Inhalation Injury & Carbon Monoxide in Burns

Meet the patient

A 48-year-old man is brought in unconscious after being rescued from a house fire in a small enclosed room. He has facial burns, singed nasal hairs, and soot in his mouth and sputum. SpO2 reads 99 per cent on 15 L of oxygen. The blood gas shows a pH of 7.20, a lactate of 11.8 mmol/L, and the CO-oximeter reads a carboxyhaemoglobin of 34 per cent — a level at which neurologic impairment is expected, with a lactate in the cyanide range.^[5][6]

Three things are true at once. His airway is swelling and will be impossible in hours; his pulse oximeter is lying to him about his oxygenation; and a second, invisible poison — cyanide — is blocking his mitochondria. The trap is to believe the reassuring SpO2 and wait on the airway. The answer is to intubate now, give 100 per cent oxygen, and reach for the hydroxocobalamin.^[5][14]

Smoke inhalation is a time-critical, multi-compartment injury that kills more fire victims than the cutaneous burn itself: most fire-related deaths occur at the scene from CO and cyanide and upper-airway obstruction, not from the burn wound. Among patients who reach a burn centre, concomitant inhalation injury carries a pooled odds ratio of 3.2 for in-hospital mortality and adds roughly 45 per cent to fluid requirements in the classic series (mean 5.76 versus 3.98 mL/kg per percentage TBSA). Three anatomically and mechanistically distinct processes coexist after any significant smoke exposure and each demands a specific intervention:^[3][9][4]

1. Supraglottic thermal injury — heat is a poor penetrant of gas; the upper airway (nasopharynx, oropharynx, supraglottic larynx) acts as a heat exchanger that cools dry inspired gas below the vocal cords. Thermal damage is therefore largely confined above the cords (the larynx takes the most intense thermal damage), producing progressive mucosal oedema that can occlude the laryngeal inlet — the single most important reason to intubate before the airway becomes impossible.^[14][17]
2. Subglottic chemical tracheobronchitis or pneumonitis — combustion generates a toxic aerosol. Water-soluble irritants (HCl, ammonia, sulphur dioxide) deposit in the upper airway causing laryngospasm and bronchospasm; lipid-soluble toxins (phosgene, nitrogen dioxide, acrolein, the aldehydes) penetrate to the alveoli, denaturing surfactant, sloughing mucosa, forming fibrin casts, and triggering an ARDS picture over the first days.^[1]
3. Systemic asphyxiant toxicity — CO and cyanide — incomplete combustion in an enclosed space generates CO (binds haemoglobin with around 200 to 250 times the affinity of O2) and cyanide (combustion of wool, silk, polyurethane, plastics — CN blocks cytochrome c oxidase). Pulse oximetry is falsely normal in CO poisoning; a high lactate (above 10 mmol/L) is the bedside surrogate for cyanide.^[5][6][1]

References18ShowHide

1. [1]Foncerrada G, Culnan DM, Capek KD, et al. Inhalation Injury in the Burned Patient Ann Plast Surg, 2018.PMID 29461292
2. [2]Rose JJ, et al. Carbon Monoxide Poisoning: Pathogenesis, Management, and Future Directions of Therapy Am J Respir Crit Care Med, 2017.PMID 27753502
3. [3]Galeiras R, Seoane-Quiroga L, Pértega-Díaz S Prevalence and prognostic impact of inhalation injury among burn patients: A systematic review and meta-analysis J Trauma Acute Care Surg, 2020.PMID 31688831
4. [4]Brusselaers N, Monstrey S, Vogelaers D, Hoste E, Blot S Severe burn injury in Europe: a systematic review of the incidence, etiology, morbidity, and mortality Crit Care, 2010.PMID 20958968
5. [5]Culnan DM, Craft-Coffman B, Bitz GH, et al. Carbon Monoxide and Cyanide Poisoning in the Burned Pregnant Patient: An Indication for Hyperbaric Oxygen Therapy Ann Plast Surg, 2018.PMID 29461288
6. [6]Baud FJ, et al. Elevated blood cyanide concentrations in victims of smoke inhalation N Engl J Med, 1991.PMID 1944484
7. [7]Weaver LK, Hopkins RO, Chan KJ, et al. Hyperbaric oxygen for acute carbon monoxide poisoning N Engl J Med, 2002.PMID 12362006
8. [8]Endorf FW, Gamelli RL Inhalation injury, pulmonary perturbations, and fluid resuscitation J Burn Care Res, 2007.PMID 17211205
9. [9]Navar PD, Saffle JR, Warden GD Effect of inhalation injury on fluid resuscitation requirements after thermal injury Am J Surg, 1985.PMID 4073365
10. [10]Desai MH, Mlcak R, Richardson J, et al. Reduction in mortality in pediatric patients with inhalation injury with aerosolized heparin/N-acetylcystine therapy J Burn Care Rehabil, 1998.PMID 9622463
11. [11]Thompson JP, Marrs TC Hydroxocobalamin in cyanide poisoning Clin Toxicol (Phila), 2012.PMID 23163594
12. [12]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
13. [13]Wong E, Dodson N, Wagner S, et al. Time to Burn? Characteristics of Hydroxocobalamin Administration in an Academic Medical Center J Pharm Pract, 2024.PMID 36318086
14. [14]Gupta K, Mehrotra M, Kumar P, et al. Smoke Inhalation Injury: Etiopathogenesis, Diagnosis, and Management Indian J Crit Care Med, 2018.PMID 29657376
15. [15]Brower RG, Matthay MA, Morris A, et al. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome N Engl J Med, 2000.PMID 10793162
16. [16]Amarasekera NN, Jha A, Charles WN, et al. Evaluating the association between bronchoscopic severity of burns-related smoke inhalation injury and clinical outcomes: A systematic review and meta-analysis Burns, 2025.PMID 41101183
17. [17]Reid A, Ha JF Inhalational injury and the larynx: A review Burns, 2019.PMID 30529118
18. [18]Weaver LK Carbon monoxide poisoning Undersea Hyperb Med, 2020.PMID 32176957