Bone WizardryMEDICAL EDUCATION
⌘ KStart free
Back
On this page
0%
Skip to lesson

Pharmacology

Toxidromes and antidotes: recognize the failing physiology

Read pupils, secretions, ventilation, ECG and acid-base findings together to recognize poisoning, select antidotes and identify urgent escalation.

An unresponsive patient may need ventilation before anyone knows the drug name. A patient who looks well after acetaminophen ingestion may already need antidotal treatment. Toxicology therefore asks two questions at once: what physiology is failing now, and what delayed injury must treatment prevent?

A toxidrome is a pattern, not a confirmatory test. Pupils, moisture, bowel activity, temperature, muscle findings and breathing must agree with the exposure and time course. Mixed ingestions, hypoxia and underlying illness can blur the pattern. A familiar pupil size must never close the differential.

Read the whole pattern, especially breathing and moisture

Start with airway patency, respiratory rate and depth, oxygenation and circulation. Check bedside glucose promptly and correct hypoglycemia; dextrose is not automatically required when glucose is normal. Obtain temperature and ECG early. Draw electrolytes, renal function and targeted tests according to the history and findings. Acetaminophen testing matters in an uncertain ingestion because early symptoms can be absent; salicylate concentrations need interpretation alongside acid-base status and clinical progression. A urine drug screen neither establishes severity nor reliably excludes every important exposure. [1] [2] [5]

Two pupils-and-moisture comparisons, with respiratory findings beside them

Small pupils: compare the chest

Opioid pattern: slow, shallow respiration and depressed consciousness. Pinpoint pupils support the diagnosis but are not mandatory; skin dryness is not a defining rule.

Cholinergic pattern: secretions, tearing, bronchorrhea and often diarrhea. Fasciculations or weakness indicate nicotinic involvement and can contribute to respiratory failure.

Large pupils: compare moisture and bowel activity

Sympathomimetic pattern: sweating, agitation, tachycardia, hypertension and hyperthermia.

Antimuscarinic pattern: dry mouth and skin, delirium, urinary retention and reduced bowel activity, often with tachycardia and hyperthermia.

Moisture helps discriminate otherwise similar patterns, but no single sign is absolute. Breathing determines an immediate treatment priority.

Sedative-hypnotic poisoning often causes depressed consciousness with relatively normal pupils. Isolated benzodiazepine poisoning differs from combinations with opioids, alcohol or other sedatives, which can produce much greater respiratory depression. Sedation is also compatible with stroke, hypoglycemia or trauma, so reassess when the pattern or response does not fit. [1] [23]

In sympathomimetic toxicity, benzodiazepines reduce agitation and excessive adrenergic activation; active cooling and assessment for seizures, rhabdomyolysis and organ injury accompany treatment. Antimuscarinic delirium also needs temperature control and supportive care. Physostigmine may be useful for a well-characterized isolated antimuscarinic exposure, but a widened QRS, suspected tricyclic ingestion or other seizure/conduction concerns change that decision. A narrow QRS alone does not establish safety. [1] [4]

Try it here · Checkpoint 1 of 3

Make your prediction before reading the choices. A first attempt is just a starting point.

Case 1

An adult found beside an opioid bottle has a pulse, a respiratory rate of 4/min and shallow breaths. Pupils are small. What is the best immediate approach?

Show answer and explanations for case 1

  1. A. Support the airway and ventilation while administering naloxone (Best answer)

    Inadequate ventilation is the immediate threat; naloxone is given alongside respiratory support rather than before all supportive care.

  2. B. Give naloxone and wait for a response before providing breaths (Why this does not fit)

    Waiting leaves severe hypoventilation untreated while the antagonist takes effect.

  3. C. Give flumazenil because all sedative poisonings share one antidote (Why this does not fit)

    Flumazenil does not reverse opioid receptors and can add risk in an uncertain exposure.

  4. D. Perform gastric decontamination before addressing breathing (Why this does not fit)

    Decontamination does not correct immediate hypoventilation and can increase aspiration risk.

Takeaway: Treat respiratory failure while reversing the suspected opioid effect.

Case sources: [1] [23]

Choose an antidote without interrupting resuscitation

Naloxone reverses opioid receptor effects, but ventilation remains the first physiological need in a patient with a pulse who is barely breathing. Give assisted breaths and naloxone while arranging emergency care. In monitored care, titrate reversal to adequate ventilation rather than demanding abrupt full arousal. Repeat doses or an infusion may be needed because the opioid can outlast naloxone. In cardiac arrest, CPR and ventilation take priority; an antidote must not delay standard resuscitation. [1] [23]

Flumazenil antagonizes the benzodiazepine binding site on the GABA-A receptor. It is not the routine answer to unexplained coma. Selected iatrogenic oversedation in a benzodiazepine-naive patient is different from chronic benzodiazepine use, a seizure history or an uncertain mixed overdose. Reversal can precipitate withdrawal seizures or expose a co-ingestant's proconvulsant effect. Support ventilation while determining whether the narrow indication is met. [1]

Organophosphates inhibit acetylcholinesterase. Atropine counters muscarinic effects; titrate it toward improved pulmonary secretions, air entry and oxygenation, rather than pupil dilation alone. The 2025 AHA guideline considers pralidoxime reasonable in life-threatening organophosphate poisoning; response depends on the compound and timing, and mortality evidence is mixed. Pralidoxime can reactivate phosphorylated enzyme before aging makes that enzyme complex resistant to reactivation.

It is particularly relevant to peripheral neuromuscular weakness. Atropine, early pralidoxime when indicated, airway care, benzodiazepines for seizures, protective equipment and decontamination can proceed concurrently. Do not wait for complete atropinization before even considering the oxime. Avoid succinylcholine in this setting because cholinesterase inhibition can prolong paralysis. [19] [1]

An ECG can identify a second mechanism hiding inside an apparent antimuscarinic overdose. Tricyclic antidepressants can cause sodium-channel blockade, producing QRS widening, hypotension and ventricular dysrhythmias. Sodium bicarbonate supplies sodium and alkalinization in clinically significant cardiotoxicity. Follow QRS, perfusion, pH, sodium and potassium to avoid excessive alkalemia or hypernatremia. A prolonged QT is a different electrical problem: sotalol has potassium-channel effects and torsades risk, whereas some other beta-blockers, especially propranolol, can also block sodium channels in overdose. Do not describe every beta-blocker as electrically identical. [1] [21]

For life-threatening beta-blocker poisoning, the 2025 AHA guideline recommends vasopressors for hypotension and high-dose insulin when hypotension is refractory to vasopressors. For life-threatening calcium-channel blocker poisoning, it recommends both vasopressors and high-dose insulin for hypotension without requiring the same prior vasopressor-failure condition. High-dose insulin requires protocolized glucose and potassium monitoring. Glucagon may improve beta-blocker-associated bradycardia and hypotension by activating its own Gs-coupled receptor and increasing cAMP, but it is not a guaranteed complete treatment for shock. Calcium has a role in calcium-channel blocker poisoning. Persistent shock despite pharmacological support may require extracorporeal life support in an appropriate center. [1]

Use time and acid-base physiology to detect delayed injury

Acetaminophen metabolism produces the reactive metabolite NAPQI, normally detoxified by glutathione. Excess exposure can exhaust that defense. Acetylcysteine replenishes protective capacity and has benefits even after the early prevention window. For a reliably timed acute ingestion, use a concentration obtained from four through 24 hours with the appropriate treatment nomogram. Do not extend a nomogram line beyond its validated time window or apply it to an intravenous dosing error.

