Abstract

Ventilator-associated pneumonia (VAP) is defined as an infection of the lung parenchyma developing during mechanical ventilation, usually after at least 2 days of positive-pressure ventilation delivered via an endotracheal tube [1, 2]. This time criterion aims to exclude pneumonias caused by infectious agents already present or incubating before mechanical ventilation is started [1]. The diagnosis of VAP is usually based on clinical, radiographic, and microbiological criteria. However, the accuracy of data on the epidemiology of VAP is limited by the lack of a gold standard for its diagnosis [3]. In most reports the incidence of VAP ranges from 8% to 28% [3]. The lower incidence is reported in studies where quantitative cultures of protected specimen brushes were used to define pneumonia [4]. The incidence seems to rise from 5% for patients receiving mechanical ventilation for 1 day to 69% for those receiving mechanical ventilation for more than 30 days, with an incremental risk of pneumonia of around 1% per day [2, 5, 6]. Some authors report that, although the cumulative risk of developing VAP increases over time, the daily hazard rate decreases after 5 days of mechanical ventilation; these authors estimate the risk per day at 3% for the first 5 days of mechanical ventilation, 2% between days 5 and 10 of mechanical ventilation and 1% between days 10 and 15 of mechanical ventilation [7]. VAP is, then, a common complication of long ICU stays. Among the causative pathogens of VAP, Gram-positive strains are common and are associated with a high mortality.

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