9-29: Smoke Inhalation

The inhalation of products of combustion may cause serious respiratory complications. As many as one-third of patients admitted to burn-treatment units have pulmonary injury from smoke inhalation. Morbidity and mortality due to smoke inhalation may exceed those attributed to the burns themselves. The death rate of patients with both severe burns and smoke inhalation exceeds 50%.

All patients in whom significant smoke inhalation is suspected must be assessed for three consequences of smoke inhalation: impaired tissue oxygenation, thermal injury to the upper airway, and injury to the lower airways and lung parenchyma. Impaired tissue oxygenation may result from inhalation of a hypoxic gas mixture, carbon monoxide or cyanide, or from alterations in V̇/Q̇ matching, and is an immediate threat to life. Immediate treatment with 100% oxygen is essential. The management of patients with carbon monoxide and cyanide poisoning is discussed in Chapter 38. The clinician must recognize that patients with carbon monoxide poisoning display a normal partial pressure of oxygen in arterial blood (PaO₂), but have a low measured (ie, not oximetric) hemoglobin saturation (SaO₂). Treatment with 100% oxygen should be continued until the measured carboxyhemoglobin level falls to less than 10% and concomitant metabolic acidosis has resolved.

Thermal injury to the mucosal surfaces of the upper airway occurs from inhalation of super-heated gases. Complications, including mucosal edema, upper airway obstruction, and impaired ability to clear oral secretions, usually become evident by 18–24 hours and produce inspiratory stridor. Respiratory failure occurs in severe cases. Early management (Chapter 37) includes the use of a high-humidity face mask with supplemental oxygen, gentle suctioning to evacuate oral secretions, elevation of the head 30 degrees to promote clearing of secretions, and topical epinephrine to reduce edema of the oropharyngeal mucous membrane. Helium-oxygen gas mixtures (Heliox) may reduce labored breathing due to critical upper airway narrowing. Close monitoring with ABGs and later with oximetry is important. Examination of the upper airway with a fiberoptic laryngoscope or bronchoscope is superior to routine physical examination. Endotracheal intubation is often necessary to maintain airway patency and is likely to be necessary in patients with deep facial burns or oropharyngeal or laryngeal edema. Tracheotomy should be avoided, if possible, because of an increased risk of pneumonia and death from sepsis.

Injury to the lower airways and lung parenchyma results from inhalation of toxic gases and products of combustion, including aldehydes and organic acids. The site of lung injury depends on the solubility of the gases inhaled, the duration of exposure, and the size of inhaled particles that transport noxious gases to distal lung units. Bronchorrhea and bronchospasm occur early after exposure along with dyspnea, tachypnea, and tachycardia. Labored breathing and cyanosis may follow. Physical examination at this stage reveals diffuse wheezing and rhonchi. Bronchiolar and alveolar edema (eg, ARDS) may develop within 1–2 days after exposure. Sloughing of the bronchiolar mucosa may occur within 2–3 days, leading to airway obstruction, atelectasis, ...