Abstract
BackgroundAcute lung injury (ALI) is a major factor determining morbidity following burns and inhalational injury. In experimental models, factors potentially contributing to ALI risk include inhalation of toxins directly causing cell damage; inflammation; and infection. However, few studies have been done in humans.MethodsWe carried out a prospective observational study of patients admitted to the NC Jaycees Burn Center who were intubated and on mechanical ventilation for burns and suspected inhalational injury. Subjects were enrolled over an 8-month period and followed till discharge or death. Serial bronchial washings from clinically-indicated bronchoscopies were collected and analyzed for markers of cell injury and inflammation. These markers were compared with clinical markers of ALI.ResultsForty-three consecutive patients were studied, with a spectrum of burn and inhalation injury severity. Visible soot at initial bronchoscopy and gram negative bacteria in the lower respiratory tract were associated with ALI in univariate analyses. Subsequent multivariate analysis also controlled for % body surface area burns, infection, and inhalation severity. Elevated IL-10 and reduced IL-12p70 in bronchial washings were statistically significantly associated with ALI.ConclusionsIndependently of several factors including initial inhalational injury severity, infection, and extent of surface burns, high early levels of IL-10 and low levels of IL-12p70 in the central airways are associated with ALI in patients intubated after acute burn/inhalation injury. Lower airway secretions can be collected serially in critically ill burn/inhalation injury patients and may yield important clues to specific pathophysiologic pathways.
Highlights
Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) occur in a substantial proportion of patients following burns and inhalational injury, and are major factors associated with morbidity and mortality
Our goal was to examine whether mediator profiles early after inhalational injury could be predictive of clinical outcomes, and if these observations could be used to develop discrete hypotheses regarding the mechanisms by which burn and inhalational injury modulate airway innate immunity
One enrolled patient was excluded from the data analysis due to lack of specimens obtained during the first 72 hours post-injury, and another 2 did not have sufficient material left for analysis, after clinical use of specimens
Summary
Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) occur in a substantial proportion of patients following burns and inhalational injury, and are major factors associated with morbidity and mortality. Risk factors for lung injury include the inhalation of products of incomplete combustion containing a variety of toxins and particulate matter, direct cell damage, inflammation, infection, edema, and immunologic changes due to burn injury [1,2,3]. Serial bronchoscopies and airway washings for clearance of soot, debris and secretions are part of supportive care [9,10,11]. Acute lung injury (ALI) is a major factor determining morbidity following burns and inhalational injury. Factors potentially contributing to ALI risk include inhalation of toxins directly causing cell damage; inflammation; and infection.
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