Review Article

Prevention of hospital-associated pneumonia and

ventilator-associated pneumonia
Marin H. Kollef, MD

Objective: To synthesize the available clinical data for the
prevention of hospital-associated pneumonia (HAP) and ventila-
tor-associated pneumonia (VAP) into a practical guideline for
clinicians.
Data Source: A Medline database and references from identi-
fied articles were used to perform a literature search relating to
the prevention of HAP/VAP.
Conclusions: There is convincing evidence to suggest that
specific interventions can be employed to prevent HAP/VAP. The
evidence-based interventions focus on the prevention of aerodi-
gestive tract colonization (avoidance of unnecessary antibiotics
and stress ulcer prophylaxis, use of sucralfate for stress ulcer
prophylaxis, chlorhexidine oral rinse, selective digestive decon-
tamination, short-course parenteral prophylactic antibiotics in
high-risk patients) and the prevention of aspiration of contami-
nated secretions (preferred oral intubation, appropriate intensive
care unit staffing, avoidance of tracheal intubation with the use of
mask ventilation, application of weaning protocols and optimal
use of sedation to shorten the duration of mechanical ventilation,
semirecumbent positioning, minimization of gastric distension,
subglottic suctioning, avoidance of ventilator circuit changes/
manipulation, routine drainage of ventilator circuit condensate).
Clinicians caring for patients at risk for HAP/VAP should promote
the development and application of local programs encompassing
these interventions based on local resource availability, occur-
rence rates of HAP/VAP, and the prevalence of infection due to
antibiotic-resistant bacteria (Pseudomonas aeruginosa, Acineto-
bacter species, and methicillin-resistant Staphylococcus aureus).
(Crit Care Med 2004; 32:1396 –1405)
KEY WORDS: hospital-acquired pneumonia; pneumonia; ventila-
tor-associated pneumonia; intensive care unit; nosocomial infec-
tion

B y definition, hospital-acquired
pneumonia (HAP) includes
any case of pneumonia that
starts ⱖ48 hrs after hospital
admission. Among intubated and me-
chanically ventilated patients, the devel-
opment of HAP 48 hrs or later is known
as ventilator-associated pneumonia
(VAP). There are approximately 300,000
cases of HAP annually in the United
States, representing roughly five to ten
cases per 1,000 hospital admissions (1).
Based on data from ⬎14,000 intensive
care unit patients in the U.S. National
Nosocomial Infection Surveillance Sys-
tem, HAP is the second most common
nosocomial infection after urinary tract
infection, affecting approximately 27% of
all critically ill patients (2).
HAP is the leading cause of mortality
attributed to nosocomial infections (2).
Approximately 60% of all deaths in pa-
tients with nosocomial infections are as-
From the Pulmonary and Critical Care Division,
Washington University School of Medicine, St. Louis,
MO.
Copyright © 2004 by the Society of Critical Care
Medicine and Lippincott Williams & Wilkins
DOI: 10.1097/01.CCM.0000128569.09113.FB
sociated with HAP/VAP, and the reported
hospital mortality rates for HAP/VAP
range from 20% to 70% (3–7). Although
patients with HAP/VAP are generally
sicker than those without the infection, it
is not simply a marker for other fatal
illnesses in these patients. “Attributable
mortality” in patients with HAP/VAP can
account for up to 50% of all mortality (8,
9). Additionally, the occurrence of HAP/
VAP has been associated with excess med-
ical care costs ranging from $5,800 to
$20,000 per case of HAP/VAP (10 –13).
Pathogenesis of HAP/VAP
An understanding of the pathogenesis
of HAP/VAP is fundamental for the devel-
opment of strategies aimed at preventing
this nosocomial infection. Risk for HAP/
VAP is determined in part by the duration
of exposure to the health care environ-
ment and the presence of host factors and
treatment-related factors that predispose
to the development of HAP/VAP (Table 1).
These risk factors predispose to the oc-
currence of HAP/VAP by increasing the
likelihood for colonization of the aerodi-
gestive tract with pathogenic bacteria
(e.g., prior antibiotic exposure) and pre-
disposing to the aspiration of contami-
nated secretions and fluids (e.g., ventila-
tor tubing condensate) (14 –17) (Fig. 1).
Additionally, risk profiles for the develop-
ment HAP/VAP have been developed to
identify patients at high risk for this nos-
ocomial infection (18). The use of such
risk profiles can assist in targeting pre-
ventive strategies, especially in the set-
ting of limited resources.
Oropharyngeal or tracheobronchial
colonization with pathogenic bacteria be-
gins with the adherence of microorgan-
isms to epithelial cells in the upper and
lower airway (19 –24). In addition to oro-
pharyngeal and tracheobronchial coloni-
zation, the stomach has been postulated
to be an important reservoir of organisms
that cause HAP/VAP, although the exact
role of the stomach in the causation of
HAP/VAP is debated (25). The importance
of the stomach as a source of pathogens
for HAP/VAP appears to be influenced by
multiple factors including the use of
medications predisposing to bacterial col-
onization (antibiotics, stress ulcer pro-
phylaxis), supine head positioning, the
administration of enteral feedings, and
the patient’s severity of illness to include

