Carbon Monoxide Poisoning

Meet the patient — three people, one house, one boiler

A whole family arrives in January with 'the flu' — headache, nausea, fatigue. The father is confused; the mother has fainted; the teenage son is asymptomatic. Their cat died last week. The symptoms improve every time they leave for work and school, and return each evening.^[10]

Three clinical questions now sit on your shoulders, and each one decides whether the family leaves hospital intact. Is the pulse oximeter lying (it can be — pulse oximetry remains elevated and fails to detect the falling true oxyhaemoglobin saturation). Is there a second toxin (in a fire victim, yes — cyanide). Will the neurological injury come back in two weeks (it may — delayed neurological sequelae follow a lucid interval of 2 to 40 days). Hold those three and every section below slots into place.^[3][12]

What CO poisoning is — and why the pulse oximeter lies

Carbon monoxide is a colourless, odourless, non-irritant gas produced by the incomplete combustion of hydrocarbons. Recognised sources include poorly functioning heating systems, indoor propane-powered forklifts, indoor burning of charcoal briquettes, riding in the back of pick-up trucks, ice-skating rinks using propane-powered resurfacing machines, and gasoline-powered generators that are not in correct locations. It accounts for thousands of deaths worldwide each year.^[3][4]

The clinical syndrome is tissue hypoxia plus poisoned oxidative metabolism: inhaled CO binds haemoglobin to form carboxyhaemoglobin (COHb) with an affinity 200 times greater than oxygen, decreasing oxygen-carrying capacity and the release of oxygen to tissues. Beyond binding many haeme-containing proteins, CO disrupts oxidative metabolism, leading to free-radical formation; once hypotension and unconsciousness occur, lipid peroxidation and apoptosis follow.^[3]

The mechanisms to name in the viva: (1) carboxyhaemoglobin formation with reduced oxygen carriage and unloading; (2) binding to many haeme-containing proteins besides haemoglobin; (3) disrupted oxidative metabolism with free-radical generation; and (4) lipid peroxidation and apoptosis after hypotensive, unconscious exposure — the substrate of the delayed neurological syndrome.^[3]

CO poisoning is a clinical diagnosis supported by COHb measurement. The diagnosis can be elusive: clinical effects are diverse and non-specific, and carboxyhaemoglobin levels do not always correlate with the degree of poisoning. In 124 CO-poisoned patients, pulse oximetry saturation stayed near 99 per cent while measured oxyhaemoglobin fell linearly with rising COHb — the pulse-oximetry gap approximated the COHb level, so pulse oximetry must be considered unreliable until the COHb level is measured.^[4][12]

Stage the patient — by severity, by COHb, by chronicity

CO poisoning is classified by clinical severity, by COHb concentration, and by whether effects are acute or delayed. None alone is sufficient — the decision to treat is clinical, supported by COHb and physiology, because COHb does not always correlate with the degree of poisoning.^[4]

^{[3] [4] [5]}

By COHb concentration — a guide, not a diagnostic threshold in isolation:^[3]

^[3]

By exposure scenario — the list that explains every cluster:^[3]

• Domestic and accidental: poorly functioning heating systems and blocked or faulty flues.
• Indoor fuel-burning devices: charcoal briquettes burned indoors, propane-powered forklifts used indoors.
• Recreation and transport: riding in the back of pick-up trucks; ice-skating rinks using propane-powered resurfacing machines.
• Generators: gasoline-powered generators that are not in correct locations — a classic post-disaster cluster.
• Fire or smoke inhalation — fire-related cases accounted for the majority of unintentional CO poisoning deaths in United States surveillance (non-fire causes comprised 40.9 per cent of deaths).^[10]
• Deliberate self-harm: vehicle exhaust or indoor charcoal — consider psychiatric presentation after stabilisation.^[3]

