microscope view of stained tissue sample

Pneumonia is the second most common nosocomial infection (after urinary tract infection) in the United States, and the leading cause of death as a result of nosocomial infection.1 It accounts for approximately 15% of all hospital-associated infections.1-3 Intubation and mechanical ventilation greatly increase the risk of bacterial pneumonia. In fact, nosocomial pneumonia that occurs in association with mechanical ventilation has become a clinical entity so well recognized that a distinct term used to describe it—ventilator-associated pneumonia (VAP)—has gained widespread acceptance.

Pathogenesis and Clinical Manifestations

Any patient in the hospital can develop nosocomial pneumonia by either aspirating contaminated substances or inhaling airborne particles. Such contaminants and particles can come from various respiratory and medical devices, the hospital environment, other patients, and even hospital staff. In general, the signs and symptoms of pneumonia may include fever, new onset of purulent sputum or change in the character of sputum, cough, dyspnea, tachypnea, rales or bronchial breath sounds, and altered mental status. X-ray findings might include new or progressive infiltrate, consolidation, cavitation, and pneumatoceles (in patients ≤1 year of age). For a detailed description of signs and symptoms, x-ray findings, and laboratory findings associated with pneumonia, the reader is referred to the NNIS Pneumonia Flow Diagram, which can be accessed at www.cdc.gov…anyPatientFlowDiagramv1.pdf.

In hospitals, aspiration occurs most frequently in patients who cannot swallow normally or when altered level of consciousness, mechanical ventilation, or a gastric or endotracheal tube causes regurgitation. A patient who is fed by someone else or who has dementia is also at increased risk. Inhalation of airborne particles occurs when contaminated droplets enter the patient’s lungs through respiratory or anesthesia equipment, ventilation systems, humidifiers, showers, or faucets, or from other people’s coughing and sneezing. Pathogens may then proliferate in the patient’s respiratory tract.

Oropharyngeal or tracheobronchial colonization by gram-negative bacilli begins with their adherence to the host’s epithelial cells. Successful epithelial adherence is determined by multiple factors related to the bacteria (eg, presence of a capsule, production of elastase or mucinase), host cell (eg, surface proteins and polysaccharides), and environment (eg, pH and presence of mucin in respiratory secretions). Some reports indicate that fibronectin can inhibit the adherence of gram-negative bacilli to host cells, whereas several conditions (eg, malnutrition, severe illness, postoperative state) can increase adherence.3

Causative Organisms

The reported distribution of etiologic agents that cause nosocomial pneumonia differs among hospitals because of different patient populations and diagnostic methods employed. In general, however, bacteria have been the most frequently isolated pathogens. Nosocomial bacterial pneumonias are frequently polymicrobial, and gram-negative bacilli are usually the predominant organisms. However, Staphylococcus aureus (particularly methicillin-resistant S. aureus) and other gram-positive cocci, including Streptococcus pneumoniae, have emerged as important isolates.3-6 In addition, Haemophilus influenzae has been isolated from mechanically ventilated patients who had pneumonia that occurred within 48 to 96 hours after intubation.7-10 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

Risk factors and host defenses that are altered by placement of an artificial airway contribute to the development of VAP once colonization occurs.

Host-Related Factors. Aspiration is common in hospitalized patients, and is the most common cause of VAP.11 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 65 years, underlying illness (particularly chronic obstructive lung disease), coma, prolonged hospitalization, and thoracic or abdominal surgery. Patients who are transported from the ICU to other areas of the hospital for testing purposes, and those who have recently completed antibiotic therapy, may also be at increased risk for VAP.12,13

Infection Control Practices. Hand washing is an important component in reducing the incidence of VAP. 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. Patients who have been treated before with antibiotics are more likely than those who have not to be infected with high-risk pathogens such as P. aeruginosa.

Endotracheal Tube Factors. 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.

The Ventilator Circuit. 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. At least four randomized controlled trials14-17 and seven observational studies18-24 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.25,26

Bacterial Colonization of the Oropharynx. Rarely, bacterial colonization of the oropharynx can also contribute to the risk of VAP. Endotracheal intubation may allow leakage around the tube of oropharyngeal secretions laden with bacteria. For this reason, continuous aspiration of subglottic secretions may reduce the incidence of VAP.

Gastrointestinal Factors. Several gastrointestinal factors are believed to increase the risk of VAP. These include the presence of a nasogastric tube, gastric alkalinization, and use of enteral feedings.

