HEALTHCARE EPIDEMIOLOGY CID 2004:38 (15 April) 1141

H E A L T H C A R E E P I D E M I O L O G Y I N V I T E D A R T I C L E
Robert A. Weinstein, Section Editor
Risk Factors for Ventilator-Associated Pneumonia:
From Epidemiology to Patient Management
Marc J. M. Bonten,
1
Marin H. Kollef,
2
and Jesse B. Hall
3
1
Department of Internal Medicine, Division of Acute Internal Medicine and Infectious Diseases, University Medical Center Utrecht, Utrecht, The Netherlands;
2
Pulmonary and Critical Care Division, Washington University School of Medicine, St. Louis, Missouri; and
3
Department of Medicine, Section of Pulmonary
and Critical Care, University of Chicago, Chicago, Illinois
Risk factors for the development of ventilator-associated pneumonia (VAP), as identied in epidemiological studies, have
provided a basis for testable interventions in randomized trials. We describe how these results have inuenced patient
treatment. Single interventions in patients undergoing intubation have focused on either reducing aspiration of oropharyngeal
secretions, modulation of colonization (in either the oropharynx, the stomach, or the whole digestive tract), use of systemic
antimicrobial prophylaxis, or ventilator circuit changes. More recently, multiple simultaneously implemented interventions
have been used. In general, routine measures to decrease oropharyngeal aspiration and antibiotic-containing prevention
strategies appear to be the most effective, and the latter were associated with improved rates of patient survival in recent
trials. These benets must be balanced against the widespread fear of emergence of antibiotic resistance. In hospital settings
with low baseline levels of antibiotic resistance, however, the benets to patient outcome may outweigh this fear of resistance.
In settings with high levels of antibiotic resistance, combined approaches of nonantibiotic using strategies and education
programs might be most benecial.
Ventilator-associated pneumonia (VAP) is the most common
lethal infection observed in patients who require treatment in
intensive care units (ICUs). VAP is dened as pneumonia oc-
curring 48 h after intubation and the start of mechanical
ventilation. This time window is important, so that any infec-
tion that is incubating at the time of admission can be excluded.
Incidences are highly inuenced by the characteristics of the
patient population studied and the criteria and techniques ap-
plied for diagnosis. When compared with combinations of clin-
ical and radiographic criteria and results of semiquantitative
culture of endotracheal aspirates, incidences based on the same
criteria with the addition of results of quantitative culture sam-
ples obtained by bronchoscopic techniques decrease by 30%
50% [1].
Most estimates of the incidence of VAP cite a rate of 10%
Received 20 October 2003; accepted 20 November 2003; electronically published 30 March
2004.
Reprints or correspondence: Dr. Marc J. M. Bonten, Dept. of Internal Medicine, Div. of
Acute Internal Medicine and Infectious Diseases, University Medical Center Utrecht,
Heidelberglaan 100, 3584 CX Utrecht, The Netherlands (m.j.m.bonten@digd.azu.nl).
Clinical Infectious Diseases 2004; 38:11419
2004 by the Infectious Diseases Society of America. All rights reserved.
1058-4838/2004/3808-0018$15.00
40% [1]. However, the denominator used to calculate rates in
these studies consisted of patients undergoing mechanical ven-
tilation for 48 h, and these incidence rates may, therefore, be
higher than the rates among general medical and surgical ICU
patients [1]. If these high incidence rates were to pertain to
the broad population of patients undergoing mechanical ven-
tilation, VAP would be one of the most common nosocomial
infections in the United States. In point prevalence studies, VAP
consistently has the highest mortality and morbidity, and it
typically prolongs the duration of hospitalization for an average
of 79 days per patient [1].
The crude mortality rate for VAP has been cited to be as
high as 70%, but there is wide recognition that not all deaths
among affected patients are the direct result of infection, but,
rather, that the infection is a marker for severity of illness. The
mortality attributable to VAP has been dened as the percentage
of deaths that would not have occurred in the absence of in-
fection. Some case-matching studies have estimated that one-
third to one-half of all VAP-related deaths are the direct result
of infection, with higher attributable mortality in cases char-
acterized by bacteremia or in which the etiologic agent is Pseu-
domonas aeruginosa or Acinetobacter species [2, 3]. However,
using similar methodology, others failed to identify attributable

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1142 CID 2004:38 (15 April) HEALTHCARE EPIDEMIOLOGY
Table 1. Risk factors for ventilator-associated pneumonia
(VAP).
