Combined thermal, chemical, and systemic toxic injury from combustion products; carries highest mortality in burn patients.
Also known as: inhalation injury, smoke inhalation, carbon monoxide poisoning, cyanide toxicity, burn-related inhalation
Overview
Multifaceted respiratory and systemic injury produced by inhalation of combustion products: thermal injury to the upper airway, chemical injury to the lower airway and parenchyma from particulates and irritant gases, and systemic asphyxiant toxicity from carbon monoxide and hydrogen cyanide.
Epidemiology
Present in 20-35% of hospitalized burn patients and 60-70% of burn fatalities. Inhalation injury is the strongest independent predictor of mortality after total burn surface area and age.
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Enclosed-space fire, prolonged exposure, loss of consciousness at scene
Burns to the face, neck, oropharynx, or upper torso
Industrial chemical fires (cyanide from plastics, isocyanates, hydrochloric acid from PVC)
House fires with synthetic materials releasing cyanide and hydrogen sulfide
Extremes of age, preexisting cardiopulmonary disease
Pathophysiology
Three injury mechanisms occur simultaneously. (1) Thermal injury — heated gases damage the supraglottic airway producing edema and obstruction (subglottic injury is rare due to heat absorption by the oropharynx, except with steam). (2) Chemical injury — particulates and irritant gases (aldehydes, oxides of nitrogen, ammonia, hydrochloric acid) damage tracheobronchial epithelium causing mucosal sloughing, bronchospasm, cast formation, and increased pulmonary vascular permeability. (3) Systemic asphyxiation — carbon monoxide binds hemoglobin with ~250x the affinity of O2 (left-shifts the O2-Hb curve and impairs delivery); hydrogen cyanide blocks cytochrome c oxidase causing tissue hypoxia despite adequate O2 delivery.
Clinical presentation
Symptoms
Hoarseness, stridor, dysphagia from upper airway edema
Cough productive of carbonaceous sputum
Dyspnea, wheezing, chest tightness
Headache, dizziness, nausea, altered mental status (CO and cyanide toxicity)
Signs / physical exam
Facial burns, singed nasal vibrissae or eyebrows, soot in nares or oropharynx
Carbonaceous sputum
Hoarseness or stridor, drooling
Wheezing, rhonchi, decreased breath sounds
Cherry-red skin is RARE in CO poisoning (postmortem finding); cyanide produces an unreliable bitter-almond odor
Classic findings
Patient pulled from house fire with soot in nares, hoarse voice, and altered mental status — assume thermal upper airway injury and CO/CN toxicity.
Differential diagnosis
Cutaneous burn without inhalation injury — Burn surface area without facial soot, singed nasal hair, or carbonaceous sputum; SpO2 normal
ARDS from other causes — Bilateral infiltrates after another insult (sepsis, trauma) without inhalation history; carboxyhemoglobin normal
Acute methemoglobinemia — Cyanosis unresponsive to O2 with chocolate-brown blood; oximetry reads ~85% regardless of true SaO2; treat with methylene blue
Toxic gas exposure (chlorine, ammonia, phosgene) — Industrial or chemical exposure history; chest CT shows similar tracheobronchitis pattern
Anaphylaxis — Urticaria, angioedema, hypotension after allergen exposure; responds to epinephrine
Diagnostic workup
Diagnostic criteria
Diagnosis is clinical: enclosed-space fire exposure + ≥1 of facial burns, singed nasal hair, carbonaceous sputum, hoarseness/stridor, hypoxia, or altered mental status. Bronchoscopy grades severity (Abbreviated Injury Score 0-IV).
