Abstract
Background. Ventilator-associated pneumonia (VAP) is a leading cause of morbidity and mortality in intensive care unit (ICU) patients, encompassing up to 15% of all hospital acquired infections. Our hospital implemented a facility-wide conversion from a low-volume high-pressure polyvinyl cuffed endotracheal tube (PV-cuffed ETT) to a high-volume low-pressure (HVLP) polyurethane-cuffed endotracheal tube (PU-cuffed ETT) in an effort to reduce the incidence of VAP. Methods. We completed an IRB approved, retrospective chart review comparing the number of episodes of VAP 12 months preceding and following the introduction of a new ETT. A diagnosis of VAP was made based upon the guidelines of our institution, consistent with the Center of Disease Control and Prevention definition. Results. The number of patients developing VAP the year after the ETT conversion reduced to 32 (16.3%) from 68 (24.7%) the year before the conversion (). The rate of VAP was reduced by 56% per ventilator day after the implementation of the PU-cuffed ETT (). No significant differences were observed in length of hospital stay, length of mechanical ventilation, or mortality before or after the conversion. Conclusions. We found that HVLP PU-cuffed ETTs were associated with a statistically significant reduction of VAP in the adult ICUs.
Highlights
Ventilator-associated pneumonia (VAP) is a healthcareassociated infection that commonly causes morbidity and mortality in mechanically ventilated patients [1]
Patients were evenly distributed between the groups based on demographics and baseline characteristics (Table 1); there was a significant difference in weight between the patients before and after the endotracheal tube (ETT) conversion (76.9 kg versus 81.7 kg (P = 0.016))
The median number of intensive care unit (ICU) days was significantly less in the year after the conversion to the PU- ETTs compared to the year before (11 days versus 17 days (P = 0.002))
Summary
Ventilator-associated pneumonia (VAP) is a healthcareassociated infection that commonly causes morbidity and mortality in mechanically ventilated patients [1]. Tracheal intubation impairs the cough reflex, injures the tracheal epithelial surface, facilitates entry of bacteria into the airway by aspiration of subglottic secretions, and allows formation of a bacterial biofilm on the ETT surface. The combination of these factors puts the mechanically ventilated patient at great jeopardy of developing VAP. Ventilator-associated pneumonia (VAP) is a leading cause of morbidity and mortality in intensive care unit (ICU) patients, encompassing up to 15% of all hospital acquired infections.
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