Risk factor class, type OR (95% CI) Reference
Nonmodiable risk factors
Patient-related risk factor
COPD 1.9 (1.42.6) [13]
18.3 (3.889.8) [14]
Organ System Failure Index of 12 10.2 (4.523) [15]
Age of 160 years 5.1 (1.914.1) [15]
Coma 40.3 (3.3423.1) [16]
ARDS 9.7 (1.659.2) [17]
Head trauma 5.2 (0.930.3) [17]
Male sex 2 (1.52.7) [18]
Intervention-related risk factor
Neurosurgery 10 (1.664.9)
a
[17]
Thoracic surgery 2.16 [19]
ICP monitor 4.2 (1.710.5) [20]
Transportation out of ICU 3.8 (2.85.5) [18]
Reintubation 5.94 (1.2722.71) [21]
Modiable risk factors
Intervention-related risk factor
Use of H
2
-antagonist 2.5 (1.25) [20]
2.33 [19]
Use of antacids 20 [19]
Use of sucralfate 3.44 [19]
24-h circuit changes, compared
with 48-h circuit changes 2.3 (1.24.7) [20]
Use of antibiotics 3.1 (1.46.9) [15]
2.3 [19]
0.1 (0.010.7) [22]
Supine position 2.9 (1.36.6) [15]
Receipt of enteral nutrition 31.2 (3.3294.8) [16]
Failed subglottic aspiration 5.3 (1.222.6) [22]
Intracuff pressure of !20 cm H
2
O 4.2 (1.115.9) [22]
Tracheostomy 3.1 (2.24.5) [20]
Aerosol treatment 1.9 (1.42.5) [20]
NOTE. ARDS, acute respiratory distress syndrome; COPD, chronic ob-
structive pulmonary disease; ICP, intracranial pressure; ICU, intensive care
unit.
a
Only associated with increased risk for VAP caused by Acinetobacter
baumannii.
mortality due to VAP [47] or due to bacteremia [8]. VAP has
also been associated with increased health care costs, with es-
timated incremental health care costs of $11,897 per episode
of VAP [9] and estimated cost-savings of $13,340 for every
episode of VAP that is prevented [10].
Despite the importance of preventing nosocomial infections,
available information suggests that the number of such infec-
tions is on the increase, resulting in warnings from professional
and national agencies to refocus efforts on their prevention [11,
12]. In this review, we describe how determination of risk fac-
tors for the development of VAP in epidemiological studies has
led to interventions tested in randomized trials and how the
results of these trials have inuenced patient management.
PATHOGENESIS
For nosocomial respiratory tract infections to occur, the delicate
balance between host defenses and microbial propensity for
invasion must shift in favor of the capability of pathogens to
establish pneumonia. Risk for these infections is determined in
part by the duration of exposure to the health care environment
and in part by a number of host factors and treatment-related
factors that have been identied in the literature (table 1). To
consider methods to prevent these infections, it is useful to
separate host- and treatment-related factors into modiable
and nonmodiable groups. Most importantly, pathogens must
reach the lower airways. This usually occurs after aspiration of
oropharyngeal uids containing potential pathogens, and,
therefore, colonization at this site is almost a prerequisite for
the development of VAP. In addition, microorganisms may be
introduced directly by inhalation into the lower airways as a
result of contamination of medical equipment, and they may
reach the lungs after hematogenous spread, although these
routes of infection are probably much less common. Host de-
fenses may be impaired because of multiple disease-related al-
terations or even genetic predisposition, although genetic fac-
tors have yet to be explicitly dened.
