Eduovisual
Emergency & Toxicology
Carbon monoxide poisoning: recognition and management
— Binds hemoglobin with ~240× affinity of O₂ → forms carboxyhemoglobin (COHb) → ↓ oxygen-carrying capacity
— Shifts oxyhemoglobin curve leftward → impairs O₂ offloading at tissues
— Binds cytochrome c oxidase → inhibits mitochondrial oxidative phosphorylation (delayed neurologic injury)
— Triggers lipid peroxidation, NO release, neutrophil activation → reperfusion-style CNS injury
— Faulty furnaces, gas water heaters, wood stoves (winter peak, "whole family sick")
— Indoor generators after power outage (hurricanes, ice storms)
— Charcoal grills used indoors, hibachi
— House fires (combine CO + cyanide toxicity + thermal injury)
— Motor vehicle exhaust in enclosed garage (suicide attempt)
— Methylene chloride (paint stripper) — metabolized to CO in liver → delayed/prolonged COHb elevation
— Multiple household members or coworkers with simultaneous headache, nausea, dizziness
— Symptoms improve when away from home/workplace and recur on return
— Pet also acting ill
— Smoke inhalation victim with altered mental status, lactic acidosis, or soot
— Unexplained syncope, seizure, or coma in winter
Board pearl: A patient presenting in winter with "flu-like illness" — headache, nausea, malaise — but no fever and multiple affected household members is CO until proven otherwise. Order a COHb level before sending home; do not anchor on viral syndrome. Pulse oximetry will be falsely normal because standard SpO₂ cannot distinguish COHb from O₂Hb.
— <10%: often asymptomatic (chronic smokers baseline 5–10%)
— 10–20%: headache (most common symptom), mild dyspnea on exertion
— 20–30%: throbbing headache, nausea, vomiting, dizziness, impaired judgment, visual disturbance
— 30–40%: confusion, weakness, tachypnea, tachycardia, syncope
— 40–50%: ataxia, syncope, seizures
— >50%: coma, cardiovascular collapse, death
— "Headache and nausea that improves at work, returns at home"
— Family of four in ED with simultaneous headaches after first cold night with furnace on
— Firefighter pulled from burning building, GCS 10, lactate 8
— Suicide attempt found in running car in closed garage
— Heating source (furnace age, last inspection), generator use, indoor cooking
— Onset relative to environment (home vs work vs car)
— Co-victims (humans AND pets — birds and small mammals fall ill first)
— Recent CO detector alarm ignored
— Methylene chloride exposure (paint/finish stripping) → suspect ongoing endogenous CO production for hours
— Pregnancy status (fetal Hb binds CO even more avidly)
— Smoking status (baseline COHb confounder)
— Cognitive deficits, parkinsonism, personality change, incontinence, gait disorder
— Occurs in 10–30%; risk factors include LOC during exposure, age >36, prolonged exposure
Key distinction: "Cherry-red" skin is a classic but unreliable late/postmortem finding — do not rely on it. Most living CO patients look pale or cyanotic, not cherry-red. Board answers favor headache + altered mentation + normal SpO₂ + elevated COHb, not skin color.
— Tachycardia, tachypnea (compensation for tissue hypoxia)
— Hypotension in severe cases — myocardial depression + vasodilation
— Temperature usually normal (helps differentiate from sepsis/influenza)
— SpO₂ falsely normal — standard 2-wavelength pulse oximetry reads COHb as O₂Hb
— Spectrum: mild HA → confusion → ataxia → seizure → coma
— Cerebellar signs, dysmetria
— Focal deficits mimicking stroke (basal ganglia and white matter most vulnerable)
— Mini-Cog or orientation testing — subtle cognitive deficits common and prognostic
— Retinal hemorrhages (flame-shaped) — severe exposure
— Ischemic-pattern ECG changes even in young patients
— New-onset arrhythmias, hypotension
— Pulmonary edema (cardiogenic from myocardial stunning, or noncardiogenic)
— Tachypnea; if smoke inhalation: soot in airway, singed nasal hairs, hoarseness, stridor → airway threat
— Pale or cyanotic (not cherry-red in vivo)
— Bullae or blistering at pressure points (immobile from coma) — classic
— Rhabdomyolysis from prolonged immobility
— Look for burns, soot, carbonaceous sputum → also consider cyanide co-toxicity
— Persistent lactic acidosis after correcting hypoxia/hypotension is a cyanide red flag
CCS pearl: On exam, order continuous cardiac monitoring, IV access ×2, 100% non-rebreather O₂ immediately, then fingerstick glucose, 12-lead ECG, and a focused neuro exam. Document GCS and any LOC during exposure — these drive disposition and hyperbaric oxygen (HBO) eligibility. Reassess neuro status every 15–30 minutes; subtle deterioration is your trigger to escalate.