A two-hour concentration cannot simply be plotted on the four-hour line. An uncertain time or repeated supratherapeutic ingestion needs a different assessment using concentrations and liver injury markers. Start treatment without waiting for delayed results when indicated, and do not stop solely because a preset infusion duration has elapsed. [2]

Parent alcohol versus downstream injury
ExposureMetabolite and organ patternWhat treatment must accomplish
MethanolFormate-associated acidosis and visual injuryFomepizole prevents further toxic metabolism; severe findings, including new visual deficits, require urgent dialysis assessment
Ethylene glycolGlycolate contributes to acidosis; oxalate can bind calcium and injure kidneysFomepizole plus severity-based dialysis assessment; urine crystals are neither required nor independently diagnostic

Early parent alcohol may increase the osmol gap before substantial acidosis develops. Later metabolism can reduce that gap while the anion gap rises. Neither a normal osmol gap nor absent crystals excludes a late presentation. Fomepizole inhibits alcohol dehydrogenase; it prevents additional metabolite production but does not instantly eliminate existing acids. Dialysis decisions use the actual poison, clinical injury, acid-base status and antidote availability. Methanol and ethylene glycol thresholds are not interchangeable, and published anion-gap formulas may differ in whether potassium is included. [20] [6] [7]

Salicylates stimulate respiratory drive and disrupt oxidative metabolism. A low PCO2 and low bicarbonate may represent simultaneous respiratory alkalosis and anion-gap metabolic acidosis, even when pH appears near normal. Interpret serial concentrations with symptoms, renal function and pH; falling blood concentration alone does not prove improving tissue toxicity. Alkalinization helps reduce tissue entry and increase renal elimination, with potassium correction essential to successful urine alkalinization.

Altered mental status, new oxygen requirement or failure of standard treatment can justify dialysis even below the highest concentration thresholds. If intubation becomes unavoidable, loss of compensatory hyperventilation can rapidly worsen acidemia, requiring a deliberate ventilation plan. [5] [25]

Try it here · Checkpoint 2 of 3

Make your prediction before reading the choices. A first attempt is just a starting point.

Case 13

An adult presents four hours after a reliably timed single acute acetaminophen ingestion. The concentration is 185 µg/mL, and the patient feels well. What is indicated?

Show answer and explanations for case 13

  1. A. Begin acetylcysteine (Best answer)

    At four hours, 185 µg/mL exceeds the US/Canada treatment line of 150 µg/mL. Begin acetylcysteine even though early poisoning can be asymptomatic.

  2. B. Repeat the concentration at eight hours before deciding whether to treat (Why this does not fit)

    The valid four-hour concentration already meets treatment criteria; repeating it should not delay acetylcysteine.

  3. C. Withhold acetylcysteine if the current aminotransferases are normal (Why this does not fit)

    Normal early liver tests do not override a concentration above the treatment line.

  4. D. Give activated charcoal as the only toxin-directed treatment (Why this does not fit)

    Charcoal may have a selected decontamination role, but it does not replace acetylcysteine once treatment criteria are met.

Takeaway: Use exposure timing and concentration before symptoms of liver injury emerge.

Case sources: [2] [34]

Separate dissolved oxygen, hemoglobin function and cellular use

Standard pulse oximetry and arterial PO2 answer different questions. Methemoglobin contains oxidized ferric iron that cannot carry oxygen normally. A patient exposed to dapsone or a local oxidizing anesthetic may have cyanosis, dark brown blood and a pulse oximeter reading that remains near the mid-80s despite a normal arterial PO2. Confirm with co-oximetry. [30] [28] [29] Methylene blue supports reduction of methemoglobin but is contraindicated in G6PD deficiency because of reduced effectiveness and hemolysis risk. It also has a clinically relevant serotonergic interaction warning. Seek toxicology guidance for alternatives or refractory illness. [8]

Carbon monoxide impairs oxygen transport and delivery. Ordinary pulse oximetry may look reassuring; measure carboxyhemoglobin with co-oximetry and provide high-concentration oxygen. A low level after time on oxygen does not reconstruct the peak exposure or exclude serious poisoning. Severe neurologic or cardiac findings warrant hyperbaric treatment assessment. CDC recommends a more aggressive approach in pregnancy, where hyperbaric oxygen is the treatment of choice even with less severe poisoning; involve the relevant specialists promptly. [3]

Cyanide inhibits cellular oxygen utilization. Enclosed-space fire exposure with soot, altered mental state, shock and marked lactate elevation supports empiric hydroxocobalamin while resuscitation continues. Hydroxocobalamin binds cyanide to form cyanocobalamin. Lactate is supportive, not uniquely diagnostic, and a confirmatory cyanide assay must not delay treatment in a compelling presentation. Carbon monoxide and cyanide can coexist; a modest carboxyhemoglobin result after oxygen does not settle that distinction.

Nitrite-based antidotes create methemoglobin, an additional oxygen-transport concern in smoke exposure. Sodium thiosulfate supplies sulfur for rhodanese-mediated conversion of cyanide to thiocyanate. AHA considers it a possible adjunct to hydroxocobalamin; with concurrent carbon monoxide poisoning, thiosulfate alone is a reasonable alternative when hydroxocobalamin is unavailable. This is a conditional choice, not proof of equal effectiveness. [32] [1] [15] [3]

Connect the remaining antidotes to what they actually reverse

Isoniazid poisoning can cause refractory seizures by interfering with pyridoxal phosphate-dependent GABA synthesis. Pyridoxine restores the needed cofactor, alongside standard seizure and airway treatment. [31] In a symptomatic adult with a known isoniazid dose, the label describes initial IV pyridoxine gram-for-gram with the ingestion; for an unknown adult dose, it describes an initial 5 g.

