Sher Mohammad and authors look at smoke inhalation affecting airways, with a brief focus on carbon monoxide and hydrogen cyanide poisoning
Smoke inhalation injury is a major determinant of morbidity and mortality in a fire victim. It is a complex multifactorial injury affecting the airway, however in a short time it can become a complex life-threatening systemic disease affecting every organ in the body.
Up to 30% of all flame burns presentations may suffer with smoke inhalation injury and in higher proportions if facial burns are present. It carries a high mortality and is the most common cause of death at the incident of fire. Inhalation injury increases the risk of death from a burn many times. Respiratory complications are more than 70% and the risk of ARDS is 20%. Patients younger than 10 years and older than 65 are at risk. Likewise, physical or cognitive disability will contribute towards mortality.
In order to understand the pathophysiology, clinical presentation and the management of smoke inhalation injury, we will briefly mention the components of smoke first. For the sake of completion, we will briefly explain carbon monoxide and cyanide poisoning as well.
Components of smoke
Smoke is a product of combustion, which is composed of air borne solids, liquid particles and gases that are mixed with entrained air. The composition of smoke depends on materials present, the availability of O2 and the nature of combustion. The amount of smoke is less if the temperature generated is high and the O2 is in abundance. The products that are produced as a result of flame burn include chemicals that will cause chemical damage to the respiratory tract. Other products include CO and HCN, which results in systemic toxicity. Here is a list of chemicals/poisons produced as a result of flame burns.
- Aldehydes are produced from wood and paper.
- NO2 is produced from fabric.
- H2, Cl2, and SO2 are produced when rubber is burnt.
- N2 containing material will yield NH3.
- Synthetic materials such as furnishings, plastics and vinyl will produce hydrogen cyanide.
- NH3 will combine with H2O to form alkali e.g. NH4 OH
- H2, Cl2, and SO2 will combine with H2O to form acids e.g.HCl and H2SO4
Alkalis and acids will result in chemical burns of the throat, larynx and trachea. Hydrogen cyanide and CO are known asphyxiants and result in carbon monoxide and cyanide poisoning.
Smoke inhalation injury is caused by the inspiration of steam, superheated gases, or toxic, often incomplete products of combustion.
So smoke inhalation results in three physiological types of injury
- Thermal injury predominantly to the upper airway:
The heating capacity of steam is 4000 times that of hot dry air and thus causes tissue damage, even with momentary contact. Major pathophysiological change is the development of oedema in the respiratory tract. The upper airway including tongue, throat and glottis could be injured by superhot steam, of these the most fatal is the glottic oedema.
- Chemical injury to the upper and lower respiratory tract: Particles up to 10µm size will be entrained in nostrils and nasopharynx while particles of 1-2µm will reach up to alveoli.
The toxic chemicals can lead to chemical injury causing bronchoconstriction. Proteolytic elastases damage the lung parenchyma leading to the release of inflammatory mediators which increase the trans-vascular flux of fluids resulting in pulmonary oedema and atelectasis.
- Systemic effects of toxic gases such as CO and HCN: Early deaths in fire are predominantly due to hypoxia, which results from a lethal synergistic effect of low O2 levels (due to massive O2 consumption during combustion) and inhalation of high concentrations of CO and HCN (both result in inability of O2 consumption at mitochondrial level).
Systemic effects happen as a result of CO ad HCN poisoning leading to hypoxia.
Mechanism of systemic toxicity
If the victim of burns is in a closed space, the concentration of O2 could be as low as 10%. Products of incomplete combustion cause hypoxia, the main toxic compound in fire deaths is carbon monoxide (80% of fire deaths by fire gases). CO is a the main culprit which causes hypoxia by three mechanisms. Firstly, CO attaches itself to Hb more avidly(250 times) as compared to O2. Secondly, it shifts the Hb-O2 curve to the left decreasing unloading of O2 to the tissues. Thirdly, it inhibits the binding of O2 with cytochrome oxidase, mitochondrial enzyme needed in cellular utilization of O2.
Smoke inhalation is one of the most common cause of cyanide poisoning which is 20 times more toxic than CO. Hydrogen cyanide is a colourless gas with a bitter almond odour which cannot be detected by humans