Guias Americanas de Ventilación Mecánica en QUEMADOS

PRACTICE GUIDELINES
American Burn Association Practice Guidelines

for Prevention, Diagnosis, and Treatment of
Ventilator-Associated Pneumonia (VAP)
in Burn Patients
Michael J. Mosier, MD, Tam N. Pham, MD
The purpose of this guideline is to review the available published literature on ventilatorassociated pneumonia (VAP) as it pertains to the burn patient. It provides an evidencebased recommendation for the prevention, diagnosis, and treatment of VAP in adult
burn patients. This guideline is designed to assist all healthcare providers caring for
adult burn patients with suspected VAP. Summary recommendations were made using
the following grading scale: grade Asupported by at least one well-designed prospective trial with clear-cut results; grade Bsupported by several small prospective trials
with a similar conclusion; and grade Csupported by a single small prospective trial,
retrospective analyses, cases studies, and expert opinions based on investigators practices. (J Burn Care Res 2009;30:910 928)
RECOMMENDATIONS
Standards
There are insufficient data to support a management
standard ventilator-associated pneumonia (VAP) at
this time.
Guidelines
Mechanically ventilated burn patients are at high
risk for developing VAP, with the presence of
inhalation injury as a unique risk factor in this
patient group.
VAP prevention strategies should be used in mechanically ventilated burn patients.
Clinical diagnosis of VAP can be challenging in
mechanically ventilated burn patients where systemic inflammation and acute lung injury are
prevalent. Therefore, a quantitative strategy,
From the University of Washington Burn Center and Department

of Surgery, Division of Burns/Trauma, Harborview Medical
Center, Seattle, Washington.
Address correspondence to Tam N. Pham, MD, University of
Washington Burn Center, Harborview Medical Center, 325
Ninth Avenue, Box 359796, Seattle, Washington 98104.
Copyright 2009 by the American Burn Association.
1559-047X/2009
DOI: 10.1097/BCR.0b013e3181bfb68f
910
when available, is the preferable method to confirm the diagnosis of VAP.

An 8-day course of targeted antibiotic therapy is
generally sufficient to treat VAP; however, resistant Staphylococcus aureus and Gram-negative
bacilli may require longer treatment duration.
OVERVIEW
Purpose
The purpose of this guideline is to review the available
published literature on VAP as it pertains to the burn
patient. It provides evidence-based recommendations for the prevention, diagnosis, and treatment of
VAP in adult burn patients.
Users
This guideline is designed to assist all healthcare providers caring for adult burn patients with suspected VAP.
Clinical Problem
Hospital-associated pneumonia is the second most
common nosocomial infection (most common infection in mechanically ventilated patients) in the
United States. Recent reviews indicate that between
10 and 20% of patients receiving 48 hours of mechanical ventilation will develop VAP. VAP has been
Journal of Burn Care & Research