— Measured on arterial OR venous blood (venous is acceptable and equivalent for COHb)
— Normal: <3% nonsmokers, <10% smokers
— Level reflects exposure at time of draw — do not delay O₂ therapy to obtain it
— Level decreases rapidly once 100% O₂ started; correct for time/treatment when interpreting
— Reads COHb as oxyhemoglobin → falsely reassuring 98–100%
— Same trap as methemoglobinemia (SpO₂ falsely ~85%)
— PaO₂ is normal (dissolved O₂ unaffected) — another trap
— Calculated O₂ saturation from PaO₂ also misleading; must measure with co-oximeter
— Metabolic acidosis with elevated lactate indicates tissue hypoxia / severe poisoning
— Lactate >10 with smoke inhalation → strong suspicion for concurrent cyanide toxicity
Board pearl: A patient with headache, normal SpO₂ 99%, normal PaO₂ 95 mmHg, but lactate 6 and COHb 32% — the dissolved oxygen is fine; the problem is oxygen delivery and utilization. Always order co-oximetry when CO is on the differential; it is the only blood test that directly measures COHb.
— Half-life on room air: ~4–5 hours
— Half-life on 100% non-rebreather O₂: ~60–90 minutes
— Half-life on hyperbaric O₂ at 2.5–3 ATA: ~20–30 minutes
— Methylene chloride exposure: COHb may continue to rise for hours after removal because liver keeps generating CO endogenously — repeat levels mandatory
— Non-contrast CT head: bilateral globus pallidus hypodensities are classic (delayed finding)
— MRI more sensitive: globus pallidus, hippocampus, subcortical white matter demyelination
— Imaging findings on initial CT predict delayed neurologic sequelae
— May reveal global hypokinesis (CO-induced cardiomyopathy), usually reversible
— Tracks delayed neuropsychiatric syndrome (DNS)
— Useful for return-to-work/school decisions
Key distinction: A normal initial head CT does not rule out delayed neurologic injury. Globus pallidus lesions appear over days. Counsel every moderate-severe CO patient about DNS risk before discharge and arrange neurocognitive follow-up at 1–2 months.
— Intubate if GCS ≤8, airway burns, respiratory failure, or unable to protect airway
— Mechanical ventilation with FiO₂ 1.0
— Mild: headache, nausea, dizziness; COHb <25%; no LOC, no neuro deficits, no cardiac ischemia, normal acid-base
— Moderate: COHb 25–40%, or any neurologic symptoms beyond HA/dizziness, mild metabolic acidosis
— Severe: COHb >40%, LOC, seizure, coma, focal neuro deficit, cardiac ischemia/arrhythmia, pH <7.1, pregnancy with COHb >15–20%, persistent neuro deficits despite NRB
— Mild + asymptomatic after 4–6 hr NRB + COHb <5% + normal exam → discharge with safety counseling
— Moderate → admit for monitoring, continue NRB until COHb <5% and symptoms resolved
— Severe → consider hyperbaric oxygen (HBO) and ICU admission
— LOC at any time during/after exposure
— Neurologic signs (seizure, focal deficit, abnormal cerebellar exam, cognitive impairment)
— Cardiac ischemia (elevated troponin, ischemic ECG)
— COHb >25% (>20% in pregnancy)
— Severe metabolic acidosis (pH <7.1)
— Pregnancy with COHb >15–20% or any fetal distress
— Age >36 with prolonged exposure
— Symptoms persisting after 4–6 hours of normobaric O₂
Step 3 management: Decision to transfer for HBO is a time-critical interfacility transfer decision — call the chamber while resuscitating. Don't withhold normobaric O₂ during transport; continue 100% NRB en route. Document GCS, COHb, troponin, pregnancy status — these drive the receiving team's plan.