Delivery, repeat dosing and pediatric treatment require a toxicology protocol, not extrapolation of an adult amount. Sulfonylurea hypoglycemia may recur after dextrose stimulates further endogenous insulin release; octreotide suppresses that secretion. Its role is different from replacing glucose immediately or treating an exogenous insulin depot. Continued observation is necessary. [9] [17]

Unfractionated heparin: protamine
Positively charged protamine binds negatively charged heparin. The label states that 1 mg protamine neutralizes at least 100 USP heparin units; the amount needed falls as heparin is cleared. Calculate reversal from recent exposure and time; give it very slowly, with no more than 50 mg during any 10-minute period under the cited label, because hypotension and severe reactions can occur. Reversal of enoxaparin anti-Xa activity is incomplete. [10] [27]
Major warfarin bleeding: four-factor PCC plus intravenous vitamin K
PCC rapidly supplies clotting factors; vitamin K restores ongoing synthesis. Vitamin K alone acts too slowly for intracranial hemorrhage. [11]
Severe iron poisoning: deferoxamine
Systemic toxicity after iron ingestion can require iron chelation. A transient improvement after gastrointestinal symptoms does not guarantee safety. [33] [12]
Lead: exposure control and severity-specific chelation
Succimer is an oral option in selected nonencephalopathic children with sufficiently high blood lead levels. Encephalopathy requires inpatient specialist-directed parenteral therapy, often dimercaprol followed by calcium disodium EDTA. Disodium EDTA is not interchangeable and can cause fatal hypocalcemia. [13] [14]
Life-threatening digoxin toxicity: digoxin immune Fab
Fab binds circulating digoxin. Treat dangerous arrhythmias or other severe toxicity based on the clinical picture; total digoxin measurements after Fab can mislead. Follow potassium and watch for loss of digoxin's therapeutic effects. [24]

Finally, distinguish serotonin toxicity from neuroleptic malignant syndrome using exposure and motor findings. Serotonergic toxicity often develops rapidly after a relevant drug change and features clonus, hyperreflexia, agitation and sweating. Ocular clonus means rhythmic involuntary ocular oscillation, not simply slow eye motion. Dopamine-blocking drug exposure with generalized sustained rigidity, fever and autonomic instability suggests NMS. Linezolid can contribute through reversible MAO inhibition, particularly with serotonergic co-medication. [26] Both require stopping causative drugs and urgent supportive care; fever alone cannot distinguish them. [16] [22]

Activated charcoal is a selective decontamination tool, not a universal antidote. Consider substance, timing, expected benefit and airway protection. The 2026 toxicology collaborative finds no role for charcoal in iron, methanol or ethylene glycol poisoning. An unprotected airway creates aspiration risk. Timing depends on the poison and formulation; a universal one-hour cutoff is inappropriate. [34] Early poison-center or toxicologist involvement helps coordinate these decisions while resuscitation continues. [18]

Try it here · Checkpoint 3 of 3

Make your prediction before reading the choices. A first attempt is just a starting point.

Case 28

A patient taking warfarin has an intracranial hemorrhage and INR of 6.7. Four-factor PCC is available. Which reversal approach is preferred?

Show answer and explanations for case 28

  1. A. Withhold warfarin and wait for the next routine INR (Why this does not fit)

    Intracranial hemorrhage requires urgent reversal rather than passive clearance alone.

  2. B. Four-factor PCC plus intravenous vitamin K (Best answer)

    PCC supplies immediate factor replacement while vitamin K supports sustained synthesis after the infused factors decline.

  3. C. Vitamin K alone because rapid factor replacement is unnecessary (Why this does not fit)

    Vitamin K acts too slowly as the sole reversal strategy for this critical-site major bleed.

  4. D. Protamine alone (Why this does not fit)

    Protamine reverses heparin, not warfarin's suppression of vitamin K-dependent factor synthesis.

Takeaway: Major warfarin bleeding needs immediate and sustained reversal.

Case sources: [11]

Match each pattern to the treatment decision

Case 2

A patient with a suspected long-acting opioid exposure initially breathes normally after naloxone but becomes somnolent with a respiratory rate of 6/min 40 minutes later. What best explains the course?

Show answer and explanations for case 2

  1. A. Delayed benzodiazepine absorption as the established sole cause (Why this does not fit)

    A sedative co-ingestion remains possible, but the initial naloxone response followed by recurrent hypoventilation after a long-acting opioid points to antagonist wear-off.

  2. B. Precipitated opioid withdrawal as the best explanation (Why this does not fit)

    Withdrawal usually produces arousal and autonomic symptoms rather than recurrent depressed ventilation.

  3. C. Naloxone-induced pulmonary edema as the leading explanation (Why this does not fit)

    Pulmonary edema is a possible complication, but the described recurrence of somnolence and slow breathing without new lung findings better fits persistent opioid action.

  4. D. The opioid effect can persist after naloxone has worn off (Best answer)

    Recurrent respiratory depression can require repeat antagonist dosing or an infusion with continued monitoring.

Takeaway: Initial reversal is not evidence that the exposure has ended.

Case sources: [23] [1]

Case 3

A 28-year-old has agitation, tachycardia, hypertension, mydriasis and profuse sweating after stimulant use. Which toxidrome best fits?

Show answer and explanations for case 3

  1. A. Opioid toxicity (Why this does not fit)

    Profound respiratory depression and reduced consciousness would be more characteristic than this activated, sweating pattern.

  2. B. Isolated benzodiazepine toxicity (Why this does not fit)

    Benzodiazepines generally depress consciousness rather than produce this hyperadrenergic examination.

  3. C. Sympathomimetic toxicity (Best answer)

    The combination of adrenergic activation and sweating fits the reported exposure and examination.

  4. D. Antimuscarinic toxicity (Why this does not fit)

    Antimuscarinic poisoning can share mydriasis and tachycardia, but dry skin and reduced bowel activity are more characteristic.

Takeaway: Compare moisture and mental state when tachycardia and pupil dilation overlap.

Case sources: [1] [4]

Case 4

After taking an excessive amount of a sedating antihistamine, a patient becomes delirious. The mouth is dry, pupils are dilated, bowel sounds are reduced and the bladder is distended. Which mechanism best explains the pattern?

Show answer and explanations for case 4

  1. A. Selective enhancement of GABA-A signaling alone (Why this does not fit)

    That mechanism can cause sedation but does not explain this full peripheral antimuscarinic constellation.

  2. B. Muscarinic receptor antagonism (Best answer)

    The linked dry mucosa, urinary retention, reduced gut activity and delirium fit an antimuscarinic effect.

  3. C. Acetylcholinesterase inhibition (Why this does not fit)

    Excess acetylcholine usually produces secretions and gastrointestinal activity rather than this dry, retained pattern.

  4. D. Pure mu-opioid receptor agonism (Why this does not fit)

    Opioid toxicity primarily threatens ventilation and usually causes depressed consciousness rather than this characteristic delirium pattern.

Takeaway: Use several organ findings to identify the receptor pattern.

Case sources: [4]

Case 5

An unresponsive patient with an uncertain medication exposure has a bedside glucose of 29 mg/dL. Airway support is underway. Which action addresses an immediately reversible cause of brain dysfunction?

Show answer and explanations for case 5

  1. A. Administer glucose promptly and recheck the response (Best answer)

    Severe hypoglycemia can independently cause coma and needs immediate correction alongside ongoing resuscitation.

  2. B. Wait for a comprehensive urine drug screen (Why this does not fit)

    A screening result does not justify delaying correction of a measured dangerous glucose concentration.

  3. C. Give flumazenil before glucose because the exposure is unknown (Why this does not fit)

    Unknown exposure is a reason for caution with flumazenil, not a reason to postpone glucose.

  4. D. Assume the glucose value is irrelevant if pupils are small (Why this does not fit)

    Pupil size does not exclude hypoglycemia or mixed pathology.

Takeaway: Treat measured hypoglycemia; do not let a suspected toxidrome override it.

Case sources: [1] [17]

Case 6

A previously healthy adult with no benzodiazepine use or seizure history has excessive respiratory depression after a documented isolated procedural midazolam dose. Ventilation is supported. Which statement about flumazenil is correct?

