Ventilator-associated pneumonia (VAP) is defined as nosocomial pneumonia in a patient on mechanical ventilatory support (by endotracheal tube or tracheostomy) for >48 hours. For many years, VAP has been diagnosed by the clinical criteria published by Johanson et al1 in 1972. The criteria include the appearance of a new or progressive pulmonary infiltrate, fever, leukocytosis, and purulent tracheobronchial secretions; but these criteria are nonspecific. In the mechanically ventilated patient, fever might be caused by a drug reaction, extrapulmonary infection, blood transfusion, or extrapulmonary inflammation. Pulmonary infiltrates can be due to pulmonary hemorrhage, chemical aspiration, pleural effusion, congestive heart failure, or tumor. Both fever and pulmonary infiltrates occur in the fibroproliferation of late acute respiratory distress syndrome, atelectasis, and pulmonary embolism, as well as in VAP. Cultures of tracheal aspirates are not very useful in establishing the cause of VAP,2 because, although such cultures are highly sensitive, their specificity is low­ even when they are cultured quantitatively.3

Getting to the Source

The agents that are reported to cause nosocomial pneumonia differ between hospitals secondary to different patient populations and diagnostic methods utilized. In general, bacteria have been the most frequently isolated pathogens. Nosocomial bacterial pneumonias are frequently polymicrobial, and gram-negative bacilli are usually the causative organisms. Recently, Staphylococcus aureus (particularly methicillin-resistant S. aureus) and other gram-positive cocci, including Streptococcus pneumoniae, have emerged as causative organisms. In addition, Haemophilus influenzae has been isolated from mechanically ventilated patients who had pneumonia that occurred within 48 to 96 hours after intubation.4 In hospitals participating in the NNIS, Pseudomonas aeruginosa, Enterobacter species, Klebsiella pneumoniae, Escherichia coli, Serratia marcescens, and Proteus species comprised 50% of the isolates from cultures of respiratory tract specimens obtained from patients for whom nosocomial pneumonia was diagnosed by using clinical criteria; S. aureus accounted for 16%, and H. influenzae, for 6%.5

Risk factors and host defenses that are altered by placement of an artificial airway contribute to the development of VAP once colonization occurs. Aspiration is common in hospitalized patients and is the most common cause of VAP.6 Patients with a documented history of aspiration and those who are immunocompromised are at increased risk for VAP. Additional host-related risk factors for VAP include age more than 70 years, underlying illness (particularly those patients with chronic pulmonary pathophysiology), coma, prolonged hospitalization, and thoracic or abdominal surgery. Patients who are transported from the critical care environment to other areas of the hospital for diagnostic evaluation and those who have recently completed a course of antibiotic therapy can also be at increased risk for VAP.7 The administration of antibiotics in the ICU is also an important factor in the development of VAP. Prior antibiotic therapy can lead to the emergence of antibiotic-resistant strains of bacteria.

Direct effects of an endotracheal tube include mucosal injury, impaired mucociliary function, and reduction in upper airway defenses due to an ineffective cough mechanism. The presence of an endotracheal tube might contribute indirectly to the risk of VAP by creating binding sites for bacteria in the bronchial tree and by increasing mucus secretion. Stagnation of secretions promotes the growth and proliferation of bacterial pathogens. In addition, the endotracheal tube can serve as a reservoir for bacteria that are inaccessible to host defense systems. The tube also keeps the vocal cords from approximating, which contributes to the aspiration process and the development of VAP. A growing body of evidence has demonstrated that bacterial colonization of the gastrointestinal tract, with subsequent aspiration around the endotracheal tube cuff, is a major source of VAP.

Another consideration regarding the development of VAP includes the ventilator circuit. At least four randomized controlled trials7-10 provide evidence that increasing the time between ventilator circuit changes can decrease the rate of VAP. Despite variation in the types of ventilator circuits, criteria for the diagnosis of VAP, type of humidifiers, and the frequency of circuit changes in these four studies, a meta-analysis of the four trials supports the use of less frequent ventilator circuit changes.

Gastrointestinal factors and body position also can play a role in the development of VAP. Several gastrointestinal factors are believed to increase the risk of VAP: the presence of a nasogastric tube, gastric alkalinization, and use of enteral feedings. Also the supine position can predispose some intubated patients to aspiration of gastric contents. This can occur even if the endotracheal tube cuff is inflated. Some authorities believe that the risk of aspiration and VAP can be reduced by keeping the head of the patient’s bed at an angle of 45° or more.11-12 In addition, continuous lateral rotational therapy or use of a vibration bed has been utilized to improve mucociliary clearance and facilitate drainage of pulmonary secretions.