— Mechanism: mass-action displacement of CO from hemoglobin; also delivers dissolved O₂ to tissues
— Delivery: non-rebreather mask (NRB) at 15 L/min with reservoir bag inflated, tight seal
— Intubated patients: FiO₂ 1.0, PEEP as needed
— Duration: continue until COHb <5% AND symptoms resolved (minimum 4–6 hours typical for mild cases)
— Do not use nasal cannula or simple face mask — inadequate FiO₂
— 2.5–3.0 ATA for 90–120 minutes, typically 1–3 sessions
— Accelerates CO elimination AND addresses mitochondrial/inflammatory injury
— Reduces incidence of delayed neuropsychiatric sequelae (Weaver trial: 25% → 10% at 6 weeks)
— IV crystalloid for hypotension; avoid over-resuscitation if pulmonary edema present
— Treat seizures with benzodiazepines (lorazepam 2–4 mg IV); avoid phenytoin first-line
— Treat acidosis by improving oxygenation/perfusion, not bicarbonate (lactate clears with O₂)
— Continuous cardiac monitoring; treat arrhythmias per ACLS
— Hydroxocobalamin 5 g IV over 15 min (preferred — binds CN⁻ to form cyanocobalamin, renally excreted)
— Avoid the nitrite component of older cyanide kits (sodium nitrite induces methemoglobinemia → worsens O₂ delivery in CO co-poisoning)
— Sodium thiosulfate is safe adjunct
Board pearl: In a house-fire victim with soot, altered mentation, and lactate >10, give 100% O₂ + hydroxocobalamin empirically. Do not wait for cyanide levels and do not use nitrites. This combination addresses both toxins without worsening oxygen delivery.
— Monoplace chamber: single patient, pressurized with 100% O₂; limits hands-on access
— Multiplace chamber: multiple patients + attendants breathe air, patient breathes O₂ via hood/mask; preferred for critically ill, intubated, or unstable patients
— Pressure: 2.4–3.0 ATA; treatment 90–120 minutes
— Typically 1 session for moderate poisoning; up to 3 within 24 hours for severe
— Tympanic membrane exam — risk of barotrauma; consider myringotomy in obtunded/intubated
— Chest x-ray to rule out pneumothorax (absolute contraindication until chest tube placed — gas expansion on decompression)
— Glucose check (hypoglycemia worsened under pressure in diabetics)
— Remove transdermal patches, jewelry, restricted-airflow materials
— Ensure IV lines, ETT cuff filled with saline not air
— Absolute: untreated pneumothorax
— Relative: severe COPD with bullae, recent ear/sinus surgery, claustrophobia, pregnancy considerations (HBO is actually indicated, not contraindicated, in pregnancy with CO)
— Middle ear barotrauma (most common), sinus squeeze
— Pulmonary O₂ toxicity (rare, dose-related)
— CNS O₂ toxicity → seizures (~1–2%, usually self-limited)
— Reversible myopia
CCS pearl: If your facility lacks a chamber, arrange transfer early but never delay 100% NRB. Stabilize airway, ensure no pneumothorax on CXR, and send copies of COHb trend, ECG, troponin, β-hCG, and neuro exam with the patient. Document the time of last 100% O₂ initiation — receiving team needs it.