1396 Crit Care Med 2004 Vol. 32, No. 6

hemodynamic instability and the require- The relative importance of oropharyn- aeruginosa, Enterobacter species, Kleb-
ment for vasopressors (14, 25). geal colonization over that of gastric col- siella pneumoniae, Acinetobacter spe-
onization in the development of VAP has cies, and methicillin-resistant Staphylo-
been strongly suggested in studies using coccus aureus (31–33). Anaerobic
Table 1. Risk factors predisposing to hospital- rigorous culture methods to sequence bacteria seem to play a very limited role
associated and ventilator-associated pneumoniaa bacterial colonization in these locations in VAP, although they appear to be com-
and their relationship to VAP (26, 27). monly associated with aspiration pneu-
Witnessed aspirationb Bacteria can also gain entry into the monia in nonintubated patients (34, 35).
Chronic obstructive pulmonary diseasec
Administration of antacids or histamine type-2
lower respiratory tract of patients
antagonistsc through inhalation of aerosols generated
primarily by contaminated nebulization Nonpharmacologic Approaches
Supine positioningb
Comab devices (28). When this occurs, it is usu- to Prevent HAP/VAP
Enteral nutritionb ally related to lapses in proper infection
Nasogastric tubeb In general, nonpharmacologic ap-
Reintubationb
control procedures (29, 30).
proaches to the prevention of HAP/VAP
Tracheostomyb,c are more easily applied compared with
Patient transportb
Acute respiratory distress syndromeb,c Pathogens pharmacologic approaches and may be
Prior antibiotic exposurec performed at less expense. Additionally,
Age ⬎60 yrsc Infectious organisms that commonly the nonpharmacologic approaches usu-
Head traumab result in HAP are generally different from ally target the prevention of aspiration
Presence of intracranial pressure monitoringb
those that are most commonly associated whereas pharmacologic approaches focus
a
These risk factors are associated with hospital- with community-acquired pneumonia. on the prevention of colonization with
associated pneumonia by logistic regression analy- Gram-negative aerobes comprise the ma- pathogenic bacteria (Fig. 2) (14, 36).
sis (Ref. 17); bpredispose to aspiration of contami- jority of HAP infections (2); the individ- Avoidance of Tracheal Intubation/
nated secretions; cpredispose to colonization of the ual organisms that are commonly associ- Noninvasive Positive Pressure Ventila-
aerodigestive tract with pathogenic bacteria. ated with HAP/VAP are Pseudomonas tion. Intubation and mechanical ventila-

Figure 1. Pathogenesis of bacterial hospital-associated and ventilator-associated pneumonia.

