Ventilator-associated pneumonia in a surgical intensive care unit: epidemiology, etiology and comparison of three bronchoscopic methods for microbiological specimen sampling

Citation
Hj. Woske et al., Ventilator-associated pneumonia in a surgical intensive care unit: epidemiology, etiology and comparison of three bronchoscopic methods for microbiological specimen sampling, CRIT CARE, 5(3), 2001, pp. 167-173
Citations number
19
Categorie Soggetti
Aneshtesia & Intensive Care
Journal title
CRITICAL CARE
ISSN journal
1466609X → ACNP
Volume
5
Issue
3
Year of publication
2001
Pages
167 - 173
Database
ISI
SICI code
1466-609X(2001)5:3<167:VPIASI>2.0.ZU;2-F
Abstract
Background: Ventilator-associated bacterial pneumonia (VAP) is a important intensive care unit (ICU) acquired infection in mechanically ventilated pat ients. Early and correct diagnosis of VAP is difficult but is an urgent cha llenge for an optimal antibiotic treatment. The aim of the study was to eva luate the incidence and microbiology of ventilator-associated pneumonia and to compare three quantitative bronchoscopic methods for diagnosis. Methods: A prospective, open, epidemiological clinical study was performed in a surgical ICU. In a prospective study, 279 patients admitted to a 14-be d surgical ICU during a 1-year period were evaluated with regard to VAP. Th ree quantitative culture bronchoscopic techniques for identifying the etiol ogical agent were compared [bronchoalveolar lavage (BAL), protected specime n brush (PSB) and bronchoscopic tracheobronchial secretion (TBS)]. Results: Among 103 long-term ventilated patients, 49 (48%) developed one or more VAPs (a total of 60 VAPs). The incidence was 24 VAPs per 100 ventilat ed patients or 23 VAPs per 1000 ventilator days. BAL, PSB and TBS with quan titative measurements were equivalent in identifying the bacterial etiology . The VAP was caused predominantly by Staphylococcus aureus in 38% of cases , followed by Pseudomonas aeruginosa in 10%, Haemophilus influenzae in 10% and Klebsiella sp. in 9%. We did not find an increased mortality rate in pa tients undergoing long-term ventilation who acquired VAP in comparison with patients without VAP. Conclusion: For the identification of the microbiological etiology of VAP, one of three available bronchoscopic methods analysed by quantitative measu rements is sufficient. In our study, quantitative bronchoscopic tracheal se cretion analysis was very promising. Before accepting this method as a stan dard technique, other studies will have to confirm our results.