Smoke Inhalation

Juan C. Martinez, MD, FAAP

Introduction/Etiology/Epidemiology

•Smoke inhalation affects a small population of pediatric patients admitted for burns. In a retrospective review of 5,959 pediatric patients admitted to Parkland Burn Center over 35 years, inhalation injury was identified in 3.1% of burned individuals.

•Smoke inhalation injury can involve the upper airway (supraglottic), lower airway (infraglottic), or lung parenchyma. The degree of airway injury depends on the duration of smoke exposure and the composition of the smoke. Toxic combustion products are simple asphyxiants, irritant toxins, and chemical asphyxiants.

•Flame and inhalation injuries are more common in older children, according to some large series.

•Inhalation injury with burns significantly increases the odds of mortality to 14:1.

•Toxic by-products of smoke—carbon monoxide and cyanide—are primarily responsible for mortality. Other potential smoke compounds that may contribute to pathologic findings include acrolein/propanol, aldehydes, ammonia, hydrogen chloride, hydrogen sulfide, phosgene, and sulfur dioxide.

Pathophysiology

•Mouth breathing promotes laryngeal and large-airway damage.

•Injury can be classified as upper-airway thermal injury, chemical irritation of the respiratory tract, or systemic toxic gas toxicity.

•The main pathologic features are bronchospasm, pulmonary edema, bronchopneumonia, and ventilation-perfusion mismatch.

•Systemic inflammatory response syndrome is promoted by excess formation of reactive oxygen species.

•Carbon monoxide is likely the primary cause of death in most cases.

•Carbon monoxide and cyanide gas exposure, derived from sources such as nylon, silks, and plastics, contribute to death.

•Airway necrosis contributes to poor mucociliary clearance and infection.

•Small-airway obstruction predominates, with mucus plugging and bacterial infection common manifestations.