Crit Care Med 2004 Vol. 32, No. 6 1397


Figure 2. The relationship between pathogenesis and preventive strategies for hospital-associated
pneumonia (HAP) and ventilator-associated pneumonia (VAP). *Prevention strategies that should be
limited to specific patient populations according to available clinical data.
tion are, by definition, prerequisites for
the development of VAP. Unnecessary in-
tubation, therefore, should be avoided at
all times. Noninvasive positive-pressure
ventilation using a full-face or nasal mask
can be used as an alternative ventilation
mode in many patients with acute respi-
ratory failure. The beneficial effects of
noninvasive positive-pressure ventilation
on the development of VAP and patient
survival have been determined in ran-
domized trials for patients with various
medical conditions including acute exac-
erbations of chronic obstructive pulmo-
nary disease and acute lung injury with
hypoxic respiratory failure and in immu-
nosuppressed patients with pulmonary
infiltrates and respiratory failure (37–
41). The beneficial influence of noninva-
sive positive-pressure ventilation on VAP
and hospital mortality rate has been fur-
ther demonstrated in a recent large ob-
servational study of patients experiencing
exacerbations of chronic obstructive pul-
monary disease and pulmonary edema
(42).
Shortening the Duration of Mechani-
cal Ventilation. Several studies have
identified an association between the du-
ration of mechanical ventilation and the
development of VAP (43, 44). As a result,
strategies to reduce patient exposure to
this risk factor may decrease the risk for
development of VAP. Examples of strate-
gies with the potential to shorten the
duration of mechanical ventilation are
protocols aimed at limiting the adminis-
1398
tration of sedation (45) and accelerated
weaning from mechanical ventilation us-
ing either weaning protocols or early at-
tempts at spontaneous breathing (46).
The goal of these strategies is to mini-
mize the patient’s exposure to endotra-
cheal intubation with its inherent risk of
aspiration of contaminated secretions.
Appropriate Staffing Levels in the In-
tensive Care Unit. Nursing and respira-
tory therapy staffing levels may influence
the length of stay of patients in intensive
care units, with an inverse relationship
between the adequacy of staffing levels
and duration of stay and subsequent de-
velopment of HAP/VAP (47, 48). With in-
creased workloads for registered nurses
and the reliance on less trained health
care personnel for the delivery of care,
there is concern that lapses in infection
control will occur, resulting in greater
rates of nosocomial infection (49 –53).
Availability of staff to participate in man-
datory training aimed at preventing HAP/
VAP appears to also be important for the
prevention of this nosocomial infection
(16).
Subglottic Suctioning. Secretions are
common in the upper airways of intu-
bated patients. Additionally, secretions
appear to pool above the endotracheal
tube cuff allowing for leakage of contam-
inated secretions into the lower airway
(54). In four studies, the effect of using an
endotracheal tube that has a separate
dorsal lumen, which allows continuous
aspiration of the subglottic secretions,
was compared with that of a conventional
endotracheal tube (55–58). Although the
four randomized, controlled studies
showed a beneficial effect of continuous
suctioning of subglottic secretions on the
incidence of VAP, none of the studies
showed a corresponding effect on mortal-
ity rate, length of stay in the intensive
care unit, or duration of mechanical ven-
tilation.
Oral (Nonnasal) Intubation. Nasotra-
cheal intubation has been identified as a
risk factor promoting the development of
VAP and sinusitis (59, 60). Nasal obstruc-
tion with an endotracheal tube or feeding
tube prevents the clearance of secretions
from the sinuses resulting in the devel-
opment of sinusitis. Aspiration of infected
secretions from the sinuses into the
lower respiratory tract can overwhelm lo-
cal host defense mechanisms allowing
VAP to occur (61). Available investiga-
tions and experience suggest that the pre-
ferred route of tracheal and gastric intu-
bation is via the oropharynx and not the
nasopharynx to prevent both hospital-
associated sinusitis and HAP/VAP.
Avoid Unnecessary Manipulation/
Changes of the Ventilator Circuit. The
role of ventilator tubing changes in pre-
venting pneumonia among mechanically
ventilated patients has been extensively
investigated. Initial studies evaluating
contamination of mechanical ventilator
circuits with heated water humidifiers
have shown that neither the rate of bac-
terial contamination of inspiratory-phase
gas nor the incidence of pneumonia was
significantly increased when tubing was
changed more frequently (62, 63). This
finding has been confirmed in more re-
cent observational and randomized trials
(64 – 67). Therefore, the previous recom-
mendations of the Centers for Disease
Control to change ventilator circuits rou-
tinely on the basis of duration of use
should be changed to one that is based on
visual contamination of the ventilator
circuit with blood, emesis, or purulent