Body Position. The supine position may 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. In addition, continuous lateral rotational therapy or use of a bed that rotates the patient continuously from side to side has been purported to improve mucociliary clearance and facilitate drainage of pulmonary secretions.

Preventive Strategies

Several preventive strategies can be recommended.

Noninvasive Positive-Pressure Ventilation. 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.32-34 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.

Reduction of Time on Ventilator and Prevention of Unplanned Extubation. One of the simplest methods to reduce VAP risk is to extubate patients as soon as possible. As numerous randomized14-17 and observational18-24 studies have shown, 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.

Reduction of Bacterial Colonization. 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. Hand washing should be performed whether or not gloves are worn. In addition to hand washing, universal precautions should be observed. Gloves should be worn if contact with respiratory secretions or contaminated objects is anticipated. Gowns are useful if it is expected that the health care worker’s clothes may be soiled. The cornerstone of the successful implementation of universal precautions is regular changing of gloves and gowns. Gloves and gowns should be changed and hands should be washed after any contaminating event before touching any other patient, object, or environmental surface.

If stress bleeding prophylaxis is warranted, such as for patients who remain intubated for long periods of time, then either sucralfate or H2 antagonists may be used. According to the American Thoracic Society (ATS),27 comparative data from randomized trials suggest a trend toward reduced VAP with sucralfate, but there is a slightly greater rate of clinically significant gastric bleeding, compared with H2 antagonists. If needed, stress bleeding prophylaxis with either H2 antagonists or sucralfate is acceptable.

A novel approach to the reduction of bacterial colonization (and hence VAP risk) is selective digestive decontamination. This procedure has been evaluated in mechanically ventilated patients in Europe.28 In selective digestive decontamination, a nonabsorbable antibiotic paste is applied locally to the oropharynx and is administered via nasogastric tube three to four times per day. Unfortunately, the results of clinical trials investigating the usefulness of selective digestive decontamination in reducing the risk of VAP have been mixed.

Reduction of Aspiration of Oropharyngeal Secretions. Because aspiration of oropharyngeal secretions is a primary mechanism for the development of VAP, strategies that reduce aspiration may significantly reduce the risk of VAP. Endotracheal cuff pressures should be checked periodically to make sure that a pressure of at least 20 cm water is maintained. The incidence of VAP increases when endotracheal cuff pressures fall below 20 cm water.29 Finally, it is important to perform thorough oral suctioning whenever endotracheal tubes are repositioned to reduce the pooling of secretions above the tube.

Reduction of Aspiration of Gastric Secretions. Several strategies can be used to reduce the potential for introduction of gastrointestinal contents and microorganisms into the respiratory tract. Elevating the head of the patient’s bed 30° to 45°, particularly if being fed enterally, may help avoid gastric reflux and reduces the risk of aspiration. Nasogastric tubes, if used, should be removed as soon as possible.

Enteral nutrition has been considered a risk factor for the development of hospital-acquired pneumonia, primarily because of an increased risk of aspiration of gastric contents.30,31 However, parenteral nutrition is associated with greater risks for intravascular device–associated infections, complications of line insertions, and loss of intestinal villous architecture, which may facilitate enteral microbial translocation.30 According to the ATS, based on the weight of current evidence, a strategy of early enteral feeding (eg, Day 1 of intubation and ventilation) is associated with a greater risk for ICU-acquired VAP than later enteral feeding (eg, Day 5 of intubation and ventilation).27

Heated Humidifiers Versus Heat and Moisture Exchangers. Many hospitals prefer heat and moisture exchangers, because they can provide some humidity to the patient but produce no condensate and, hence, are believed to be associated with a lower risk for VAP than are heated humidifiers. Clinical studies evaluating this issue, however, have provided mixed results.35-37

Early Tracheostomy. The endotracheal tube may 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.38

New Products. A preventive strategy gaining momentum is the use of new endotracheal tubes designed to reduce the risk of VAP. Of many on the market, the most well-known tube is Mallinckrodt’s Hi Lo Evac® Endotracheal Tube, which has a separate suction lumen that allows for continuous suctioning of subglottic secretions, thereby preventing aspirated bacteria from around the cuff to travel into the lower respiratory tract. This feature makes the tube ideal for critical care and long-term intubations. In one study performed in cardiac surgery patients, the risk of VAP with the Hi Lo was approximately 50% lower than that with a conventional endotracheal tube.39

In December 2006, Kimberly-Clark launched its Microcuff® endotracheal tube, a device designed to reduce the leakage of potentially infectious secretions into the lungs, thereby reducing the risk of VAP. The sealing capability of the tube is created by its unique cuff, which is made with an advanced microthin polyurethane material. While conventional polyvinyl chloride cuffs create folds and channels when inflated, which allow fluid to leak past the cuff, the cuff on the Microcuff Endotracheal Tube minimizes channel openings and creates an effective tracheal seal. The cuff length and shape of Microcuff Endotracheal Tubes are also designed for better contact with tracheal contours to increase protection against fluid leakage.

