The 3 primary mechanisms that lead to injury in SI are thermal damage, asphyxiation, and pulmonary irritation. Thermal damage Thermal damage usually is limited to the oropharyngeal area. This is due to the poor conductivity of air and the high amount of dissipation that occurs in the upper airways. Animal experiments have shown that if air at 142C is inhaled, then by the time it reaches the carina it will have cooled to 38C. Steam, volatile gases, explosive gases, and the aspiration of hot liquids provide some exceptions, as moist air has a much greater heat-carrying capacity than dry air.
Tissue hypoxia can occur secondary to several mechanisms. Combustion utilizes oxygen, which in a closed space may be consumed, significantly decreasing the ambient concentration of oxygen to as low as 10-13%. The decrease in fraction of inspired oxygen (FIO2) leads to hypoxia, despite adequate circulation and oxygen-carrying capacity. Carbon monoxide (CO) causes tissue hypoxia by decreasing the oxygen-carrying capacity of the blood. Hemoglobin binds CO with an affinity more than 200 times greater than the affinity for oxygen.
O also causes a left shift in the oxyhemoglobin saturation dissociation curve. CO has been shown to bind to the cytochrome oxidase chain in vitro. Finally, CO decreases myocardial contractility. Combustion of plastics, polyurethane, wool, silk, nylon, nitriles, rubber, and paper products can lead to the production of cyanide (CN) gas. Consider CN toxicity in all SI patients with CNS or cardiovascular findings. CN is a chemical asphyxiant that interferes with cellular metabolism by binding to the ferric ion on cytochrome a3, subsequently halting cellular respiration.
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