secretions (68). This change may reduce
the overall occurrence of VAP, minimize
health care exposure to infectious aero-
sols that occur with circuit manipulation,
and result in cost savings.
Drain Ventilator Circuit Condensate/
Use of Heat and Moisture Exchangers.
The contaminated condensate within
ventilator circuits may predispose to
HAP/VAP and serve as a reservoir for the
spread of nosocomial pathogens through-
out an intensive care unit (69). Based on
these observations, a scheduled approach
Crit Care Med 2004 Vol. 32, No. 6
to the removal of tubing condensate, with
its proper disposal, should be employed
in all treatment areas where patients re-
ceive mechanical ventilation. The trans-
port of contaminated condensate from
one patient room to an another within a
common collection container should be
avoided as this can result in outbreaks of
VAP due to antibiotic-resistant bacteria
(16). Condensate accumulation can be re-
duced to a great extent with the applica-
tion of heat and moisture exchangers,
thereby potentially reducing the risk of
VAP (70, 71). This may explain the lower
incidence of late-onset VAP observed in
one randomized trial comparing humid-
ification with a heat and moisture ex-
changer compared with conventional
heat-water humidification (72). Routine
monitoring of all ventilator circuits for
the accumulation of condensate and ex-
peditious removal of condensate are im-
portant measures to prevent the develop-
ment of VAP.
Semierect Positioning. Aspiration of
upper airway secretions is a common
event even in normal healthy adults (73).
Among mechanically ventilated patients,
supine positioning has been shown to be
an independent risk factor for the devel-
opment of VAP (74). Studies employing
radiolabeled enteral feeding solutions in
ventilated patients have demonstrated
that aspiration of gastric contents occurs
to a significantly greater degree when pa-
tients are in the supine position com-
pared with the semirecumbent position
(75–77). One randomized trial demon-
strated a three-fold reduction in the inci-
dence of VAP and a trend toward a re-
duced hospital mortality rate in patients
treated in the semirecumbent position
(maintained at 45°) compared with pa-
tients treated completely supine (78). Of
note, the occurrence of VAP among pa-
tients in the supine position was strongly
associated with the simultaneous admin-
istration of enteral nutrition.
Avoidance of Large Gastric Volumes.
Several studies have found an association
between the aspiration of gastric contents
and VAP, suggesting that the avoidance of
gastric overdistention may reduce the oc-
currence of this complication (79, 80).
Unfortunately, the optimal approach for
providing nutrition to mechanically ven-
tilated patients remains undefined. Cur-
rently available measures aimed at avoid-
ing gastric overdistention include
reducing the use of narcotics and anti-
cholinergic agents, monitoring gastric
residual volumes following the adminis-
Crit Care Med 2004 Vol. 32, No. 6
tration of intragastric feeding solutions,
using gastrointestinal motility agents,
supplying enteral nutrition with smaller
bore feeding tubes, and administering
feeding solutions directly into the small
bowel instead of the stomach (14, 15).
A recent analysis examined ten studies
comparing gastric feeding with small
bowel feeding of critically ill patients
(81). In general, this analysis found that
small bowel feeding was associated with a
reduction in gastroesophageal regurgita-
tion, an increase in protein and calories
delivery to patients, and a shorter time to
achieving the target dose of nutrition.
Compared with gastric feeding, when the
results of seven randomized trials were
aggregated statistically, small bowel feed-
ing was associated with an overall reduc-
tion in pneumonia (81). However, there
was no difference in mortality rates be-
tween the two groups. However, delaying
the administration of enteral feedings in
some patient may also prevent the occur-
rence of HAP/VAP (82).
Biofilm Prevention Technology. Bio-
films form on surfaces such as an endo-
tracheal tube when they are encountered
by bacteria that “settle” on that surface,
up-regulating genes involved in matrix
production (83). The colonies of bacteria
forming the biofilm and detaching from
it are under the control of chemical sig-
nals of the same type that regulates
quoron sensing, and these regulatory
molecules guide the formation of the
slime-enclosed microcolonies and water
channels that makeup the biofilm (84).
Certain bacteria such as Pseudomonas
species appear to be more capable of
forming biofilms, especially in the pres-
ence of abnormal airway mucosa as exists
in patients with cystic fibrosis (24). The
recognition of biofilms on the surface of
endotracheal tubes has resulted in the
development of other novel approaches
aimed at limiting their formation. These
include the use of surface coatings that
impede bacterial adherence, oxygen-
plasma processing of the polyvinyl chlo-
ride, and the administration of nebulized
antibiotics (84 – 89). Unfortunately, none
of these approaches has been subjected to
clinical investigation, and it is also not
