What is the pathophysiology of smoke inhalation in the lower lung areas?

Updated: Oct 15, 2021
  • Author: Keith A Lafferty, MD; Chief Editor: Joe Alcock, MD, MS  more...
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Inhalation of toxic products triggers a cascade of effects in the lower lung areas, such as the following [13] :

  • Activation of the body's inflammatory response system

  • Direct tissue injury

  • Mucus oversecretion

  • Acute bronchospasm or bronchorrhea

Activation of polymorphonuclear neutrophils (PMNs), resident alveolar macrophages, increased activity of systemic interleukin (IL)–1, IL-6, IL-8, and tumor necrosis factor alpha (TNF-α) and neutrophilic infiltration are suggested to mediate the physiopathologic changes that subsequently lead to atelectasis and impaired mucociliary function. [7] In addition, humoral mediators such as prostanoids and leukotrienes produce reactive oxygen species and proteolytic enzymes, which contribute to the development of pulmonary edema and the formation of airway fibrin clots and hypoxemia.

Supporting the importance of the inflammatory response in tissue destruction, some studies have shown that administration of the cyclooxygenase inhibitor ibuprofen reduced the lung lymph flow in animals with smoke inhalation. [14, 15]

The direct injury is a consequence of the size of the particle, its solubility in water, and its acid-base status. Ammonia produces alkaline injury, while sulfur dioxide and chlorine gas cause acid injuries. Other chemicals act via different mechanisms; for instance, acrolein causes free radical formation and protein denaturation. [16]

The solubility of the substance in water determines the location of injury and timing of symptoms. Highly soluble substances such as acrolein, sulfur dioxide, ammonia, and hydrogen chloride cause injury to the upper airway and cause immediate symptoms. Substances with intermediate solubility, such as chlorine and isocyanates, cause both upper and lower respiratory tract injury with more delayed symptoms. Phosgene (a colorless gas with oxidant properties) and oxides of nitrogen have low water solubility and cause diffuse parenchymal injury, with symptoms sometimes delayed up to a day or more.

Days after the injury, the risk of bacterial infection increases markedly. Ciliary function is impaired, leading to accumulation of airway debris. Macrophages within the alveoli are destroyed, allowing bacteria to proliferate. Disruption of the epithelial barrier by ulcerations and necrosis further facilitates the development of pneumonia.

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