Pathophysiology of Ventilator-Associated Pneumonia

Abstract

Ventilator-associated pneumonia (VAP) is a frequent complication of mechanical ventilation with an incidence that ranges between 9% and 70% [1–4]. VAP seems to be particularly frequent in patients with acute respiratory distress syndrome (ARDS) in whom several local and systemic factors apparently predispose its development [5]. Crude mortality rates of VAP varies from 25% to 50% [6–7], while mortality directly attributable is 27% [8]. Clinical and radiological parameters are not very specific to diagnose VAP [9]. Among several prognostic factors, both inappropriate and prior antibiotic therapy have a particular importance and they indirectly highlight the need for a correct clinical and microbiological diagnosis of pneumonia [3, 7, 10–12]. Most of our knowledge about VAP comes from clinical and or microbiological studies that have been published in the last decade. However, the histology of VAP has been only known in recent years mainly through immediate post-mortem studies that have been performed to validate techniques used to elicit microbial diagnosis of pneumonia in mechanically ventilated patients [13–24]. These studies have extensively investigated the lungs of patients mechanically ventilated for several days and along with experimental models of pneumonia [25–27] have allowed to describe the peculiar histological and microbiological characteristics and interactions of human VAP. From this information important clinical implications have been concluded.