Enlarge

Who gets poisoned, and why the whole household matters

United States surveillance (2005 to 2018) quantifies the burden of unintentional CO poisoning. Annually: about 39.5 poison-centre exposure calls per million population nationally, 56.5 emergency-department visits per million across 17 states, 7.3 hospitalizations per million in 26 states, and 3.3 deaths per million nationally. Non-fire-related cases comprised 74.0 per cent of ED visits, 60.1 per cent of hospitalizations, and 40.9 per cent of deaths. Cases peaked in winter — notably January and December. Children aged 0 to 9 years had the highest rates of poison-centre exposures and ED visits; adults older than 80 had the highest rates of hospitalization and death; deaths occurred more often among men and in the Midwest region. Headache, nausea, and dizziness or vertigo were the most reported symptoms.^[10]

Populations at highest risk:^[5][10]

^{[3] [5] [10]}

Pathophysiology — four mechanisms, and the oxygen that drives treatment

CO is inhaled, binds haemoglobin to form carboxyhaemoglobin with an affinity 200 times greater than oxygen, and reduces both oxygen-carrying capacity and oxygen release to tissues — tissue hypoxia follows.^[3]

1. Carboxyhaemoglobin formation. The 200-to-1 affinity ratio means even modest inhaled CO occupies haemoglobin, and the dissociation of oxygen at tissue level is further impaired by the decreased release of oxygen.^[3]

2. Binding beyond haemoglobin. CO binds many haeme-containing proteins — not only haemoglobin — extending the injury to multiple organ systems.^[3]

3. Disrupted oxidative metabolism and free radicals. CO disrupts oxidative metabolism, leading to the formation of free radicals — one reason clinical effects can be acute or delayed.^[3]

4. The secondary injury wave — why the delayed syndrome happens. Ischaemia occurs with CO poisoning when loss of consciousness is accompanied by hypotension, producing ischaemia in the arterial border zones of the brain. Once hypotension and unconsciousness occur, lipid peroxidation and apoptosis follow — the substrate of the delayed neurological syndrome that emerges after a lucid interval of 2 to 40 days, with diffuse demyelination in the brain.^[3]

Why oxygen is the cornerstone — the kinetic rationale for treatment:^[3]

^[3]

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Clinical presentation — a chameleon that hides as the flu

Clinical effects can be diverse: headache, dizziness, nausea, vomiting, syncope, seizures, coma, dysrhythmias, and cardiac ischaemia. Severe toxicity generally affects the nervous and cardiovascular systems, and effects can be acute or delayed — the diagnosis is often missed because the symptoms are non-specific and access to specialised tools is limited.^[4][13]

Symptoms by COHb band:^[3]

• COHb 15 to 30 per cent — non-specific: headache, dizziness, nausea, fatigue, impaired manual dexterity.
• Ischaemic heart disease at COHb 1 to 9 per cent — chest pain and decreased exercise duration.
• COHb 30 to 70 per cent — loss of consciousness and eventually death.^[3]

In poison-centre exposure data, headache, nausea, and dizziness or vertigo were the most reported symptoms — precisely the profile mistaken for viral illness.^[10]

Delayed neurological sequelae (DNS). Following resolution of acute symptoms there may be a lucid interval of 2 to 40 days before DNS develops, with diffuse demyelination in the brain accompanied by lethargy, behaviour changes, forgetfulness, memory loss, and parkinsonian features. Seventy-five per cent of patients with DNS recover within 1 year.^[3]

• Cognitive: forgetfulness, memory loss, impaired concentration.
• Affective and behavioural: lethargy, behaviour changes.
• Motor: parkinsonian features.
• Other: toxic or ischaemic peripheral neuropathies are associated with CO exposure in humans and animals.^[3]

Imaging. White-matter damage in the centrum semiovale and periventricular area and abnormalities in the globus pallidus are the abnormalities most commonly seen on MRI following CO exposure. Neuropsychological abnormalities with chronic exposure are found even when MRI and magnetic resonance spectroscopy are normal.^[3]

Pregnancy. CO poisoning during pregnancy may cause deleterious effects to the fetus. Hyperbaric oxygen therapy in pregnancy is proven to be safe and is considered beneficial, reducing the severity of fetal injuries — but the COHb level that should trigger HBO in pregnant patients remains an open question.^[11]

