Smoke Inhalation Lung Injury: An Update

Smoke inhalation injury, either by itself or in the presence of a burn, is now well-recognized to result in severe lung-induced morbidity and mortality. The most common cause of death in burn centers is now respiratory failure.1–3 Overall, burn tragedies in history have markedly improved our knowledge of this injury (Table ​(Table1).1). Although smoke inhalation injury has been present since ancient times, it was probably the use of chemical warfare agents in World War I that first initiated the interest. Table 1 Notable events leading to smoke inhalation knowledge In 1915, the German army released aerosolized chlorine into the air toward the Allied troops. The response, upon breathing, was severe airway irritation with coughing, and severe exposure led to pulmonary edema and death. Filtering the gases with an activated charcoal filter removed the chlorine from the air,4,5 a method of decreasing lung damage. Phosgene gas, a component of smoke, was purified and also used as a chemical warfare agent along with mustard gas, also leading to lung damage.4 Phosgene is a common component of smoke today in any fire. The Cleveland Clinic Fire, in 1929, was caused by burning x-ray film. The cause of the many respiratory deaths was considered to be the released toxin, nitrogen dioxide, again a component of smoke in fires today.6 Skin burns were frequently absent and management of the lung injury became a priority for burn teams. The pulmonary pathology after smoke exposure was considered to be slough of the large- and small-airway mucosa causing obstruction to breathing. It was not until after the Coconut Grove Night Club Fire in 1942 that a surge of research in the pathophysiology of smoke inhalation developed.7,8 In this tragedy, hundreds of people were involved, many dying rapidly from apparent respiratory failure in the absence of burns. Others initially survived only to die later of what appeared to be pneumonia.7,8 Of importance was the fact that victims, not dead on arrival, appeared to be stable until 12- to 24-hours later, at which point the respiratory distress developed.7–9 Bronchial obstructions which developed, now recognized to be the result of the delayed airways mucosal slough, were caused by toxins that carried carbonaceous particles. Carbon monoxide poisoning was then well understood, so the initial use of oxygen was already established.9 By the mid-1940s, World War II was underway, and the risks of lung damage from closed-space fires were well recognized. Dr Oliver Cope, at the Massachusetts General Hospital, was instrumental in describing the pathology, time course, and the treatment of the severe cases of smoke inhalation injury. Respiratory assistance was recognized as a key factor in survival.9 The late effect on the airways and alveoli of smoke exposure was not yet appreciated, as ventilator assistance was not yet a tool used for longer-term survival. It was not until the use of blood-gas analysis in the late 1960s, that a clearer pattern of basic pathophysiology was determined along with the establishment of critical care medicine.10 The adult respiratory distress syndrome (ARDS) was also becoming recognized in the 1960s, and alveolar edema and collapse were recognized.11 It was still to be determined that smoke inhalation was mainly a large- and small-airway injury, although ARDS remained an alveolar damage process. Also, the role of bacteria in the lungs after inhalation injury became better recognized.12,13 A burst of research activity from the late 1970s and early 1980s better defined the chemical toxins found in smoke, including cyanide. Advances in the field of toxicology and the composition of aerosols provided the tools for research in the area. Identification of gas and particle phases of smoke and its components allowed for fairly accurate cause-and-effect hypotheses.11–16 The advances were followed by more active research on particle size and distribution in the lung. It was not appreciated until later that the particles carried gas phase toxins, which then deposited on the tracheal bronchial tree leading to the airways injury. The potentiating effect of a smoke injury on burn morbidity and mortality was well described in the 1980s. The mechanism of this potentiating effect still remains poorly understood.17–20 Overall, uncovering the physiologic changes in the lung evolved stepwise through fairly recent history (Table ​(Table22).21–23 Table 2 Historic progression of known physiologic changes in smoke injury Through the 1990s to the present, the research focus in this area has been to better define the biochemical and cell biologic changes, occurrence of which would explain the recognized physiologic changes. The products of airway inflammation, characteristics of smoke injury, have been of particular interest.24–29 Proinflammatory cytokines and free oxygen radicals have been demonstrated to play a significant role in both the lung and systemic response to smoke. More recently, apoptosis or programmed cell death has been found in the injured airways epithelium.28 The Station Nightclub Fire in Rhode Island in 2005 and the 9/11 World Trade Center tragedy in 2001 have led to a number of observations, stimulating further research.29,30 However, it is fair to state that the recently identified cell biologic and cell genetic changes have not yet altered the clinical management. The identified physiologic changes have, however, played a major role in improving management, thereby leading to a decrease in mortality and morbidity.