RISK FACTORS
Many risk factors for the development of VAP have been iden-
tied. They can be differentiated into modiable and non-
modiable risk factors and into patient-related and treatment-
related risk factors (table 1). Nonmodiable patient-relatedrisk
factors include male sex, preexisting pulmonary disease, coma,
AIDS, head trauma, and multipleorgan system failure. Non-
modiable treatment-related risk factors include the necessity
of neurosurgery, monitoring of intracranial pressure, reintu-
bation, or transportation out of ICU. However, observational
studies cannot distinguish causation from noncausal associa-
tion. Ultimate proof of causalityand, thus, of the potential
for modulation to prevent infectionshould be provided by
empirical testing in prospective trials. Some of the modiable
risk factors have been subjected to empirical testing and will
be discussed here. To get a rough estimate of the magnitude
of preventive efcacy, we have pooled data from specic in-
terventions and calculated relative risk reductions (and 95%
CIs) of the pooled data (table 2).
PATIENT-RELATED RISK FACTORS
AND INTERVENTION STRATEGIES
Intubation. Intubation and mechanical ventilation are, by
denition, prerequisites for the development of VAP. Unnec-

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HEALTHCARE EPIDEMIOLOGY CID 2004:38 (15 April) 1143
Table 2. Relative risk (RR) reductions of pooled data of different intervention strategies for ventilator-associated pneumonia (VAP).
Preventive strategy, reference(s)
No. of
studies
No. of patients
with VAP/total
no. of patients
RR reduction
(95% CI)
Study
group
Control
group
Selective digestive decontamination
Oropharyngeal, intestinal, and systemic prophylaxis vs. control [23] 16 226/1437 493/1446 0.54 (0.450.63)
Oropharyngeal, and intestinal prophylaxis vs. control [23] 10 89/624 165/638 0.45 (0.280.62)
Oropharyngeal, intestinal, and systemic prophylaxis vs. systemic prophylaxis [23] 6 107/475 195/640 0.26 (0.090.43)
Oropharyngeal prophylaxis vs. control [2426] 3 13/125 70/181 0.73 (0.50.96)
Oropharyngeal and systemic prophylaxis vs. control [27] 1 13/58 23/30 0.71 (0.510.83)
Systemic prophylaxis vs. control [28] 1 12/50 25/50 0.52 (0.150.73)
Stress ulcer prophylaxis
Sucralfate vs. ranitidine [29] 8 160/914 202/911 0.21 (0.050.38)
Postpyloric vs. gastric feeding [30] 7 60/221 81/227 0.24 (0.010.41)
Semirecumbent vs. supine patient position [31, 32] 2 15/151 19/156 0.18 (0.390.76)
Subglottic aspiration [3336] 4 45/425 81/421 0.45 (0.230.61)
essary intubation, therefore, should be avoided at all times.
Noninvasive positive-pressure ventilation (NIPPV) using a face
mask could be used as an alternative ventilation mode in ICU
patients. The benecial effects of NIPPV on the development
of VAP and on patient survival have been determined in ran-
domized trials involving patients with acute exacerbations of
chronic obstructive pulmonary disease [37], acute respiratory
failure [38], and, in immunosuppressed patients with pulmo-
nary inltrates, fever and respiratory failure [39]. Relative risk
reductions from these individual studies range from 0.67 to
0.87. Nasotracheal intubation clearly is a risk for the devel-
opment of nosocomial sinusitis and should, therefore, be
avoided as well. Moreover, sinusitis was associated with an
increased OR for VAP of 3.8 in one study [40].
Duration of mechanical ventilation. Several studies have
identied the duration of ventilation as an important deter-
minant for the development of VAP. The risk of VAP does not
appear to be constant over the time of ventilation. In a large
cohort study, the risk was estimated to be 3% per day in the
rst week, 2% per day in the second week, and 1% per day in
the third week and beyond [41]. As a result, strategies to reduce
the duration of ventilation may decrease the risk for devel-
opment of VAP, especially when they reduce time on the ven-
tilator in the rst week or two of support. Examples of such
strategies are protocols to improve methods of sedation ad-
ministration [42, 43] and to accelerate weaning, either by pro-
tocolized methods [44] or by using noninvasive ventilation
[45]. Furthermore, stafng levels may inuence the length of
stay of patients in the ICU, with an inverse relationshipbetween
adequacy of stafng levels and the duration of stay and sub-
sequent development of VAP [46, 47].
