Smoke inhalation and carbon monoxide poisoning

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Carbon monoxide binds haemoglobin with high affinity and also disrupts cellular oxygen use, so oxygen content and tissue delivery fall despite a deceptively normal PaO2. Neurological and myocardial tissues are especially vulnerable. Delayed neuropsychiatric problems can emerge after apparent recovery, although no single bedside value predicts them reliably.

Smoke is chemically variable. Irritant gases and particulates injure airway epithelium, impair mucociliary clearance and create oedema, bronchospasm, casts or acute lung injury over hours. Cyanide may be generated when nitrogen-containing materials burn in an enclosed space and causes cellular hypoxia with profound lactate elevation and collapse.

The central decisions are whether to secure the airway before it becomes impossible, whether toxic gas exposure needs antidote or hyperbaric specialist discussion, and how long to observe for evolving pulmonary, cardiac or neurological injury. Exact antidote and referral thresholds are volatile and must come from live TOXBASE, NPIS and local major-burns pathways.

Key points

Smoke injury can combine upper-airway thermal damage, lower-airway chemical injury, carbon monoxide poisoning, cyanide toxicity, bronchospasm, trauma and cutaneous burns.
An enclosed fire, loss of consciousness, neurological symptoms or several co-exposed household members should raise concern even when the patient looks pink and pulse oximetry seems normal.
Standard pulse oximetry cannot distinguish oxyhaemoglobin from carboxyhaemoglobin reliably, while PaO2 measures dissolved oxygen and may remain normal in serious carbon monoxide poisoning.
Give the highest available inspired oxygen concentration promptly; do not wait for the carboxyhaemoglobin result and do not use a conventional saturation target during active carbon monoxide treatment.
Carboxyhaemoglobin falls after removal and oxygen, and its value correlates imperfectly with tissue injury; symptoms, exposure, cardiac findings, acidosis and vulnerability guide severity.
Hoarseness, stridor, drooling, soot in the mouth, facial burns and progressive swelling warrant early expert intubation because oedema and fluid resuscitation can make a later airway much harder.
Severe lactic acidosis, cardiovascular collapse or coma after an enclosed-space fire suggests possible cyanide toxicity; seek immediate TOXBASE advice and do not wait for a cyanide assay.
ECG changes and troponin elevation can reveal carbon-monoxide myocardial injury, particularly in older people or those with coronary disease, and change monitoring intensity.
Pregnancy lowers the threshold for specialist discussion because fetal carboxyhaemoglobin can rise higher and clear more slowly than maternal levels.
Routine antibiotics and corticosteroids do not prevent smoke-inhalation complications; treat established infection or a specific airway indication instead.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Enclosed-space fire

Smoke concentration, heat and incomplete combustion are greatest indoors, combining airway irritants with carbon monoxide and sometimes cyanide exposure.

Faulty combustion appliances

Boilers, heaters, generators and charcoal used with poor ventilation can produce occult carbon monoxide exposure without visible smoke or airway burns.

Industrial and chemical fire

Burning plastics, wool, foam and industrial materials release complex irritant gases and may generate cyanide or other systemic toxins.

Host and exposure factors

Exposure duration, loss of consciousness, pregnancy and underlying cardiac or respiratory disease increase harm at a given environmental concentration.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Thermal upper-airway injury
Hot gases and steam damage supraglottic tissue, with evolving oedema capable of making later airway access difficult.
2
Chemical lower-airway injury
Soot and soluble irritants damage bronchial epithelium, impair cilia and trigger bronchospasm, mucus and delayed sloughing.
3
Carbon monoxide hypoxia
Carbon monoxide binds haemoglobin and cellular haem proteins, reducing oxygen carriage, hindering unloading and impairing mitochondrial use despite normal arterial oxygen tension.
4
Cyanide cellular toxicity
Cyanide inhibits mitochondrial oxidative metabolism, causing severe lactic acidosis and cardiovascular collapse despite available blood oxygen.
5
Delayed inflammatory injury
Airway debris, permeability oedema and systemic reperfusion effects can worsen respiratory and neurological function after initial rescue.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Threatened upper airwayRed flag

Voice change, stridor, dysphagia, drooling, tongue or oropharyngeal swelling, facial or neck burns and increasing work of breathing predict a narrowing airway. Absence of external burns does not guarantee safety.