Conclusion

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. A strategy that does not involve purchasing equipment is staff education. Zack et al40 showed a 58% reduction in VAP rates after implementing an educational program.

Phyllis C. Braun, PhD, and John D. Zoidis, MD, are contributing writers for RT.

References

  1. Patel PJ, Leeper KV, McGowan JE. Epidemiology and microbiology of hospital-acquired pneumonia. Semin Respir Crit Care Med. 2002;23:415-425.
  2. American Thoracic Society. Hospital-acquired pneumonia in adults: diagnosis, assessment of severity, initial antimicrobial therapy, and preventative strategies. A consensus statement. Am J Respir Crit Care Med. 1995;153:1711-1725.
  3. Centers for Disease Control and Prevention. National Nosocomial Infections Surveillance (NNIS) system report, data summary from January 1992 through June 2004, issued October 2004. Am J Infect Control. 2004;32:470-485.
  4. Centers for Disease Control and Prevention. Guidelines for prevention of nosocomial pneumonia. MMWR. 1997;46:1-79.
  5. Schalberg DR, Culver DH, Gaynes RP. Major trends in the microbial etiology of nosocomial infection. Am J Med. 1991;91:72S-75S.
  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;139:877-884.
  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;142:523-528.
  8. Giantsou E, Liratzopoulos N, Efraimidou E, et al. Both early-onset and late-onset ventilator-associated pneumonia are caused mainly by potentially multiresistant bacteria. Intensive Care Med. 2005;31:1488-1494.
  9. American Thoracic Society. Hospital-acquired pneumonia in adults: diagnosis, assessment of severity, initial antimicrobial therapy, and preventive strategies. A consensus statement, American Thoracic Society, November 1995. Am J Respir Crit Care Med. 1995;153:1711-1725.
  10. Craven DE, Steger KA. Epidemiology of nosocomial pneumonia. New perspectives on an old disease. Chest. 1995;108(suppl):1S-16S.
  11. Bonten MJ, Kollef MH, Hall JB. Risk factors for ventilator-associated pneumonia: from epidemiology to [atient management. Clin Infect Dis. 2004;38:1141-1149.
  12. Noor A, Hussain SF. Risk factors associated with the development of ventilator-associated pneumonia. J Coll Physicians Surg Pak. 2005;15:92-95.
  13. Bercault N, Wolf M, Runge I, Fleury JC, Boulain T. Intrahospital transport of critically ill ventilated patients: a risk factor for ventilator-associated pneumonia—a matched cohort study. Crit Care Med. 2005;33:2471-2478.
  14. Craven DE, Kunches LM, Kilinsky V, Lichtenberg DA, Make BJ, McCabe WR. Risk factors for pneumonia and fatality in patients receiving continuous mechanical ventilation. Am Rev Respir Dis. 1986;133:792-796.
  15. Dreyfuss D, Djedaini K, Weber P, et al. Prospective study of nosocomial pneumonia and of patient and circuit colonization during mechanical ventilation with circuit changes every 48 hours versus no change. Am Rev Respir Dis. 1991;143:738-743.
  16. Kollef MH, Shapiro SD, Fraser VJ, et al. Mechanical ventilation with or without 7-day circuit changes. A randomized controlled trial. Ann Intern Med. 1995;123:168-174.
  17. Long MN, Wickstrom G, Grimes A, Benton CF, Belcher B, Stamm AM. Prospective, randomized study of ventilator-associated pneumonia in patients with one versus three ventilator circuit changes per week. Infect Control Hosp Epidemiol. 1996;17:14-19.
  18. Lareau SC, Ryan KJ, Diener CF. The relationship between frequency of ventilator circuit changes and infectious hazard. Am Rev Respir Dis. 1978;118:493-496.
  19. Hess D, Burns E, Romagnoli D, Kacmarek RM. Weekly ventilator circuit changes: a strategy to reduce costs without affecting pneumonia rates. Anesthesiology. 1995;82:903-911.
