Smoke inhalation lung injury: an update

Abstract

Objectives: The purpose of this study is to present a multifaceted, definitive review of the past and current status of smoke inhalation injury. History along with current understanding of anatomical, physiology, and biologic components will be discussed.

Methods: The literature has been reviewed from the early onset of the concept of smoke inhalation in the 1920s to our current understanding as of 2007.

Results: The results indicate that the current pathophysiologic concept is of a disease process that leads to immediate and delayed pulmonary injury best managed by aggressive physiologic support. Management approaches for the biochemical changes have not kept up with current knowledge. The lung injury process is activated by toxins in the smoke's gas and particle components and perpetuated by a resulting lung inflammation. This inflammatory process becomes self-perpetuating through the activation of a large number of inflammatory cascades. In addition, smoke injury leads to significant systemic abnormalities injuring other organs and accentuating the burn injury process and subsequently leading to mediator-induced cellular injury leading potentially to multisystem organ failure.

Conclusions: Smoke inhalation injury results in the anatomic finding of denuded and sometimes sloughed airways mucosa. Physiologic findings include small airways containing fibrin casts of mucosa and neutrophils. Airway hyper-reactivity results as well, leading to further decreased collapse, causing obstruction.

Figure 1

Effect of the components of smoke on the lungs. Water-soluble gases are seen producing upper-airway irritation. The components on the carbon particles lead to more severe airways damage including cell membrane changes and, in some cases, alveolar damage. Carbon monoxide and cyanide are absorbed directly into the blood from the alveoli

Figure 2

Relationship of COHgb and O₂ breathed. The half-life of COHgb breathing room air is about 60 minutes, compared with 20 minutes breathing 100% oxygen

Figure 3

Upper-airways edema after smoke inhalation. Note the erythema and edema of supraglottic tissue and cords. Progression of edema can lead to obstruction

Figure 4

Facial burn (24 hours). Note the marked facial and oropharyngeal distortion caused by the resulting tissue edema

Figure 5

Lower airways response to smoke exposure. Note the presence of erythema and edema in airways encroaching on the airways lumen. Addition of increased mucus can lead to destruction

Figure 6

Airway lining at 3 days. Note the infiltration of inflammatory cells around airway

Figure 7

Airway lining at 5 days. Note the absence of airways epithelium and cilia severely impairing immune defenses

Figure 8

Reactive airways. Note that airways remain hyperactive in the postinhalation injury period. Peribronchial edema and inflammation is evident

Figure 9

Severe airways injury from smoke. Note the case of airways mucosa, which can break up plugging distal airways

Figure 10

Severe tracheobronchiolitis evolving to bilateral nosocomial pneumonia. Note the diffuse nature of the respiratory dysfunction

Figure 11

Neuropeptides and airway changes. Note the loss of neutral endopeptidase (NEP) activity due to epithelial damage, increases neuropeptide activity