Pulmonary infections span a wide spectrum, ranging from self-limited processes (e.g., tracheobronchitis) to life-threatening infections including both community-acquired pneumonia (CAP) and hospital-acquired pneumonia (HAP). Together, pneumonia and influenza rank as the sixth leading cause of death in the United States and lead all other infectious diseases in this respect.1 Pneumonia is the second-most-common hospital -acquired infection in the United States, accounting for 17.8% of all hospital-acquired infections and 40,000 to 70,000 deaths per year.2 HAP is the most common nosocomial infection occurring in patients requiring mechanical ventilation, developing in 6.5% of patients after 10 days and in 28% of patients after 30 days of ventilatory support.3 Patients acquiring HAP have a greater risk of mortality than comparably ill ventilated patients who do not develop pneumonia.2,4,5 Ventilator-associated pneumonia (VAP) specifically refers to a bacterial pneumonia developing in patients with acute respiratory failure who have been receiving mechanical ventilation for at least 48 hours.5 The etiologic bacteriologic agents associated with VAP typically differ based on the timing of the occurrence of the infection relative to the start of mechanical ventilation. VAP occurring within 96 hours of the onset of mechanical ventilation is usually due to antibiotic-sensitive bacteria that colonize the patient prior to hospital admission (e.g., Streptococcus pneumoniae, Haemophilus influenza, oxacillin-sensitive Staphylococcus aureus).6 VAP developing after 96 hours of ventilatory support is more often associated with antibiotic-resistant bacteria including oxacillin-resistant Staphylococcus aureus, Acinetobacter species and Pseudomonas aeruginosa. However, more recent data suggest that hospitalization and exposure to antibiotics prior to the start of mechanical ventilation are important risk factors for the occurrence of VAP attributed to antibiotic-resistant bacteria.7,8 Therefore, these risk factors should be considered when deciding on an appropriate empiric antibiotic regimen regardless of the onset of VAP. VAP and catheter-associated bloodstream infections are the leading causes of infection acquired in the intensive care unit (ICU) setting.3 Patients in the ICU have rates of HAP that are as much as five to ten rimes higher than the rates in general hospital wards.9 Additionally, like nosocomial bloodstream infections, VAP is associated with an attributable mortality beyond that accounted for by patients' severity of illness.8,10 The attributable mortality associated with VAP appears to be greatest for "high-risk" antibiotic-resistant bacteria including Pseudomonas aeruginosa and oxacillin-resistant Staphylococcus aureus.10-12 The greater hospital mortality associated with these "high-risk" pathogens has been attributed to the virulence of these bacteria and the increased occurrence of inadequate initial antibiotic treatment of VAP due to the presence of antibiotic resistance.13 This review provides an overview of the clinical importance of VAP. We then describe how this nosocomial infection influences the management and outcomes of patients with the acute respiratory distress syndrome (ARDS).
|Number of pages
|Seminars in Respiratory and Critical Care Medicine
|Published - Jan 1 2001
- Nosocomial infection
- Ventilator-associated pneumonia