Aspiration and nutrition. Aspiration of gastric or oro-
pharyngeal contents that are contaminated with colonizing
ora is important in the pathogenesis of VAP. The oropharynx
appears to be the most important source for microorganisms.
Continuous aspiration of subglottic secretions has been asso-
ciated with signicant reductions in the incidence of VAP in 2
randomized trials [33, 34] and with a strong tendency for such
a preventive effect in 2 other randomized studies [35, 36]. In
a fth study, subglottic aspiration combined with topical or-
opharyngeal antimicrobial prophylaxis signicantly reducedthe
occurrence of VAP [48]. The pooled relative risk reduction for
VAP of subglottic aspiration (without concomitant use of top-
ical antimicrobial prophylaxis) is 0.45 (95% CI, 0.070.95)
(table 2).
Supine patient positioning may also facilitate aspiration,
which may be decreased by semirecumbent positioning. Using
radioactive-labeled enteral feeding, cumulative numbers of en-
dotracheal counts were higher when patients were placed in a
completely supine position (0), compared with a semirecum-
bent position (45) [49, 50]. One randomized trial demon-
strated a 3-fold reduction in the incidence of VAP in patients
who were treated while in a semirecumbent position, compared
with patients who were treated while completely supine [31].
Of note, the occurrence of infection in patients in supine po-
sition was strongly associated with the simultaneous admin-
istration of enteral nutrition. In a second randomized trial
(which has only been published as an abstract to date), the
supine position was compared to the standard of care, which
appeared to be a head-up position of 12 [51]. In that mul-
ticenter study, a 45 patient position did not appear to be
achievable, and only a mean position of 28 was achieved,
which was not associated with a reduced incidence of VAP [32].

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1144 CID 2004:38 (15 April) HEALTHCARE EPIDEMIOLOGY
The summarized results of both trials lead to a relative risk
reduction of 0.18 (95% CI, 0.39 to 0.76) (table 2).
Stress ulcer prophylaxis. Both H
2
-antagonists and antacids
have been identied as independent risk factors for VAP. By
decreasing intragastric acidity and increasing intragastric vol-
ume (in the case of antacids), gastric colonization and aspi-
ration can be stimulated, favoring the development of VAP.
Sucralfate has been postulated as an alternative agent for stress
ulcer prophylaxis, because it does not decrease intragastric acid-
ity (as do H
2
-antagonists), nor does it increase gastric volume
signicantly (as do antacids). However, double-blind, random-
ized trials have failed to conrm the preventive effects of using
sucralfate [52, 53]. In meta-analysis, ranitidine was, when com-
pared with sucralfate, associated with a 4% higher incidence
of VAP [29]. However, ranitidine provided better prevention
against gastric bleeding in high-risk patients undergoing ven-
tilation [53]. Moreover, the presumed association between gas-
tric colonization and increased incidence of VAP has been
questioned [52, 54, 55]. The summarized results of 8 trials
comparing sucralfate with ranitidine for stress ulcer prophylaxis
yielded a relative risk reduction for VAP of 0.21 (95% CI, 0.05
0.38) (table 2). Thus, although the use of sucralfate may offer
some means of reducing the risk of VAP, as determined on the
basis of current published data, this benet may be more than
offset by increased risk of gastrointestinal hemorrhage.
Enteral nutrition. Enteral nutrition has been considered
a risk factor for the development of VAP, mainly because of an
increased risk of aspiration [56]. However, its alternative (par-
enteral nutrition) is associated with higher risks of developing
intravascular deviceassociated infections, complications of line
insertions, higher costs, and loss of intestinal villous architec-
ture, which may facilitate microbial translocation. For the latter,
it has been advised to feed critically ill patients enterally as early
as possible. However, a strategy of early (i.e., day 1 of venti-
lation) administration of enteral feeding for patients under-
going mechanical ventilation was, compared with late admin-
istration (i.e., day 5 of ventilation), associated with a higher
risk for ICU-acquired VAP [57]. In another attempt to reduce
aspiration, gastric nutrition has been compared with postpy-
loric feeding. Two studies using radioisotopes to compare the
incidence of aspiration were not conclusive [58, 59]. Seven
studies evaluated the risks for VAP in patients randomized to
receive either gastric or postpyloric feeding [30]. Although sig-
nicant differences were not demonstrated in any individual
study, postpyloric feeding was associated with a signicant re-
duction in VAP in meta-analysis (relative risk reduction, 0.24;
95% CI, 0.010.41) [30]. Few studies have evaluated the ap-
proaches of intermittent or acidied enteral feeding, and re-
ductions in the incidence of VAP have not been demonstrated
in any randomized trial [60, 61].
