Acute Salicylate Toxicity Management

Question 1: Salicylate Toxicity Treatment

Sodium bicarbonate should be titrated to serum pH 7.45-7.55 to promote urinary excretion while avoiding excessive alkalemia. 1

Activated charcoal DOES adsorb salicylates effectively and should be administered early 2
Forced diuresis is NOT first-line therapy; alkalinization of urine is the priority 2
Hemodialysis IS indicated for severe toxicity (altered mental status, severe acidosis, renal failure, pulmonary edema) 2
Whole bowel irrigation has no role in salicylate elimination 2

Snake Envenomation

Question 2: Respiratory Failure Risk

Eastern Coral snake envenomation is most likely to cause respiratory failure due to neurotoxic venom causing progressive paralysis and respiratory muscle weakness. 1

Coral snakes are elapids with neurotoxic venom, unlike pit vipers (copperhead, cottonmouth, rattlesnakes) which cause primarily local tissue destruction and coagulopathy 1
Hognose snakes are rear-fanged and rarely cause significant envenomation 1

Digoxin Toxicity

Question 3: Digifab Indication

Bidirectional ventricular tachycardia is pathognomonic for severe digoxin toxicity and requires immediate Digifab administration. 1

This life-threatening ventricular arrhythmia is an absolute indication for antidigoxin Fab antibodies 1
Other indications include: hemodynamically unstable dysrhythmias, hyperkalemia >5.5 mEq/L, and ingestion >10 mg in adults 1
Sinus bradycardia and AV blocks alone do not mandate Digifab unless hemodynamically unstable 1

Activated Charcoal Adsorption

Question 4: Charcoal Effectiveness

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

Activated charcoal does NOT effectively adsorb: metals (iron, lithium), alcohols (ethylene glycol, ethanol), hydrocarbons (toluene), or strong acids/bases 2
Acetaminophen is well-adsorbed by activated charcoal when given within 1-2 hours of ingestion 3

Methemoglobinemia

Question 5: Cyanosis with Dark Blood

Amyl nitrite is the most likely xenobiotic causing methemoglobinemia, presenting with cyanosis despite oxygen therapy, low pulse oximetry, and chocolate-brown blood. 1

This clinical presentation is classic for methemoglobinemia 1
Nitrites and nitrates are well-known methemoglobin-inducing agents 1
Treatment is methylene blue 1-2 mg/kg IV 1

Anion Gap Acidosis

Question 6: Normal Anion Gap

Isopropanol overdose produces a normal anion gap metabolic acidosis.

Isopropanol is metabolized to acetone (not an acid), causing osmolar gap without anion gap 2
Ethylene glycol, methanol, salicylates, and iron all cause elevated anion gap metabolic acidosis 2

Mushroom Toxicity

Question 7: Hepatotoxic Mushroom

Amatoxin is the mushroom toxin known to cause severe hepatotoxicity.

Amatoxin (from Amanita phalloides) causes delayed hepatotoxicity and is the leading cause of mushroom-related deaths
Coprine causes disulfiram-like reaction with alcohol
Ibotenic acid causes CNS effects
Orellanine causes delayed renal toxicity
Psilocybin causes hallucinations

Opioid Withdrawal

Question 8: Withdrawal Syndrome

Opioid withdrawal is the most likely diagnosis based on myalgias, GI symptoms, anxiety, tachycardia, hypertension, rhinorrhea, mydriasis, and piloerection 36 hours after last opioid dose.

Timeline fits opioid withdrawal (typically 6-12 hours for short-acting, peaks 36-72 hours)
Normal temperature excludes ethanol withdrawal (which causes hyperthermia in severe cases)
Mydriasis is characteristic of opioid withdrawal (vs. miosis in intoxication)
Benzodiazepine withdrawal would include seizures and more severe autonomic instability

Acetaminophen Nomogram

Question 9: Nomogram Application

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

The nomogram is ONLY valid for: acute single ingestion, known time of ingestion 4-24 hours prior, and reliable serum level 3
Cannot be used for: chronic ingestions, unknown time, extended-release formulations, or presentations >24 hours 3
The other options fail criteria: comatose with unknown time, chronic ingestion (3 days), presentation >24 hours, or vague timing 3

Cyanide Poisoning

Question 10: Physiological Manifestations

Elevated serum lactate is consistent with cyanide poisoning due to inhibition of cellular respiration and shift to anaerobic metabolism. 1

Cyanide causes elevated (not decreased) central venous oxygen saturation due to inability of tissues to extract oxygen 1
Metabolic acidosis with elevated anion gap (not normal) occurs 1
Treatment is hydroxocobalamin and 100% oxygen 1

Antimuscarinic Toxidrome

Question 11: Anticholinergic Agent

Jimson weed ingestion causes an antimuscarinic toxidrome.

Jimson weed (Datura stramonium) contains tropane alkaloids (atropine, scopolamine)
Classic presentation: "hot as a hare, blind as a bat, dry as a bone, red as a beet, mad as a hatter"
Kratom causes opioid-like effects, methamphetamine is sympathomimetic, psilocybin is hallucinogenic

Isoniazid Toxicity

Question 12: Refractory Seizures

Pyridoxine (vitamin B6) is most helpful for persistent seizures after isoniazid overdose despite benzodiazepine therapy.

