Shutterstock/Around the World Photos
We published “Don’t Get Burned” in September 2025t about airway management for burn patients. The focus was making the decision to intubate or not and being ready in case the patient’s condition worsened. This one is not exactly Part Two, rather it is a deeper dive into what damage has been caused by the burn or inhalation and the various causes of hypoxia these patients suffer from.
In this piece we will talk about three causes of hypoxia for burn patients: acute respiratory distress syndrome (ARDS), carbon monoxide poisoning, and hydrogen cyanide poisoning.
Damage…
Damage to the lungs and airways occurs through a few different pathways.
- Direct thermal burns from the inhalation of superheated gases.
- Inhalation of carbonaceous materials.
- Systemic effects of inhaled asphyxiants: carbon monoxide (CO) and hydrogen cyanide (HCN).
This tells us that these patients are suffering from a combination of destruction of the airways, contamination of the airways that generates more damage, and an inability to deliver oxygen to tissues.
To make matters worse, burns lead to a massive release of inflammatory mediators and cytokines.1-2 This leads to damage to and destruction of the vascular endothelium and endothelial glycocalyx, which results in increased vascular permeability (read: leak).1-2 This can spell disaster for the lungs since much of the damaged endothelium and capillaries communicate directly with the alveoli.
The ensuing pulmonary edema and alveolar damage results in the inability to adequately oxygenate.1-2 Increased resistance and low pulmonary compliance from the edema and alveolar damage make it progressively more difficult for the patient to generate adequate minute volume and thereby bring in less and less oxygen.
This is the ARDS we all know and love (but not really), at its most basic level. If ARDS was the only challenge to overcome, then this would be a useless article. Burned tissue not only swells, but eschar is very stiff and non-compliant, which also gets progressively worse.
Circumferential chest/torso burns are particularly difficult.3 The resulting stiffness from the eschar acts like a constricting band around the chest wall, limiting the essential bellows function to allow the lungs to fill with air.3
In some cases that constriction is severe enough to require an escharotomy. This procedure entail making incisions along midaxillary line and subcostal margins to allow the chest to expand and restore normal ventilation.3
The Vent Strategy
Keeping in mind that these patients are incredibly complex, the overall strategy for mechanical ventilation is focused on lung protection. The ARDSnet strategy of using 6-8cc/kg of ideal body weight to calculate the needed tidal volume is still a cornerstone of ventilation for the burn patient.4-5
There really is no special maneuver, mode, or approach that has shown a specific benefit for burn patients. Therefore, it is prudent to keep the strategy simple and approach vent management for these patients as you would any other ARDS patient:4-5
- Low tidal volume ventilation (6-8cc/kg)
- Reasonable PEEP titrations that prevent derecruitment of good alveoli, recruits collapsed alveoli, and does not put the pPLAT above 30.
- Controlling plateau pressures (pPLAT) to stay less than 30 to the greatest degree possible.
- Allow for permissive hypercapnia, an expected by-product of ARDS and low tidal volume ventilation (target a pH greater than 7.2).
The vent strategy is to keep the patient ventilated and attempt to move as much oxygen as possible into the blood stream to be delivered to the tissues. It can slow the progression of ARDS and lessen the severity if the strategy is such that it does not cause strain and worsen the cycle of inflammation and edema formation.4-5
Moving oxygen into the bloodstream is only half of the battle for a burn patient.
Asphyxiants and Hypoxias
The physical damage of inhalation injuries is easy to isolate to the lungs (generally). The patient has to contend with two specific hypoxia challenges of the four types of hypoxia:6
- hypoxic hypoxia – a lack of oxygen in the arterial system.
- stagnant hypoxia – a lack of forward flow to the tissues.
- histotoxic hypoxia – inability of the cells to use oxygen for normal metabolism.
- anemic hypoxia – a lack of oxygen carrying capacity.
The hypoxia from ARDS leaves the patient with a lack of oxygen delivery to the tissues because of the difficulty in facilitating diffusion of oxygen into the blood due to the damage to the alveolar capillary membranes and pulmonary edema.
The other form of hypoxia that the burn patient must overcome is histotoxic hypoxia. A dwelling fire (or any fire which involves the combustion of synthetic materials) allows for the formation of hydrogen cyanide (HCN) in addition to carbon monoxide (CO).7-8
When synthetic materials like vinyl, wool, plastic, etc. burn, they produce HCN as a byproduct. The production of HCN does not stop when the flames go out, HCN and CO are still produced from the smoldering embers.7-8
Both compounds negatively impact oxygenation. CO primarily keeps oxygen from binding to hemoglobin (forming carboxyhemoglobin (COHb)and therefore it cannot be transported to the tissue beds.6-8
HCN on the other hand inhibits cellular respiration and the formation of adenosine triphosphate (ATP) by inhibiting the action of complex IV in the respiratory chain, specifically it inhibits the enzyme cytochrome c oxidase (COX).7-8 This inhibition effectively halts oxidative phosphorylation and the production of ATP.