Modulation of colonization. Colonization of the upper
respiratory tract is a prerequisite for the development of VAP.
Oropharyngeal colonization, either present on admission or
acquired during the ICU stay, has been identied as an inde-
pendent risk factor for the development of VAP caused by
enteric gram-negative bacteria and P. aeruginosa [54]. Modu-
lation of oropharyngeal colonization, either by antibiotics [24
27] or chlorhexidine therapy [62], appears to be an effective
measure to prevent VAP. Combined results of 3 studies of top-
ical oropharyngeal antibiotics showed a relative risk reduction
for VAP of 0.73 (95% CI, 0.500.96).
Oropharyngeal decontamination is, together with gastric
and intestinal decontamination, one of the components of
selective decontamination of the digestive tract (SDD). SDD
has been associated with signicant reductions in the inci-
dence of VAP in most studies [23], although the methodo-
logical study quality appeared to be inversely related to the
magnitude of the preventive effects [63]. Of note, the pre-
ventive effects of SDD for VAP are considerably lower in ICUs
with high endemic levels of antibiotic resistance [6467], and,
in such settings, SDD will increase the selective antibiotic
pressure for drug-resistant microorganisms [6871]. The
pooled data from 15 studies comparing patients who received
the full SDD regimen with control patients yielded a relative
risk reduction for VAP of 0.54 (95% CI, 0.450.63) [63] (table
2). Pooled data from 5 studies comparing patients who re-
ceived the full SDD regimen with a control group of patients
receiving systemic prophylaxis yielded a smaller relative risk
reduction for VAP (0.26; 95% CI, 0.090.43), whereas data
from 10 studies comparing only patients who received topical
prophylaxis with control patients yielded a relative risk re-
duction for VAP of 0.45 (95% CI, 0.280.62) [23].
In addition to prevention of VAP, signicant reductions of
ICU-mortality in patients receiving SDD have been reported
recently. After stratication based on APACHE II scores, Krue-
ger et al. [72] randomized 265 patients in a double-blind design
to receive a regimen containing intravenous ciprooxacin for
4 days, as well as topical colistin and gentamicin applied to the
nostrils, mouth, and stomach. Control patients received intra-
venous and topical placebo. The overall relative risk for ICU
mortality was 0.76 (95% CI, 0.531.09), but, in the subgroup
of patients with APACHE II scores of 2029, the relative risk
was 0.51 (95% CI, 0.30.88) [72]. In a second study, an im-
pressive relative risk reduction in both ICU (36%) and hospital
mortality (23%) for patients receiving SDD was demonstrated
[73]. With almost 1000 patients enrolled, this was the largest
trial of SDD performed thus far. The reduction in the mortality
rate reported was the highest in any individual trial and even
exceeded the most positive predictions for mixed populations
in meta-analyses. Moreover, patients receiving SDD had a

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HEALTHCARE EPIDEMIOLOGY CID 2004:38 (15 April) 1145
shorter length of ICU stay, and fewer patients acquired colo-
nization with antibiotic-resistant, gram-negative bacteria. Of
interest, patients were not individually randomized to receive
SDD or not, but 2 identical wards were randomized in an open
design, and all admitted patients received the standard of care
in their unit. If possible, patients were randomized to 1 of the
2 wards. However, because no cross-over was performed, it
cannot be completely excluded that structural differences be-
tween the 2 wards might have inuenced patient care. There-
fore, these exciting ndings should be conrmed. It is impor-
tant to note that rate of colonization with drug-resistant,
gram-negative bacteria and vancomcyin-resistant enterococci
at the start of study and at the time of patient admission were
very low, and none of the patients were colonized with meth-
icillin-resistant Staphylococcus aureus [73].
