The Daily Differential — Sunday, April 19, 2026

2 of 5

Carbon Monoxide Poisoning

Carbon monoxide (CO) poisoning is common, easy to miss, and can be fatal or cause delayed neurocognitive injury. Pulse oximetry can be misleadingly normal,...

At the Bedside

Suspect CO in: headache, dizziness, nausea, malaise, syncope, confusion, chest pain, or multiple patients from the same environment; consider house fires, heaters, generators, garage exposure.
Key exam findings: nonspecific neurologic findings, tachycardia, altered mental status; “cherry red skin” is rare and not reliable.
Testing:
Carboxyhemoglobin (COHb) by co-oximetry on venous or arterial blood.
Normal pulse ox does not exclude CO poisoning.
ECG and troponin if symptomatic, older patient, or concern for ischemia.
Consider lactate, CMP, CBC; pregnancy test when relevant.
Initial management:
Remove from exposure and give 100% oxygen immediately.
Monitor cardiac rhythm and mental status.
Treat co-exposures from smoke inhalation as indicated (cyanide, airway injury).
Hyperbaric oxygen (HBO) considerations:
Indications vary, but commonly include: loss of consciousness, persistent neurologic deficits, significant cardiac ischemia, severe acidosis, pregnancy with symptomatic exposure, or very high COHb levels.
Do not delay high-flow oxygen while arranging transfer.
Disposition:
Mild, asymptomatic, improving patients may be discharged after symptom resolution, normal exam, and safe environment.
Admit/transfer for neurologic symptoms, ischemia, pregnancy, severe exposure, or need for HBO.

A Classic Presentation

A family of four presents from a cabin with headaches, nausea, and dizziness after running a propane heater overnight. One child is confused and tachycardic. Pulse oximetry reads 99% on room air, but co-oximetry shows elevated carboxyhemoglobin. All patients are placed on 100% oxygen, ECG and troponin are obtained, and the confused child is transferred for hyperbaric consultation.

Study Directive

Memorize the common exposure clues: garages, heaters, house fires, generators.
Practice interpreting a CO poisoning workup: pulse ox, co-oximetry, ECG, troponin, lactate.
Write out your HBO consultation triggers from memory.
Review the difference between CO poisoning vs smoke inhalation vs cyanide toxicity.

Key Medications

Oxygen: 100% via nonrebreather or endotracheal tube if needed; use the highest FiO2 feasible.
There is no antidote other than oxygen; HBO protocols vary by center—check local hyperbaric medicine guidance.

High-Yield Pearls

Pulse ox lies: It cannot distinguish oxyhemoglobin from carboxyhemoglobin.
Neuro/cardiac injury matter most: symptoms and end-organ effects guide severity more than the COHb number alone.
Pregnancy increases risk: fetal hemoglobin binds CO strongly, and fetal elimination is slower.

Board Question

Which statement about carbon monoxide poisoning is most accurate?

ANormal pulse oximetry excludes the diagnosis
BCarboxyhemoglobin is best measured by standard pulse oximetry
C100% oxygen is the initial treatment
DCherry red skin is a sensitive diagnostic finding

Reveal answer

Correct: C

The immediate treatment is high-flow 100% oxygen, which accelerates CO elimination. Standard pulse oximetry can be normal despite significant poisoning, and cherry red skin is rarely seen.

Recent Literature

Review or guideline Carbon Monoxide Poisoning: Pathogenesis, Management, and Future Directions of Therapy
Am J Respir Crit Care Med, 2017 · cited 811×
Recent clinical Suicide by Inhalation of Carbon Monoxide Produced by Mixing Formic Acid and Sulfuric Acid: Case Report and Review of the Literature
Am J Forensic Med Pathol, 2026

3 of 5

Cyanide Toxicity and Poisoning

Cyanide poisoning can cause rapid cardiovascular collapse and death, especially after smoke inhalation or industrial exposure. It causes cellular hypoxia...

