What is the most likely etiology of syncope and collapse after caustic agent ingestion?

Medical Toxicology Examination Questions - Answers

Question 1: Acute Salicylate Toxicity Treatment

Activated charcoal should be administered as first-line therapy for acute salicylate ingestion when the patient presents within 1-2 hours of ingestion. The correct answer is that sodium bicarbonate should be titrated to serum pH 7.45-7.55 for alkalinization therapy.

• Activated charcoal effectively adsorbs salicylates and should be given early (within 1-2 hours) after ingestion 1
• Sodium bicarbonate therapy aims to alkalinize both serum and urine to enhance salicylate elimination by ion trapping 1
• The target serum pH is 7.45-7.55 to promote urinary excretion while avoiding excessive alkalemia 2
• Forced diuresis is NOT recommended as first-line therapy and has fallen out of favor due to risks of fluid overload 1
• Hemodialysis is reserved for severe cases with altered mental status, severe acidosis, or very high salicylate levels, but salicylates ARE dialyzable 1
• Whole bowel irrigation is not standard therapy for salicylate toxicity 1

Question 2: Snake Envenomation and Respiratory Failure

Eastern Coral snake envenomation is most likely to cause respiratory failure among the listed options.

• Coral snakes are elapids with neurotoxic venom that can cause progressive paralysis and respiratory muscle weakness leading to respiratory failure 2
• Copperhead, cottonmouth, and prairie rattler are all pit vipers (crotalids) that primarily cause local tissue destruction, coagulopathy, and systemic effects but rarely respiratory failure 2
• Hognose snakes are generally not medically significant 2

Question 3: Digoxin Toxicity and Digifab Indication

Bidirectional ventricular tachycardia is an indication to administer digitalis antibody (Digifab) fragments in this patient with digoxin toxicity.

• The American Heart Association recommends antidigoxin Fab antibodies for patients with severe cardiac glycoside toxicity 2
• Bidirectional ventricular tachycardia is a life-threatening ventricular arrhythmia pathognomonic for severe digoxin toxicity and requires immediate Digifab administration 2
• Other indications include severe bradycardia, AV nodal blockade, and hemodynamically unstable ventricular arrhythmias 2
• Sinus bradycardia and sinus tachycardia alone are not absolute indications unless associated with hemodynamic instability 2
• AV nodal reentry tachycardia and atrial fibrillation with RVR are not typical presentations of digoxin toxicity 2

Question 4: Activated Charcoal Adsorption

Acetaminophen is most likely to be adsorbed by activated charcoal among the listed options.

• Activated charcoal effectively adsorbs most organic compounds including acetaminophen 2
• Charcoal should NOT be administered for ingestions of caustic substances, metals (iron), or hydrocarbons (toluene) 2
• Ethylene glycol, lithium, and other small molecules or ions are poorly adsorbed by activated charcoal 2
• Iron is a metal and not adsorbed by charcoal 2

Question 5: Methemoglobinemia

Amyl nitrite is the most likely xenobiotic ingested in this patient presenting with cyanosis, hypoxia refractory to oxygen, and dark blood.

• The clinical presentation of cyanosis despite high-flow oxygen, low pulse oximetry readings, and chocolate-brown appearing blood is classic for methemoglobinemia 2
• Amyl nitrite (and other nitrites/nitrates) are known to cause methemoglobinemia 2
• These agents are sometimes abused as inhalants ("poppers") 2
• The other listed agents do not typically cause methemoglobinemia 2

Question 6: Normal Anion Gap Metabolic Acidosis

Isopropanol overdose would be expected to produce a normal anion gap metabolic acidosis.

• Isopropanol is metabolized to acetone, which does not produce an anion gap acidosis 1
• Ethylene glycol, methanol, and salicylates all cause elevated anion gap metabolic acidosis 1
• Iron toxicity also produces an elevated anion gap acidosis 1

Question 7: Hepatotoxic Mushroom Toxin

Amatoxin is known to cause hepatotoxicity among the listed mushroom toxins.

• Amatoxins (found in Amanita phalloides and related species) cause severe hepatotoxicity and are the leading cause of fatal mushroom poisoning 2
• Orellanine causes nephrotoxicity, not primarily hepatotoxicity 2
• Coprine causes disulfiram-like reactions with alcohol 2
• Ibotenic acid and psilocybin cause primarily neurological effects 2

Question 8: Opioid Withdrawal

Opioid withdrawal is the most likely diagnosis in this patient presenting 36 hours after last opioid dose with characteristic symptoms.