Show answer and explanations for case 6

  1. A. It is equally appropriate for every unexplained coma (Why this does not fit)

    Uncertain co-ingestants and dependence can make empiric reversal dangerous.

  2. B. It directly antagonizes opioid receptors (Why this does not fit)

    Naloxone is the opioid antagonist; flumazenil acts at the benzodiazepine site.

  3. C. Its use eliminates the need to support ventilation (Why this does not fit)

    Antidotal treatment does not replace airway and respiratory support during depression.

  4. D. It can be considered in this carefully selected iatrogenic exposure (Best answer)

    Known isolated benzodiazepine exposure with contraindications excluded differs from an uncertain overdose.

Takeaway: Flumazenil has a narrow useful setting, not a general coma indication.

Case sources: [1]

Case 7

A patient who takes clonazepam daily is found obtunded beside several medication bottles, including a tricyclic antidepressant. What best explains avoiding empiric flumazenil?

Show answer and explanations for case 7

  1. A. Direct potentiation of tricyclic sodium-channel blockade by receptor binding (Why this does not fit)

    The main concern is loss of benzodiazepine anticonvulsant effects and precipitated withdrawal, rather than flumazenil directly binding cardiac sodium channels.

  2. B. Reduced renal clearance of clonazepam after flumazenil (Why this does not fit)

    Flumazenil reverses receptor effects. A renal clearance interaction is not the mechanism of the seizure risk.

  3. C. It may precipitate withdrawal seizures and expose proconvulsant co-ingestant effects (Best answer)

    Chronic benzodiazepine use and possible tricyclic ingestion both increase concern for harm from reversal.

  4. D. Recurrent sedation alone is the principal reason to avoid it here (Why this does not fit)

    Recurrent sedation requires monitoring, but dependence and a proconvulsant co-ingestant create the more serious seizure and arrhythmia concerns.

Takeaway: Dependence and uncertain proconvulsant exposure make benzodiazepine reversal hazardous.

Case sources: [1]

Case 8

A patient with suspected amitriptyline ingestion has hypotension, delirium and a QRS duration of 148 ms. Which treatment targets the demonstrated cardiotoxic mechanism?

Show answer and explanations for case 8

  1. A. Intravenous magnesium as the sole treatment for the conduction abnormality (Why this does not fit)

    Magnesium is useful for torsades, but the demonstrated QRS widening and hypotension call for sodium bicarbonate for sodium-channel blockade.

  2. B. Intravenous sodium bicarbonate with ECG and electrolyte monitoring (Best answer)

    A widened QRS and hypotension suggest sodium-channel blockade; sodium loading and alkalinization can improve conduction and perfusion.

  3. C. Physostigmine solely to reverse delirium (Why this does not fit)

    The conduction abnormality and suspected tricyclic exposure make this an inappropriate isolated-delirium strategy.

  4. D. Procainamide to treat the broad-complex rhythm (Why this does not fit)

    Additional sodium-channel blockade can worsen tricyclic cardiotoxicity. Sodium loading and alkalinization address the demonstrated mechanism.

Takeaway: An apparent antimuscarinic syndrome can contain a life-threatening sodium-channel effect.

Case sources: [1] [4]

Case 9

A delirious patient after an uncertain antihistamine ingestion has dry skin and mydriasis. ECG shows QRS duration of 126 ms. Which finding argues against physostigmine?

Show answer and explanations for case 9

  1. A. The widened QRS suggests an additional conduction-toxic mechanism (Best answer)

    QRS widening changes the risk assessment; the exposure cannot be treated as uncomplicated isolated antimuscarinic delirium.

  2. B. Dry skin proves physostigmine is safe regardless of ECG (Why this does not fit)

    A compatible peripheral sign does not override a cardiac contraindication concern.

  3. C. Mydriasis excludes any sodium-channel blockade (Why this does not fit)

    A drug can produce both antimuscarinic findings and sodium-channel toxicity.

  4. D. Urinary retention requires immediate cholinesterase inhibition in every case (Why this does not fit)

    Supportive measures and cardiac risk assessment take precedence over automatically reversing one symptom.

Takeaway: Evaluate the ECG and exposure context before considering physostigmine.

Case sources: [4]

Case 10

A worker exposed to an organophosphate insecticide develops tearing, diarrhea, copious respiratory secretions and fasciculations. Which paired treatment strategy is appropriate while respiratory support proceeds?

Show answer and explanations for case 10

  1. A. Naloxone alone because both syndromes can have small pupils (Why this does not fit)

    Opioid reversal does not address bronchorrhea, diarrhea and fasciculations from excess acetylcholine.

  2. B. Pralidoxime only after all atropine dosing has been completed (Why this does not fit)

    The therapies can be coordinated early; waiting for a fixed completed atropine sequence can lose time before aging.

  3. C. Flumazenil plus charcoal before airway support (Why this does not fit)

    These choices do not target the organophosphate mechanism and would delay immediate respiratory care.

  4. D. Atropine for muscarinic effects and early pralidoxime when indicated for enzyme reactivation (Best answer)

    The secretions and neuromuscular findings reflect different consequences of acetylcholinesterase inhibition and need complementary treatment.

Takeaway: Treat muscarinic and nicotinic toxicity concurrently with resuscitation.

Case sources: [1] [19] [34]

Case 11

During treatment of organophosphate poisoning, a patient remains hypoxic with copious bronchial secretions despite some increase in heart rate. Which finding should guide further atropine titration most directly?

Show answer and explanations for case 11

  1. A. A fixed total dose regardless of examination (Why this does not fit)

    Organophosphate atropine requirements vary; ongoing pulmonary findings guide treatment.

  2. B. Normalization of serum acetylcholinesterase before any additional dose (Why this does not fit)

    Clinical resuscitation should not wait for a laboratory value to normalize.

  3. C. Pulmonary secretions, air entry and oxygenation (Best answer)

    The dangerous muscarinic pulmonary effects are key clinical endpoints; a faster pulse alone does not establish adequate treatment.

  4. D. Pupil dilation alone (Why this does not fit)

    Pupil size can lag or reflect local exposure and is not a sufficient pulmonary treatment endpoint.

Takeaway: Treat the lungs rather than chasing a pupil or pulse target alone.

Case sources: [1] [19]

Case 12

A patient with organophosphate poisoning is being considered for pralidoxime. Why does early administration matter?

Show answer and explanations for case 12

  1. A. Progressive depletion of pralidoxime from the body before the first dose (Why this does not fit)

    The timing issue concerns chemical stabilization of the inhibited enzyme, not elimination of an antidote that has not been given.

  2. B. Aging can make the phosphorylated enzyme complex resistant to reactivation (Best answer)

    Pralidoxime can reactivate susceptible inhibited enzyme before this chemical change; timing depends on the specific exposure.

  3. C. Delayed muscarinic receptor downregulation that prevents atropine binding (Why this does not fit)

    Aging describes the phosphorylated cholinesterase complex; it does not change atropine's receptor target.

  4. D. Irreversible nicotinic receptor destruction by the oxime (Why this does not fit)

    Pralidoxime targets inhibited cholinesterase. It does not work by destroying nicotinic receptors.

