The aim of this study was to determine the incidence, the organisms responsible for and the impact on outcome of nosocomial tracheobronchitis (NTB) in the intensive care unit (ICU).This prospective observational cohort study was conducted in a 30-bed medical/ surgical ICU over a period of 6.5 yrs. All patients ventilated for w48 h were eligible. Patients with nosocomial pneumonia (NP) without prior NTB were excluded. Patients with first episodes of NTB were compared with those without NTB by univariate analysis.The study diagnosed 201 (10.6%) cases of NTB. Pseudomonas aeruginosa was the most common bacteria. NP rates were similar in patients with NTB compared with patients without NTB. Even in the absence of subsequent NP, NTB was associated with a significantly higher length of ICU stay and duration of mechanical ventilation in both surgical and medical populations. Mortality rates were similar in NTB patients without subsequent NP compared with patients without NTB. Antimicrobial treatment in NTB patients was associated with a trend to a better outcome.Nosocomial tracheobronchitis is common in mechanically ventilated intensive care unit patients. In this population, nosocomial tracheobronchitis was associated with longer durations of intensive care unit stay and mechanical ventilation. Further studies are needed to determine the impact of antibiotics on outcomes of patients with nosocomial tracheobronchitis.
Cellular events that occur in status asthmaticus (SA) remain poorly investigated. Autopsy studies frequently emphasized about the presence of eosinophils in bronchial airway wall, whereas recent studies reported increased number of neutrophils in patients dying of sudden-onset fatal asthma. Mucus plugs occluding the bronchial lumen are almost constant features during SA. Bronchial lavage (BL) may be useful to remove mucus plugs in cases of atelectasis and/or refractory SA. We investigated the contribution of different cell types and cellular mediators (neutrophil elastase, eosinophil cationic protein [ECP], histamine, interleukin-8 [IL-8]) to the pathogenesis of SA. We studied 16 BL from eight patients undergoing mechanical ventilation (MV) for SA (time interval from onset of MV = Day 0 to Day 11), four BL from patients undergoing MV without preexisting respiratory disease (V), 11 BL from patients with stable asthma (A) and eight BL from healthy controls (C). SA exhibited higher number and percentage of neutrophils (81.5 +/- 4.5%) than V (44.3 +/- 12.2) (p < 0.05), A (6.9 +/- 2.7) and C (9.5 +/- 3.8) (p < 0.0001), and higher number of eosinophils than V, A, and C (p < 0.01). Neutrophil elastase, ECP, and IL-8 levels were dramatically increased in SA. Histamine was higher in SA than in C and V (p < 0.05). Bronchial neutrophilia was not related to concomitant bacterial infection as bacteriological cultures were positive in only three BL. Eosinophils, mast cells and histamine were higher in BL performed within the first 48 h of MV (p < 0.05) than in BL performed later on. Our results indicate that bronchial inflammation in SA differs from bronchial inflammation in mild asthma. Persistent bronchial neutrophilia is associated with increased eosinophils and mast cells in the early phase of SA. Neutrophils may result in tissue damage and participate to the shedding of the epithelium in SA.
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