Volume 30, Number 6
traditionally defined as an infection occurring 48

hours after hospital admission in a mechanically ventilated patient with a tracheostomy or endotracheal
tube.1 In early 2007, the Centers for Diseases Control (CDC) revised their definition for diagnosing
VAP.2 These latest criteria state that there is no minimum period that the ventilator must be in place to
diagnose VAP. Those who develop VAP are twice as
likely to die compared with similar patients without
VAP, and patients with VAP have significantly longer
intensive care lengths of stay, associated with an additional $40,000 in hospital charges.3,4
Injured patients have the highest risk of developing
VAP of any individual hospital patient population.
Reports from single center studies estimate the incidence of VAP as 22.1 to 26 per 1000 ventilator days
in burn patients.57 The National Nosocomial Infections Surveillance System reports the median rate of
11.4 VAP per 1000 ventilator days for patients in
trauma intensive care units (ICUs), higher than surgical ICUs, and more than double that seen in medical (3.7) or coronary care ICUs (4.0).4,8 These data
are consistent with findings of a large Canadian study
where burns had the highest relative risk of VAP (5.1,
95% CI: 1.517.0), followed by trauma (5.0, 95% CI:
1.9 13.1), compared with the medical ICU reference group.9
Ultimately, improving our management of this disease is not only medically important but also may
carry financial implications for burn centers in the
United States. Despite multiple studies indicating
that burn patients have unique risk factors for developing VAPincluding inhalation injury, prolonged
mechanical ventilation, and intensive care length of
staythe Centers for Medicare and Medicaid services
are considering cessation of reimbursements for services related to this potentially preventable complication. In a letter to the Department of Health, the
American Burn Association has expressed strong concerns about the inclusion of VAP into the list of
healthcare-associated infections because of the underlying nature of the admitting conditions in burn patients
that factor into the development of pneumonia.
The following recommendations were developed
using burn-specific and general critical care literature,
where appropriate, to assist providers in tailoring approaches to the prevention, diagnosis, and treatment
of VAP with an understanding of pathogenesis, risk
factors, and challenges specific to the burn patient.
Mosier and Pham
911
tions involving the key words burns, thermal injury, and pneumonia, nosocomial, hospitalacquired, ventilator-associated/acquired, burn
bacterial pneumonia, burn fungal pneumonia.
Additional publications were retrieved by evaluating references from the available articles. They were collectively reviewed, and summary recommendations were
made using the following grading scale (Table 1): grade
Asupported by at least one well-designed prospective
trial with clear-cut results; grade Bsupported by several small prospective trials with a similar conclusion;
grade Csupported by a single small prospective trial,
retrospective analyses, cases studies, and expert opinions
based on investigators practices.
SCIENTIFIC FOUNDATION
VAP Pathogenesis and the Role of
Inhalation Injury
VAP often results from microbial invasion of the normally sterile lower respiratory tract and lung parenchyma by aspiration, and less commonly from bloodstream spread or by direct extension of adjacent
infection. Principle defenses against infection in the host
include glottis closure, cough reflexes, mucociliary
clearance mechanisms, and immune cells-mediated responses to eliminate infection. Comparison of bacterial
DNA samples from broncheoalveolar lavages to organisms present on patients tongues has demonstrated that
the oropharynx is a potential reservoir for VAP.10 Because oropharyngeal colonization is often present on
Table 1. Grading of scientific evidence*
Level of Evidence
Class I: large prospective
clinical trial
Class II: small prospective
clinical trial (low power)
Recommendation
Grade Level
Grade A: supported by at least
one large prospective clinical
trial with clear-cut results
Grade B: supported by several
small prospective clinical
trials that support a similar
conclusion
Grade C: supported by a single
small prospective trial,
retrospective studies, and
consensus expert opinions
PROCESS
Class III: retrospective

analytical study,
contemporaneous
controls
Class IV: retrospective
analytical study,
historical controls
Class V: case series, expert
opinions
A Medline search of the English-language literature was

conducted for the years 1966 to 2008 for all publica-
* Adapted from Sackett DL. Rules of evidence and clinical recommendations on the use of antithrombotic agents. Chest. 1989;95(Suppl):25 45.

November/December 2009
912 Mosier and Pham
admission, or subsequently acquired in the ICU, this

risk factor is ubiquitous in critically ill patients.11,12
The stomach and sinuses are potential reservoirs of
bacteria. The stomach often becomes colonized with
Gram-negative bacteria during critical illness, and enteric Gram-negative bacteria are among the most frequent microorganisms isolated from cultures of patients with VAP. The gastropulmonary hypothesis
postulates that colonization of the stomach leads to
colonization of the lower respiratory tract from sustained microaspiration of contaminated oropharyngeal or gastric secretions around the endotracheal
tube cuff.13 After entry into the respiratory tract, infection can evolve in the setting of impaired host defenses, a challenge by a highly virulent pathogen, or
an overwhelming inoculum.14,15
Intubation and mechanical ventilation negate many
of the normal respiratory tract defenses against infection, bypassing the glottis barrier, with leakage of contaminated secretions around the endotracheal tube cuff,
and pooling into lower airways. The mechanically ventilated patient is unable to clear their own secretions, has
impaired mucociliary clearance, and is subjected to repeated inoculations despite suctioning.
The cumulative incidence of VAP increases with
the duration of mechanical ventilation, with the
highest risk of VAP early, at an estimated incidence
of 3% per day during the first 5 days, decreasing to
2% per day on days 5 to 10, and to 1% per day after
10 days.9,16 By definition, early-onset VAP occurs
within the first 4 days, in which normal mouth flora
or community-acquired pathogens typically predominate. In contrast, late-onset pneumonia (defined as 5
days and beyond) is predominantly caused by multidrug resistant (MDR) Gram-negative organisms and
methicillin-resistant S. aureus (MRSA).17 Identified
patient, injury, and intervention factors that predispose the mechanically ventilated patients to develop
VAP are summarized in Table 2.
Burn injury is a strong predictor of VAP, and the
intubation process itself contributes to the risk of infection. Multiple reports have documented the effect of
prehospital and emergency intubation in addition to the
presence of an endotracheal tube as contributing to
pneumonia.18 22 Cutaneous thermal injury can also
cause pulmonary dysfunction.23,24 In patients with
large burns (2530% TBSA), increased capillary permeability occurs not only at the injured site but also in
remote organ systems.2527 At 48 hours after injury,
tumor necrosis factor, interleukin-6, and interleukin-8
are elevated in the systemic circulation and at distant
sites, including the lung. Furthermore, these perturbations are temporally correlated to impairment in lung
Table 2. Identified independent factors for ventilatorassociated pneumonia9,22,244 252