Systemic antibiotics. The role of systemic antibiotics in
the development of VAP is unclear. In one study, prior ad-
ministration of antibiotics had an adjusted OR of 3.1 (95% CI,
1.46.9) for development of VAP [15]. Moreover, antibiotics
clearly predispose patients to subsequent colonization and in-
fection with antibiotic-resistant pathogens [74]. In contrast,
prior antibiotic exposure conferred protection (risk ratio, 0.37;
95% CI, 0.270.51) for VAP in another study [41]. Preventive
effects of intravenous antibiotics were evaluated in only 1 ran-
domized trial: administration of cefuroxime at the time of in-
tubation reduced the incidence of VAP in patients with closed
head injury [28]. Moreover, further circumstantial evidence for
efcacy of systemic antibiotics also follows from the results of
meta-analyses of SDD, which have suggested that the intra-
venous component of SDD is essential for improved patient
outcome [23, 75].
Ventilator circuitrelated factors. Although the majority
of VAP episodes likely arise from aspiration of contaminated
secretions around the endotracheal tube, in some circum-
stances, colonization of the ventilator circuit undoubtedly leads
to lower airway contamination and, eventually, pneumonia. A
large number of studies have been conducted to determine the
magnitude of risk related to a number of ventilator circuit
factors and management strategies. A large number of pro-
spective, randomized trials have shown that the frequency of
ventilator circuit change does not affect the incidence of VAP
[76, 77]. Use of passive humidiers with or without ltering
capacity has been shown to decrease circuit colonization by
bacteria, but it has not been shown to reduce the incidence of
VAP, and, with regard to infection control, there is no benet
to changing passive humidiers any more frequently than every
48 h [7882].
Combined interventions. Although the optimal approach
to reducing VAP is unclear, recent studies indicate that edu-
cating health care workers who care for patients who are re-
ceiving mechanical ventilation can decrease VAP rates [8387].
In times of limited resources, focusing health care workers
efforts on the prevention of VAP is important, especially given
the association between inadequate stafng in the ICU setting
and the occurrence of nosocomial infection [47, 8890]. In
addition, there are data supporting the benet of education-
based infection-control interventions targeting regional health
care systems [91].
Recently, an education-based program with multiple inter-
ventions has been shown to reduce the occurrence of VAP at
an academic medical center [84]. The centerpiece of this ed-
ucational initiative was a 10-page self-study module, including
information on the following topics related to VAP: (1) epi-
demiology and scope of the problem, (2) risk factors, (3) eti-
ology, (4) denition, (5) methods to decrease risk, (6) proce-
dures for collecting suctioned sputum specimens, and (7)
clinical and economic outcomes inuenced by VAP [84]. (The
study module and self-examinations can be obtained as a CD-
ROM through the Association for Professionals in Infection
Control and Epidemiology.) Risk factors for VAP that were
specically addressed included those promoting aspiration (su-
pine positioning and gastric overdistention) and those associ-
ated with bacterial colonization of the upper airway and stom-
ach (prior antibiotic exposure and the use of stress ulcer
prophylaxis). A section from the self-study module outlining
specic risk-reduction strategies addressed in the infection-
control policy is shown in table 3 [84, 92]. This integrated
education-based system aimed at reducing VAP was subse-
quently taken to 2 community hospitals and a pediatric hospital
for implementation [92]. Relative reductions in the occurrence
of VAP of 38%61% occurred in the hospitals that imple-
mented this education-based program as part of their man-
datory training for patient care providers [92].
Although multiple interventions to reduce VAP are available,
studies show that they are not being widely implemented. Cook
et al. [93] compared Canadian and French ICUs with regard
to the use of 7 strategies to control secretions and care for
ventilator circuits to prevent VAP and to reduce overall health
care costs. Adherence to specic prevention guidelines for VAP
was more common among French ICUs (64% vs. 30%; P p
), but rates were low in both countries. These investigators .002
also found that published recommendations did not appear to
substantially affect whether prevention interventions were used
within individual ICUs. Similarly, a European survey found that
37% of ICU practitioners were not following published rec-
ommendations for the prevention of VAP [94]. The most com-
mon reasons for nonadherence were disagreement with the
interpretation of clinical trial ndings (35%), lack of resources
(31%), and costs associated with the implementation of specic
interventions (17%).