Differential — the rule that catches the most cases

CO poisoning is a chameleon — symptoms are non-specific and overlapping. Consider CO whenever multiple people in the same environment develop similar symptoms and when symptoms resolve on leaving the environment, particularly in winter.^[4][10]

^{[3] [4] [6] [9]}

The clinical decision rule that catches the most cases: CO poisoning is the diagnosis in any patient with non-specific neurological or cardiovascular symptoms that improve when they leave their home or workplace and recur on return — particularly in winter (January and December are the peak months), and particularly when multiple cohabitants are affected.^[10]

Bedside assessment — the first 15 minutes decide the case

The first 15 minutes at the bedside decide the case.^[4]

1. Scene safety and environmental history. Ask: what fuel sources are in the dwelling (heating system, propane devices, charcoal, generator)? Are other family members or pets ill? Was there a fire? The recognised sources — poorly functioning heating systems, indoor propane devices, indoor charcoal briquettes, pick-up trucks, ice-rink resurfacers, misplaced generators — should be sought explicitly. Escalate to the fire service or public health if a domestic source is identified.^[3]

2. Primary survey (ABCDE). Severe cases reach the resuscitation bay as syncope, seizure, coma, dysrhythmia, or cardiac arrest. Pulse oximetry is unreliable — in confirmed CO poisoning it stayed near 99 per cent while true oxyhaemoglobin saturation fell; the gap approximated the COHb level. Treat the patient, not the SpO2 reading, until the COHb level is measured.^[12]

3. Focused history. Time of onset, time of removal from exposure, duration of any loss of consciousness (hypotension plus unconsciousness defines the ischaemic, lipid-peroxidation phase), source, co-injuries in fire victims, past medical history (ischaemic heart disease, pregnancy), and psychiatric history in deliberate exposure.^[3]

4. Targeted examination.^[4]

• Neurological — conscious level, cerebellar dysfunction (in the Weaver randomised trial, cerebellar dysfunction before treatment was strongly associated with cognitive sequelae), focal deficit, cognitive screen.
• Cardiovascular — perfusion, blood pressure, careful ECG review for ischaemia and dysrhythmia; cardiac ischaemia is a described effect of severe toxicity.
• Respiratory — soot in the nasopharynx, hoarseness, or stridor after smoke inhalation raises concomitant airway injury and cyanide concern.
• Mental state and psychiatric screen — deliberate exposure requires protection of the patient after stabilisation.^[1][4]

5. Bedside tests.^[6]

• Capillary glucose — altered consciousness demands exclusion of hypoglycaemia.
• 12-lead ECG — ischaemia and dysrhythmias are described cardiac effects.
• Point-of-care lactate — in pure cyanide poisoning a plasma lactate of 8 mmol/L or more was 94 per cent sensitive and 70 per cent specific for a toxic blood cyanide concentration; immediate and serial lactate measurement is useful in assessing severity. The study excluded fire victims, so the threshold must be interpreted with caution at the fire scene.^[6]

6. Reassessment on oxygen. The cornerstone of treatment is 100 per cent oxygen using a tight-fitting mask for greater than 6 hours; failure to improve as expected should prompt reconsideration of the diagnosis, the severity, or a concomitant toxin or injury.^[3]

Investigations — the COHb level, interpreted with humility

Carboxyhaemoglobin is the key measurement, but it is only one piece of the picture. Blood carboxyhaemoglobin levels have real limitations as a diagnostic technique, and levels do not always correlate with the degree of poisoning. Order the measurement, but interpret it in clinical context — and never delay oxygen for it.^[4][13]

Carboxyhaemoglobin measurement:^[3]

• The single most important test. COHb is measured by multi-wavelength spectrophotometry (co-oximetry) on a blood sample; in the pulse-oximetry-gap study, arterial blood gas analysis included direct spectrophotometric determination of oxyhaemoglobin and carboxyhaemoglobin saturations.^[12]
• Interpretation — COHb 15 to 30 per cent gives non-specific symptoms; ischaemic heart disease may suffer chest pain at 1 to 9 per cent; 30 to 70 per cent leads to loss of consciousness and eventually death. Levels do not always correlate with the degree of poisoning.^[3]
• Timing — measure early, but treatment should never wait for the result: oxygen is the cornerstone and is started on suspicion.^[3]