  20. Thompson RE. Incidence of ventilator-associated pneumonia (VAP) with 14-day circuit change in a subacute environment. Respir Care. 1996;41:601-606.
  21. Kotilainen HR, Keroack MA. Cost analysis and clinical impact of weekly ventilator circuit changes in patients in intensive care unit. Am J Infect Control. 1997;25:117-120.
  22. Fink JB, Krause SA, Barrett L, Schaaff D, Alex CG. Extending ventilator circuit change interval beyond 2 days reduces the likelihood of ventilator-associated pneumonia. Chest. 1998;113:405-411.
  23. Han JN, Liu YP, Ma S, et al. Effects of decreasing the frequency of ventilator circuit changes to every 7 days on the rate of ventilator-associated pneumonia in a Beijing hospital. Respir Care. 2001;46:891-896.
  24. Lien TC, Lin MY, Chu CC, Kuo BI, Wang ED, Wang JH. Ventilator-associated pneumonia with circuit changes every 2 days versus every week. Zhonghua Yi Xue Za Zhi (Taipei). 2001;64:161-167.
  25. Hess DR, Kallstrom TJ, Mottram CD, Myers TR, Sorenson HM, Vines DL. Care of the ventilator circuit and its relation to ventilator-associated pneumonia. Respir Care. 2003;48:869-879.
  26. Branson RD. The ventilator circuit and ventilator-associated pneumonia. Respir Care. 2005;50:774-785.
  27. American Thoracic Society. Guidelines for the management of adults with hospital-acquired, ventilator-associated, and healthcare-associated pneumonia. Am J Respir Crit Care Med. 2005;171:388-416.
  28. Mayhall CG. Nosocomial pneumonia. Diagnosis and prevention. Infect Dis Clin North Am. 1997;11:427-457.
  29. Grap MJ, Munro CL. Ventilator-associated pneumonia: clinical significance and implications for nursing. Heart Lung. 1997;26:419-429.
  30. Tablan OC, Anderson LJ, Besser R, Bridges C, Hajjeh R. Guidelines for preventing health-care–associated pneumonia, 2003: recommendations of the CDC and the Healthcare Infection Control Practices Advisory Committee. MMWR Recomm Rep. 2004;53:1-36.
  31. Pingleton SK, Hinthorn DR, Liu C. Enteral nutrition in patients receiving mechanical ventilation: multiple sources of tracheal colonization include the stomach. Am J Med. 1986;80:827-832.
  32. Antonelli M, Conti G, Esquinas A, et al. A multiple-center survey on the use in clinical practice of noninvasive ventilation as a first-line intervention for acute respiratory distress syndrome. Crit Care Med. 2007;35:18-25.
  33. George DL, Falk PS, Wunderink RG, et al. Epidemiology of ventilator-acquired pneumonia based on protected bronchoscopic sampling. Am J Respir Crit Care Med. 1998;158:1839-1847.
  34. Meduri GU. Noninvasive positive pressure ventilation in chronic obstructive pulmonary disease patients with acute exacerbation. Crit Care Med. 1997;25:1631-1633.
  35. Lorente L, Lecuona M, Jiménez A, Mora ML, Sierra A. Ventilator-associated pneumonia using a heated humidifier or a heat and moisture exchanger: a randomized controlled trial [ISRCTN88724583]. Crit Care. 2006;10:R116.
  36. Boots RJ, George N, Faoagali JL, Druery J, Dean K, Heller RF. Double-heater-wire circuits and heat-and-moisture exchangers and the risk of ventilator-associated pneumonia. Crit Care Med. 2006;34:687-693.
  37. Lacherade JC, Auburtin M, Cerf C, et al. Impact of humidification systems on ventilator-associated pneumonia: a randomized multicenter trial. Am J Respir Crit Care Med. 2005;172:1276-1282.
  38. Ramirez P, Ferrer M, Torres A. Prevention measures for ventilator-associated pneumonia: a new focus on the endotracheal tube. Curr Opin Infect Dis. 2007;20-190-197.
  39. Kollef MH, Skubas MJ, Sundt TM. A randomized clinical trial of continuous aspiration of subglottic secretions in cardiac surgery patients. Chest. 1999;116:1339-1346.
  40. 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.