Inhalation Injury in Burns
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Direct answer
Carbon monoxide lies to a pulse oximeter: carboxyhaemoglobin absorbs light identically to oxyhaemoglobin, so the saturation reads reassuringly high while the patient is tissue-hypoxic — 100% oxygen is the treatment, reducing the half-life of carboxyhaemoglobin from roughly 4–6 hours on room air to about 60–90 minutes. Inhalation injury in burns spans three components: supraglottic thermal injury (oedema threatening the airway), carbon monoxide and cyanide poisoning (systemic asphyxiants), and lower airway injury from smoke and chemicals (chemical tracheobronchitis and pneumonia). Diagnosis rests on the setting (enclosed-space fire), signs (singed nasal vibrissae, carbonaceous sputum, hoarseness, stridor, facial burns) and bronchoscopy; management rests on a low threshold for early intubation before oedema closes the airway, high-concentration oxygen, supportive ventilation, and increased fluid resuscitation volumes.
What you must remember
- The triad of inhalation injury components: upper airway thermal injury (heat exchange in the pharynx usually protects the cords and below — except steam, which carries far more heat energy), carbon monoxide and cyanide poisoning, and lower airway chemical injury from products of combustion.
- Carboxyhaemoglobin: pulse oximetry is falsely normal; co-oximetry is required. Half-life about 4–6 hours on room air, roughly 60–90 minutes on 100% oxygen, about 20–30 minutes under hyperbaric conditions; symptoms begin with headache and nausea around 10–20%, confusion at 30–40%, coma and seizures above roughly 50%.
- Hyperbaric oxygen is considered for carboxyhaemoglobin above about 25%, neurological deficits, loss of consciousness, or pregnancy, provided the patient is haemodynamically stable and burns manageable.
- Cyanide poisoning from burning plastics (especially in enclosed industrial or house fires): high lactate (often above 10 mmol/L), a metabolic acidosis out of proportion, and a near-normal PaO2 — treat with hydroxocobalamin (or the classic antidote kits) in suspected cases.
- Clinical predictors: enclosed-space fire, altered consciousness, singed nasal hairs, carbonaceous sputum, hoarseness, stridor (a late, ominous sign), facial and neck burns, and tachypnoea; bronchoscopy confirms and grades injury (carbonaceous deposits, erythema, oedema, mucosal sloughing).
- Early elective intubation before transfer or resuscitation: oedema progresses over hours, and the swollen burn airway is the surgical airway nobody wants in an emergency; the cuffed tube also permits ventilation of the injured lower airways.
- Inhalation injury raises burn fluid requirements (commonly 30–50% above calculated Parkland volumes) and is the strongest driver of burn mortality after burn size and age.
- Escalation options in severe lower airway injury: lung-protective ventilation, aggressive airway toilet, bronchodilators, mucolytics and humidification, sometimes nebulised heparin and N-acetylcysteine in some burn centres.
How to work through it
A woman is pulled from a burning kitchen, face blackened, coughing carbon-flecked sputum and speaking hoarsely. First, the airway decision: hoarseness plus carbonaceous sputum plus facial burns means early intubation now, while anatomy is still recognisable — not after two hours of resuscitation fluid have turned the glottis into a slit. Second, the asphyxiants: she is confused; a co-oximeter shows carboxyhaemoglobin of 32%, and the lactate is elevated enough to worry about cyanide. Treatment runs in parallel — 100% oxygen by non-rebreather (or via the ventilator once intubated), hydroxocobalamin for suspected cyanide, and discussion of hyperbaric therapy, which in practice is rarely feasible in a major burn needing surgery. Third, the lungs: bronchoscopy shows carbonaceous deposits and erythema down to segmental bronchi, confirming lower airway injury; ventilation is lung-protective from the start, airway toilet and physiotherapy are scheduled, and the fluid chart is watched carefully — she will need more than calculated volume, delivered without drowning the lung. Over the following days the enemies are retained secretions, atelectasis and pneumonia; tracheostomy is considered if the ventilator course looks prolonged. Each step buys the mucosa the one to two weeks it needs to regenerate.
Where students slip
Two facts separate the well-taught answer. First, the oximeter: candidates quote a falling saturation as a sign of carbon monoxide poisoning, but the saturation is misleadingly normal — only co-oximetry (arterial blood gas with carboxyhaemoglobin measurement) reveals it, and that "oximeter lies" line is precisely what examiners want. Second, the steam exception: hot dry air exchanges its heat in the upper airway, but steam delivers latent heat below the cords, so only steam (and explosions or chemical fumes) classically injures the lower airway directly. Third, stridor: treating hoarseness as the early sign and stridor as the late one — by the time stridor appears, the airway is nearly lost; waiting for it is the error the scenario is built to catch.
Frequently asked questions
Why is pulse oximetry unreliable in carbon monoxide poisoning?
Carboxyhaemoglobin and oxyhaemoglobin absorb similar wavelengths of light, so the oximeter overestimates true oxygen saturation; only co-oximetry measures carboxyhaemoglobin directly.
How does 100% oxygen change carboxyhaemoglobin half-life?
From roughly 4–6 hours on room air to about 60–90 minutes on 100% inspired oxygen, and shorter under hyperbaric conditions — which is why high-flow oxygen starts at the scene.
Which findings on bronchoscopy indicate inhalation injury?
Carbonaceous debris coating the airway, mucosal erythema and oedema, ulceration or sloughing, and increased secretions — bronchoscopy is the diagnostic standard and grades severity.
When is hyperbaric oxygen therapy considered?
For carboxyhaemoglobin above about 25%, neurological signs or loss of consciousness, and pregnant patients, provided the burn itself can be safely managed alongside or within the chamber.
How does inhalation injury alter burn fluid resuscitation?
It increases requirements — commonly 30–50% above formula-predicted volumes — because of the added inflammatory capillary leak, while demanding close monitoring to avoid worsening the lung injury.