SummaryVentilator-associated pneumonia is common, difficult to diagnose, affects the most vulnerable of patients and carries a high mortality. During prolonged mechanical ventilation the oropharynx, sinuses, dentition and stomach of critically ill patients become colonised with pathogenic bacteria. Colonised secretions pool in the oropharynx and subglottic space. These secretions repeatedly gain access to the lower airways by leakage past the tracheal tube cuff. If host defence mechanisms are overwhelmed, multiplication occurs in the lower respiratory tract producing an inflammatory response in the bronchioles and alveoli. The inflammatory response is characterised by capillary congestion, leucocyte and macrophage infiltration and fibrinous exudation into the alveolar spaces. If this inflammatory response occurs more than 48 h after intubation, it is called ventilatorassociated pneumonia. Prevention depends on reducing upper airway and gastrointestinal reservoirs of bacteria, reducing or abolishing aspiration of these bacteria past the tracheal tube cuff and enhancing bacterial clearance from the lower airways. Despite an increased understanding of the pathogenesis and diagnosis of ventilator-associated pneumonia (VAP), prevention has remained problematic. There is now good evidence for continuous leakage of infected secretions past the tracheal tube cuff being responsible for VAP. As a result, VAP strikes critically ill patients and increases their morbidity and mortality. The aim of this review is to discuss the diagnosis and pathogenesis of VAP, including a brief review of natural defence mechanisms. The review also covers the prevention of VAP with special reference to new developments aimed at reducing aspiration past the cuff.
Definition