Perhaps the most effective means of preventing VAP caused by exogenous microorganisms is consistent and thorough hand washing. All health care personnel should wash hands before and after contact with patients. Hands should also be washed before and after contact with the patient’s respiratory equipment—and anything else in the patient’s room—and after contact with respiratory secretions. Hands should be washed even when gloves are worn. In addition to hand washing, universal precautions should be observed: Gloves should be worn if contact with respiratory secretions or contaminated equipment is anticipated and gowns are useful if it is expected that the health care worker’s clothes could be soiled. The keystone of the successful implementation of universal precautions is regular changing of gloves and gowns.

To help prevent ventilator-associated pneumonia, clinicians caring for patients who are receiving mechanical ventilation should participate in programs aimed at its prevention. These programs may be part of a more general local effort directed at preventing nosocomial infections. Use of noninvasive positive-pressure ventilation (NIPV) might offer several advantages over endotracheal intubation, including reduced risk of VAP. The potential advantages of NIPV include flexibility of use; avoidance of complications associated with the use of endotracheal tubes, such as pneumonia and sinusitis; preservation of the ability to speak and swallow; and improved patient comfort.13-14

Choosing the Right Patients

Patient selection is important when considering the use of NIPV. Not all patients are candidates for noninvasive ventilation. The patient must be alert and cooperative. One of the simplest methods to reduce VAP risk is to extubate patients as soon as possible. The longer an endotracheal tube remains in place, the greater the risk of developing VAP. The patient’s readiness for weaning and the appropriateness of spontaneous breathing trials should be assessed on a daily basis. In addition, it is important to take precautions to prevent accidental extubation because reintubation may increase the risk of VAP.

A new, novel approach to reducing VAP is an attempt to reduce the aspiration of oropharyngeal secretions. Because aspiration of oropharyngeal secretions is a primary mechanism for the development of VAP, strategies that reduce aspiration might significantly reduce the risk of VAP. Endotracheal cuff pressures should be checked periodically to make sure that a pressure of at least 20 cm H2O is maintained, as the incidence of VAP increases when endotracheal cuff pressures fall below that point.15 Finally, it is important to perform thorough oral suctioning whenever endotracheal tubes are repositioned to reduce the accumulation of secretions above the tube. A preventive strategy gaining momentum is the use of new endotracheal tubes designed to reduce the risk of VAP—endotracheal tubes that have a separate suction lumen, which allows for continuous suctioning of subglottic secretions. This action prevents aspirated bacteria from around the cuff from traveling into the lower respiratory tract. This feature makes the tube ideal for critical care patients and long-term intubations. In one study performed in cardiac surgery patients, the risk of VAP with this tube was approximately 50% lower than that with a conventional endotracheal tube.16

The endotracheal tube can contribute to the pathogenesis of VAP by eliminating natural defense mechanisms, thereby allowing the entry of bacteria by the aspiration of subglottic secretions or the formation of biofilm on the endotracheal tube itself. It has been suggested that substitution of the endotracheal tube by early tracheostomy might reduce the risk of VAP. Whereas aspiration of subglottic secretions might be an effective measure with little risk, decontamination or exhaustive control of the sealing of the cuff has not demonstrated a positive risk-benefit ratio. The benefit of early tracheostomy in reducing VAP is still controversial.17 Moller and colleagues,18 using a retrospective study design, examined the potential benefit of early tracheostomy (<7 days) versus late tracheostomy in severely injured surgical SICU patients. Patients with late tracheostomy had significantly higher rates of VAP (42.3% versus 27.2%, P <0.05), duration of mechanical ventilation, and length of ICU stay. The authors18 suggest that if patients will require prolonged ventilation (>7 days), the tracheostomy should be performed between day 3 and 7. In a trial of 60 trauma patients randomized to early tracheostomy by Barquist and coworkers,19 the study was terminated as the intervention had no effect on mortality, rates of VAP, ICU stay, or other outcomes. A systematic review and meta-analysis by Griffiths and colleagues20 from 406 patients in five studies also reported no reduction in pneumonia, mortality, ventilator days, or length of ICU stay.

VAP remains an important cause of morbidity and mortality in hospitalized patients. By implementing a variety of strategies proven to reduce the risk of VAP, health care personnel can decrease the occurrence of VAP and improve patient outcomes. These simple and effective strategies are designed to prevent aspiration and reduce bacterial colonization.21 A strategy that does not involve purchasing equipment is staff education. Zack et al22 showed a 58% reduction in VAP rates after implementing an educational program. Reducing mortality due to ventilator-associated pneumonia requires an organized process that guarantees early recognition of pneumonia and consistent application of the best evidence-based practices. The “ventilator bundle” is a series of interventions related to ventilator care that, when implemented together, will achieve significantly better outcomes than when implemented individually. The key components of the ventilator bundle are:

  • elevation of the head of the bed
  • daily “sedation vacations” and assessment of readiness to extubate
  • peptic ulcer disease prophylaxis
  • deep venous thrombosis prophylaxis

Education, proper patient position, and meticulous hand washing can reduce the occurrence of VAP. Early ventilatory liberation and interventions to improve mucokinesis and secretions removal, such as early tracheotomy, can also reduce the incidence of VAP. The respiratory care therapist plays a major part in helping reduce the number of VAP cases in their institution.

