fire and smoke inhalation exposures

Fires are a leading cause of injury and death around the world. Smoke inhalation can cause damage to the respiratory tract and have systemic consequences. Injury severity depends on the ignition source, duration of exposure, and size of particles in the smoke. Generation of reactive oxygen species creates cytokine release that triggers an inflammatory cascade throughout the exposed airway. In addition, the balance between coagulation factors and antifibrinolysis becomes unstable, affecting alveolar homeostasis. This combination can lead to capillary leak and airway edema, impaired ciliary function, and bronchospasm. Patients who are exposed to fire must be examined and monitored closely to determine the extent and location of their injuries, including the airways. Injuries to the upper airway are primarily due to thermal exposure as a result of effective heat exchange and can result in airway edema, erythema, and ulcers. Close attention must be paid to patients with inhalation and burn injury, as fluid needed to treat shock and/or accommodate transdermal water loss can accelerate edema. Impaired ciliary function can affect mucous clearance, with atelectasis, pneumonia, and/or airway obstruction. Injuries to the tracheobronchial tree are usually caused by the chemicals generated by the smoke and should be considered in patients with wheezing and cough, particularly if cough produces dark, soot-containing secretions. Parenchymal injury is not immediately seen, unless there is severe damage or a delay in presentation. It is usually detected by impaired oxygenation from ventilation/perfusion mismatch due to alveolar fibrin deposition. Attention to systemic toxicity is imperative.

Carbon monoxide poisoning is a frequent cause of death in smoke inhalation injury. Carbon monoxide is a colorless, odorless gas with an affinity for hemoglobin more than 200 times higher than that of oxygen. Carboxyhemoglobin severely impairs the release of oxygen at the tissues and use of oxygen in mitochondria, leading to profound tissue hypoxia. Conventional two-wavelength pulse oximetry cannot differentiate between carboxyhemoglobin and oxyhemoglobin and therefore is insufficient to detect the presence of carboxyhemoglobin. All patients who present after inhalation injury or house fires should receive high-flow oxygen irrespective of  SpO2  or PaO2 and have the carboxyhemoglobin level sent through a co-oximetry panel (Figure 1) to exclude carbon monoxide toxicity (choice B is correct).

Head CT scanning can be considered in patients who present with an altered level of consciousness to evaluate for occult injury. However, this should be performed after determining the extent of carbon monoxide poisoning through co-oximetry (choice A is incorrect). Thorax CT scanning can be useful to determine the extent of parenchymal injury after the patient is stabilized and the extent of carbon monoxide poisoning is known (choice C is incorrect).

Hyperbaric oxygen is reserved for patients with a carbon monoxide level >25% or who are pregnant with a carbon monoxide level >20% (choice D is incorrect). Rapid assessment of the carbon monoxide level is important because transfer to a center for hyperbaric therapy may be necessary. In addition, all patients suspected of having carbon monoxide poisoning from smoke inhalation should be evaluated for cyanide poisoning, given the high likelihood of it occurring during a fire. The gaseous form of cyanide, hydrogen cyanide, is a colorless gas with a bitter almond smell. Arterial blood gas measurements with elevated lactate levels and elevated anion gap metabolic acidosis are seen. Bright red venous blood should raise suspicion of cyanide poisoning. A minimal difference between arterial and venous PO2 are also seen. Emergency consultation with a toxicologist should be performed and antidote immediately administered, as cyanide toxicity is rapidly fatal if not treated. Hydroxocobalamin is the antidote, should be considered in any patient being treated for smoke inhalation, and should be administered in severe cases (cardiac decompensation and/or arrest), even if laboratory confirmation is not yet attained.