Host Factors
Burns and trauma
Severe critical illness
Age 60 yr
Acute respiratory distress
syndrome
Chronic obstructive pulmonary
disease
Serum albumin 2.2 g/dL
Multiple organ dysfunction
Large-volume gastric
aspiration
Gastric colonization and
elevated pH
Upper respiratory tract
colonization
Sinusitis
Intervention Factors
Mechanical ventilation 2 d
Re-intubation
Supine head position
Paralytic agents, continuous
intravenous sedation
Positive end-expiratory
pressure
Frequent ventilator circuit
changes
4 units of blood products
transfused
Histamine 2-blockers,
antacids
Nasogastric tube
Prior antibiotic therapy
Transport out of the intensive
care unit
physiology and predict subsequent nosocomial lung

infection.28
Approximately 10 to 20% of burn patients are also
victims of inhalation injury, and the incidence increases with increasing burn size.29 Inhalation injury
is an important predictor of prolonged ventilator dependence, increased length of hospitalization, and
death.30 33 Inhalation injury is differentiated into 3
distinct types: 1) systemic injury by inhalation of poisonous substance (ie, carbon monoxide), 2) upper
airway heat injury, and 3) lower airway chemical injury. Hot air causes thermal injury to the upper tract
epithelium, whereas smoke particles can cause extensive injury to the lower respiratory epithelium and
pulmonary parenchyma.34,35 After significant smoke
inhalation, the ciliary function of the respiratory lining ceases.36 Epithelial cells immediately separate
from the basement membrane, and intracellular
bonds are disrupted.36,37
As with edema in the burn wound, the local injury
to the mucosa of the airway initiates an inflammatory
cascade, with edema formation and increased blood
flow to the respiratory tree.38 41 Leakage of plasma
proteins from the pulmonary microvasculature into
the interstitial and alveolar spaces leads to exudate
formation. These exudates congeal with neutrophils
and necrotic cellular debris to form fibrin casts, partially or fully obstructing the airways and causing
bronchoconstriction.42,43 Release of the proteolytic
enzymes and oxidants initiated by the acute inflam-

Volume 30, Number 6
matory response destroys the lung parenchyma and

increases the microvascular permeability, further
propagating edema formation and decreasing gas exchange.41,44 51 Surfactant is also diminished, resulting in alveolar collapse and a decrease in lung compliance.40,52 At the molecular level, smoke inhalation
induces a massive influx of alveolar leukocytes that are
primed for an early, enhanced lipopolysaccharideactivated cytokine response compared with alveolar
leukocytes isolated from cutaneous burn patients or
uninjured controls.53
As a result, burn patients with inhalation injury
frequently develop pulmonary complications, including reactive airway disease, acute respiratory distress
syndrome (ARDS), and pneumonia.54 VAP is
thought to be a common complication of ARDS:
between 34 and 70% of patients with ARDS develop
VAP.55 60 At autopsy, as many as 73% of patients
with a premortem diagnosis of ARDS also have histological evidence of pneumonia.61 VAP concurrent
with ARDS is typically late onset, caused by resistant
bacteria, and can be polymicrobial. VAP diagnosis in
patients with ARDS is often difficult because of the
lack of specificity of clinical criteria alone to diagnose
VAP concurrent to ARDS, thus, bronchoscopic evaluation has been used in many studies.58 60,62,63
VAP Prevention Strategies

Considerable efforts have been devoted in critical care
research to VAP prevention, although relatively few
reports have focused specifically on burn patients.
Nevertheless, many of these findings are applicable to
the mechanically ventilated burn patient and form the
basis of our recommendations (Table 3).
Mosier and Pham
913
Necessity and Duration of Mechanical Ventilation.