— Higher baseline cardiopulmonary disease → less reserve; symptoms appear at lower COHb levels
— Increased risk of myocardial ischemia, arrhythmia, and delayed neuropsychiatric sequelae
— Age >36 with prolonged exposure is itself an HBO indication in some protocols
— More vulnerable to falls and syncope-related injury at presentation — survey for occult trauma
— Higher rate of unrecognized chronic low-level CO exposure from old heating systems → consider home inspection referral
— Cognitive baseline often unclear — obtain collateral from family, prior records; subtle DNS may be missed
— Polypharmacy: review β-blockers (mask tachycardia compensation), anticoagulants (intracranial bleeding risk if fall)
— Does not directly affect CO elimination (CO is exhaled via lungs, not renally cleared)
— Rhabdomyolysis from prolonged immobility can precipitate AKI — aggressive isotonic fluids, monitor CK, K⁺
— Hydroxocobalamin (for concurrent cyanide) is renally excreted but no dose adjustment needed; expect red discoloration of urine and skin for days
— Contrast for neuroimaging — weigh risk; non-contrast CT/MRI usually sufficient
— Methylene chloride exposure: hepatic metabolism produces CO; impaired liver may slow conversion, altering kinetics — still monitor for prolonged COHb elevation
— Coagulopathy increases bleed risk if HBO-related trauma (myringotomy, barotrauma)
— Alcoholic patients: concurrent ethanol/methanol; check anion gap and osmolar gap
Step 3 management: In any elderly CO patient with ischemic ECG changes or troponin elevation, treat as acute coronary syndrome equivalent in terms of monitoring and follow-up — telemetry admission, cardiology input, and outpatient stress imaging once recovered. Long-term mortality is elevated independent of initial COHb.
— Fetal hemoglobin binds CO with higher affinity than adult Hb; fetal COHb peaks later and clears slower than maternal
— Fetal COHb may be 10–15% higher than maternal at equilibrium
— Maternal symptoms underestimate fetal risk — a "mildly symptomatic" mother may have a severely affected fetus
— Indications for HBO are broader in pregnancy:
— Any maternal symptoms with COHb >15–20%
— Any sign of fetal distress (non-reassuring tracing, decreased movement, IUFD)
— Maternal LOC, neuro signs, or cardiac ischemia regardless of COHb
— HBO is safe in pregnancy for CO poisoning — benefit outweighs theoretical risk
— Continue 100% NRB for ≥5× the time needed to normalize maternal COHb (because fetal clearance lags) — typically 4× longer than for nonpregnant patient
— Continuous fetal monitoring ≥20 weeks gestation
— Outcomes: increased risk of stillbirth, anatomic malformations (if first trimester exposure), cerebral palsy, low birth weight
— Higher minute ventilation per kg → faster uptake of CO; symptoms at lower exposure durations
— Often present with vague GI complaints (nausea, vomiting) → misdiagnosed as gastroenteritis, especially if siblings also affected
— Lower threshold for HBO; LOC, seizure, or persistent neuro signs are clear indications
— School-age children: assess for cognitive/behavioral DNS at 1–2 months; coordinate with pediatrician and school
— Infants in car seats during exhaust exposure (running car) are highest risk in family
Board pearl: A pregnant woman in winter with headache and nausea — even if COHb is "only" 18% — gets HBO referral. The fetus is the limiting factor, and obstetric outcomes drive the decision more than the maternal number.
— Onset 2–40 days after apparent recovery (lucid interval)
— Manifestations: cognitive impairment, memory loss, parkinsonism, dystonia, gait disorder, urinary incontinence, personality change, depression, psychosis
— Pathology: bilateral globus pallidus necrosis, subcortical white matter demyelination
— Incidence: 10–30% overall; up to 40% in severe cases
— Risk factors: age >36, LOC during exposure, prolonged exposure, abnormal initial neuro exam, severe acidosis
— Recovery: ~75% improve over 1 year, but residual deficits common
— Myocardial injury (elevated troponin in 30–40% of moderate-severe cases)
— CO-induced cardiomyopathy (usually reversible)
— Arrhythmias, including atrial fibrillation, ventricular tachycardia
— Independent predictor of long-term mortality even in young patients
— Seizures, status epilepticus
— Anoxic brain injury, persistent vegetative state in severe cases
— Cortical blindness, peripheral neuropathy
— Rhabdomyolysis → AKI
— Compartment syndrome from prolonged immobility
— Pulmonary edema (cardiogenic or noncardiogenic)
— Pressure-point skin bullae
— Retinal hemorrhages, hearing loss
— In pregnancy: stillbirth, anomalies, neurodevelopmental delay
— Acute mortality 1–3% in hospitalized cases; higher with concurrent smoke/cyanide
— All-cause mortality at 7 years elevated even after apparent recovery — emphasize follow-up
Key distinction: DNS is distinct from persistent neurologic sequelae (deficits that never resolved from the acute event). DNS implies interval recovery followed by deterioration. Any patient with LOC during CO exposure should be specifically counseled and scheduled for cognitive reassessment.