At the Bedside

When to suspect:
House fire/smoke inhalation, enclosed-space fires, industrial exposure, ingestion of cyanide salts, certain chemicals.
Sudden collapse, severe neurologic symptoms, hypotension, seizure, cardiac arrest, or profound lactic acidosis.
Pathophysiology clue: Blocks cytochrome oxidase in the electron transport chain → cells cannot use oxygen → anaerobic metabolism and lactic acidosis.
Testing:
Diagnosis is largely clinical; cyanide levels are rarely rapidly available and should not delay treatment.
Very high lactate is a major clue in smoke inhalation or toxic exposure.
ABG/VBG, lactate, ECG, CMP, co-oximetry; consider coexisting CO poisoning.
Initial management:
Remove from exposure, give oxygen, support airway/breathing/circulation.
Aggressive fluid resuscitation and vasopressors as needed.
Early toxicology/poison center consultation.
Antidotal therapy:
Preferred in many settings: Hydroxocobalamin.
Other regimens exist, but hydroxocobalamin is common in smoke inhalation because it avoids inducing methemoglobinemia.
Disposition:
ICU for significant exposure, acidosis, hypotension, neurologic symptoms, or antidote administration.
Observe only if minimal exposure and fully asymptomatic with reassuring workup.

A Classic Presentation

A 42-year-old woman is rescued from a house fire with soot in her nares, confusion, hypotension, and a lactate of 14 mmol/L. Co-oximetry shows elevated carboxyhemoglobin, but her shock seems out of proportion to the CO level. The team gives 100% oxygen, intubates for airway protection, and administers hydroxocobalamin for suspected cyanide toxicity.

Study Directive

Memorize the classic smoke inhalation toxic bundle: CO + cyanide + airway injury.
Build a mental trigger list for hydroxocobalamin indications.
Practice differentiating cyanide vs CO vs methemoglobinemia using oxygenation and lactate patterns.
Review how hydroxocobalamin interferes with lab assays and why that matters in the ED.

Key Medications

Hydroxocobalamin: 5 g IV over ~15 minutes; may repeat 5 g once if needed. It can discolor skin/urine and interfere with some lab tests.
Sodium thiosulfate: dosing varies by protocol; commonly used as adjunct in some regimens. Check toxicology/institutional reference if used.
Sodium nitrite: generally avoided in smoke inhalation or significant CO co-exposure because it induces methemoglobinemia and worsens oxygen delivery.

High-Yield Pearls

Think cellular asphyxiation: cyanide prevents oxygen utilization, not oxygen delivery.
Lactate is a clue: marked lactic acidosis is a major bedside red flag.
Treat empirically when high-risk: do not wait for confirmatory cyanide levels.

Board Question

A patient rescued from an enclosed-space house fire has severe lactic acidosis and hypotension. Which treatment is most appropriate?

ASodium nitrite first
BHydroxocobalamin
CFlumazenil
DFomepizole

Reveal answer

Correct: B

Hydroxocobalamin is the preferred empiric antidote for suspected cyanide poisoning, especially in smoke inhalation. Sodium nitrite can worsen oxygen delivery by causing methemoglobinemia and is less desirable in this setting.

Recent Literature

Review or guideline 2023 American Heart Association Focused Update on the Management of Patients With Cardiac Arrest or Life-Threatening Toxicity Due to Poisoning: An Update to the American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Circulation, 2023 · cited 144×
Recent clinical Recommendations from the Clinical Toxicology Recommendations Collaborative on the administration of activated charcoal in acute oral overdose
Clin Toxicol (Phila), 2026

Full text · open access

4 of 5

Dieting Agents - DNP, Diuretics, and Thyroid Supplements

Misuse of dieting agents can cause life-threatening hyperthermia, arrhythmias, electrolyte derangements, and endocrine crises. These exposures are often...