Naturally, reducing the need for intubation and mechanical ventilation is highly desirable, because this
process alone increases the risk of VAP 6-fold to 21fold.22,64 Unnecessary intubations should be
avoided, whereas necessary intubations should be
performed under controlled conditions as much as
possible, because an increased incidence of VAP has
been documented with field and emergency department intubations compared with the ICU setting.18
Furthermore, avoiding accidental tube dislodgement
and emergency reintubation also decreases VAP incidence.22,65,66 Presence of a cuff leak over 10 to 15%
has been suggested as a simple screening test to limit
reintubation for laryngeal edema and postextubation
stridor and may be particularly useful in the burn patient
with extensive head and neck edema following burn
resuscitation. However, the absence of a cuff leak later in
hospitalization is not necessarily a contraindication to
removal of the endotracheal tube.6770 Daily interruption of sedation and weaning protocols are established
strategies to reduce the duration of mechanical ventilation in ICU patients.65,66,7175 Although very few burn
patients were included in these studies, centers that have
adopted the practice of daily spontaneous breathing trials report an improvement in extubation rates without
an increase in reintubation rates.74,76 78 These strategies are applicable to mechanically ventilated burn patients as well. Thus, we recommend daily interruption of
sedation and daily spontaneous breathing trial. Recommendation grade: A.
Use of Specialized Endotracheal Tubes. Specialized endotracheal tubes that reduce the bacterial inoculum may prove particularly beneficial in subsets of
Table 3. Recommended ventilator-associated pneumonia prevention strategies

Level of
Evidence
Study Population
Sources
Avoid unnecessary intubation and re-intubation

Implement ventilator weaning and sedation protocols
Use of specialized endotracheal tubes
Topical oral antisepsis (eg, Chlorhexidine)
Use oral route for endotracheal and gastric tubes
Continuous suctioning of subglottic secretions
Semirecumbent patient positioning with enteral nutrition
Avoid unnecessary red blood cell transfusions
Class I
Class I
Class I
Class I
Class II
Class I
Class I
Class I
1, 18, 22, 65, 66, 253

65, 66, 7178
89
11, 118123, 254
255257
7984
90, 9294, 99, 258
126130
Heat-moisture exchangers to reduce tubing condensate,

emptying of tubing condensate, and avoidance
of unnecessary ventilator circuit changes
Infection control measures and intensive care unit surveillance
Class I
Medical, surgical, and trauma

Medical and surgical
Medical and surgical
Medical, surgical, trauma,
and burns

and burns
1, 72, 135, 140, 253
Strategy
Class I
References
66, 136, 138140
914 Mosier and Pham
patients who need prolonged mechanical ventilation.

Tubes with continuous aspiration of subglottic secretions have reduced the incidence of early-onset VAP
in several studies.79 84 Silver impregnated endotracheal tubes are theoretically attractive because of the
broad-spectrum antimicrobial activity of silver85 and
prevention of bacterial adhesion and biofilm formation.86 88 Use of a silver-coated endotracheal tubes
was recently evaluated in the NASCENT randomized
trial of 9417 patients across 54 centers in North
America, showing a 35.9% relative risk reduction in
VAP from an incidence of 7.5 to 4.8% in a mixed ICU
population of patients expected to require intubation
for 24 hours.89 At this time, we consider specialized
endotracheal tubes an option in the management of
mechanically ventilated burn patients, until confirmatory evidence supports their benefit in the burn population. Recommendation grade: A.
Reducing Aspiration From Gastrointestinal
Tract Sources. The supine position and simultaneous administration of enteral nutrition are considered risk factors for the development of VAP due to
an increased risk of aspiration of gastric contents.90,91
Patients fed enterally in the supine position have as
much as a 50% incidence of VAP compared to 5% in
those kept in the semirecumbent position.90,9294
Thus, we recommend maintaining mechanically ventilated burn patients in the semirecumbent position,
especially when enterally fed. Recommendation
grade: A.
Under fasting conditions, gastric sterility is maintained by an acidic pH. Clinical evidence suggests
that a gastric pH of 3.5 prevents bacterial colonization, whereas a pH 4.0, potentiated by many common ICU practices such as stress-ulcer prophylaxis
and continuous enteral nutrition, is associated with
clinically important bacterial colonization and a
higher incidence of nosocomial pneumonia in many,
but not all reports.55,9598
Joint Commission on Accreditation of Healthcare
Organizations core measures currently mandate
stress ulcer prophylaxis on ventilated patients; however, with improvement in resuscitation and hemodynamic monitoring, clinically important stress gastritis is now a rare event in the burn ICU. Early and
aggressive enteral nutrition is also likely to provide
some level of protection against stress gastritis and is
likely to be partly responsible for the significantly decreased incidence of gastric ulceration in burn patients; however, although gastric feeds may offer a
degree of protection against stress gastritis, duodenal
feeds may not. Thus, a conflict exists between increasing gastric pH to decrease the risk for stress gastritis