Arterial blood gas and lactate:^[6]

• Lactate — immediate and serial plasma lactate measurement is useful in assessing the severity of cyanide poisoning (≥8 mmol/L was 94 per cent sensitive, 70 per cent specific for toxic cyanide in non-fire victims); lactate correlated positively with anion gap and inversely with pH and systolic blood pressure in cyanide-poisoned patients.^[6]

ECG and troponin: cardiac ischaemia and dysrhythmias are described effects of CO toxicity, and severe toxicity generally affects the nervous and cardiovascular systems — obtain an ECG in every case.^[4]

Beta-HCG in any woman of reproductive age — pregnancy changes management: hyperbaric oxygen is considered safe and beneficial in pregnancy, and the fetus is at particular risk.^[11]

Brain imaging — MRI: white-matter damage in the centrum semiovale and periventricular area and abnormalities in the globus pallidus are most commonly seen on MRI following CO exposure. Neuropsychological abnormalities with chronic exposure are found even when MRI is normal.^[3]

^{[3] [4] [6] [12] [1] [3]}

Resuscitation — 100 per cent oxygen from the first breath

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The resuscitation task is twofold: restore oxygen delivery, and exclude or treat concomitant threats (cyanide in fires, trauma, burns, airway injury).^[4]

The first 5 minutes:^[3]

1. 100 per cent oxygen using a tight-fitting mask from the moment poisoning is suspected — the cornerstone of treatment, continued for greater than 6 hours. Do not wait for the COHb result.
2. Remove from the environment — and confirm rescuer safety before entry.
3. Assess ABCDE — airway, breathing, circulation, disability (conscious level, pupils, glucose), exposure (search for burns, trauma, soot, stridor).
4. IV access and monitoring — remembering pulse oximetry remains unreliable until the COHb level is known.^[12]
5. Capillary glucose, COHb measurement, blood gas with lactate, ECG, and beta-HCG in women of reproductive age.^[4][6]

Cardiopulmonary arrest considerations. Standard advanced life support applies, with pure-oxygen ventilation. In fire victims, treat suspected concomitant cyanide poisoning with an antidote: prehospital hydroxocobalamin achieved return of spontaneous circulation in 21 of 38 patients found in cardiac arrest in the Paris Fire Brigade experience, and 9 of 12 initially haemodynamically unstable patients recovered systolic blood pressure after the start of hydroxocobalamin infusion.^[8]

Seizure control and airway. Seizures and coma are described effects of severe toxicity; treat supportively — oxygen, airway protection as clinically required, glucose exclusion of hypoglycaemia — and treat convulsions per standard protocols. Treatment of CO poisoning consists of oxygen therapy and supportive care, with hyperbaric oxygen in selected cases.^[4][5]

Definitive management — normobaric oxygen, then HBO in selected patients

Definitive management is normobaric 100 per cent oxygen, supportive care, and — in selected cases — hyperbaric oxygen therapy.^[5]

The randomised-trial evidence for hyperbaric oxygen (HBO). In the Weaver double-blind randomised trial, patients with symptomatic acute CO poisoning received three chamber sessions within a 24-hour period — either three hyperbaric-oxygen treatments or one normobaric-oxygen treatment plus two sessions of normobaric room air. Cognitive sequelae at six weeks were less frequent with HBO: 19 of 76 patients (25.0 per cent) versus 35 of 76 (46.1 per cent), P equals 0.007, with benefit apparent at 6 weeks and 12 months. Cerebellar dysfunction before treatment predicted cognitive sequelae (odds ratio 5.71).^[1] The 2011 Cochrane review identified six trials (1361 participants): two found benefit at one month and four did not; pooled analysis gave an odds ratio of 0.78 (95 per cent CI 0.54 to 1.12) without statistical significance, with marked methodological and statistical heterogeneity and design flaws in all trials. Existing randomised trials do not establish whether HBO reduces adverse neurologic outcomes.^[2]