clear whether such technologies will in-
fluence the adherence of airway secre-
tions on the surface of endotracheal
tubes.
Hand Washing/Disinfection. Patho-
gens causing HAP/VAP, such as Gram-
negative bacilli and S. aureus, are ubiq-
uitous in health care settings, especially
in intensive critical units. Transmission
of these microorganisms to patients fre-
quently occurs via health care person-
nel’s hands that become contaminated or
transiently colonized with the microor-
ganisms. Procedures such as tracheal
suctioning and manipulation of ventila-
tor circuits or endotracheal tubes in-
crease the opportunity for cross-contam-
ination with these pathogens. The risk of
cross-contamination can be reduced by
using aseptic technique and sterile or dis-
infected equipment when appropriate and
eliminating pathogens from the hands of
personnel. The use of alcohol-based
foams and lotions allows hand disinfec-
tion to occur more efficiently (90, 91).
The use of these methods has been advo-
cated as a means to increase compliance
among health care providers with hand
disinfection before patient contacts (92).
Pharmacologic Approaches
Avoid Unnecessary Use of Stress Ulcer
Prophylaxis. Both histamine type-2 an-
tagonists and antacids are recognized to
be appropriate measures for stress ulcer
prophylaxis and risk factors for VAP (93–
95). The risk of VAP is increased by de-
creasing intragastric acidity, which can
result in greater gastric colonization with
pathogenic bacteria. Additionally, intra-
gastric volumes may be increased with
the administration of antacids promoting
aspiration and the development of VAP.
Sucralfate has been advocated as an alter-
native, but potentially less active, agent
for stress ulcer prophylaxis that does not
decrease intragastric acidity and does not
increase gastric volume significantly
(96 –98).
Decolonization of the Aerodigestive
Tract. Colonization of the upper respira-
tory tract is an important prerequisite for
the development of VAP. Oropharyngeal
colonization, either present on admission
or acquired during hospitalization, has
been identified as an independent risk
factor for the development of VAP caused
by enteric Gram-negative bacteria and P.
aeruginosa (98). Modulation of oropha-
ryngeal colonization, either with antibi-
otics (99 –102) or chlorhexidine (103),
appears to be an effective measure to pre-
vent VAP. However, the main limitation
to the routine use of these agents has
been the emergence of bacterial resis-
tance (104). Therefore, oropharyngeal de-
contamination has been limited to spe-
cific populations at high risk for VAP and
1399
to control outbreaks of antibiotic-resis-
tant bacteria (105).
Selective decontamination of the di-
gestive tract (SDD) combines oropharyn-
geal decontamination with gastric decon-
tamination and systemic administration
of antimicrobials. Several recent meta-
analyses have demonstrated that the use
of SDD is associated with significant re-
ductions in the incidence of VAP and
lower rates of hospital mortality, espe-
cially among surgical patients (106, 107).
A recent study of SDD among surgical
patients with a low prevalence of coloni-
zation with resistant bacteria (e.g., van-
comycin-resistant enterococci, methicil-
lin-resistant S. aureus) found a
statistically significant reduction in mor-
tality rate without increasing overall col-
onization with resistant bacteria (108).
However, like with antimicrobial oropha-
ryngeal decontamination, SDD carries
the potential risk of promoting more
widespread antibiotic resistance (109).
Therefore, the use of SDD should be care-
fully monitored for the emergence of an-
timicrobial resistance.
Prophylactic Antibiotics. A recent
study found that prolonged use of pro-
phylactic antibiotics in trauma patients
was associated with the delayed onset of
HAP/VAP, an increased incidence of
pneumonia caused by antibiotic-resistant
Gram-negative bacteria, and an increased
overall incidence of nosocomial infec-
tions (110). This study confirms the po-
tential harm of prolonged prophylactic
antibiotics and suggests that the duration
of prophylactic therapy in this patient
population must be critically reevaluated
because it may have a significant impact
on the infectious morbidity and the costs
associated with the care of trauma pa-
tients. However, prophylactic parenteral
antibiotics may play a role in the preven-
tion of HAP/VAP among specific high-risk
populations including patients with head
trauma or coma (111). Therefore, pro-
phylactic antibiotics should be employed
in appropriate high-risk patients (e.g.,
trauma, severe head injury, coma, high-
risk surgical procedures) generally for
ⱕ24 hrs following surgery or the initial
trauma.
Antibiotic Class Switch. Predominant
use of a single drug class for the treat-
ment of Gram-negative bacterial infec-
tions has been associated with the emer-
gence of antibiotic-resistant infections
including HAP/VAP (112). One strategy
designed specifically to minimize antimi-
crobial resistance while ensuring ade-
1400
quate empirical antimicrobial coverage is
the practice of a scheduled antibiotic