At the Bedside

DNP (2,4-dinitrophenol):
Uncouples oxidative phosphorylation → extreme heat generation, tachycardia, diaphoresis, acidosis, rhabdomyolysis, multiorgan failure.
Suspect with severe hyperthermia and a history of online weight-loss products.
Diuretics abuse:
Common in eating disorders/weight cutting.
Findings: dehydration, orthostasis, hypokalemia, hyponatremia, metabolic alkalosis, AKI, arrhythmia risk.
Thyroid supplement/thyrotoxicosis from supplements:
Exogenous T3/T4 or adulterated “thyroid support” products can cause tachycardia, tremor, anxiety, diarrhea, weight loss, heat intolerance.
Severe cases can progress to thyroid storm.
Workup:
Vital signs, temperature, ECG.
CMP, Mg, Phos, CK, renal function, VBG/ABG if severe, lactate if ill.
TSH and free T4/T3 if thyrotoxicosis suspected.
Urinalysis for dehydration/rhabdo; pregnancy test as appropriate.
Initial management:
DNP hyperthermia: aggressive cooling, sedation, IV fluids, treat rhabdo, ICU.
Diuretic abuse: volume repletion, electrolyte correction, cardiac monitoring if severe hypokalemia/QT issues.
Thyroid excess: beta-blockade, supportive care, treat precipitating causes; consider thyroid storm pathway if severely ill.
Disposition:
DNP exposures generally require ICU.
Significant electrolyte abnormalities, arrhythmias, or inability to ensure safe follow-up warrant admission.
Psychiatric/eating disorder assessment may be needed.

A Classic Presentation

A 24-year-old man arrives with a temperature of 41.2°C, tachycardia, diaphoresis, and confusion after taking an online “fat burner” for weight loss. Labs show metabolic acidosis and elevated CK. He is aggressively cooled, given IV fluids, and admitted to the ICU for suspected DNP toxicity.

Study Directive

Make a 3-column comparison of DNP vs diuretic abuse vs thyroid supplement toxicity: mechanism, vital sign pattern, labs.
Practice a hyperthermia algorithm and identify where toxicologic hyperthermia fits.
Review the electrolyte patterns of diuretic abuse and how they affect ECG.
Memorize when to use beta-blockade in thyrotoxicosis and when to escalate to thyroid storm care.

Key Medications

Active cooling and IV fluids are core therapy for DNP; there is no proven antidote.
Propranolol for symptomatic thyrotoxicosis: 10–40 mg PO every 6–8 hours if stable; IV dosing for thyroid storm is protocol-dependent.
Esmolol infusion may be used in severe thyrotoxicosis/thyroid storm; dosing varies widely—check protocol/reference.
Potassium repletion: dose depends on severity/route; use institutional protocol and telemetry for significant deficits.
Magnesium sulfate if torsades/QT issues or severe deficiency: standard ED dosing often 1–2 g IV.
Thionamides are for endogenous thyroid hormone overproduction; exogenous thyroid ingestion may respond less predictably—consult endocrinology/toxicology.

High-Yield Pearls

DNP = dangerous hyperthermia: think “metabolic furnace.”
Diuretic abuse often hides in eating disorders: check electrolytes and ECG.
Thyroid supplements are not benign: exogenous hormone can mimic thyroid storm.

Board Question

Which dieting agent is most associated with severe hyperthermia due to uncoupling of oxidative phosphorylation?

AFurosemide
BLevothyroxine
CDNP
DOrlistat

Reveal answer

Correct: C

DNP is a classic uncoupler of oxidative phosphorylation, producing profound heat generation, acidosis, and rhabdomyolysis. This is a medical emergency requiring rapid cooling and ICU-level care.

5 of 5

Dieting Agent - Stimulant Toxicity and Poisoning

Weight-loss stimulants and “energy” supplements can cause sympathomimetic toxicity, hyperthermia, arrhythmias, agitation, and seizures. Many products are...