— GCS ≤13 or any persistent altered mentation
— Seizure during or after presentation
— Hemodynamic instability requiring vasopressors
— Cardiac ischemia (elevated troponin, ischemic ECG)
— Arrhythmia requiring monitoring or intervention
— Severe metabolic acidosis (pH <7.1, lactate >8) not rapidly resolving
— Intubation for any reason (airway burn, respiratory failure, coma)
— Concurrent severe smoke inhalation
— Post-HBO patients with severe initial presentation
— Moderate poisoning with symptoms but stable hemodynamics
— COHb 25–40% with neurologic symptoms (HA, dizziness) without focal signs
— Elderly with comorbid cardiopulmonary disease
— Pregnancy with COHb >10–15% even if mildly symptomatic
— Suicide attempt — requires medical stabilization + psychiatric clearance
— Hyperbaric medicine / poison control (1-800-222-1222) — call early for any moderate-severe case
— Cardiology — elevated troponin, arrhythmia, ischemic ECG
— Neurology — seizure, focal deficit, persistent altered mentation
— Obstetrics — any pregnant patient, fetal monitoring
— Burn surgery — concomitant burns or smoke inhalation with airway concern
— Psychiatry — intentional exposure (suicide attempt)
— Pediatrics + CPS — pediatric exposure with neglect concerns
— Asymptomatic for ≥4 hours on 100% NRB
— COHb <5% (or returned to chronic smoker baseline)
— Normal neurologic exam, normal ECG, normal lactate
— Safe disposition (CO source identified and remediated, or patient not returning to it)
— Written instructions including DNS red flags and 24-hour follow-up plan
CCS pearl: Always call Poison Control — they document, advise on HBO transfer, and track outbreaks (a cluster of CO cases may indicate a building or community source requiring public health response).
— Co-exposure in fire victims; combustion of plastics, wool, silk
— Severe lactic acidosis (lactate >10), normal-to-high SvO₂ (impaired tissue extraction)
— "Bitter almond" breath (only ~50% can detect)
— Treatment: hydroxocobalamin (avoid nitrites if CO co-poisoning)
— Causes: dapsone, benzocaine sprays, nitrates, aniline dyes
— SpO₂ saturates near 85% regardless of true O₂ status (vs CO where SpO₂ is falsely normal)
— Chocolate-brown blood; cyanosis unresponsive to oxygen
— Treatment: methylene blue 1–2 mg/kg IV (avoid in G6PD deficiency)
— Sewer, manure pit, oil/gas industry
— "Knockdown" — rapid LOC; rotten egg smell (lost at high concentrations due to olfactory fatigue)
— Inhibits cytochrome oxidase like cyanide
— Treatment: 100% O₂, supportive; nitrites controversial
— Displace ambient O₂; hypoxia without metabolic poisoning
— COHb normal; PaO₂ may be low
— Euphoria, ataxia; chronic abuse → renal tubular acidosis
— No COHb elevation
— Pinpoint pupils, respiratory depression, response to naloxone
— May coexist with CO if found in enclosed space with running car
— Mixed respiratory alkalosis + anion-gap metabolic acidosis, tinnitus, hyperthermia
— Different vignette, but altered mental status overlap
Key distinction: In fire victim with persistent lactic acidosis after oxygenation/hemodynamic correction, think cyanide co-poisoning. CO alone is unlikely to keep lactate elevated once COHb falls — cyanide does.
