Inhalation Injury 

Although children are less likely than adults to experience significant smoke inhalation, it remains a serious and life-threatening problem in the pediatric population. Management of a child with burns and a coexistent inhalation injury requires a cohesive team of pediatric intensive care physicians, nurses, and burn specialists. Although children with burns have traditionally been cared for in adult burn units, the increased availability of physicians, nurses, and ancillary staff trained in the care of severely ill pediatric patients make the pediatric intensive care unit a superior environment. Understanding that children are not merely small adults is critical to preventing therapeutic errors that can result in disastrous iatrogenic complications.

The heat generated during combustion can cause significant thermal injury to the upper airway. Particulate matter produced during combustion (soot) can mechanically clog and irritate the airways, causing reflex bronchoconstriction. Noxious asphyxiant gases released during thermal decomposition include carbon monoxide (CO) and hydrogen cyanide. Other byproducts produced by combustion of furniture and cotton (aldehydes) or rubber and plastics (chlorine gas, ammonia, hydrocarbons, various acids, ketones) produce injury. Exposure to metal fumes and fluorocarbons, systemic toxins typically released during industrial fires, is rare in the pediatric population. Children are less likely to be affected by systemic toxins than by toxins from household products and products of smoke, including CO and cyanide poisoning.

Routine use of smoke and CO detectors in the home is designed to decrease the risk of injury by permitting early escape. However, the risk for smoke inhalation remains high in the pediatric population, and ongoing prevention efforts are important.

Inhalation injury occurs in 3 ways: (1) by cell injury and pulmonary parenchymal damage by irritants, (2) hypoxemia by interruption of oxygen delivery by asphyxiants, and (3) end organ damage by systemic absorption through the respiratory tract.

Respiratory embarrassment can be broadly categorized as the result of thermal or chemical damage to the epithelial surfaces of the intrathoracic and extrathoracic airways. Secondary insult with bacterial pneumonia may occur days after inhalation, causing further cytotoxic damage. Ciliary function is impaired, leading to accumulation of airway debris. The inflammatory cascade initiates neutrophil infiltration. Macrophages within the alveoli are destroyed, allowing bacteria to proliferate. Lack of an intact epithelial barrier further facilitates the development of pneumonia.

Hypoxemia results from a decrease in inspired oxygen concentration at the scene of injury, a mechanical inability to exchange gas because of airway obstruction or parenchymal pulmonary disease, and inhibition of oxygen delivery and tissue use by toxins. With the advent of sophisticated intensive care support, patients who survive the acute injury and are successfully transported to an ICU now rarely die from isolated pulmonary disease. However, the presence of multiorgan dysfunction, a common sequela of hypoxia, substantially raises morbidity and mortality.

Because CO does not directly injure the lung, its toxic effect results from a displacement of oxygen from hemoglobin-binding sites, thereby decreasing the oxygen-carrying capacity of the blood. It not only has a 250-fold increased affinity for hemoglobin than oxygen but also shifts the oxyhemoglobin dissociation curve to the left. The leftward shift of the oxyhemoglobin dissociation curve results in further tissue hypoxia because the hemoglobin is less able to unload oxygen. CO reacts with myoglobin to further impair oxygen uptake by decreasing facilitated diffusion of oxygen into muscle. CO also interacts with several heme-containing enzymes of the electron transport chain, further impairing tissue oxygen availability.

Cyanide causes tissue asphyxiation through the inhibition of intracellular cytochrome oxidase. It blocks the final step in oxidative phosphorylation and prevents mitochondrial oxygen use. Affected cells convert to anaerobic metabolism, and lactic acidosis ensues. The organs most sensitive to cellular hypoxia are the CNS and the heart. The CNS reacts to low concentrations of cyanide through hyperventilation, thereby increasing exposure if the route is by inhalation.

Frequency

United States

Burns in children are 2.5 times more likely to occur by scalding rather than flame exposure. Hence, the percentage of children who experience respiratory symptoms after burns is less than that of adults who are more often exposed to smoke-producing flames. About 50% of all burn deaths are related to inhalation injuries. Early hypoxemia is a contributor to over 50% of smoke inhalation deaths, with CO intoxication accounting for as much as 80% of the fatalities.

Mortality/Morbidity

Inhalation injury significantly increases the morbidity and mortality of burns. Small children are especially vulnerable because they are less likely to escape a confined space and also have a higher minute ventilation, which increases exposure to smoke and other toxins released during pyrolysis. In addition, their relatively smaller airways will be more severely affected by airway edema and obstructing material.

Bacterial pneumonia often complicates inhalation injury within 4-5 days of presentation. This additional cellular damage can cause significant mortality days to weeks after the initial injury.

Children with acute pulmonary injury secondary to toxic inhalations generally do well once supported through the initial inflammation and damage. Most of the pulmonary damage is self-limited and resolves within 2-3 days. The degree of recovery depends on the extent of the pulmonary parenchymal injury and subsequent hypoxic damage to the organs.

Residual reactive airway disease, bronchiectasis, bronchiolitis obliterans, and interstitial fibrosis have been reported. However, the cause-and-effect relationships between toxic exposure and pulmonary sequelae remain controversial and unproven.

Airway hyperreactivity generally improves over several months following inhalation injury. However, some authors documented long-term respiratory symptoms such as cough, wheeze, and shortness of breath even after mild inhalation injury, indicating a more prolonged nature of the lung injury. The long-term effects of inhaled toxins on pulmonary function are not yet determined.

CO intoxication is a particularly serious consequence of smoke inhalation and may account for as much as 80% of fatalities from inhalation injury. Most patients who arrive alive to the emergency department make a full recovery. However, up to one third of patients with significant CO exposure develop a secondary syndrome of long-term neurologic dysfunction within 1-3 weeks after exposure. Higher cortical functions seem most severely affected. Whether the use of hyperbaric oxygen (HBO) therapy alters the outcome of delayed-onset neurologic dysfunction due to CO poisoning remains controversial. Approximately one third of patients with smoke inhalation from domestic fires also have high blood cyanide levels.