With improvements in the treatment of burn shock and sepsis, inhalation injury has emerged as the main cause of mortality in the burn patient. 24 Despite advances in respiratory support, smoke inhalation injury significantly increases mortality; half of all fire-related deaths are due to smoke inhalation. Inhalation injuries are associated with closed-space fires, and conditions that decrease mentation—such as overdose, alcohol intoxication, drug abuse, and head injury. Exposure to smoke includes exposure to heat, particulate matter, and toxic gases.11
There is general consensus that direct thermal injury is limited to the upper airway. Thermal injuries below the vocal cords occur only in cases of steam inhalation.
Smoke contains particulate matter, usually less than 0.5 pm in size, which is formed from incomplete combustion of organic material. Small particles may reach the terminal bronchioles, where they can initiate an inflammatory reaction leading to bronchospasm and edema.
Toxic inhalants are divided into three large groups: tissue asphyxiants, pulmonary irritants, and systemic toxins. The two major tissue asphyxiants are carbon monoxide and hydrogen cyanide.
Carbon monoxide poisoning is a well-known consequence of smoke inhalation injury.11 Severe carbon monoxide poisoning will produce brain hypoxia and coma. Comatose patients lose airway protective mechanisms, which may result in aspiration, thus further exacerbating the pulmonary injury from smoke inhalation. All patients with suspected carbon monoxide exposure should be started on 100% oxygen by non-rebreathing mask. Further details of treatment of carbon dioxide poisoning are discussed in Chap 198.
Hydrogen cyanide is formed when nitrogen-containing polymers—such as wool, silk, polyurethane, or vinyl—are burned. Cyanide binds to and disrupts mitochrondrial oxidative phosphorylation, leading to profound tissue hypoxia. Further discussion of management of cyanide poisoning is discussed in Chap 182.
Inhalation injury damages endothelial cells, produces mucosal edema of the small airways, and decreases alveolar surfactant activity leading to bronchospasm, airflow obstruction, and atelectasis. With time, tracheal and bronchial epithelial sloughing occurs. As these patients are resuscitated with large quantities of fluid for their burn injury, pulmonary edema develops. Hence, the potential for adult respiratory distress syndrome (ARDS) from inhalation injury should be recognized and careful fluid management instituted with emphasis on hemodynamic monitoring.
Bronchospasm may occur early, but lower airway edema is usually not clinically evident for up to 24 h. Upper airway edema, however, can occur rapidly. Although the injury is mainly to the airways, pulmonary vascular changes do occur. There is no single method capable of demonstrating the extent of inhalation injury. Diagnosis of smoke inhalation is made from the history of a fire in an enclosed space and physical signs that include facial burns, singed nasal hair, soot in the mouth or nose, hoarseness, carbonaceous sputum, and expiratory wheezing. Carboxyhemoglobin levels are useful to document prolonged exposure within an enclosed space with incomplete combustion. The chest radiograph may be normal initially; bronchoscopy and radionuclide scanning are useful in determining the full extent of injury.
Treatment of suspected inhalation injury should be instituted prior to definitive diagnosis. Humidified oxygen (100%) should be administered by mask. Arterial blood gases including carboxyhemoglobin levels should be obtained. In suspected cases, control of upper airway is achieved by prompt endotracheal intubation. Indications for intubation include (1) full-thickness burns of the face or perioral region, (2) circumferential neck burns, (3) acute respiratory distress, (4) progressive hoarseness or air hunger, (5) respiratory depression or altered mental status, and (6) supraglottic edema and inflammation on bronchoscopy.
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