• The clinical presentation of myalgias, nausea, vomiting, diarrhea, anxiety, tachycardia, hypertension, rhinorrhea, mydriasis, and piloerection is classic for opioid withdrawal 2
• The timeline of 36 hours after last dose is consistent with short-acting opioid withdrawal 2
• Temperature is typically normal in opioid withdrawal, distinguishing it from other conditions 2
• Benzodiazepine and ethanol withdrawal typically present with tremor and risk of seizures 2
• Cocaine withdrawal presents with hypersomnia and depression, not these symptoms 2

Question 9: Rumack-Matthew Nomogram Application

A patient who presents 8 hours after an acute ingestion of 15g acetaminophen with an acetaminophen concentration of 200 mcg/mL can have the Rumack-Matthew nomogram applied.

• The Rumack-Matthew nomogram is only valid for acute, single-time-point ingestions with known time of ingestion between 4-24 hours post-ingestion 2
• The nomogram cannot be used for chronic ingestions, unknown time of ingestion, or presentations outside the 4-24 hour window 2
• Patients with chronic supratherapeutic ingestion require different management approaches 2
• The nomogram is not reliable when time of ingestion is unknown or when presentation is delayed beyond 24 hours 2

Question 10: Cyanide Poisoning Manifestations

Elevated serum lactate is consistent with cyanide poisoning among the listed options.

• Cyanide inhibits cytochrome oxidase, causing cellular hypoxia and shift to anaerobic metabolism with resultant lactic acidosis 2
• Lactic acidosis is a sensitive and specific finding in cyanide poisoning 2
• Central venous oxygen saturation is typically INCREASED (not decreased) because tissues cannot utilize oxygen 2
• Metabolic acidosis with ELEVATED anion gap (not normal) is expected 2
• The American Heart Association recommends hydroxocobalamin and 100% oxygen for cyanide poisoning 2

Question 11: Antimuscarinic Toxidrome

Jimson weed ingestion is expected to cause an antimuscarinic toxidrome.

• Jimson weed (Datura stramonium) contains tropane alkaloids (atropine, scopolamine) that cause classic anticholinergic/antimuscarinic effects 2
• The antimuscarinic toxidrome includes mydriasis, dry skin, hyperthermia, tachycardia, urinary retention, and altered mental status 2
• Methamphetamine causes sympathomimetic toxidrome 2
• Kratom causes opioid-like effects 2
• Psilocybin causes hallucinogenic effects 2

Question 12: Isoniazid Overdose Treatment

Pyridoxine (vitamin B6) may be most helpful for persistent seizures after tuberculosis medication (isoniazid) overdose despite benzodiazepine therapy.

• Isoniazid depletes pyridoxine, leading to decreased GABA synthesis and refractory seizures 2
• Pyridoxine should be administered gram-for-gram equal to the amount of isoniazid ingested, or 5 grams IV if amount unknown 2
• Benzodiazepines remain first-line, but pyridoxine addresses the underlying mechanism 2

Question 13: Opioid Toxicity

Naloxone should initially be administered in low doses and uptitrated is the true statement regarding opioid agonist toxicity.

• Starting with low doses of naloxone (0.04-0.4 mg) and titrating to adequate respiratory effort (not full reversal) prevents acute withdrawal and agitation 2
• Bradypnea is NOT the primary cause of hypoventilation; decreased respiratory drive is 2
• Miosis alone is not sufficient to diagnose opioid intoxication as other conditions can cause pinpoint pupils 2
• Identifying the specific opioid is not critical for initial diagnosis and management 2

Question 14: Beta-Blocker Seizures

Propranolol ingestion is most likely to cause seizures among the listed beta-blockers.

• Propranolol is lipophilic and crosses the blood-brain barrier, causing CNS effects including seizures 2
• Membrane-stabilizing activity (sodium channel blockade) also contributes to seizure risk 2
• Other listed beta-blockers are less lipophilic or have different properties making seizures less likely 2

Question 15: Carboxyhemoglobin Half-Life with 100% Oxygen

The half-life of carboxyhemoglobin with a 100% nonrebreather mask is approximately 90 minutes.

• Room air: ~5-6 hours 2
• 100% oxygen via nonrebreather: ~90 minutes 2
• Hyperbaric oxygen: ~20-30 minutes 2
• The American Heart Association states that hyperbaric oxygen may be helpful for severe carbon monoxide poisoning 2

Question 16: Coral Snake Bite Management

The patient should be observed for at least 6 hours and can be discharged if he remains asymptomatic after this coral snake bite.

• Coral snake envenomation can have delayed onset of symptoms (up to 12-24 hours) 2
• Minimal or absent local findings are typical with coral snakes, unlike pit vipers 2
• If the patient remains completely asymptomatic after observation, discharge with strict return precautions is reasonable 2
• Antivenom is indicated if signs of envenomation develop (neurological symptoms, respiratory compromise) 2

Question 17: Torsades de Pointes Risk

Sotalol has the greatest risk of torsades de pointes among the listed antihypertensive agents.