Isoniazid depletes pyridoxine, causing GABA deficiency and refractory seizures
Dose: gram-for-gram matching of isoniazid ingested, or 5g IV if amount unknown
Pyridoxine allows GABA synthesis to resume

Opioid Toxicity

Question 13: Opioid Clinical Toxicity

Naloxone should initially be administered in low doses (0.04-0.4 mg) and uptitrated to adequate respiratory effort to prevent acute withdrawal and agitation. 1

Decreased respiratory drive (not just bradypnea) is the primary cause of hypoventilation 1
Miosis alone is insufficient for diagnosis (also seen with cholinergics, pontine hemorrhage)
Identifying specific agent is NOT critical for emergency management 1
Acute vision loss is not a direct effect of opioid use 1

Beta-Blocker Seizures

Question 14: Seizure Risk

Propranolol is most likely to cause seizures due to its lipophilic properties allowing blood-brain barrier penetration and CNS effects. 1

Propranolol is highly lipophilic, causing membrane-stabilizing effects and CNS toxicity 1
Other beta-blockers listed are less lipophilic with lower seizure risk 1

Carbon Monoxide Half-Life

Question 15: Carboxyhemoglobin Elimination

The half-life of carboxyhemoglobin with a 100% nonrebreather mask is approximately 90 minutes. 1

Room air: 4-6 hours
100% oxygen via nonrebreather: 90 minutes 1
Hyperbaric oxygen: 20-30 minutes 1

Coral Snake Bite Management

Question 16: Asymptomatic Snake Bite

The patient should be observed for at least 6 hours and can be discharged if he remains asymptomatic after this coral snake bite. 1

Coral snake envenomation may have delayed onset of symptoms (up to 12 hours) 1
Antivenom is indicated only if signs of envenomation develop (neurological symptoms, respiratory compromise) 1
Suction devices and local antivenom injection are contraindicated 1

Torsades de Pointes Risk

Question 17: QT Prolongation

Sotalol has the greatest risk of torsades de pointes due to its class III antiarrhythmic properties that prolong the QT interval. 1

Sotalol is a beta-blocker with potassium channel blocking effects 1
QT prolongation significantly increases torsades risk 1
Other agents listed do not significantly prolong QT 1

Acute Aspirin Overdose

Question 18: Initial Management

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

Activated charcoal effectively adsorbs salicylates when given early (<1-2 hours) 2
Patient is awake and able to protect airway, making charcoal safe 2
Hemodialysis is reserved for severe toxicity (not yet present) 2
Gastric lavage is not indicated 2

Hyperbaric Oxygen Indications

Question 19: Carbon Monoxide Treatment

Syncope is an indication for hyperbaric oxygen therapy in carbon monoxide exposure, as it indicates severe toxicity with altered mental status. 1

Indications include: syncope, altered mental status, cardiovascular instability, pregnancy with any symptoms, and carboxyhemoglobin >25% 1
Pregnancy with carboxyhemoglobin >5% is NOT an absolute indication unless symptomatic 1
Headache alone is insufficient 1
Metabolic alkalosis is not an indication 1

Body Packer Management

Question 20: Drug Packet Ingestion

Whole bowel irrigation with polyethylene glycol is the most appropriate next step for an asymptomatic body packer.

Whole bowel irrigation is treatment of choice for asymptomatic body packers 1
Endotracheal intubation only needed if toxicity develops from packet rupture 1
Surgery reserved for obstruction, perforation, or severe toxicity 1
Activated charcoal ineffective for intact packets 1

SSRI Overdose

Question 21: Paroxetine Overdose Testing

Serum acetaminophen level is needed to guide management in an asymptomatic intentional overdose patient.

Co-ingestion of acetaminophen is common in intentional overdoses and may be asymptomatic initially
Paroxetine levels are not clinically useful
Urine drug screens do not change management
Asymptomatic SSRI overdose requires observation and co-ingestion screening

Alpha-2 Agonist Mechanism

Question 22: Sympathetic Outflow Reduction

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

Alpha-2 agonists (clonidine, dexmedetomidine) work via central presynaptic receptors
This mechanism reduces sympathetic outflow and lowers blood pressure
Alpha-1 agonists increase blood pressure via vasoconstriction

Serotonin Syndrome

Question 23: Hyperthermia and Clonus

Phenelzine (MAOI) exposure is the most likely causative agent for this presentation of hyperthermia, altered mental status, autonomic instability, mydriasis, hyperreflexia, and clonus. 1

This clinical presentation is classic for serotonin syndrome 1
MAOIs like phenelzine are high-risk agents for serotonin syndrome 1
Hyperthermia (42°C), clonus, and hyperreflexia are key diagnostic features 1
Methamphetamine would cause sympathomimetic toxidrome without clonus 1

Severe Ethanol Withdrawal Prediction

Question 24: Delirium Tremens Risk

Seizure prior to presentation or during ED course is predictive of severe ethanol withdrawal and progression to delirium tremens. 1

History of withdrawal seizures is the strongest predictor of progression to severe withdrawal 1
Presence of withdrawal symptoms despite elevated ethanol concentration indicates severe physiological dependence 1
CIWA score guides treatment but doesn't predict progression 1

Caustic Ingestion with Cardiac Arrest

Question 25: Syncope After Caustic Ingestion

Hydrofluoric acid is the most likely etiology of syncope and collapse after caustic agent ingestion, causing systemic fluoride toxicity with severe hypocalcemia and hyperkalemia leading to cardiac arrest. 1

Hydrofluoric acid causes systemic fluoride toxicity 1
Fluoride binds calcium and causes life-threatening hypocalcemia 1
Hyperkalemia from cellular toxicity contributes to dysrhythmias 1
Calcium administration is critical in treatment 1
Other caustics (ammonia, bleach, lye, hydrogen peroxide) cause local tissue injury but not the same systemic electrolyte derangements causing cardiac arrest 4

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

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