Takeaway: Enzyme aging explains urgency without inventing one universal time cutoff.

Case sources: [19]

Case 14

A patient has taken excessive acetaminophen doses for three days for dental pain and now has increased aminotransferases. The last dose was two hours ago. Why is plotting the concentration on the acute-ingestion nomogram inappropriate?

Show answer and explanations for case 14

  1. A. The nomogram is valid only when the patient has jaundice (Why this does not fit)

    Jaundice is not required for the acute nomogram; the repeated dosing pattern is the problem.

  2. B. A two-hour interval since the last dose converts three days of dosing into a single ingestion (Why this does not fit)

    The last dose does not erase earlier exposure or redefine it as a reliably timed acute event.

  3. C. Increased aminotransferases prove acetylcysteine can no longer help (Why this does not fit)

    Acetylcysteine may remain beneficial after injury has begun; abnormal tests do not make treatment futile.

  4. D. Repeated supratherapeutic ingestion does not fit the nomogram's timing assumptions (Best answer)

    Assessment instead uses the exposure pattern, acetaminophen concentration and liver injury findings to guide acetylcysteine.

Takeaway: Repeated ingestion needs its own assessment rather than a forced nomogram plot.

Case sources: [2]

Case 15

A patient after suspected methanol ingestion has blurred vision, severe anion-gap acidosis and worsening mental status. Fomepizole is started. What additional action is warranted?

Show answer and explanations for case 15

  1. A. Exclude methanol if the osmol gap has fallen (Why this does not fit)

    As parent methanol is metabolized, the osmol gap may fall despite worsening metabolite toxicity.

  2. B. Substitute activated charcoal for extracorporeal treatment (Why this does not fit)

    Charcoal does not effectively address this toxic alcohol burden or its severe systemic consequences.

  3. C. Arrange urgent hemodialysis assessment and treatment (Best answer)

    New visual deficits and severe clinical toxicity are dialysis indications; blocking further metabolism does not eliminate existing toxic metabolites.

  4. D. Wait for fomepizole to immediately reverse all visual injury (Why this does not fit)

    Fomepizole prevents further metabolite formation but does not guarantee rapid reversal of established injury.

Takeaway: Methanol-associated visual injury calls for elimination treatment as well as enzyme blockade.

Case sources: [6] [20] [34]

Case 16

After suspected antifreeze ingestion, a patient has severe metabolic acidosis, hypocalcemia, calcium oxalate crystalluria and stage 3 acute kidney injury. Which treatment pair is most appropriate?

Show answer and explanations for case 16

  1. A. Fomepizole alone with serial laboratory reassessment (Why this does not fit)

    Metabolism blockade is needed, but stage 3 AKI is already a clinical indication for extracorporeal treatment.

  2. B. Fomepizole and urgent hemodialysis (Best answer)

    The pattern supports ethylene glycol toxicity with severe renal injury; preventing metabolism and extracorporeal treatment address different needs.

  3. C. Hemodialysis without continued alcohol-dehydrogenase inhibition (Why this does not fit)

    Dialysis addresses existing toxin/metabolites; continued antidotal blockade, adjusted for dialysis, limits further toxic metabolism.

  4. D. Bicarbonate and calcium replacement without antidote or dialysis (Why this does not fit)

    Supportive correction does not stop toxic metabolism or meet the elimination need created by severe renal injury.

Takeaway: Severe renal injury distinguishes this exposure from uncomplicated early toxic-alcohol ingestion.

Case sources: [7] [20]

Case 17

A patient presents late after a credible toxic-alcohol exposure with marked anion-gap acidosis but a normal osmol gap. Which interpretation is best?

Show answer and explanations for case 17

  1. A. A normal osmol gap does not exclude poisoning after parent alcohol has been metabolized (Best answer)

    Toxic acidic metabolites may predominate later, so clinical findings and targeted testing remain essential.

  2. B. Normal osmol gap rules out both methanol and ethylene glycol at every time point (Why this does not fit)

    This ignores the changing parent-alcohol and metabolite concentrations over time.

  3. C. The anion gap must be an analyzer error because the osmol gap is normal (Why this does not fit)

    The gaps measure different phenomena and can diverge during metabolism.

  4. D. Dialysis decisions should use one shared threshold for every toxic alcohol (Why this does not fit)

    EXTRIP recommendations differ by poison, antidote and clinical severity.

Takeaway: Interpret gaps as time-dependent findings, not binary exclusion tests.

Case sources: [6] [7] [20]

Case 18

A patient with tinnitus and vomiting after aspirin exposure has pH 7.46, PCO2 22 mm Hg, bicarbonate 15 mmol/L and an anion gap of 23 mmol/L. Which interpretation best fits?

Show answer and explanations for case 18

  1. A. Isolated chronic respiratory alkalosis with renal compensation (Why this does not fit)

    Renal compensation can lower bicarbonate, but the increased anion gap and acute salicylate syndrome support an additional metabolic acidosis.

  2. B. Isolated anion-gap metabolic acidosis with appropriate respiratory compensation (Why this does not fit)

    Winter's estimate is 1.5 × 15 + 8 = 30.5 mm Hg, approximately 28.5 to 32.5. The measured PCO2 of 22 is lower, indicating an additional respiratory alkalosis.

  3. C. Anion-gap metabolic acidosis with superimposed respiratory acidosis (Why this does not fit)

    A superimposed respiratory acidosis would produce PCO2 above expected compensation; it is substantially below expected here.

  4. D. Respiratory alkalosis with anion-gap metabolic acidosis (Best answer)

    The PCO2 is lower than expected compensation for the low bicarbonate, indicating an additional primary respiratory alkalosis.

Takeaway: Check compensation and the anion gap rather than reading pH alone.

Case sources: [25]

Case 19

A patient with salicylate concentration of 65 mg/dL develops confusion despite bicarbonate therapy. What is the best escalation?

Show answer and explanations for case 19

  1. A. Stop treatment if the next concentration is slightly lower (Why this does not fit)

    A falling serum value does not independently establish improving tissue toxicity or neurologic safety.

  2. B. Increase sedation to suppress hyperventilation while awaiting the next level (Why this does not fit)

    Suppressing respiratory compensation can worsen acidemia. New confusion in salicylate poisoning warrants urgent elimination assessment.

  3. C. Urgent hemodialysis while continuing appropriate supportive treatment (Best answer)

    Altered mental status is a severity-based dialysis indication even below the highest concentration threshold.

  4. D. Continue bicarbonate alone until the concentration exceeds 100 mg/dL (Why this does not fit)

    Waiting for a numerical threshold disregards a current clinical indication for dialysis.

Takeaway: Clinical deterioration can outweigh a concentration-based shortcut.

Case sources: [5]

Case 20

A patient taking dapsone has cyanosis and dyspnea. Pulse oximetry remains 85% on oxygen, arterial PO2 is normal and blood appears dark brown. Which test best resolves the discrepancy?

Show answer and explanations for case 20

  1. A. An arterial blood gas that calculates saturation from PO2 alone (Why this does not fit)

    Calculated saturation assumes normal hemoglobin. Co-oximetry directly measures abnormal hemoglobin fractions and resolves this discrepancy.

