What causes ventilator associated
pneumonia
The principal risk factor for the development of ventilator
associated pneumonia is the presence of an endotracheal tube.
These tubes interfere with the normal protective upper airway
reflexes, prevent effective coughing, and encourage
microaspiration of contaminated pharyngeal contents. The
importance of the endotracheal tube is emphasised by the
incidence of pneumonia being significantly lower for
non-invasive ventilation via a tight fitting facemask.
Reintubation after unsuccessful extubation also increases the
risk of pneumonia.
Most cases are caused by microaspiration of contaminated
oropharyngeal secretions.9 The oropharynx becomes rapidly
colonised with aerobic Gram negative bacteria after illness,
antibiotic treatment, or hospital admission as a result of
alterationsin host defences and subsequent changesin bacterial
adherence to mucosal surfaces. These contaminated secretions
pool above the cuff of the trachea or tracheostomy tube and
slowly gain access to the airway via folds in the wall of the
cuff.A bacterial biofilm, which is impervious to systemic
antibiotics, gradually forms on the inner surface of the
endotracheal tube and serves as a nidusfor infection.Ventilator
cycling propels pathogen rich biofilm and secretionsto the distal
airways. The size of the biofilm and the virulence of the bacteria
within it contribute to the risk of infection, but it is the host’s
immune response that determines whether parenchymal infection
and ventilator associated pneumonia will develop.
Critical illness is associated with immunosuppression, and this
increases susceptibility to nosocomial infection.Neutrophils
are central to the body’s response to most bacterial infections,
and mechanically ventilated patients have neutrophil dysfunction
and impaired phagocytosis. Recent work by Morris and
colleagues examined neutrophil function in patients with a high
clinical suspicion of ventilator associated pneumonia. They
found that patients had significantly reduced phagocytic activity
secondary to the overexpression of the inflammatory
anaphylotoxin C5a, excess levels of which cause neutrophil
dysfunction.Further work by the same group suggests that
this C5a driven immunosuppression precedes the acquisition
of nosocomial infection and is not merely a coincidental
finding.