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1146 CID 2004:38 (15 April) HEALTHCARE EPIDEMIOLOGY
Table 3. Section from the self-study module for the prevention of ventilator-associated pneumonia (VAP).
How do I reduce the risk of VAP in my patients?
The primary intervention to prevent any nosocomial infection is hand washing. Careful infection-control practices related to respiratory
care are also essential to preventing VAP. Health care workers should use the following recommendations for all patients receiving
mechanical ventilation.
To prevent bacterial colonization of the aerodigestive tract:
Meticulous hand hygiene with the use of soap and water or a waterless hand antiseptic agent is essential before and after ventilator
contact or patient suctioning;
Do not change ventilator circuits and/or in-line suction catheters unless visibly soiled or malfunctioning;
Do not use HMEs for patients with excessive secretions or hemoptysis (be sure to provide alternative form of humidication);
Change HMEs every 24 h or when visibly soiled with secretions;
Drain condensate from ventilator circuits per policy, using appropriate technique to avoid contamination of the circuit.
To prevent aspiration of contaminated secretions:
Maintain adequate ventilation and cuff pressure;
Place ventilated patients in semirecumbent position with head of bed elevated to 30, as tolerated, even during transport;
Drain ventilator circuit condensate before repositioning patient;
To avoid gastric distention monitor gastric residual volumes before initiating gastric feedings via nasogastric, orogastric, or percutaneous
gastrostomy tubes:
Remove nasogastric tubes as soon as possible.
To reduce risk of VAP when suctioning a ventilated patient:
Use clean gloves for in-line suctioning and sterile gloves for single use catheter suctioning;
Do not store catheter where it can become contaminated or contaminate clean supplies;
Oral suction catheters (e.g., Yankauer) should be stored in a nonsealed paper or plastic bag when not in use;
Do not lay suction catheters on ventilator;
Suction when necessary. Frequent unnecessary suctioning may introduce organisms into the lower respiratory tract.
Other key points to reduce the risk of VAP include the following:
Avoid nasal intubation;
Adequately secure endotracheal tube and take necessary measures to prevent accidental extubation;
Avoid overuse of multiple antibiotics;
Limit stress ulcer treatment if possible;
Use daily chlorhexidine oral rinse (only for patients undergoing cardiothoracic surgery);
Provide immunizations (e.g., inuenza, pneumococcus, and Haemophilus inuenzae B).
NOTE. Presented with permission from [92]. HME, heat moisture exchanger.
CONCLUSIONS
As summarized in table 2, along with routine measures to di-
minish aspiration, antimicrobial prophylaxis appears an effec-
tive strategy for preventing VAP. Importantly, in most studies
assessing antimicrobial prophylaxis, VAP was diagnosed with
bronchoscopic techniques, thereby minimizing the risk that the
prophylactic antibiotics induced false-negative results of diag-
nostic cultures. Unfortunately, antibiotic resistance has become
so prevalent in many ICUs that the benets of prophylactic
use of antibiotics for patients could be overcome by the in-
creased selective pressure for antibiotic-resistant pathogens. The
latter has been an important argument against the widespread
use of such strategies [95, 96]. Moreover, the long-term effects
of prophylactic antibiotic use on resistance development are
unclear. On the other hand, improved patient survival resulting
from antimicrobial prophylaxis, as has been suggested by 2
recent studies [72, 73], would necessitate a reappraisal of this
balance. If these ndings are conrmed in other settings, their
application could well be advised, especially for high-risk pa-
tients in settings with low levels of antibiotic resistance or when
specic problem antibiotic-resistant pathogens are encoun-
tered. It is therefore imaginable that, in the near future, baseline
levels of antibiotic resistance will determine which infection-
prevention strategies should be used. In settings with high levels
of antibiotic resistance, a combined approach of different non
antibiotic using strategies in combination with education pro-
grams for health care workers might be most benecial.
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