  2. B. Co-oximetry measuring methemoglobin (Best answer)

    The findings suggest dysfunctional hemoglobin despite preserved dissolved oxygen; co-oximetry identifies the abnormal hemoglobin fraction.

  3. C. Repeat standard pulse oximetry alone until it becomes normal (Why this does not fit)

    Ordinary pulse oximetry cannot reliably quantify methemoglobin and does not resolve the mechanism.

  4. D. Use arterial PO2 alone to exclude any oxygen-transport problem (Why this does not fit)

    PO2 measures dissolved oxygen, not whether hemoglobin carries oxygen normally.

Takeaway: Normal dissolved oxygen does not prove normal hemoglobin function.

Case sources: [8] [28] [29] [30]

Case 21

A patient with symptomatic methemoglobinemia has known G6PD deficiency. Which treatment warning is essential?

Show answer and explanations for case 21

  1. A. Methylene blue is contraindicated because of hemolysis risk and impaired reducing capacity (Best answer)

    G6PD deficiency limits the NADPH-dependent reduction pathway and increases concern for hemolysis; specialist alternatives are needed.

  2. B. G6PD deficiency guarantees an enhanced response to methylene blue (Why this does not fit)

    The biochemical limitation reduces reliable effectiveness rather than improving it.

  3. C. Higher methylene blue doses always overcome the deficiency safely (Why this does not fit)

    Dose escalation does not erase the contraindication or hemolysis risk.

  4. D. A normal arterial PO2 means symptomatic methemoglobinemia never needs treatment (Why this does not fit)

    Dissolved oxygen can be normal while hemoglobin-mediated oxygen delivery is impaired.

Takeaway: Antidote selection can depend on the patient's reducing pathways.

Case sources: [8]

Case 22

After an enclosed-space fire, a patient has soot in the mouth, hypotension, altered mental status and lactate of 14 mmol/L. Carboxyhemoglobin is 8% after high-concentration oxygen. Which decision is most appropriate?

Show answer and explanations for case 22

  1. A. Exclude cyanide because carboxyhemoglobin is only 8% (Why this does not fit)

    Carboxyhemoglobin measures a different toxic exposure and has already been affected by oxygen therapy.

  2. B. Wait for a confirmatory cyanide concentration before any antidote (Why this does not fit)

    Rapid confirmatory testing is often unavailable, and delay can be dangerous in a compelling severe presentation.

  3. C. Assume the lactate proves cyanide is the sole cause (Why this does not fit)

    Lactate supports concern but is not specific; hypoperfusion and coexisting injuries can contribute.

  4. D. Treat suspected cyanide toxicity with hydroxocobalamin while continuing resuscitation and CO assessment (Best answer)

    The exposure and severe findings support empiric treatment; the postoxygen CO result neither excludes earlier CO toxicity nor explains away cyanide concern.

Takeaway: Smoke poisoning may involve both impaired transport and impaired cellular oxygen use.

Case sources: [15] [3]

Case 23

Two people from the same poorly ventilated room develop headache and confusion. Standard pulse oximetry is 99%. What is the best next oxygen-related assessment and treatment?

Show answer and explanations for case 23

  1. A. Wait outdoors without evaluation because all symptoms resolve immediately (Why this does not fit)

    Neurologic symptoms warrant assessment; leaving the source is necessary but does not establish recovery.

  2. B. Use a normal arterial PO2 alone to rule out poisoning (Why this does not fit)

    Dissolved oxygen may be preserved despite impaired oxygen carriage and delivery.

  3. C. Provide high-concentration oxygen and measure carboxyhemoglobin with co-oximetry (Best answer)

    The shared exposure suggests CO; a normal ordinary pulse oximeter reading does not exclude it.

  4. D. Exclude CO because the pulse oximeter is normal (Why this does not fit)

    Standard pulse oximetry cannot reliably distinguish oxyhemoglobin from carboxyhemoglobin.

Takeaway: Choose the test that measures abnormal hemoglobin, not merely dissolved oxygen.

Case sources: [3]

Case 24

A patient with metoprolol poisoning remains bradycardic and hypotensive despite initial stabilization and vasopressor support. Which therapy is recommended for persistent life-threatening hypotension?

Show answer and explanations for case 24

  1. A. Use glucagon alone before considering further circulatory support (Why this does not fit)

    Glucagon is a reasonable adjunct, but it has variable efficacy and should not delay indicated treatment of vasopressor-refractory hypotension.

  2. B. High-dose insulin with protocolized glucose and potassium monitoring (Best answer)

    Insulin can support myocardial function in severe beta-blocker poisoning; monitoring addresses predictable metabolic complications.

  3. C. Use intravenous calcium as the sole additional treatment (Why this does not fit)

    Calcium may be reasonable in selected beta-blocker poisoning, but high-dose insulin is the recommended therapy for this persistent hypotension after vasopressors.

  4. D. Use intravenous lipid emulsion as the routine next treatment (Why this does not fit)

    The AHA considers its usefulness uncertain in refractory beta-blocker shock. The stated high-dose-insulin recommendation is better supported.

Takeaway: High-dose insulin treats poisoned myocardial function, with active metabolic monitoring.

Case sources: [1]

Case 25

A patient after sotalol overdose has bradycardia and a markedly prolonged QT interval. Which additional mechanism distinguishes sotalol from a purely beta-receptor-blocking drug?

Show answer and explanations for case 25

  1. A. Potassium-channel effects that prolong repolarization (Best answer)

    Sotalol's class III activity explains QT prolongation and torsades risk in addition to beta-blockade.

  2. B. Fast sodium-channel blockade slowing ventricular depolarization (Why this does not fit)

    That would primarily widen QRS and can occur with some other beta-blockers, especially propranolol. Sotalol's class III action prolongs repolarization.

  3. C. L-type calcium-channel blockade slowing AV conduction (Why this does not fit)

    Calcium-channel inhibition can slow nodal conduction, but it is not sotalol's class III mechanism underlying prolonged QT.

  4. D. Inhibition of the sodium-potassium ATPase (Why this does not fit)

    That is the cardiac glycoside target, not sotalol's potassium-channel repolarization effect.

Takeaway: QRS widening and QT prolongation point to different electrical mechanisms.

Case sources: [21] [1]

Case 26

A patient after a large isoniazid ingestion has recurrent seizures despite initial benzodiazepine treatment and airway support. Which specific therapy addresses the metabolic mechanism?

Show answer and explanations for case 26

  1. A. Fomepizole (Why this does not fit)

    Alcohol dehydrogenase inhibition does not restore the cofactor needed for GABA synthesis here.

  2. B. Protamine (Why this does not fit)

    Protamine binds heparin and has no role in correcting isoniazid-associated cofactor depletion.

  3. C. Flumazenil (Why this does not fit)

    Benzodiazepine antagonism could undermine seizure treatment and does not correct the isoniazid mechanism.

  4. D. Pyridoxine (Best answer)

    Replacement supports pyridoxal phosphate-dependent GABA synthesis impaired by isoniazid toxicity.