Indications for hyperbaric oxygen remain debated. The 2015 Handbook review states the indications for treatment with hyperbaric oxygen to decrease the COHb half-life remain controversial; the 2022 Emergency Medicine review notes the efficacy of hyperbaric oxygen is unclear and even the appropriate therapy is widely debated. The 2025 Diagnostics review concludes hyperbaric oxygen therapy remains the primary treatment but is not always accessible. Decisions are therefore clinical and local — loss of consciousness, neurological deficit, cardiac ischaemia, and pregnancy weigh toward hyperbaric discussion, but no universally accepted COHb threshold can be quoted from the trial evidence.^[3][4][13]

Continued normobaric 100 per cent oxygen. The cornerstone for treatment is 100 per cent oxygen using a tight-fitting mask for greater than 6 hours; normobaric oxygen is the standard therapy.^[3][4]

Supportive care: treatment consists of oxygen therapy, supportive care, and in selected cases hyperbaric oxygen therapy. Children, pregnant women, and patients with underlying cardiovascular disease deserve particular attention.^[5]

Antidotes — only for concomitant cyanide in fire victims. Cyanide poisoning treatment is based on excellent supportive care with adjunctive antidotal therapy; multiple antidotes exist, vary in regional availability, and all currently marketed antidotes appear to be effective. Pure CO poisoning has no antidote beyond oxygen.^[9]

Stepwise management and disposition

For an adult presenting with suspected CO exposure:^[3]

1. Confirm safety of rescuers and environment. Remove from source. Apply 100 per cent oxygen by tight-fitting mask — before blood tests, and continued for greater than 6 hours.
2. Primary survey (ABCDE) — noting pulse oximetry is unreliable until COHb is measured.^[12]
3. History — exposure timing and source, loss of consciousness (hypotension plus unconsciousness defines the severe ischaemic phase), comorbidity (ischaemic heart disease), pregnancy.^[3]
4. First-line investigations — COHb measurement, blood gas with lactate, ECG, glucose, beta-HCG.^[4][6]
5. Disposition decision:^[4]

^{[3] [4] [11]}

Pre-arrival for HBO — telephone the receiving hyperbaric centre early; transport with continued high-concentration oxygen. Access to hyperbaric oxygen is a real constraint — it is not always available.^[13]

Time-to-treatment rule. Prognosis is influenced by exposure severity and delayed treatment, which increases the risk of neurological damage — early detection is vital for preventing long-term complications.^[13]

The scenarios examiners set

• Fire or smoke-inhalation victims. The most clinically dangerous scenario because of concomitant cyanide poisoning. Cyanide's primary target of toxicity is mitochondrial cytochrome oxidase; common features include altered mental status, seizures, and lactic acidosis. Always consider cyanide in any fire victim with altered consciousness or profound lactic acidosis. Treatment combines excellent supportive care with adjunctive antidotal therapy.^[9]

• Pregnancy. CO poisoning during pregnancy may cause deleterious effects to the fetus. Hyperbaric oxygen therapy in pregnancy is proven safe and considered beneficial, reducing the severity of fetal injuries; the COHb level that should trigger HBO in pregnant patients remains an open question — organisations are advised to develop their own protocols.^[11]

• Paediatrics. Children are particularly at risk of adverse outcomes from CO toxicity, and US surveillance found the highest rates of poison-centre exposure calls and ED visits in children aged 0 to 9 years. Presentation is non-specific; oxygen and supportive care as in adults, with hyperbaric oxygen in selected cases.^[5][10]

• Suicide attempt with vehicle exhaust or indoor charcoal. After medical stabilisation, the patient requires psychiatric evaluation and observation under safe conditions; deliberate exposure must be assumed in indoor charcoal and exhaust presentations.^[3]

• Occupational and environmental clusters. Indoor propane-powered forklifts, ice-skating rinks with propane-powered resurfacing machines, and poorly functioning heating systems are recognised sources; multiple casualties from the same dwelling are a public-health incident — evacuate, inspect, and notify public health. Winter months (January and December) carry the highest burden.^[3][10]