Lower-airway injuryRed flag

Cough, wheeze, carbonaceous sputum, hypoxaemia, coarse breath sounds and rising secretion burden may evolve after an initially normal examination. Bronchial casts and acute lung injury can cause later deterioration.

Carbon monoxide syndromeRed flag

Headache, dizziness, nausea, weakness, confusion, ataxia, syncope, seizures, coma, chest pain or arrhythmia after combustion exposure are non-specific but important. Clustered symptoms in co-occupants strongly support a shared source.

Cardiac toxicityRed flag

Ischaemic chest discomfort, hypotension, dysrhythmia, ECG change or troponin rise suggests myocardial injury from hypoxic stress. Symptoms can be subtle in older adults and those with diabetes.

Possible cyanide toxicityRed flag

Rapid collapse, coma, seizures, severe hypotension and marked lactic acidosis after an enclosed fire, particularly with soot or very high smoke burden, warrant immediate toxicology-guided antidote consideration.

Vulnerable exposureRed flag

Pregnant people, fetuses, infants, older adults, and patients with anaemia or cardiopulmonary disease may have severe effects at lower measured carboxyhaemoglobin and deserve cautious specialist assessment.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Exposure and scene historyFirst step
Why
Define likely toxicants, dose and risk to others.
Interpretation and limitations
Record enclosed versus open fire, duration, loss of consciousness, fuel and materials, rescue delay, protective equipment and co-exposed people. Contact emergency or public-health services if an ongoing source threatens others.
02
Co-oximetry carboxyhaemoglobin
Why
Confirm carbon monoxide uptake using direct multiwavelength measurement.
Interpretation and limitations
Interpret timing, oxygen already given and smoking status. A low value after treatment does not exclude important earlier exposure, and a high value alone does not determine neurological outcome or hyperbaric eligibility.
03
Blood gas, pH and lactate
Why
Assess ventilation, acidosis and possible cellular hypoxia.
Interpretation and limitations
PaO2 may be normal in CO poisoning. Marked lactate and acidaemia after an enclosed fire increase concern for cyanide, shock or seizures; evaluate all mechanisms and trend response.
04
ECG and cardiac troponin
Why
Detect myocardial ischaemia, injury or dysrhythmia.
Interpretation and limitations
New ST-T changes, arrhythmia or troponin rise warrants monitored care and cardiology or toxicology discussion. Normal initial tests may need repeating when symptoms or exposure are significant.
05
Serial airway and respiratory assessment
Why
Identify evolving oedema or lower-airway failure before collapse.
Interpretation and limitations
Trend voice, stridor, secretions, respiratory effort, gas exchange and flow-volume limitation. A reassuring first examination cannot exclude progression over the next several hours.
06
Chest radiograph or CT
Why
Evaluate pulmonary injury, aspiration and associated trauma.
Interpretation and limitations
Early imaging may be normal. New bilateral opacities support pulmonary oedema or acute lung injury but are non-specific; CT is reserved for a question that changes management.
07
Flexible bronchoscopy
Why
Grade and clear significant lower-airway soot, oedema or casts in selected patients.
Interpretation and limitations
Bronchoscopy is performed by experienced teams when findings will guide ventilation or toilet. A normal laryngoscopy does not fully assess distal airway injury.
08
Pregnancy and fetal assessment
Why
Recognise a fetus at risk from prolonged carbon monoxide exposure.
Interpretation and limitations
Establish pregnancy sensitively and involve obstetric and toxicology teams. Maternal improvement and carboxyhaemoglobin do not by themselves prove fetal safety; gestation-specific monitoring follows local protocol.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Simple thermal burns

External burns may occur without significant inhalation, while a normal skin examination does not exclude toxic smoke exposure.

Asthma or COPD exacerbation

Smoke can trigger genuine bronchoconstriction, but soot, enclosed exposure, neurological symptoms and co-oximetry indicate additional inhalational toxicity.

Metabolic or toxic encephalopathy

Alcohol, sedatives, hypoglycaemia and head injury can explain confusion after a fire and should be assessed alongside carbon monoxide.

Cyanide toxicity

Severe cardiovascular collapse and lactic acidosis after enclosed synthetic-material fire raise cyanide in addition to carbon monoxide.

