, vertigo, vomiting, hyperthermia.
Blood Gas: Respiratory Alkalosis (central stimulation) followed by High Anion Gap Metabolic Acidosis.
Management:
- Activated Charcoal (multi-dose may be useful).
- Urinary Alkalinization: Keep K+ > 4.0 mmol/L to ensure successful alkalinization.
- Hemodialysis: If CNS changes, pulmonary edema, renal failure, or very high levels (>7.2 mmol/L or >100 mg/dL).

Toxic Alcohols (Methanol & Ethylene Glycol)

Methanol: Found in windshield washer fluid. Metabolized to Formic Acid. Causes blindness (“snowstorm vision”).
Ethylene Glycol: Found in antifreeze. Metabolized to Oxalic Acid. Causes renal failure (calcium oxalate crystals in urine).
Management:
- Antidote: Fomepizole (Alcohol dehydrogenase inhibitor). Ethanol is a second-line alternative.
- Hemodialysis: For severe acidosis, renal failure, or visual changes.
- Cofactors: Folate (Methanol); Thiamine/Pyridoxine (Ethylene Glycol).

Carbon Monoxide (CO)

Source: Fires, faulty heaters, indoor combustion.
Presentation: Headache (“flu-like” in winter), nausea, confusion, cherry-red skin (rare/late).
Diagnosis: Co-oximetry (standard SpO2 is normal).
Management:
- 100% Oxygen via non-rebreather mask.
- Hyperbaric Oxygen indications: Pregnancy (fetal Hgb binds CO avidly), CO level >25%, syncope, ischemia, neurological deficits.

Canadian Guidelines & Resources

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Key Canadian Resource: In any complex poisoning case, the Medical Expert collaborates by consulting the regional Poison Control Centre.

Access: Most provinces can be reached at 1-844-POISON-X.
Units: Always use SI Units (mmol/L) for the MCCQE1. Be comfortable converting if necessary, but expect SI units in the stem.
Naloxone Kits: Widely available in Canadian pharmacies and community centers without a prescription as part of harm reduction strategies.

Key Points to Remember for MCCQE1

Don’t forget Glucose: Altered mental status = Check capillary glucose.
Don’t forget Pregnancy: All females of reproductive age with overdose need a beta-hCG.
ECG is vital: Look for QRS > 100ms in TCA overdose (Treat with Sodium Bicarbonate).
Digoxin Toxicity: Visual changes (yellow halos), scooped ST segments. Treat with Digoxin Immune Fab (DigiFab).
Beta-Blocker/Ca-Channel Blocker: Bradycardia + Hypotension. Treat with High-Dose Insulin Euglycemia, Glucagon, Calcium, Lipids.
Cyanide: House fire victim with lactate > 10 mmol/L. Treat with Hydroxocobalamin.

Sample Question

Stem

A 24-year-old female presents to the Emergency Department with complaints of ringing in her ears, nausea, and vomiting. She admits to intentionally ingesting a “bottle of painkillers” approximately 6 hours ago because of a breakup.

Vitals:

Temp: 38.1°C
HR: 110 bpm
BP: 118/70 mmHg
RR: 26 bpm
O2 Sat: 98% on room air

Physical Exam: She appears anxious and slightly diaphoretic. Chest is clear. Abdomen is soft but tender in the epigastrium. Neurological exam is non-focal, GCS 15.

Investigations:

Na+: 140 mmol/L
K+: 3.2 mmol/L
Cl-: 100 mmol/L
HCO3-: 14 mmol/L
Creatinine: 90 µmol/L
ABG: pH 7.46, pCO2 20 mmHg, pO2 95 mmHg

Which one of the following is the most appropriate initial pharmacological intervention to enhance the elimination of the toxin?

Options

Click to reveal the answer and explanation

Explanation

The correct answer is:

B. Intravenous Sodium Bicarbonate

Reasoning: The clinical presentation is classic for Salicylate (Aspirin) toxicity.

Symptoms: Tinnitus (ringing in ears), nausea, vomiting, hyperthermia (uncoupling of oxidative phosphorylation), and tachypnea.
Lab Findings: The ABG shows a primary Respiratory Alkalosis (pCO2 20 mmHg) driven by direct stimulation of the respiratory center, co-existing with a Metabolic Acidosis (Anion Gap = 140 - (100 + 14) = 26). The pH is alkalemic (7.46) because the respiratory drive often predominates early.
Management: Urinary alkalinization with IV Sodium Bicarbonate is the mainstay of treatment to enhance elimination. Salicylates are weak acids; alkalinizing the urine traps the salicylate ion in the renal tubules (ion trapping), preventing reabsorption and increasing excretion. Note: Hypokalemia (K+ 3.2) must be corrected to successfully alkalinize the urine.

Why other options are incorrect:

A. Fomepizole: Antidote for toxic alcohols (Methanol, Ethylene Glycol), not salicylates.
C. Oral Activated Charcoal: While useful for decontamination if given early, the question asks for intervention to enhance elimination. Furthermore, at 6 hours post-ingestion, the utility is debated, though salicylates can delay gastric emptying. However, urinary alkalinization is the specific elimination technique.
D. N-acetylcysteine: Antidote for Acetaminophen toxicity. While she took “painkillers” and APAP level should be checked, the clinical picture fits salicylates specifically.
E. Hemodialysis: Indicated for severe salicylate toxicity (e.g., altered mental status, pulmonary edema, renal failure, or very high serum levels). This patient is GCS 15 with no organ failure yet; medical management is the first step.

References

Rosen’s Emergency Medicine: Concepts and Clinical Practice. 9th ed. Philadelphia, PA: Elsevier; 2018.
Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 9th ed. New York, NY: McGraw-Hill Education; 2020.
Poison and Drug Information Service (PADIS). Alberta Health Services. Link to resource
Medical Council of Canada. MCCQE Part I Objectives: Poisoning. mcc.ca
Juurlink DN. The management of salicylate poisoning. CMAJ. 2016;188(16):1177. doi:10.1503/cmaj.151460.