— Most common misdiagnosis in mild CO; winter timing, headache, malaise, nausea
— Distinguishing features: no fever in CO, multiple simultaneous household cases, symptoms tied to location, normal WBC, elevated COHb
— Recurrent headaches that resolve when away from home should prompt CO testing
— Chest pain, dyspnea, ischemic ECG, elevated troponin — but CO causes all of these in young patients without CAD
— Coronary angiography may be needed if presentation is ambiguous; CO can also unmask underlying CAD
— Focal deficits, altered mentation — but CO often produces symmetric basal ganglia injury and bilateral findings
— Imaging clarifies; CO MRI shows bilateral globus pallidus
— New-onset seizure in adult — always check COHb, glucose, sodium, tox screen
— Altered mental status, acidosis — fingerstick glucose is mandatory early
— Fever distinguishes; LP if meningismus
— Patients with chronic low-level CO exposure often labeled with depression, chronic fatigue, fibromyalgia before diagnosis is made — environmental history is key
— Headache, nausea, dyspnea at altitude; resolves with descent/O₂; no COHb elevation
Step 3 management: In an outpatient clinic, the patient with "recurrent flu" every winter that resolves when traveling needs a CO investigation — order COHb same-day and refer for home CO detector check and furnace inspection. Public health may need notification if a rental property has a defective system affecting other tenants.
— Identify the source: furnace, water heater, generator, vehicle, charcoal, stove
— Engage local fire department or gas utility for home inspection (often free)
— Do not allow patient to return to unremediated environment — admit or arrange alternate housing
— Public health notification for shared housing (apartments, dormitories)
— Install battery- or hardwired CO detectors on every level of home, near sleeping areas
— Test monthly; replace batteries annually; replace unit every 5–7 years
— Required by law in many states for rental properties
— Never run generators indoors, in garages (even with door open), or within 20 feet of windows
— Never use gas oven or stove for heating
— Never use charcoal grills or hibachis indoors
— Annual professional inspection of furnaces, chimneys, water heaters
— Don't idle car in garage even briefly
— No specific long-term medications for CO itself
— Continue management of revealed comorbidities (CAD if troponin rose, asthma if smoke-related)
— Antidepressant or trauma-focused care if suicide attempt
— Baseline cognitive screen before discharge (orientation, recall, attention)
— Neuropsychiatric reassessment at 1–2 months and 6 months — DNS surveillance
— Provide written list of DNS red flags: new memory loss, gait change, personality change, incontinence — return immediately
— Repeat ECG, troponin trend; outpatient cardiology referral if elevated
— Consider stress imaging once recovered if cardiac involvement
Board pearl: Discharge "back to the same home with the same furnace" is the most common patient-safety failure in CO cases. Document source remediation explicitly in the chart.
— 24–72 hours: primary care or ED follow-up — assess symptom resolution, ensure CO source remediated, screen for early DNS
— 1–2 weeks: cognitive screen (MoCA or similar), depression screen (PHQ-9), review CO detector installation
— 1–2 months: formal neuropsychological testing if any persistent symptoms or severe initial poisoning — peak window for DNS detection
— 6 months: final cognitive reassessment; return-to-work clearance if occupation-relevant (pilots, drivers, surgeons)
— Symptom diary: headache, memory, mood, sleep, gait
— Functional status: ADLs, work performance, school performance in children
— Repeat ECG if initial ischemia; echo at 4–6 weeks if cardiomyopathy noted
— Repeat MRI brain if new neuro symptoms emerge — bilateral globus pallidus, white matter changes
— Cognitive rehabilitation (occupational therapy, speech-language pathology) for memory/executive dysfunction
— Physical therapy for parkinsonism, gait, balance
— Vocational rehabilitation if persistent deficits
— Mental health support — depression, PTSD, anxiety common after severe poisoning, especially fire survivors
— Avoid driving until cognitive and visual function clear
— Pilots, commercial drivers, heavy machinery operators — formal clearance required
— Detailed anatomy ultrasound, growth scans, antenatal testing
— Pediatric neurodevelopmental follow-up of the infant after delivery
— Anyone exposed to same source should have COHb checked even if asymptomatic
— Counsel about shared-risk environment
Step 3 management: Build follow-up around DNS surveillance — the patient who looks well at discharge can deteriorate at 3 weeks. A scheduled 1-month neurocognitive visit is the single highest-yield intervention in moderate-severe CO discharge planning.