Pulse-oximetry reassurance

Conventional saturation may appear normal in carbon monoxide poisoning; exposure history and co-oximetry distinguish true oxygen carriage impairment.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01AirwaySecure an evolving inhalation-injury airwayFirst stepHoarseness, stridor, oral burns, swelling, respiratory fatigue or a high-risk enclosed fire.

1Move to a monitored resuscitation area, give high-concentration oxygen, remove contaminated clothing when relevant and call senior anaesthesia, critical care and the burns service early.
2Assess mouth, voice, neck, breathing effort and associated facial trauma repeatedly; do not rely on one normal laryngoscopic view or chest radiograph.
3Intubate early using the local difficult-airway plan when progression is likely, with smaller tubes, videolaryngoscopy, fibreoptic or front-of-neck rescue equipment selected by experts.
4After securing the airway, use lung-protective ventilation, humidification and secretion clearance; arrange bronchoscopy when distal injury or casts are clinically important.

02Carbon monoxideTreat systemic carbon monoxide toxicityCompatible combustion exposure with symptoms or elevated co-oximetry.

1Give the highest feasible inspired oxygen concentration immediately and continue while assessing neurological state, glucose, ECG, troponin, blood gas, lactate and co-exposures.
2Discuss severe neurological features, loss of consciousness, cardiac injury, major acidosis, pregnancy or persistent symptoms with NPIS and a hyperbaric service under current arrangements.
3Base hyperbaric referral on the whole clinical picture and live guidance, not a single carboxyhaemoglobin threshold; transport and airway safety remain part of the decision.
4Before discharge, ensure the exposure source is made safe, give written advice about recurrent or delayed neurological symptoms and arrange follow-up when clinically indicated.

03CyanideRespond to suspected fire-related cyanideEnclosed-fire collapse, severe lactic acidosis, shock, coma or seizures unexplained by carbon monoxide alone.

1Continue high-concentration oxygen and full resuscitation while contacting TOXBASE or NPIS; do not delay treatment to obtain a rarely timely cyanide concentration.
2Give hydroxocobalamin when the live toxicology protocol and clinical probability support it, recording timing because it alters colour-based laboratory tests and dialysis alarms.
3Treat seizures, shock and severe metabolic derangement in critical care, reassessing for trauma, burns, carbon monoxide and other inhaled toxins in parallel.
4Avoid methaemoglobin-forming antidotes unless specifically directed by toxicology because additional impairment of oxygen carriage is hazardous when carbon monoxide coexists.

04ObservationChoose monitoring and discharge safelyThe airway is stable and immediate resuscitation is complete.

1Observe high-risk exposures for evolving airway, pulmonary, neurological and cardiac features with duration based on symptoms, investigations and toxicology advice.
2Admit patients with oxygen need, abnormal consciousness, cardiac injury, significant acidosis, airway findings, pregnancy concerns or unsafe social and exposure circumstances.
3Discharge only when clinically well with a safe environment, responsible supervision when needed, clear return precautions and appropriate primary-care or specialist follow-up.

Key medicines and prescribing safety4 treatments · regimens, roles and cautions

Accelerate carbon monoxide elimination and treat concurrent hypoxaemia from inhalation injury.

High-concentration oxygen

Give 100% inspired oxygen by a tight-fitting reservoir mask or secured airway, then follow toxicology advice for duration and weaning.

Do not use standard pulse oximetry to judge response during CO poisoning. Fire safety, airway patency and ventilatory support remain essential; hyperbaric decisions need specialist discussion.

Bind cyanide in severe suspected or confirmed cyanide toxicity from smoke exposure.

Hydroxocobalamin

For known or suspected cyanide poisoning, give an adult 5 g intravenously over 15 minutes. Depending on poisoning severity and clinical response, a second 5 g may be given over 15 minutes to 2 hours; the maximum total dose is 10 g. Give with decontamination and supportive care and follow live TOXBASE or NPIS advice.

Draw a cyanide sample first only if this causes no treatment delay. Monitor renal function because oxalate nephropathy and acute kidney injury are reported. Expect transient hypertension, red skin or urine, colorimetric laboratory interference and possible dialysis blood-leak alarms; it does not replace airway and circulatory support.