class switch (113, 114). This strategy has
been associated with reductions in the
occurrence of VAP when increasing
emergence of resistance to the baseline
antibiotic class was recognized as the
stimulus for the drug class switch (113).
However, more general strategies pro-
moting antimicrobial heterogeneity (i.e.,
antibiotic cycling, antibiotic rotation)
should only be employed as part of a
wider effort aimed at preventing antimi-
crobial resistance. This recommendation
is based on the inconsistent results re-
garding the influence of these practices
on antimicrobial resistance and the oc-
currence of nosocomial infections includ-
ing HAP/VAP (114 –117). Practices focus-
ing on antimicrobial heterogeneity
without the application of other strate-
gies aimed at preventing the emergence
of antibiotic-resistant infections (e.g.,
short-course antibiotic therapy, appropri-
ate hand disinfection) have the risk of
simply increasing resistance to subse-
quently introduced antimicrobial drug
classes (112, 118).
Shorter Courses of Empirical Antibi-
otic Therapy. Shortening the duration of
empirical antibiotic therapy may be a
valuable approach for reducing subse-
quent hospital-associated infections, in-
cluding HAP/VAP, that are caused by an-
tibiotic-resistant bacteria (119 –121).
Recently, the results of a large random-
ized trial comparing 8 days of adequate
antibiotic therapy for VAP to 15 days of
treatment were reported (122). Despite
similar efficacy, the longer course of an-
tibiotic therapy was associated with sta-
tistically greater emergence of multiply
resistant bacteria. These data suggest
that shorter empirical courses of antibi-
otic therapy for VAP and other infections
are safe and can decrease the emergence
of bacterial resistance and subsequent in-
fections due to antibiotic-resistant bacte-
ria (122, 123).
Vaccines. Various vaccination pro-
grams in adults and children have been
demonstrated to be successful in reduc-
ing the incidence of pneumonia caused
by specific pathogens, including Hae-
mophilus influenzae, Streptococcus
pneumoniae, and the influenza virus
(124 –126). These pathogens are major
causes of health care-associated pulmo-
nary infection and can predispose pa-
tients to developing respiratory failure
and the subsequent development of HAP/
VAP. At least one study showed that the
use of a vaccine directed against a respi-
ratory pathogen in a high-risk population
reduced subsequent hospitalization for
pneumonia, supporting the benefit of this
intervention (126). Unfortunately, vac-
cines directed against the pathogens as-
sociated with HAP/VAP possessing long-
term efficacy are not currently available
for clinical use (127).
Avoidance of Red Blood Cell Transfu-
sions. The transfusion of packed red
blood cells has been associated with seri-
ous nosocomial infections including VAP
(18, 128 –130). In one study, transfusion
of packed red blood cells was found to be
an independent risk factor for the devel-
opment of VAP (131). These data suggest
that the unnecessary transfusion of
packed red blood cells should be avoided
in hospitalized patients in order to reduce
the risk of nosocomial infections includ-
ing HAP/VAP.
Barriers to Implementation of
Prevention Strategies
Although the prevention of hospital-
associated infections, including HAP/
VAP, is advocated as an important man-
agement objective for all hospitals,
barriers exist to the implementation of
such interventions. Cook et al. (132)
compared Canadian and French intensive
care units regarding the use of seven
strategies to control secretions and care
for ventilator circuits to prevent VAP and
reduce overall health care costs. Adher-
ence to specific prevention guidelines for
VAP was statistically more common
among French intensive care units (64%
vs. 30%, p ⫽ .002), but rates were low in
both countries. These investigators also
found that published recommendations
did not appear to substantially affect
whether prevention interventions were
used within individual intensive care
units. Similarly, two European surveys
conducted among physicians and nurses,
respectively, found that 37.0% of inten-
sive care unit physicians and 22.3% of
nurses were not following published rec-
ommendations for the prevention of VAP
(133, 134). The most common reasons for
nonadherence were disagreement with
the interpretation of clinical trials, lack of
resources, fear of potential adverse
events, and costs associated with the im-
plementation of specific interventions.
Cook et al. (135) also surveyed clini-
cians to determine the reasons for the
lack of use of semirecumbency to prevent
HAP. Nurses perceived that the main de-
Crit Care Med 2004 Vol. 32, No. 6
terminant of semirecumbency was physi- fied barriers to semirecumbency related (e.g., decubitus ulcers), safety (e.g., slid-
cians’ orders, whereas intensivists per- to useful alternative positions (e.g., lat- ing out of the bed), and available re-
ceived that the main determinant was eral position), contraindications (e.g., he- sources (e.g., insufficient beds facilitating
nursing preference. Participants identi- modynamic instability), risk of harm semirecumbency). When made aware of