Kenneth Miller, MEd, RRT-NPS, is clinical educator for respiratory care, Lehigh Valley Hospital, Allentown, Pa. For further information contact [email protected].


  1. Johanson WG Jr, Pierce AK, Sanford JP, Thomas GD. Nosocomial respiratory infections with gram-negative bacilli. The significance of colonization of the respiratory tract. Ann Intern Med. 1972;77:701-6.
  2. Meduri GU. Diagnosis of ventilator-associated pneumonia. Infect Dis Clin North Am. 1993;7:295-329.
  3. Jourdain B, Novara A, Joly-Guillou M-L, et al. Role of quantitative cultures of endotracheal aspirates in the diagnosis of nosocomial pneumonia. Am J Respir Crit Care Med. 1995;152:241-6.
  4. Patel PJ, Leeper KV, McGowan JE. Epidemiology and microbiology of hospital-acquired pneumonia. Semin Respir Crit Care Med. 2002;23:415-425.
  5. National Nosocomial Infections Surveillance (NNIS) System Report, data summary from January 1992 through June 2004, issued October 2004. Am J Infect Control. 2004;32:470-85.
  6. Fagon JY, Chastre J, Domart Y, et al. Nosocomial pneumonia in patients receiving continuous mechanical ventilation. Prospective analysis of 52 episodes with use of a protected specimen brush and quantitative culture techniques. Am Rev Respir Dis. 1989;139:877-84.
  7. Torres A, Aznar R, Gatell JM, et al. Incidence, risk, and prognosis factors of nosocomial pneumonia in mechanically ventilated patients. Am Rev Respir Dis. 1990;142:523-8.
  8. Kollef MH. Prolonged use of ventilator circuits and ventilator-associated pneumonia: a model for identifying the optimal clinical practice. Chest. 1998;113:267-9.
  9. Kollef MH, Prentice D, Shapiro SD, et al. Mechanical ventilation with or without daily changes of in-line suction catheters. Am J Respir Crit Care Med. 1997;156:466-72.
  10. Kollef MH, Shapiro SD, Boyd V, et al. A randomized clinical trial comparing an extended-use hygroscopic condenser humidifier with heated-water humidification in mechanically ventilated patients. Chest. 1998;113:759-67.
  11. Djedaini K, Billiard M, Mier L, et al. Changing heat and moisture exchangers every 48 hours rather than 24 hours does not affect their efficacy and the incidence of nosocomial pneumonia. Am J Respir Crit Care Med. 1995;152:1562-9.
  12. Niederman MS, Craven DE. Devising strategies for preventing nosocomial pneumonia—should we ignore the stomach? Clin Infect Dis. 1997;24:320-3.
  13. Cook DJ, Reeve BK, Guyatt GH, et al. Stress ulcer prophylaxis in critically ill patients: resolving discordant meta-analyses. JAMA. 1996;275:308-14.
  14. Girou E, Schortge F, Delclaux C, et al. Association of noninvasive ventilation with nosocomial infections and survival in critically ill patients. JAMA. 2000;284:2361-7.
  15. Lessard MR. Noninvasive ventilation in the ICU/La ventilation non invasive aux soins intensifs. Can J Anesth. 2001;48:R2-7.
  16. Georges H, Leroy O, Guery B, Alfandari S, Beaucaire G. Predisposing factors for nosocomial pneumonia in patients receiving mechanical ventilation and requiring tracheotomy. Chest. 2000;118:767-74.
  17. Kollef MH, Skubas NJ, Sundt TM. A randomized clinical trial of continuous aspiration of subglottic secretions in cardiac surgery patients. Chest. 1999;116:1339-46.
  18. Moller MG, Slaikeu JD, Bonelli P, Davies AT, Hoogeboom JE, Bonnell BW. Early tracheostomy versus late tracheostomy in the surgical intensive care unit. Am J Surg. 2005;189:293-6.
  19. Barquist ES, Amortegui J, Hallal A, et al. Tracheostomy in ventilator dependent trauma patients: a prospective, randomized intention-to-treat study. J Trauma. 2006;60:91-7.
  20. Griffiths J, BarberVS, Morgan L, et al. Systematic review and meta-analysis of studies of the timing of tracheostomy in adult patients undergoing artificial ventilaton. BMJ. 2005;330:1243-6.
  21. MacIntyre NR. Ventilator-associated pneumonia: the role of ventilator management strategies. Respir Care. 2005;50:766-72.
  22. Zack JE, Garrison T, Trovillion E, et al. Effect of an education program aimed at reducing the occurrence of ventilator-associated pneumonia. Crit Care Med. 2002;30:2407-12.