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BACKGROUND

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Fire-related injuries constitute a major health hazard in the United States. It is estimated there is a civilian fire death every 175 minutes, and a civilian death from a home fire every 208 minutes in the United States.1 It is also a leading cause of pediatric accidental injury and death. In 2009, burn-related fatalities were the sixth leading cause of accidental injury-related death in children under 19 years, and the third leading cause between the ages of 1 and 9 years.2 The injury to the skin can be just one facet of the potentially multisystem insults that occur. Smoke inhalation is the leading cause of death in house fires, with mortality rates of approximately 5% to 8%.3 The focus of this chapter is inhalation injury associated with fires and incomplete combustion, specifically, thermal airway injuries, smoke inhalation, carbon monoxide (CO), and cyanide poisoning. Dermal burns are discussed in Chapter 162.

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PATHOPHYSIOLOGY

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The upper airways and the trachea can dissipate heat very effectively and direct thermal injury is not common. However, when it does occur, injury is often limited to structures above the carina.4 Swelling of these structures ensues in the hours following the injury and can result in critical upper airway obstruction.

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Even without skin burns or upper airway injury, significant lower airway involvement can occur in a child who inhales toxic particles in smoke. Irritants and gases can also cause direct mucosal injury, inflammation, edema, interference with surfactant production, and loss of normal protective ciliary action. Materials and fabrics found in homes and buildings can release respiratory irritant gases and particles from combustion. Respiratory irritants include hydrogen chloride, chlorine, phosgene, acrolein, ammonia, isocyanates, and nitrogen oxides.5 Irritants that are highly water soluble (ammonia, hydrogen chloride) and larger particles (>10 μm) will primarily affect mucous membranes and upper airways. Lower water soluble irritants (chlorine, phosgene) and smaller particles (<2 μm), can reach the lower airways and lung parenchyma, and can cause delayed injury. Some gases, such as nitrous oxide or sulfur dioxide, can combine with lung water to form acids which can cause corrosive injury to the bronchial tree.6 The high minute ventilation characteristic of children puts them at increased risk for smoke inhalation injury as compared to adults.7

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Some gases, such as methane, can act as simple asphyxiants by displacing oxygen. Others, such as carbon monoxide (CO) and cyanide, act as systemic toxicants. Exposure to combustion or smoke in a closed or partially closed space puts the patient at high risk for CO and cyanide poisoning. CO is a colorless, odorless gas produced from the incomplete combustion of carbon-containing substances. Other important sources of CO exposure include car exhaust fumes, furnaces, and wood-burning stoves. Epidemics tend to occur in winter months or with natural disasters associated with power outages. Alternative methods of heating and cooking and snow-obstructed motor vehicle exhaust systems are more common under these conditions.8-10

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CO is a tissue asphyxiant that disrupts both hemoglobin’s oxygen-carrying capacity and cellular metabolism. CO binds to hemoglobin with an affinity 200 to 300 times greater than that of oxygen. ...

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