• Cyanide co-toxicity in fires. Prehospital hydroxocobalamin has 8 years of Paris Fire Brigade experience in smoke inhalation-associated cyanide poisoning (101 patients; survival 41.7 per cent among the 72 with known status; return of spontaneous circulation in 21 of 38 found in cardiac arrest; adverse events limited to red or pink coloration of urine or skin and rash) — its risk-to-benefit ratio renders it suitable for prehospital use. Studied intravenous dosing in the safety trial ranged from 2.5 g up to 10 g, infused over 7.5 to 30 minutes; the most common drug-related effects were self-limiting chromaturia and reddening of the skin, with a transient blood-pressure rise. Multiple antidote classes exist and vary in regional availability.^[7][8][9]

Complications

Cardiovascular: cardiac ischaemia and dysrhythmias are described clinical effects; severe toxicity generally affects the nervous and cardiovascular systems.^[4]

Neurological — the delayed neurological syndrome (DNS): after a lucid interval of 2 to 40 days, diffuse demyelination in the brain produces lethargy, behaviour changes, forgetfulness, memory loss, and parkinsonian features; 75 per cent of patients with DNS recover within 1 year. Peripheral neuropathies, both toxic and ischaemic, are associated with CO exposure.^[3]

Pregnancy-specific: deleterious effects on the fetus; hyperbaric oxygen reduces the severity of fetal injuries.^[11]

Prognosis and disposition

Prognosis is influenced by exposure severity and delayed treatment — delayed treatment increases the risk of neurological damage, and early detection is vital for preventing long-term complications.^[13]

Outcome data:^[1][10]

• Cognitive sequelae after symptomatic acute poisoning — in the Weaver randomised trial, cognitive sequelae at six weeks occurred in 46.1 per cent of the normobaric-oxygen group versus 25.0 per cent of the hyperbaric group (P equals 0.007), with benefit persisting to 12 months; cerebellar dysfunction before treatment multiplied the odds of cognitive sequelae (odds ratio 5.71).^[1]
• Delayed neurological syndrome — follows a lucid interval of 2 to 40 days; 75 per cent of patients with DNS recover within 1 year.^[3]
• Population mortality — United States surveillance recorded 3.3 unintentional CO-poisoning deaths per million population annually (2005 to 2018), with falling rates over the period; adults older than 80 carried the highest death rates.^[10]

Disposition:^[4]

• Mild, non-specific symptoms without loss of consciousness — 100 per cent oxygen by tight-fitting mask and clinical observation.
• Loss of consciousness, seizures, coma, cardiac ischaemia, or dysrhythmias — 100 per cent oxygen, supportive care, and early discussion of hyperbaric oxygen; access is a genuine constraint.
• Pregnancy — 100 per cent oxygen; hyperbaric oxygen is safe and beneficial in pregnancy; involve obstetric services.^[11]

Special populations

• Pregnancy. Hyperbaric oxygen therapy in pregnancy is proven to be safe and is considered beneficial, reducing the severity of fetal injuries; the COHb level that should trigger HBO in pregnant patients remains an open question, and organisations are encouraged to develop their own protocols.^[11]
• Paediatrics. Children are particularly at risk of adverse outcomes; the highest rates of poison-centre exposures and ED visits were in children aged 0 to 9 years in US surveillance. Household exposure is often shared — siblings and parents need assessment.^[5][10]
• Older adults. Adults older than 80 had the highest rates of hospitalization and death in US surveillance; deaths occurred more often among men.^[10]
• Ischaemic heart disease. Chest pain and decreased exercise duration can appear at COHb between 1 and 9 per cent — cardiac symptoms at seemingly trivial COHb levels are a real phenomenon and mark risk.^[3]
• Deliberate self-harm. Vehicle-exhaust and indoor-charcoal presentations must be assumed deliberate until proven otherwise; protect the patient during admission and arrange psychiatric evaluation after stabilisation.^[3]

Evidence, guidelines, and regional differences

Landmark trials and reviews:^[1]