• Sotalol is a beta-blocker with class III antiarrhythmic properties that prolongs the QT interval 2
• QT prolongation from sotalol significantly increases risk of torsades de pointes 2
• The other agents listed do not typically cause significant QT prolongation 2

Question 18: Acute Aspirin Overdose Management

Activated charcoal is the suggested first step in management for this patient presenting 30 minutes after 7g aspirin ingestion.

• For a 60 kg person, 7g represents approximately 117 mg/kg, which is a potentially toxic dose 1
• Activated charcoal should be administered within 1-2 hours of ingestion to prevent absorption 1
• The patient is awake and oriented, making activated charcoal administration safe 1
• Hemodialysis is reserved for severe toxicity with altered mental status, severe acidosis, or very high levels 1
• Forced diuresis is not first-line therapy 1
• Gastric lavage is rarely indicated and not preferred over activated charcoal 3

Question 19: Hyperbaric Oxygen Indication for Carbon Monoxide

Syncope is an indication for hyperbaric oxygen therapy in the setting of carbon monoxide exposure.

• The American Heart Association states that hyperbaric oxygen may be helpful for acute carbon monoxide poisoning in patients with severe toxicity 2
• Syncope, altered mental status, cardiovascular instability, and pregnancy are considered indications for hyperbaric oxygen 2
• Carboxyhemoglobin level alone is not the sole determinant; clinical presentation matters more 2
• Headache alone without other severe symptoms is not an absolute indication 2

Question 20: Body Packer Management

Whole bowel irrigation with polyethylene glycol is the most appropriate next step for this body packer with drug packets visible on abdominal x-ray.

• The abdominal x-ray shows multiple radiopaque foreign bodies consistent with drug packets 2
• Whole bowel irrigation is the treatment of choice for body packers who are asymptomatic 2
• Endotracheal intubation is only needed if the patient develops toxicity from packet rupture 2
• Surgical intervention is reserved for signs of obstruction, perforation, or packet rupture with severe toxicity 2
• Activated charcoal is not effective for this indication 2

Question 21: Paroxetine Overdose Evaluation

Serum acetaminophen level is needed to guide management in this patient with intentional paroxetine overdose.

• In any intentional overdose, co-ingestion of acetaminophen must be ruled out due to its delayed toxicity and specific antidote availability 2
• Paroxetine (SSRI) overdose typically has a benign course when taken alone 2
• No specific testing for paroxetine levels is clinically useful 2
• Urine drug screens do not change acute management 2

Question 22: Alpha-2 Agonist Mechanism

Alpha-2-adrenergic agonist has the greatest potential to activate presynaptic autoreceptors, inhibit norepinephrine release, and decrease sympathetic outflow.

• Alpha-2 agonists (like clonidine) work centrally to decrease sympathetic outflow 2
• Activation of presynaptic alpha-2 receptors inhibits norepinephrine release 2
• This mechanism results in decreased blood pressure and heart rate 2

Question 23: Serotonin Syndrome

Phenelzine (MAOI) is the most likely causative agent for this presentation of hyperthermia, agitation, mydriasis, hyperreflexia, and clonus.

• The clinical presentation of hyperthermia (42°C), altered mental status, autonomic instability, mydriasis, hyperreflexia, and clonus is classic for serotonin syndrome 2
• MAOIs like phenelzine are high-risk agents for serotonin syndrome, especially when combined with other serotonergic agents 2
• Clonus is a key distinguishing feature of serotonin syndrome 2
• Methamphetamine would cause sympathomimetic toxidrome without clonus 2
• Diphenhydramine causes anticholinergic toxidrome 2

Question 24: Severe Ethanol Withdrawal Predictor

Seizure prior to presentation or during ED course is predictive of severe ethanol withdrawal (progression to delirium tremens).

• History of withdrawal seizures is the strongest predictor of progression to severe withdrawal and delirium tremens 2
• Presence of withdrawal symptoms despite elevated ethanol concentration indicates severe physiological dependence 2
• CIWA score helps guide treatment but is not the best predictor of progression 2
• History of blackouts relates to drinking patterns but not withdrawal severity 2

Question 25: Caustic Ingestion with Cardiac Arrest

Hydrofluoric acid is the most likely etiology of syncope and collapse with the rhythm strip showing what appears to be a wide-complex rhythm after caustic agent ingestion.

• Hydrofluoric acid causes systemic fluoride toxicity leading to severe hypocalcemia and hyperkalemia, which can cause cardiac arrest 2
• The mechanism involves fluoride binding calcium and causing life-threatening electrolyte disturbances 2
• Calcium administration is critical in hydrofluoric acid exposure 2
• Other caustic agents (ammonia, bleach, lye, hydrogen peroxide) primarily cause local tissue injury without the same systemic cardiac effects 2, 3
• The American Heart Association recommends calcium administration for cardiac arrest associated with hyperkalemia or hypocalcemia 2