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Ventilator-Associated Pneumonia PreventionVentilator-Associated Pneumonia Prevention: We Still Have a Long Way to Go! FREE TO VIEW

Marin H. Kollef, MD, FCCP
Author and Funding Information

From the Division of Pulmonary and Critical Care Medicine, Washington University School of Medicine.

CORRESPONDENCE TO: Marin H. Kollef, MD, FCCP, Division of Pulmonary and Critical Care Medicine, Washington University School of Medicine, 660 S Euclid Ave, Campus Box 8052, St Louis, MO 63110; e-mail: mkollef@dom.wustl.edu


FUNDING/SUPPORT: Dr Kollef’s effort was supported by the Barnes-Jewish Hospital Foundation.

FINANCIAL/NONFINANCIAL DISCLOSURES: The author has reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2014;146(4):873-874. doi:10.1378/chest.14-1066
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Published online

In this issue of CHEST (see page 890), Hurley1 performed a multilevel random effects analysis examining topical antibiotics (TAs) for the prevention of ventilator-associated pneumonia (VAP). Because TA use can confer herd protection in the ICU similar to vaccination programs in the community, contextual influences resulting from a population-based intervention cannot be estimated from a single trial. However, multilevel random effects analysis allows the estimation of contextual effects. Hurley1 found that the baseline incidence of VAP derived from observational studies was lower (23.7%; 95% CI, 20.6%-27.2%) than that in studies of TAs using concurrent control groups that either did or did not receive topical placebo (38% [95% CI, 29%-48%] vs 33% [95% CI, 20%-50%], respectively). This observed contextual influence could potentially inflate the apparent effect of TAs, especially within studies using topical placebo. The clinical importance of this observation is illustrated by investigations showing that TAs can promote the emergence of antimicrobial resistance and increase the burden of resistance genes in the gut biome of patients in the ICU.2,3 Without knowing the overall influence of TAs on antimicrobial resistance progression and clinical outcomes, their routine use cannot be endorsed, especially in areas where antibiotic resistance is already a clinically important problem.

Hurley’s1 analysis also emphasizes the importance of continuing to investigate VAP as well as other ICU-acquired infections to optimize strategies for their prevention and treatment. There has been a sense in the United States that VAP is a vanishing condition, with reported mean national rates within medical and surgical ICUs of 1.9 and 3.8 per 1,000 ventilator-days, respectively.4 This is in stark contrast to rates of VAP reported internationally in excess of 20 per 1,000 ventilator-days.4 Moreover, a recent prospective surveillance study of VAP conducted in the United States, Europe, South America, and Asia found the rates of VAP, and more importantly VAP due to Pseudomonas aeruginosa, to be similar across continents (VAP rates, 13.5%, 19.4%, 13.8%, and 16.0%, respectively; P aeruginosa VAP rates, 4.1%, 3.4%, 4.8%, and 4.6%, respectively).5 Furthermore, prior antimicrobial use and a high proportion of antimicrobial resistance in the community or hospital unit, both common exposures globally, were identified as risk factors for both VAP due to multiple drug-resistant pathogens and colonization with P aeruginosa.5

One of the most important explanations for the discrepancy regarding previously reported rates of VAP between the United States and the rest of the world is the method of surveillance used. We previously showed that the Centers for Disease Control and Prevention surveillance method markedly underestimated the occurrence of microbiologically confirmed VAP.6 This had led the Centers for Disease Control and Prevention to adopt a new method of ICU surveillance that uses ventilator-associated conditions (VACs) to monitor the quality of ICU care.7 The concern with shifting away from VAP as an important disease process within the ICU setting is that it may result in a reduced emphasis on the prevention of VAP and could have unforeseen consequences, especially as more and more VAP is caused by antibiotic-resistant pathogens.8 Moreover, simply changing ICU surveillance to VACs does not guarantee that the quality of ICU care will improve. The simple criteria used to define VACs (changes in positive end-expiratory pressure and Fio2 after periods of stability) exposes these surveillance criteria to “definitional gaming,” whereby hospitals may manipulate their rates of VACs by adjusting their use of positive end-expiratory pressure and Fio2.