As we know, ATP is the currency of energy in the body and without its organs cease to function as does the entire human body. The patient suffers from a predictable metabolic acidosis and eventually succumbs.
The one-two punch of CO and HCN poisoning presents us with quite the challenge to restore oxygenation as they both inhibit it at the mitochondrial level. It is worth noting that the literature is inconclusive as to which substance is “more lethal” although death from CO poisoning is more common.
However, studies have shown fatalities from smoke inhalation where the HCN level was elevated and CO level was below 50%, as well as victims with elevated CO levels and no detectable HCN levels.8
CO poisoning is treated with oxygen therapy or hyperbaric oxygen therapy while HCN poisoning responds to any one of the four currently available antidotes, some of which may or may not be available in the prehospital setting.7
Conclusion
ARDS physically impacts the patient’s ability to move oxygen molecules from the atmosphere into the blood stream. HCN and CO poisoning affect the patient’s ability to use the oxygen that does make it into the blood stream to create ATP and keep the machine running. Add to this the poor hemodynamic state a burn patient presents with and the prehospital team is left to contend with a maximally complicated and fragile patient.
References
1. Albright JM, Davis CS, Bird MD, et al. The acute pulmonary inflammatory response to the graded severity of smoke inhalation injury. Crit Care Med. 2012 Apr;40(4):1113-21. doi: 10.1097/CCM.0b013e3182374a67. PMID: 22067627; PMCID: PMC3290689.
2. Niu Z, Ding Z, Chan Y, et al. Clinical characteristics and predictors of burn complicated with smoke inhalation injury: A retrospective analysis. Exp Ther Med. 2022 Nov 9;24(6):758. doi: 10.3892/etm.2022.11694. PMID: 36561970; PMCID: PMC9748657.
3. Chung KK, Rhie RY, Lundy JB, et al. A Survey of Mechanical Ventilator Practices Across Burn Centers in North America. J Burn Care Res. 2016 Mar-Apr;37(2):e131-9. doi: 10.1097/BCR.0000000000000270. Erratum in: J Burn Care Res. 2017 Mar 1;38(2):134. doi: 10.1097/BCR.0000000000000521. PMID: 26135527; PMCID: PMC5312724.
4. Bittner E, Sheridan R. Acute Respiratory Distress Syndrome, Mechanical Ventilation, and Inhalation Injury in Burn Patients. Surg Clin North Am. 2023 Jun;103(3):439-451. doi: 10.1016/j.suc.2023.01.006. Epub 2023 Mar 21. PMID: 37149380; PMCID: PMC10028407.
5. Schultz MJ, Horn J, Hollmann MW, et al. Ventilation practices in burn patients-an international prospective observational cohort study. Burns Trauma. 2021 Dec 16;9:tkab034. doi: 10.1093/burnst/tkab034. PMID: 34926707; PMCID: PMC8676707.
6. Hirota K. Hypoxia-dependent signaling in perioperative and critical care medicine. J Anesth. 2021 Oct;35(5):741-756. doi: 10.1007/s00540-021-02940-w. Epub 2021 May 18. PMID: 34003375; PMCID: PMC8128984.
7. Lawson-Smith P, Jansen EC, Hyldegaard O. Cyanide intoxication as part of smoke inhalation–a review on diagnosis and treatment from the emergency perspective. Scand J Trauma Resusc Emerg Med. 2011 Mar 3;19:14. doi: 10.1186/1757-7241-19-14. PMID: 21371322; PMCID: PMC3058018.
8. Tabian D, Bulgaru Iliescu D, Iov T, Barna B, Toma SI, Drochioiu G. Hydrogen cyanide and carboxyhemoglobin assessment in an open space fire-related fatality. J Forensic Sci. 2021 May;66(3):1171-1175. doi: 10.1111/1556-4029.14649. Epub 2020 Dec 28. PMID: 33369895; PMCID: PMC8246848.
Cody Winniford is a flight paramedic and base manager in Baltimore, MD. He has a passion for sharing his professional experience in EMS and management. Cody’s clinical and leadership development background spans both military and civilian settings and has served in several capacities as a leader and prehospital clinician. He specializes in air medical and critical care transport, as well as organizational development and leadership development. He is an active speaker on various leadership and clinical topics and is an established and successful educator for prehospital clinicians of all levels. He has a passion for human performance improvement and the mental health and performance aspects of prehospital care.