Relieve clinically important bronchospasm produced by irritant lower-airway exposure.

Inhaled salbutamol

Administer by the current acute bronchospasm protocol, repeating according to response, heart rate, potassium and lactate where severe.

Tachycardia and lactic acidosis can complicate assessment. Wheeze relief does not treat airway oedema, casts, carbon monoxide toxicity or cyanide poisoning.

Treat a bacterial complication rather than sterile chemical pneumonitis.

Antibiotics

No prophylactic regimen is indicated; treat documented pneumonia using local severity, microbiology, allergy and antimicrobial-stewardship guidance.

Early fever and radiographic change can be inflammatory. Obtain cultures when appropriate and reassess because unnecessary antibiotics add toxicity and resistance without preventing infection.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Delayed airway obstruction

Progressive supraglottic oedema can convert a stable voice and airway into rapidly difficult intubation, and increasing the burden of otherwise local respiratory disease.

Acute respiratory distress syndrome

Chemical epithelial and endothelial injury can cause delayed diffuse oedema, shunt and need for ventilation, with severity determined by its extent and the patient's underlying reserve.

Cardiac ischaemia and arrhythmia

Reduced oxygen delivery and direct cellular toxicity stress myocardium, causing infarction, dysfunction or lethal rhythm disturbance.

Delayed neurological sequelae

Cognitive, mood, movement and gait problems may emerge after an apparent recovery from carbon monoxide exposure.

Pneumonia and airway plugging

Mucosal slough, impaired cilia and thick soot-laden secretions cause obstruction, atelectasis and secondary infection, particularly when baseline cardiopulmonary reserve is limited.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Repeat voice, stridor, oropharyngeal swelling, secretion burden, work of breathing, gas exchange and airway pressures because oedema and casts can evolve after admission.
Trend neurological status with a documented cognitive and focal examination; recurrent confusion, personality change, gait problem or memory impairment needs reassessment.
Use continuous cardiac monitoring for significant exposure and repeat ECG or troponin when symptoms, initial abnormalities or toxicology guidance warrant it.
Trend pH, lactate, carboxyhaemoglobin and oxygen delivery in their timing context, without treating laboratory normalisation as proof that all tissue injury has resolved.
In pregnancy, follow obstetric advice for fetal assessment and observation; maternal saturation and symptom resolution are insufficient standalone fetal endpoints.
For ventilated lower-airway injury, monitor peak pressures, compliance, secretions, atelectasis and developing acute respiratory distress, escalating according to critical-care protocols.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

PaO2 answers the wrong CO question

The arterial oxygen tension reflects oxygen dissolved in plasma, not haemoglobin occupied by carbon monoxide. It can look normal while oxygen content and cellular use are impaired.

Measured COHb is a moving target

Time outside the source and supplemental oxygen lower carboxyhaemoglobin before blood is drawn. Clinical severity cannot be reconstructed from a late number without the exposure timeline.

Soot is a warning, not a grading system

Soot around the nose or mouth supports smoke exposure, but its absence does not exclude distal chemical injury or toxic gas absorption. Serial physiology remains more important.

The airway can worsen during resuscitation

Inflammation and fluid administration increase oedema. A cooperative patient with a hoarse voice may become a very difficult intubation, which is why early senior review matters.

One fire can produce several toxidromes

Carbon monoxide, cyanide, irritant gases, hypoxia and trauma can coexist. Treating one confirmed abnormality should never close the search for the others.

11Common pitfallsFrequent interpretation and management errors.

01
Reassuring a symptomatic fire survivor because standard pulse oximetry or PaO2 is normal.
02
Waiting for carboxyhaemoglobin before starting high-concentration oxygen.
03
Using a late low carboxyhaemoglobin value to dismiss a serious earlier exposure.
04
Delaying expert intubation until progressive upper-airway oedema makes the procedure much harder.
05
Treating a single carboxyhaemoglobin threshold as an automatic hyperbaric decision.
06
Waiting for cyanide laboratory confirmation despite shock and severe lactate elevation after an enclosed fire.
07
Giving routine steroids or antibiotics to prevent complications without a defined indication.
08
Discharging to the same unsafe appliance or building without ensuring the exposure source has been addressed.