Abstract
BACKGROUND: Ventilator-associated pneumonia (VAP) is common in critically injured patients. The pathogenesis of VAP is not completely understood. We hypothesized that mechanically ventilated trauma patients who develop pneumonia have a progressive increase in pathogen burden over the course of ventilation until a threshold for symptomatic pneumonia is reached, leading to clinical suspicion of VAP. METHODS: Critically injured adults ventilated for more than two successive days were enrolled. Patients underwent daily surveillance mini-bronchoscopic alveolar lavage (mBAL) while ventilated for 14 days or until extubation. Standard semi-quantitative cultures were performed, and the investigators were blinded to the results. Standard patient management was performed by the clinical team. Patients suspected of having VAP by the clinical team underwent bronchoscopic bronchoalveolar lavage (bBAL) and semi-quantitative culture, with VAP defined as clinical symptoms plus >10(4) colony-forming units (CFU) of bacteria. Standard statistical analysis for non-parametric data was performed. RESULTS: The 37 patients enrolled were ventilated for a median of nine days. While ventilated, 23 patients met the criteria for a clinical suspicion of VAP, of which two were too ill for bronchoscopy. Thus, 21 patients underwent bBALs because of a suspicion of VAP, and 13 (35%) were positive, with >10(4) CFU of one or more pathogens, and were treated for pneumonia. The bacterial burden on mBAL remained <10(4) CFU during ventilation for 32% of patients. None developed clinical symptoms of VAP. Two-thirds (67%) had an mBAL bacterial burden of >10(4) CFU without clinical suspicion of VAP. Half (56%) of positive surveillance cultures were followed by clinical VAP, confirmed by bBAL, all of which had identical pathogens on mBAL and bBAL. Almost half (44%) of the patients with positive surveillance mBALs never developed clinical VAP. CONCLUSION: A significant percentage of critically injured, ventilated adults develop high bacterial burdens in the lungs early in their course, and many clear these bacteria without developing VAP. Further study is needed to identify the factors causing progression to VAP.