Table 2. Prevention protocol for hospital-associated pneumonia and ventilator-associated pneumonia (VAP) at Barnes-Jewish Hospitala

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 heat moisture exchangers (HMEs) for patients with excessive secretions or hemoptysis (be sure to provide alternative form of
humidification).
Change HMEs every 24 hrs 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 at least 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
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., influenza, Pneumococcus, Haemophilus B)
a
This protocol was employed in the prevention programs described in Refs. 16 and 137.

Figure 3. Results of a mandatory education program for the prevention of hospital-associated pneumonia and ventilator-associated pneumonia (VAP) carried
out in three hospitals employing the recommendations outlined in Table 2 (137). The arrow indicates the introduction of the intervention.

Crit Care Med 2004 Vol. 32, No. 6 1401


T
here is convincing
evidence to sug-
gest that specific
interventions can be em-
ployed to prevent hospi-
tal-associated pneumonia
and ventilator-associated
pneumonia.
the evidence, all participants endorsed
the use of semirecumbency. The use of
standardized orders for patient position-
ing was recently shown to increase
awareness of the importance of this in-
tervention and to increase compliance
with semirecumbency (136).
CONCLUSIONS
Although the optimal approach to re-
ducing VAP is unclear, recent studies in-
dicate that mandatory education of
health care workers caring for mechani-
cally ventilated patients can decrease
overall VAP rates (Table 2, Fig. 3) (16,
137). Among the available interventions,
shortening the duration of mechanical
ventilation and providing measures to
prevent the aspiration of contaminated
secretions appear to be most important.
Given the evidence supporting greater
morbidity rate, hospital mortality rate,
and medical care costs among patients
developing HAP/HAP, the prevention of
this nosocomial infection should be an
important priority in the hospital setting.
However, it is important to note that in-
terventions focusing on the prevention of
early-onset HAP/VAP (i.e., occurring
within the first 5 days of hospitalization)
attributed to antibiotic-sensitive bacteria
may not be associated with reduced mor-
tality rate, especially if these infections
are treated with appropriate antibiotic
regimens (14, 138). Nevertheless, clini-
cians caring for patients at risk for devel-
oping HAP/VAP should ensure that infec-
tion prevention programs are in place
within their hospitals. These programs
should target HAP/VAP, as well as other
important hospital-associated infections,
incorporating interventions that have
been demonstrated to be successful and
1402
are achievable with the available local
hospital resources.
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