Takeaway: Refractory isoniazid seizures require the missing cofactor as well as seizure support.

Case sources: [9] [31]

Case 27

A postoperative patient has major bleeding during an unfractionated heparin infusion. The infusion is stopped. Which antidote and mechanism are appropriate?

Show answer and explanations for case 27

  1. A. Four-factor PCC to replace depleted vitamin K-dependent factors (Why this does not fit)

    That replacement strategy is used for warfarin-associated major bleeding; it does not directly neutralize the active heparin infusion.

  2. B. Idarucizumab to bind the anticoagulant (Why this does not fit)

    Idarucizumab specifically binds dabigatran, not unfractionated heparin.

  3. C. Protamine, which binds heparin through opposite electrical charges (Best answer)

    Protamine neutralizes recent heparin exposure; dosing and slow administration require attention to avoid additional harm.

  4. D. Vitamin K to restore hepatic coagulation-factor synthesis (Why this does not fit)

    Vitamin K is used for vitamin K antagonists. Heparin acts through antithrombin and is neutralized by protamine.

Takeaway: Direct heparin neutralization differs from replacing vitamin K-dependent factors.

Case sources: [10] [11]

Case 29

A child with a confirmed iron-tablet ingestion develops severe vomiting followed by hypotension and metabolic acidosis. Which specific antidote should be considered with intensive supportive care?

Show answer and explanations for case 29

  1. A. Deferoxamine (Best answer)

    Systemic iron toxicity can require chelation with deferoxamine in addition to resuscitation.

  2. B. Activated charcoal as the sole definitive treatment (Why this does not fit)

    Charcoal does not reliably bind iron and cannot replace treatment of systemic toxicity.

  3. C. Succimer as the routine acute iron antidote (Why this does not fit)

    Succimer is used for selected other metals, particularly lead, rather than standard acute iron reversal.

  4. D. Calcium disodium EDTA (Why this does not fit)

    This chelator has a role in lead poisoning, not as the standard antidote for systemic acute iron toxicity.

Takeaway: Match chelation to the metal and systemic severity.

Case sources: [12] [18] [33] [34]

Case 30

A child with a very high blood lead concentration develops encephalopathy. The team plans specialist-directed inpatient chelation. Which preparation distinction is essential?

Show answer and explanations for case 30

  1. A. All products labeled EDTA are clinically interchangeable (Why this does not fit)

    Their calcium content and associated risks differ, making this substitution dangerous.

  2. B. Oral succimer alone is always sufficient for encephalopathy (Why this does not fit)

    Severe neurologic lead toxicity requires inpatient specialist-directed treatment, often parenteral combinations.

  3. C. Exposure remediation can wait indefinitely once chelation starts (Why this does not fit)

    Continued exposure can undermine treatment and must be addressed along with chelation.

  4. D. Calcium disodium EDTA must not be confused with disodium EDTA (Best answer)

    Disodium EDTA can cause fatal hypocalcemia; the calcium-containing preparation used in lead protocols is different.

Takeaway: Metal chelation requires the correct formulation as well as the correct drug family.

Case sources: [13] [14]

Case 31

A patient with severe digoxin poisoning has ventricular dysrhythmia and hyperkalemia. Which antidote directly binds the responsible cardiac glycoside?

Show answer and explanations for case 31

  1. A. Pyridoxine (Why this does not fit)

    Pyridoxine addresses isoniazid-associated cofactor dysfunction, not digoxin binding.

  2. B. Fomepizole (Why this does not fit)

    Blocking alcohol dehydrogenase does not neutralize digoxin or treat its pump inhibition.

  3. C. Digoxin immune Fab (Best answer)

    Fab binds digoxin and is indicated for life-threatening toxicity; potassium and clinical response need continued monitoring.

  4. D. Protamine (Why this does not fit)

    Protamine binds heparin rather than cardiac glycosides.

Takeaway: Life-threatening glycoside toxicity has a binding antidote.

Case sources: [24]

Case 32

A 42-year-old patient taking sertraline develops agitation, diaphoresis, hyperreflexia and inducible ankle clonus within a day of starting linezolid. Which diagnosis best fits?

Show answer and explanations for case 32

  1. A. Uncomplicated benzodiazepine sedation (Why this does not fit)

    The examination shows neuromuscular excitation and autonomic activation rather than isolated sedation.

  2. B. Serotonin toxicity (Best answer)

    The relevant exposure plus clonus and hyperreflexia with autonomic findings strongly supports serotonin toxicity.

  3. C. Neuroleptic malignant syndrome from dopamine blockade (Why this does not fit)

    No dopamine-blocking exposure is specified, and clonus with hyperreflexia favors serotonin toxicity over typical generalized NMS rigidity.

  4. D. Pure antimuscarinic poisoning (Why this does not fit)

    Dry skin, reduced bowel activity and urinary retention would better support that pattern; sweating and clonus point elsewhere.

Takeaway: Exposure plus clonus is more discriminating than fever alone.

Case sources: [16] [22] [26]

Case 33

Several days after a substantial haloperidol dose increase, a patient develops fever, altered mental status, generalized sustained rigidity and autonomic instability. Which diagnosis is most consistent?

Show answer and explanations for case 33

  1. A. Neuroleptic malignant syndrome (Best answer)

    Dopamine-blocking exposure with the characteristic rigidity and systemic findings supports NMS and requires stopping the drug and urgent care.

  2. B. Serotonin toxicity proven solely by fever (Why this does not fit)

    Fever is nonspecific; the dopamine-blocking exposure and sustained rigidity favor NMS in this stem.

  3. C. Opioid poisoning (Why this does not fit)

    The exposure and generalized rigidity with fever do not fit the usual opioid respiratory-depression pattern.

  4. D. Isolated hypoglycemia without checking glucose (Why this does not fit)

    Glucose should be checked, but that possibility does not explain away this characteristic drug-associated syndrome.

Takeaway: Use drug history and motor findings to separate hyperthermic medication syndromes.

Case sources: [22] [16]

Case 34

A deeply somnolent patient arrives shortly after an uncertain ingestion and cannot protect the airway. Which statement about activated charcoal is correct?

Show answer and explanations for case 34

  1. A. Give charcoal through a nasogastric tube before protecting the airway (Why this does not fit)

    A gastric tube does not protect the airway from aspiration. Stabilization and airway assessment come first.

  2. B. Give an antiemetic and then administer oral charcoal while the patient remains obtunded (Why this does not fit)

    An antiemetic does not restore airway-protective reflexes or remove aspiration risk.

  3. C. Treat every early ingestion with charcoal once an airway is secured (Why this does not fit)

    Airway protection addresses one hazard. Substance, expected adsorption, timing and clinical benefit still determine whether charcoal is appropriate.

  4. D. Do not give charcoal through an unprotected airway; assess whether it is indicated after stabilization (Best answer)

    Aspiration risk and the actual substance matter, and charcoal is not routine for every ingestion.

Takeaway: Stabilization and a favorable risk-benefit assessment come before charcoal.

Case sources: [18] [34]

Case 35

A child with accidental sulfonylurea exposure has recurrent hypoglycemia after initial intravenous dextrose. Which additional treatment targets continued insulin secretion?