— Many states require reporting of CO poisoning to public health departments — facilitates source investigation, outbreak detection, regulatory action
— Workplace exposures: report to OSHA if occupational
— Pediatric exposures suggesting neglect (parents using indoor charcoal heat despite warnings, ignored detector alarms, repeated exposures): mandatory CPS referral
— Suspected elder abuse/self-neglect with unsafe housing: APS referral
— Medical stabilization first; then psychiatric evaluation prior to discharge
— Involuntary hold may be required if patient refuses care and remains a danger
— Means restriction counseling — remove access to running cars in closed garages, generators
— Most dangerous handoff: ED to home discharge with unremediated source → repeat poisoning of patient and family
— Verify source identified, inspection arranged, and habitable alternate environment available before discharge
— Provide written safety instructions in patient's preferred language
— Document that all household members were tested/offered testing
— HBO transfer for a confused/altered patient: emergency exception applies; document inability to consent and best-interest decision; contact surrogate when possible
— Pregnant patient refusing HBO: respect autonomy after thorough counseling about fetal risk; document discussion; involve ethics if needed
— Low-income housing disproportionately affected — old heating systems, no detectors
— Power-outage events disproportionately affect medically vulnerable populations relying on generators
— Advocate for CO detector legislation and free-distribution programs
— Time of exposure, time of removal, time of 100% O₂ initiation, COHb trend, neuro exam timestamps — all required for HBO billing and medicolegal defense
Board pearl: Failure to identify and remediate the CO source before discharge is a patient-safety sentinel event when it leads to readmission or death.
Key distinction: The exam loves the normal SpO₂ + elevated lactate + normal PaO₂ triad in a winter headache vignette — that's CO until you co-oximeter it.
— "A mother brings her 3 children to the ED in January with headache, nausea, and dizziness. Symptoms began this morning after they woke. All are afebrile. SpO₂ 99% on RA."
— Best next step: 100% non-rebreather O₂ and co-oximetry COHb level
— Trap answer: acetaminophen and discharge with viral syndrome diagnosis
— "Firefighter pulled from a structure fire, GCS 11, lactate 12, soot in oropharynx, BP 88/50 despite fluids."
— Best treatment: 100% O₂ + hydroxocobalamin (empirical for cyanide co-toxicity)
— Trap answer: sodium nitrite (worsens O₂ delivery in CO)
— "26-year-old G2P1 at 24 weeks, COHb 18%, headache, otherwise stable."
— Best next step: HBO referral (lower threshold in pregnancy)
— Trap: discharge on NRB
— "55-year-old woman with daily morning headaches for 2 weeks; resolves at work, returns at home; husband also affected."
— Best next step: COHb level + home CO detector + furnace inspection
— Trap: migraine prophylaxis
— "Patient found in running car in closed garage, GCS 8, intubated, COHb 48%."
— Best management: 100% O₂ via ventilator, transfer for HBO, psychiatric hold once stabilized
— "Painter using paint stripper in basement, presents with HA. COHb 22%, treated with O₂, repeat level 4 h later is 28%."
— Explanation: methylene chloride → hepatic CO production continues; prolonged monitoring
— "Patient recovered 3 weeks ago from severe CO; now has new memory loss, urinary incontinence, parkinsonian gait."
— Dx: DNS; MRI shows bilateral globus pallidus / white matter changes
— "Patient with normal SpO₂ 100%, normal PaO₂, lactate 7, altered mentation in winter."
— Dx: CO poisoning; standard pulse ox cannot detect COHb
— "Severe CO, intubated, CXR shows pneumothorax."
— Best next step: chest tube before HBO
CCS pearl: On management cases, the order set is uniform: NRB 15 L → co-oximetry COHb → ECG/troponin → lactate → β-hCG → CT head if altered → call HBO/Poison Control → admit/transfer based on severity. Re-evaluate every 30 minutes.
Carbon monoxide poisoning is a winter-peaking, multi-victim, normal-SpO₂ disease in which 100% non-rebreather oxygen is started immediately, co-oximetry COHb confirms the diagnosis, and hyperbaric oxygen is reserved for severe poisoning (LOC, neuro deficit, cardiac ischemia, COHb >25%, pH <7.1, or pregnancy with COHb >15–20%) — with delayed neuropsychiatric syndrome being the long-term complication that mandates structured follow-up.
Board pearl: When the question stem has a winter setting, multiple sick people in one house, headache without fever, and a normal pulse oximetry — pick carboxyhemoglobin level and start 100% non-rebreather oxygen before anything else. That single reflex earns the point virtually every time.