• Weaver LK, Hopkins RO, Chan KJ, et al. Hyperbaric oxygen for acute carbon monoxide poisoning (NEJM 2002) — double-blind randomised trial of three hyperbaric versus normobaric sessions within 24 hours in symptomatic acute CO poisoning (76 per group, stopped at interim analysis). Cognitive sequelae at six weeks: 25.0 per cent HBO versus 46.1 per cent normobaric, P equals 0.007 (adjusted odds ratio 0.45, 95 per cent CI 0.22 to 0.92); benefit apparent at 6 weeks and 12 months.^[1]
• Buckley NA, Juurlink DN, Isbister G, et al. Hyperbaric oxygen for carbon monoxide poisoning (Cochrane 2011) — six randomised trials, 1361 participants; pooled odds ratio for neurological deficits 0.78 (95 per cent CI 0.54 to 1.12), not statistically significant, with substantial heterogeneity and methodological flaws. Existing randomised trials do not establish whether HBO reduces adverse neurologic outcomes.^[2]
• Bleecker ML. Carbon monoxide intoxication (Handbook of Clinical Neurology 2015) — mechanisms (200-fold affinity, free radicals, lipid peroxidation after hypotension and unconsciousness), COHb symptom bands, delayed neurological sequelae after a 2 to 40 day lucid interval, MRI findings, and the cornerstone of 100 per cent oxygen by tight-fitting mask for greater than 6 hours.^[3]
• Nañagas KA, Penfound SJ, Kao LW. Carbon Monoxide Toxicity (Emerg Med Clin North Am 2022) — diverse clinical effects; COHb levels do not always correlate with the degree of poisoning; normobaric oxygen is standard therapy and HBO efficacy unclear.^[4]
• Afzal M, et al. Carbon Monoxide Poisoning: Diagnosis, Prognostic Factors, Treatment Strategies (Diagnostics 2025) — diagnostic limitations of COHb levels and pulse CO-oximetry; HBOT remains the primary treatment but is not always accessible; delayed treatment worsens prognosis.^[13]

Regional differences:^[9]

• Cyanide antidotes — multiple antidotes exist and vary in regional availability; all currently marketed antidotes appear to be effective, so the local antidote is the right antidote.^[9]
• Hyperbaric oxygen access — HBOT remains the primary treatment for severe poisoning but is not always accessible; transport and chamber availability shape decisions as much as physiology.^[13]
• Pregnancy protocols — with the COHb trigger for HBO in pregnancy unsettled, organisations are advised to develop their own protocols.^[11]

Exam pearls — the mnemonic and the mantra

The mantra: oxygen from the first breath, COHb with humility, two toxins in every fire, hyperbaric oxygen debated, watch for the delayed syndrome.^[3]

^{[1] [2] [3] [9]}

Ward-round test — five stems with answers in the Reveal.^[3]

A family of four arrives in January with 'the flu'; the cat died last week; symptoms improve at work and school. What is the diagnosis, and what monitor is unreliable?ShowHide

Carbon monoxide poisoning from a faulty heating system — the winter cluster, the pet death, and improvement on leaving the building are classic, and January and December are the peak months in surveillance data. Pulse oximetry is unreliable — it overestimates true oxyhaemoglobin saturation by a gap that approximates the COHb level, so it must be interpreted with caution until the COHb level is measured. Give 100 per cent oxygen by tight-fitting mask and notify fire and public-health services to inspect the dwelling.^[3][10][12]

An obtunded fire victim has soot in the nose and profound lactic acidosis. Two diagnoses, two treatments?ShowHide

CO poisoning plus concomitant cyanide poisoning — cyanide's primary target is mitochondrial cytochrome oxidase, and altered mental status with lactic acidosis is its signature. In pure cyanide poisoning (non-fire victims), a plasma lactate of 8 mmol/L or more was 94 per cent sensitive and 70 per cent specific for a toxic blood cyanide concentration. Treat both: 100 per cent oxygen plus supportive care with adjunctive antidotal therapy — hydroxocobalamin has the prehospital fire-scene experience, with studied intravenous dosing from 2.5 g up to 10 g.^[6][7][8][9]

