The pathophysiology of inhalation injury is multifactorial. Direct thermal injury accounts for the trauma to the supraglottic region while chemical and particulate constituents of smoke contribute to the damage caused to the tracheobronchial tree and lung parenchyma. The chemical injury initiates a series of events which include the release of inflammatory mediators with subsequent increased permeability leading to edema, mucosal sloughing and cast formation. This can manifest clinically as bronchospasm, small airway occlusion and decreased pulmonary compliance all which contribute to respiratory failure .
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