Labs
Co-oximetry arterial blood gas (standard pulse oximetry does NOT distinguish carboxyhemoglobin from oxyhemoglobin)
Lactate — elevation >10 mmol/L in the absence of severe burn shock is highly suggestive of cyanide toxicity
Carboxyhemoglobin (normal <3% nonsmoker, <10% smoker; symptomatic at >10-20%; severe at >25%)
CBC, CMP, troponin, ECG (CO can cause myocardial ischemia)
Type and crossmatch, coagulation studies if surgical needs anticipated
Imaging
Chest radiograph is often normal initially even with severe inhalation injury — sensitivity is low in the first 24-48 hours
Flexible fiberoptic bronchoscopy within 24 hours is the gold standard for diagnosis and severity grading (mucosal erythema, edema, soot deposition, sloughing, ulceration)
CT chest may reveal bronchial wall thickening; reserve for diagnostic uncertainty
Diagnostic algorithm
flowchart TD
A[Fire victim<br/>enclosed space] --> B[100% non-rebreather]
B --> C{Airway signs?}
C -->|Stridor, hoarse,<br/>facial burns| D[Early intubation]
C -->|None| E[Bronchoscopy in 24 h]
B --> F[Co-oximetry ABG +<br/>lactate]
F --> G{COHb >25% or<br/>neuro/cardiac Sx?}
G -->|Yes| H[HBO therapy]
G -->|No| I[Continue normobaric O2<br/>until COHb <5%]
F --> J{Lactate >10 or<br/>persistent shock?}
J -->|Yes| K[Hydroxocobalamin 5 g IV<br/>± Na thiosulfate]
Initial management algorithm for smoke inhalation injury — addresses airway, CO, and cyanide in parallel.
Treatment
First-line
100% high-flow oxygen via non-rebreather mask immediately (reduces CO half-life from ~250 min on room air to ~70 min on 100% O2)
Early intubation for any sign of impending airway compromise (stridor, drooling, deep facial burns, voice changes) — airway edema can progress rapidly and make later intubation impossible
Nebulized therapy: albuterol for bronchospasm; nebulized heparin (5,000-10,000 units q4h) and nebulized N-acetylcysteine to reduce cast formation (per Mt Sinai/Texas burn protocols, though level of evidence is moderate)
Hydroxocobalamin 5 g IV over 15 min for suspected cyanide toxicity (preferred over sodium thiosulfate plus sodium nitrite in fire victims because nitrite-induced methemoglobinemia worsens CO physiology)
Severe CO toxicity
Hyperbaric oxygen indicated for COHb >25% (>20% in pregnancy), loss of consciousness, neurologic deficits, myocardial ischemia, or persistent symptoms after 4 hours of normobaric O2
Continue normobaric 100% O2 until COHb <5% and neurologic exam returns to baseline
Cyanide toxicity
Hydroxocobalamin 5 g IV (binds CN to form cyanocobalamin, excreted renally; turns urine and skin red-orange)
Sodium thiosulfate 12.5 g IV as adjunct
Avoid sodium nitrite in fire victims because of methemoglobinemia interaction with CO
Refractory respiratory failure
Consider ECMO referral
Prone positioning if ARDS criteria met
Complications
Upper airway obstruction (loss of airway window)
ARDS
Pneumonia (particularly Pseudomonas, MRSA) and tracheobronchitis
Anoxic brain injury and delayed neuropsychiatric sequelae of CO poisoning (weeks after exposure)
Chronic obstructive disease and bronchiectasis in survivors
PANCE pearls
Standard pulse oximetry CANNOT detect CO poisoning — it reads carboxyhemoglobin as oxyhemoglobin. Use co-oximetry.
Hyperbaric oxygen is reserved for severe CO toxicity criteria — do not delay other resuscitation for HBO.
Subglottic thermal injury is uncommon because the oropharynx absorbs heat — exception is superheated steam exposure.
Lactate >10 mmol/L in a fire victim without obvious hemorrhage is essentially diagnostic of cyanide toxicity until proven otherwise.
Fluid resuscitation in burns plus inhalation injury frequently exceeds standard Parkland formula needs; titrate to urine output 0.5 mL/kg/h and avoid over-resuscitation.
References
American Burn Association — Walker PF et al. Diagnosis and Management of Inhalation Injury: An Updated Review. Crit Care 2015;19:351 (referenced in ABA practice guidelines)
CHEST 2018 — Foncerrada G et al. Inhalation Injury in the Burned Patient. Ann Plast Surg 2018;80(3 Suppl 2):S98-S105
Undersea & Hyperbaric Med Soc — UHMS Indications for Hyperbaric Oxygen Therapy — Carbon Monoxide Poisoning (latest revision)
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