A pregnant woman has suspected CO exposure. What changes?ShowHide

The fetus is the patient too. CO poisoning during pregnancy may cause deleterious effects to the fetus. Hyperbaric oxygen therapy in pregnancy is proven to be safe and considered beneficial, reducing the severity of fetal injuries — but the COHb level that should trigger HBO in pregnant patients remains an open question, so involve obstetric and hyperbaric services early and follow a local protocol.^[11]

A patient recovers from severe CO poisoning and returns at 3 weeks with memory loss and personality change. What is this, and what does MRI show?ShowHide

Delayed neurological sequelae (DNS) — after a lucid interval of 2 to 40 days, diffuse demyelination in the brain produces lethargy, behaviour changes, forgetfulness, memory loss, and parkinsonian features. MRI most commonly shows white-matter damage in the centrum semiovale and periventricular area and abnormalities in the globus pallidus. Seventy-five per cent of patients with DNS recover within 1 year.^[3]

Why is 100 per cent oxygen the cornerstone, and what did the hyperbaric trial actually show?ShowHide

High-concentration oxygen accelerates CO clearance from haemoglobin — COHb has a short half-life, and hyperbaric oxygen decreases it further. The cornerstone of treatment is 100 per cent oxygen using a tight-fitting mask for greater than 6 hours. In the Weaver randomised trial, three hyperbaric sessions within 24 hours reduced cognitive sequelae at six weeks to 25.0 per cent from 46.1 per cent with normobaric oxygen (P equals 0.007) — but the Cochrane review of six trials found no statistically significant pooled benefit, so hyperbaric indications remain debated.^[1][2][3]

^{[1] [2] [3] [3]}

References13ShowHide

1. [1]Weaver LK, Hopkins RO, Chan KJ, et al. Hyperbaric oxygen for acute carbon monoxide poisoning N Engl J Med, 2002.PMID 12362006
2. [2]Buckley NA, Juurlink DN, Isbister G, Bennett MH, Lavonas EJ. Hyperbaric oxygen for carbon monoxide poisoning Cochrane Database Syst Rev, 2011.PMID 21491385
3. [3]Bleecker ML. Carbon monoxide intoxication Handb Clin Neurol, 2015.PMID 26563790
4. [4]Nañagas KA, Penfound SJ, Kao LW. Carbon Monoxide Toxicity Emerg Med Clin North Am, 2022.PMID 35461624
5. [5]Kao LW, Nañagas KA. Toxicity associated with carbon monoxide Clin Lab Med, 2006.PMID 16567227
6. [6]Baud FJ, Borron SW, Mégarbane B, et al. Value of lactic acidosis in the assessment of the severity of acute cyanide poisoning Crit Care Med, 2002.PMID 12352039
7. [7]Uhl W, Nolting A, Golor G, et al. Safety of hydroxocobalamin in healthy volunteers in a randomized, placebo-controlled study Clin Toxicol (Phila), 2006.PMID 16990190
8. [8]Fortin JL, Giocanti JP, Ruttimann M, Kowalski JJ. Prehospital administration of hydroxocobalamin for smoke inhalation-associated cyanide poisoning: 8 years of experience in the Paris Fire Brigade Clin Toxicol (Phila), 2006.PMID 16990192
9. [9]Borron SW, Baud FJ. Antidotes for acute cyanide poisoning Curr Pharm Biotechnol, 2012.PMID 22352728
10. [10]Shin M, Bronstein AC, Glidden E, et al. Morbidity and Mortality of Unintentional Carbon Monoxide Poisoning: United States 2005 to 2018 Ann Emerg Med, 2023.PMID 36585319
11. [11]Eleftheriou G, Butera R, Lonati D, et al. Open issues in management of carbon monoxide poisoning in pregnancy: practical suggestions J Obstet Gynaecol, 2022.PMID 35648870
12. [12]Bozeman WP, Myers RA, Barish RA. Confirmation of the pulse oximetry gap in carbon monoxide poisoning Ann Emerg Med, 1997.PMID 9360570
13. [13]Afzal M, Agarwal S, Elshaikh RH, et al. Carbon Monoxide Poisoning: Diagnosis, Prognostic Factors, Treatment Strategies, and Future Perspectives Diagnostics (Basel), 2025.PMID 40075828