At the Bedside

Common agents: caffeine, ephedra-like compounds, synephrine, yohimbine, amphetamine-like adulterants, “fat burners,” pre-workout supplements.
Presentation: agitation, anxiety, tremor, tachycardia, hypertension, mydriasis, diaphoresis, chest pain, hyperthermia, psychosis, seizures.
Workup:
Vitals including core temperature.
ECG for tachyarrhythmias, ischemia, QT/QRS issues.
Glucose, electrolytes, CK, creatinine, troponin if chest pain, pregnancy test when relevant.
Consider co-ingestants and serotonin syndrome if serotonergic symptoms are present.
Management:
Sedation is key: benzodiazepines first-line.
IV fluids, cooling if hyperthermic, treat rhabdomyolysis.
Avoid pure beta-blocker monotherapy in severe sympathomimetic toxicity; use caution with ischemia and consult toxicology.
If chest pain/vasospasm, manage as stimulant-associated ischemia; nitroglycerin may help selected patients.
Disposition:
Discharge only if symptoms fully resolve, vitals normalize, and no end-organ injury.
Admit for hyperthermia, rhabdo, chest pain/ischemia, persistent agitation, seizures, or significant arrhythmias.

A Classic Presentation

A 31-year-old woman presents with severe anxiety, tachycardia, and chest tightness after taking multiple “pre-workout” scoops plus an over-the-counter weight-loss pill. She is hypertensive, diaphoretic, and tremulous with sinus tachycardia on ECG. She improves after repeated lorazepam doses, IV fluids, and observation; troponin is negative and symptoms resolve.

Study Directive

Build a sympathomimetic toxidrome checklist from memory.
Practice distinguishing stimulant toxicity vs anticholinergic vs serotonin syndrome.
Review your ED’s preferred benzodiazepine choices and repeat-dosing strategy for agitation.
Write a one-line social history prompt that asks about pre-workout, weight-loss pills, and energy supplements.

Mechanism Pearl of the Day: Several topics today are fundamentally about oxygen and energy failure: CO prevents oxygen carriage, cyanide prevents oxygen utilization, DNP forces energy to be lost as heat by uncoupling oxidative phosphorylation, and stimulants/thyroid excess increase metabolic demand until supply fails. In toxicology, always ask whether the problem is delivery, utilization, or demand.

Key Medications

Lorazepam: 1–2 mg IV/PO/IM, repeat as needed; titrate to effect.
Diazepam: 5–10 mg IV, repeat as needed.
Midazolam: 2–5 mg IV/IM/IN, repeat as needed; often useful for severe agitation.
Nitroglycerin for stimulant chest pain/vasospasm: dosing depends on formulation; use standard ACS/chest pain protocols if BP allows.
Active cooling for hyperthermia; no antidote for most stimulant products.

High-Yield Pearls

Sedation treats the syndrome: calming the CNS lowers catecholamine-driven toxicity.
Measure temperature: hyperthermia is a major predictor of severe poisoning.
Ask specifically about supplements: “fat burners” and pre-workouts are often underreported unless directly queried.

Board Question

First-line treatment for agitation and tachycardia in stimulant toxicity is:

AHaloperidol alone
BBenzodiazepines
CPropranolol monotherapy
DPhysostigmine

Reveal answer

Correct: B

Benzodiazepines are first-line because they reduce central sympathetic outflow, agitation, and seizure risk. Pure beta-blockade is not preferred as initial monotherapy in stimulant toxicity.

Recent Literature

Recent clinical Mitigating organophosphate nerve agent, soman (GD), induced long-term neurotoxicity: Saracatinib, a Src Tyrosine Kinase inhibitor, as a potential countermeasure
J Neuroinflammation, 2025 · cited 2×

Full text · open access

TheDaily Differential

Extravasation

At the Bedside

Study Directive

Recent Literature

More in Today's Issue

Carbon Monoxide Poisoning

Cyanide Toxicity and Poisoning

Dieting Agents - DNP, Diuretics, and Thyroid Supplements

Dieting Agent - Stimulant Toxicity and Poisoning

Journal Watch

Paracetamol or Acetaminophen?

Alpha-Gal Syndrome

Podcast Picks

EMCrit 423 – Hyperbaric Therapy for Carbon Monoxide Poisoning?

Case of the Day