The continued need to focus on improved methods for the prevention of VAP, as opposed to simply switching to alternative surveillance methods, is also illustrated by several recent studies examining the inability of the VAC criteria to identify VAP. Muscedere et al9 retrospectively applied VAC criteria to data from a prospective time-series study in which VAP clinical practice guidelines were implemented in 11 ICUs. Of 1,320 patients evaluated, a VAC developed in 139 (10.5%), an infection-related VAC (IVAC) developed in 65 (4.9%), and VAP developed in 148 (11.2%). The statistical agreement (κ) between VAP and VAC was 0.18 and between VAP and IVAC, 0.19. Notably, Muscedere et al9 found that increased adherence to VAP prevention guidelines during the study was associated with decreased VAP and VAC rates but no change in IVAC rates. In a recent prospective observational study, we also observed poor sensitivity of the VAC criteria for the detection of VAP (sensitivity, 25.9%; 95% CI, 16.7%-34.5%).10 More importantly, we observed that VAP was the most common cause of VACs, and the majority of VACs were adjudicated to be nonpreventable events. These findings suggest that efforts aimed at simply improving or stabilizing oxygenation indexes during mechanical ventilation may not have an impact on the occurrence of VAP or other infection-related complications associated with mechanical ventilation.

It is unlikely that VAP will disappear as an important clinical complication of respiratory failure. Available data suggest that its occurrence is relatively uniform globally and that most of the pathogens associated with VAP are antibiotic resistant, requiring broad-spectrum antimicrobials.5,8 Given this set of circumstances, it seems logical to continue to develop enhanced strategies for the prevention of VAP. Simply increasing the use of well-established and validated prevention bundles can reduce the occurrence of VAP and seems to represent a relatively simple first step.9 TAs may still play a role in the prevention of VAP. The question is how best to apply TAs and what type of TA would be optimal for use in VAP prevention. There is increasing interest in the use of aerosolized antibiotics for the treatment and prevention of VAP to include the use of novel combinations that have an enhanced ability to minimize the development of resistance.11 Additionally, topical administration of antiseptic agents through the endotracheal tube could contribute to lowering the rates of antibiotic-resistant VAP if cost-effective approaches for their use can be developed.12

In the meantime, what should ICU clinicians and investigators do? First, they should support efforts within their own ICUs aimed at preventing VAP and other hospital-acquired infections through the use of bundles or other prevention programs. Second, antimicrobial stewardship principles should be universally promoted throughout the hospital aimed at minimizing the emergence of antibiotic resistance. Finally, research efforts focused on developing novel and effective approaches for the prevention, rapid diagnosis, and effective treatment of VAP and other antibiotic-resistant infections should be encouraged.

Acknowledgments

Role of sponsors: Barnes-Jewish Hospital Foundation provided unrestricted support for Dr Kollef’s clinical research.

Hurley JC. Ventilator-associated pneumonia prevention methods using topical antibiotics: herd protection or herd peril? Chest. 2014;146(4):890-898.
 
Oostdijk EA, de Smet AM, Blok HE, et al. Ecological effects of selective decontamination on resistant gram-negative bacterial colonization. Am J Respir Crit Care Med. 2010;181(5):452-457. [CrossRef] [PubMed]
 
Buelow E, Gonzalez TB, Versluis D, et al. Effects of selective digestive decontamination (SDD) on the gut resistome. J Antimicrob Chemother. 2014;69(8):2215-2223. [CrossRef] [PubMed]
 
Klompas M. What can we learn from international ventilator-associated pneumonia rates? Crit Care Med. 2012;40(12):3303-3304. [CrossRef] [PubMed]
 
Kollef MH, Chastre J, Fagon JY, et al. Global prospective epidemiological and surveillance study of ventilator-associated pneumonia (VAP) due toPseudomonas aeruginosa[published online ahead of print July 22, 2014]. Crit Care Med.
 
