Updated July 2026 · 10 min read
Part of the ICU Emergencies Hub — browse every related guide in one place.
"Inhalation injury" is really three different injuries wearing one name, each with its own mechanism, its own timeline, and its own treatment. The patient who looks stable in the first hour can lose their airway in the next — which is why the decisions here are about timing, not just recognition.
Hot air holds little heat and the upper airway is an efficient heat exchanger, so the thermal injury from a fire is usually confined above the vocal cords — the mouth, pharynx, and larynx (steam is the exception; it carries far more heat and can burn lower). That sounds reassuring until you remember what happens next: burned mucosa swells, and it keeps swelling as resuscitation fluids arrive. An airway that is patent and only mildly irritated on arrival can become impossible to intubate a few hours later as edema progresses.
Once intubated, protect the tube fiercely. In a face-and-neck burn the tissue will swell dramatically; a tube that dislodges may be unre-placeable. Secure it with ties rather than tape on burned skin, document the depth, and treat an unplanned extubation as a genuine emergency.
Smoke is a suspension of toxic particles and gases — aldehydes, acids, and other products of combustion that vary with what was burning. These reach the small airways and alveoli and cause a chemical injury that unfolds over hours to days: bronchospasm, mucosal sloughing that forms casts and plugs, loss of the airway's ciliary clearance, surfactant dysfunction, and an inflammatory, leaky, ARDS-like picture. Unlike the upper-airway thermal injury, this one is not fixed by an endotracheal tube — the tube protects the upper airway but the lung injury still evolves.
| Lower-airway problem | Bedside consequence |
|---|---|
| Bronchospasm | Wheeze, rising airway pressures — bronchodilators |
| Mucosal sloughing / cast formation | Plugging, atelectasis, sudden desaturation — aggressive pulmonary toilet, suctioning, sometimes bronchoscopy |
| Alveolar injury / capillary leak | Worsening oxygenation, ARDS physiology — lung-protective ventilation |
| Impaired ciliary clearance + burn immunosuppression | High risk of pneumonia over the following days |
Management is largely supportive and meticulous: lung-protective ventilation, humidification, chest physiotherapy and frequent suctioning to clear casts, bronchodilators for spasm, and — at some centers — nebulized regimens (for example heparin and N-acetylcysteine protocols) aimed at reducing cast formation. Watch closely for the pneumonia that so often follows.
The deadliest part of smoke is invisible and does not lower the SpO2 reading. Two gases poison oxygen delivery and use:
| Carbon monoxide (CO) | Cyanide (CN) | |
|---|---|---|
| Mechanism | Binds hemoglobin ~200–250× tighter than oxygen, forming carboxyhemoglobin — blood can't carry oxygen | Poisons mitochondrial cytochrome oxidase — cells can't use oxygen |
| Clue | Headache, confusion, normal-looking SpO2, elevated carboxyhemoglobin on co-oximetry | Severe lactic acidosis, cardiovascular collapse, normal or high venous oxygen saturation |
| Treatment cornerstone | High-flow 100% oxygen (hyperbaric in selected cases) | Hydroxocobalamin (antidote); supportive care |
The three injuries run on different clocks, so your priorities stack in a specific order. First, the airway — assess it immediately and secure it early if there is any suspicion of upper-airway involvement, before edema and fluids close it. Second, oxygenation and the asphyxiants — put every smoke-exposure patient on high-flow 100% oxygen from the start (this also speeds CO clearance), send co-oximetry, and keep cyanide on your differential for the crashing, acidotic patient. Third, the lung injury — anticipate that oxygenation will get worse over the first days, plan lung-protective ventilation and relentless pulmonary toilet, and expect pneumonia. Running underneath all of it is fluid resuscitation for any accompanying cutaneous burn (see the Parkland formula guide) — with the caveat that inhalation injury makes the lungs far less forgiving of over-resuscitation, so titration discipline matters even more.
On the CRNA path, the inhalation-injury patient is the archetype of the airway you must secure before it becomes unmanageable — the definition of a difficult, time-limited airway. The judgment you build deciding when to intubate the hoarse, sooty patient in the ICU is exactly the judgment anesthesia demands: read the trajectory, not the current snapshot, and act while the airway is still yours to take.
Smoke inhalation is three injuries: an upper-airway thermal burn that swells shut over hours (secure the airway early, on suspicion), a lower-airway chemical injury that evolves into ARDS-like failure over days (support, suction, expect pneumonia), and systemic asphyxiants — CO and cyanide — that poison oxygen delivery and use without dropping the pulse ox (100% oxygen, co-oximetry, keep cyanide in mind). Get the order right and you cover all three clocks.
This article is general educational information for licensed clinicians and students, not medical advice or a substitute for your institution's protocols, burn-center guidance, or a provider's orders. Always follow facility policy and verify every dose independently.
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