Show answer and explanations for case 35

  1. A. Naloxone (Why this does not fit)

    Opioid antagonism does not suppress sulfonylurea-driven pancreatic insulin release.

  2. B. Fomepizole (Why this does not fit)

    Alcohol dehydrogenase inhibition does not address pancreatic secretion caused by a sulfonylurea.

  3. C. Octreotide (Best answer)

    Octreotide suppresses endogenous insulin release and can reduce rebound hypoglycemia while glucose monitoring and replacement continue.

  4. D. Additional dextrose without considering ongoing insulin release or observation (Why this does not fit)

    Glucose is needed to correct lows, but repeated glucose alone may stimulate further insulin secretion and recurrence.

Takeaway: Correct the low glucose and suppress the mechanism causing recurrence.

Case sources: [17]

Sources

  1. AHA 2025 Guidelines: Adult and Pediatric Special Circumstances of Resuscitation (2025)

    Current critical-poisoning recommendations, especially high-dose insulin, vasopressors, sodium bicarbonate, atropine and restricted flumazenil use.

  2. Management of Acetaminophen Poisoning in the US and Canada: A Consensus Statement (2023-08-08)

    Acute ingestion nomogram eligibility, four-hour sampling, repeated ingestion and acetylcysteine continuation criteria.

  3. CDC Clinical Guidance for Carbon Monoxide Poisoning

    CO-oximetry, limits of standard pulse oximetry, effects of elapsed time and oxygen on carboxyhemoglobin, and oxygen treatment.

  4. Utah Poison Control: Physostigmine or Rivastigmine for Anticholinergic Toxicity (2024)

    Antimuscarinic delirium recognition and contraindication concerns including QRS widening and tricyclic ingestion.

  5. EXTRIP: Salicylates

    Dialysis indications based on clinical severity, including altered mental status, and continuation of bicarbonate.

  6. EXTRIP: Methanol

    New visual deficits, coma and severe acidosis as dialysis indications independent of a single concentration threshold.

  7. EXTRIP: Ethylene Glycol

    Dialysis decisions using antidote availability, severe AKI, acidosis and clinical findings; do not transfer methanol thresholds.

  8. PROVAYBLUE methylene blue prescribing information

    Acquired methemoglobinemia treatment, G6PD contraindication, hemolysis and serotonergic interaction warning.

  9. Isoniazid prescribing information

    Isoniazid poisoning and label-specific adult pyridoxine dosing; biochemical GABA explanation is supported by source 31.

  10. Protamine sulfate prescribing information

    Ionic binding of heparin and administration-related hypotension and severe reactions.

  11. 2020 ACC Expert Consensus Decision Pathway: Bleeding in Patients on Oral Anticoagulants (2020)

    Major warfarin-associated bleeding requires rapid factor replacement with four-factor PCC plus vitamin K; plasma if PCC unavailable.

  12. Deferoxamine mesylate prescribing information

    Chelation in clinically significant acute iron poisoning.

  13. ATSDR Medical Management Guidelines: Lead

    Lead exposure control, chelation thresholds, succimer and severe encephalopathy requiring inpatient parenteral chelation.

  14. CDC MMWR: Deaths Associated with Hypocalcemia from Chelation Therapy (2006)

    Calcium disodium EDTA is distinct from disodium EDTA, which can cause fatal hypocalcemia.

  15. CYANOKIT hydroxocobalamin prescribing information

    Suspected cyanide poisoning after enclosed-space smoke exposure, clinical treatment before confirmatory testing and cyanide binding.

  16. The Hunter Serotonin Toxicity Criteria (2003)

    Original derivation study identifying clonus, hyperreflexia and accompanying autonomic findings in serotonergic exposures.

  17. Utah Poison Control Fast Facts: Octreotide (2022-08-17)

    Suppression of endogenous insulin release in sulfonylurea-associated recurrent hypoglycemia and need for observation. Does not adopt the handout's absolute no-side-effects statement.

  18. AACT/EAPCCT Position Statement: Single-Dose Activated Charcoal

    Selective rather than routine charcoal, airway protection and time-dependent expected benefit.

  19. PROTOPAM pralidoxime prescribing information

    Reactivation of phosphorylated cholinesterase before aging, especially peripheral neuromuscular effects, with concomitant atropine.

  20. Fomepizole prescribing information

    Alcohol dehydrogenase inhibition limits formation of toxic methanol and ethylene glycol metabolites.

  21. Sotalol prescribing information

    Class III repolarization effects, QT prolongation and torsades distinction from sodium-channel blockade.

  22. Haloperidol prescribing information

    NMS features including hyperthermia, generalized rigidity, altered mental state and autonomic instability.

  23. Naloxone hydrochloride nasal spray prescribing information

    Emergency assistance, repeated doses and surveillance for recurrent opioid respiratory depression.

  24. DIGIFAB prescribing information

    Fab binding in life-threatening digoxin toxicity and laboratory/monitoring limitations.

  25. ACMT Management Priorities in Salicylate Toxicity (2013-03-13)

    Society guidance approved on the stated date: mixed acid-base disorders, ventilation hazards, alkalinization and potassium replacement.

  26. Linezolid prescribing information

    Reversible monoamine oxidase inhibition and serotonin toxicity with serotonergic co-medication.

  27. Lovenox prescribing information, overdose section

    Protamine provides incomplete reversal of enoxaparin anti-Xa activity; do not generalize unfractionated-heparin reversal.

  28. CDC MMWR: Severe Methemoglobinemia and Hemolytic Anemia from Aniline, Oregon 2011 (2012)

    Primary case report and CDC explanatory text supporting brown blood and pulse oximetry near 85% despite oxygen in methemoglobinemia; no recreational-drug treatment extrapolation.

  29. ATSDR Nitrate/Nitrite Toxicity: Laboratory Tests

    Co-oximetry and saturation-gap interpretation; a normal dissolved oxygen value cannot exclude abnormal hemoglobin. Archived official educational resource.

  30. Dapsone tablets prescribing information

    Oral dapsone can increase methemoglobin and cause dose-related hemolysis, greater with G6PD deficiency.

  31. Maryland Poison Center: Pyridoxine Antidote Facts (2018)

    Pyridoxal phosphate as a cofactor in glutamate-to-GABA conversion; pyridoxine antidotal mechanism. Dose details in teaching are attributed separately to the isoniazid label.

  32. Sodium thiosulfate injection prescribing information

    Sulfur donation for rhodanese-mediated conversion of cyanide to thiocyanate; clinical adjunct selection is separately paired with AHA 2025.

  33. Royal Children's Hospital Clinical Practice Guideline: Iron poisoning

    Official pediatric guideline on the latent phase after initial gastrointestinal symptoms and clinical assessment before chelation.

  34. Clinical Toxicology Recommendations Collaborative: Activated charcoal in acute oral overdose (2026-03-30)

    Original 2026 society recommendations, full abstract read: no charcoal role for methanol, ethylene glycol or iron; individualized timing and airway risk assessment.

Return to lesson title

Search Bone Wizardry

Quick links
↑ ↓ Navigate Enter Open Esc CloseBrowse the library ↗