Skrupky LP, McConnell K, Dallas J, Kollef MH. A comparison of ventilator-associated pneumonia rates as identified according to the National Healthcare Safety Network and American College of Chest Physicians criteria. Crit Care Med. 2012;40(1):281-284. [CrossRef] [PubMed]
 
Magill SS, Klompas M, Balk R, et al. Developing a new, national approach to surveillance for ventilator-associated events. Crit Care Med. 2013;41(11):2467-2475. [CrossRef] [PubMed]
 
Enne VI, Personne Y, Grgic L, Gant V, Zumla A. Aetiology of hospital-acquired pneumonia and trends in antimicrobial resistance. Curr Opin Pulm Med. 2014;20(3):252-258. [CrossRef] [PubMed]
 
Muscedere J, Sinuff T, Heyland DK, et al; Canadian Critical Care Trials Group. The clinical impact and preventability of ventilator-associated conditions in critically ill patients who are mechanically ventilated. Chest. 2013;144(5):1453-1460. [CrossRef] [PubMed]
 
Boyer AF, Schoenberg N, Babcock H, McMullen KM, Micek ST, Kollef MH. A prospective evaluation of ventilator-associated conditions and infection-related ventilator-associated conditions [published online ahead of print May 22, 2014]. Chest. doi:10.1378/chest.14-0544.
 
Montgomery AB, Rhomberg PR, Abuan T, Walters KA, Flamm RK. Amikacin/fosfomycin (5:2 ratio): characterization of mutation rates in microbial strains causing ventilator-associated pneumonia and interactions with commonly used antibiotics [published online ahead of print April 21, 2014]. Antimicrob Agents Chemother. doi:10.1128/AAC.02779-13.
 
Pinciroli R, Mietto C, Berra L. Respiratory therapy device modifications to prevent ventilator-associated pneumonia. Curr Opin Infect Dis. 2013;26(2):175-183. [CrossRef] [PubMed]
 

Figures

Tables

References

Hurley JC. Ventilator-associated pneumonia prevention methods using topical antibiotics: herd protection or herd peril? Chest. 2014;146(4):890-898.
 
Oostdijk EA, de Smet AM, Blok HE, et al. Ecological effects of selective decontamination on resistant gram-negative bacterial colonization. Am J Respir Crit Care Med. 2010;181(5):452-457. [CrossRef] [PubMed]
 
Buelow E, Gonzalez TB, Versluis D, et al. Effects of selective digestive decontamination (SDD) on the gut resistome. J Antimicrob Chemother. 2014;69(8):2215-2223. [CrossRef] [PubMed]
 
Klompas M. What can we learn from international ventilator-associated pneumonia rates? Crit Care Med. 2012;40(12):3303-3304. [CrossRef] [PubMed]
 
Kollef MH, Chastre J, Fagon JY, et al. Global prospective epidemiological and surveillance study of ventilator-associated pneumonia (VAP) due toPseudomonas aeruginosa[published online ahead of print July 22, 2014]. Crit Care Med.
 
Skrupky LP, McConnell K, Dallas J, Kollef MH. A comparison of ventilator-associated pneumonia rates as identified according to the National Healthcare Safety Network and American College of Chest Physicians criteria. Crit Care Med. 2012;40(1):281-284. [CrossRef] [PubMed]
 
Magill SS, Klompas M, Balk R, et al. Developing a new, national approach to surveillance for ventilator-associated events. Crit Care Med. 2013;41(11):2467-2475. [CrossRef] [PubMed]
 
Enne VI, Personne Y, Grgic L, Gant V, Zumla A. Aetiology of hospital-acquired pneumonia and trends in antimicrobial resistance. Curr Opin Pulm Med. 2014;20(3):252-258. [CrossRef] [PubMed]
 
Muscedere J, Sinuff T, Heyland DK, et al; Canadian Critical Care Trials Group. The clinical impact and preventability of ventilator-associated conditions in critically ill patients who are mechanically ventilated. Chest. 2013;144(5):1453-1460. [CrossRef] [PubMed]
 
Boyer AF, Schoenberg N, Babcock H, McMullen KM, Micek ST, Kollef MH. A prospective evaluation of ventilator-associated conditions and infection-related ventilator-associated conditions [published online ahead of print May 22, 2014]. Chest. doi:10.1378/chest.14-0544.
 
Montgomery AB, Rhomberg PR, Abuan T, Walters KA, Flamm RK. Amikacin/fosfomycin (5:2 ratio): characterization of mutation rates in microbial strains causing ventilator-associated pneumonia and interactions with commonly used antibiotics [published online ahead of print April 21, 2014]. Antimicrob Agents Chemother. doi:10.1128/AAC.02779-13.
 
Pinciroli R, Mietto C, Berra L. Respiratory therapy device modifications to prevent ventilator-associated pneumonia. Curr Opin Infect Dis. 2013;26(2):175-183. [CrossRef] [PubMed]
 
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