Accidental and intentional airway inhalation injuries are a major cause of death in the United States.
Toxic inhalants include asphyxiants, irritants and systemic toxins that result in airway damage, hypoxia and respiratory failure.
Tests and imaging should include arterial blood gas, carboxyhemoglobin level, chest radiograph, electrocardiogram (EKG), and may include bronchoscopy.
Attention should be focused on securing the airway, insuring adequate oxygenation, treating shock, correcting acidemia, cardiac monitoring, and administering available antidotes.
Fires kill more than 3200 and injure approximately 16,000 civilians annually in the United States1,2 via thermal, chemical and systemic injury to the airway caused by toxic inhalation of carbon monoxide (CO), cyanide (CN), and other toxins. Toxic inhalation is the major cause of death from fires with 80% of cases related to CO poisoning.3 Complications of toxic inhalation include airway damage, pneumonia, and acute respiratory distress syndrome (ARDS).4 More than 50,000 patients a year visit the emergency department with CO poisoning in the United States.5
Particles greater than 5 μm in diameter are cleared by the nasopharynx,6 but in smoke inhalation, larger particles may lodge deeper in the airway as patients breathe through the mouth.4 Thermal injuries from fires primarily affect the upper airways, as air cools as it travels to the carina. Combustion results in decreased oxygen in ambient air and asphyxiation.
Damage to the airway and lung parenchyma result in free radical formation, inflammation, increased capillary permeability, and capillary leakage. Alveoli are filled with fluid and blood. Polymorphonuclear macrophages, IL-1, IL6, IL-8, and tumor necrosis factor-α activation result in atelectasis, bronchospasm, impaired mucociliary function, and in some cases, ARDS. ARDS results from alveolar and lung endothelium capillary injury. Initially inflammation leads to increased capillary endothelial permeability resulting in accumulation of fluid in the alveoli and pulmonary edema. This leads to intrapulmonary shunting as fluid-filled alveoli are perfused but not ventilated, resulting in hypoxemia.
Toxic inhalants can be divided into asphyxiants, irritants and systemic toxins. Asphyxiants induce hypoxia, which can result in headache, dizziness, nausea, dyspnea, altered mental status, cardiac ischemia, respiratory failure, syncope, coma, and seizures. Simple asphyxiants such as helium, argon, carbon dioxide, chlorofluorocarbon refrigerants, methane, and propane displace oxygen and result in oxygen deprivation. Systemic asphyxiants such as CO, CNs, and sulfides impair oxygen transport resulting in tissue hypoxia and reduced oxidative phosphorylation and hence ATP synthesis. Irritants such as ammonia, chlorine, nitrogen oxides, and sulfur dioxide, and systemic toxins such as hydrocarbons, organophosphates, and metal fumes can cause upper and lower airway burns and destruction resulting in respiratory distress and failure.
In all cases of toxic inhalation (Table 57B–1) priorities include securing the airway and insuring adequate oxygenation, treating shock with crystalloids and vasopressors, correcting acidemia, cardiac monitoring and ...