and increasing colonization of the upper gastrointestinal tract with risk of aspiration of bacteria.
Further support for the gastropulmonary hypothesis comes from scintigraphic imaging studies, documenting that patients fed into the stomach have more
episodes of gastroesophageal regurgitation and trend
toward more microaspiration compared with patients
fed beyond the pylorus; and patients with gastroesophageal regurgitation are more likely to aspirate
than patients without.99 Three randomized controlled trials comparing gastric with postpyloric enteral feeding found an 8 to 15% absolute reduction in
VAP with postpyloric feeding. Unfortunately, they
lacked sufficient power to show a statistical significance.100 Thus, until a sufficiently powered study is
performed, a postpyloric feeding tube remains an option in mechanically ventilated burn patients receiving enteral nutrition and should be attempted if possible, given the improved tolerance and potential
decreased incidence of VAP. However, if logistically
restrictive, enteral feedings should not be delayed
while awaiting placement of a postpyloric feeding
tube. In addition, until there is better evidence about
the risk of stress gastritis with postpyloric feeding in
critically sick patients, if a patient is fed postpyloric
and remains mechanically ventilated or coagulopathic, pharmacologic stress ulcer prophylaxis should
likely be used to decrease the risk of clinically significant gastrointestinal bleeding. Recommendation
grade: A.
Role of Prophylactic Antibiotic Administration.
Modulation of oropharyngeal colonization by combinations of oral antibiotics, with or without systemic
therapy, or by selective decontamination of the gastrointestinal tract (SDD) has also been shown to reduce the frequency of VAP.101104 Fifty-eight randomized controlled trials and 12 meta-analyses have
been published focusing on SDD. The meta-analyses
have consistently demonstrated a significant reduction in pneumonia.105 The largest Cochrane metaanalysis, including 6922 patients, indicated that SDD
using parenteral and enteral antimicrobials reduced
the odds ratio (OR) for pneumonia to 0.35 (95% CI:
0.29 0.41), with similar results in trauma patients
(OR: 0.38; 95% CI: 0.29 0.50).106 SDD has also
shown a survival benefit in all meta-analyses including
parenteral and enteral antimicrobials (OR: 0.78; 95%
CI: 0.68 0.89), which shows that one life can be
saved for every 21 patients treated.
SDD has been investigated in a few trials looking
specifically at burn patients. A study from Shriners
Hospitals for Children, Galveston, examined a small
number of severely burned pediatric patients and
found no difference in pneumonia, sepsis, or mortal-

Volume 30, Number 6
ity with SDD.107 In contrast, a much larger Spanish

randomized, placebo-controlled, double-blind trial
found a mortality reduction from 27.8 to 9.4% with
SDD in the burn ICU.108
Similar to SDD is the idea of prophylactic antibiotics to decrease the incidence of VAP in areas where
the incidence is unacceptably high. In Japan, 57% of
S. aureus strains isolated from all the national hospitals are identified as MRSA, a percentage that is much
higher than any other country. This high incidence
and the increased risk inherent to patients with larger
burn size led Kimura et al at the Nippon Medical
School Hospital to undergo a prospective, randomized, placebo-controlled study of trimethoprimsulfamethoxazole (TMP-SMX) in patients with burns
20% TBSA. In 40 enrolled patients, the incidence of
MRSA pneumonia was 4.8% in the TMP-SMX group
and 36.8% in the placebo group, a statistically significant difference. Notably, no major side effects of
therapy with TMP-SMX were observed, and there
was no increased resistance to TMP-SMX. Their results combined with SDD, which typically targets
Gram-negative organisms, suggest a significant potential reduction in the incidence of VAP in severely
burned patients.109
Unfortunately, the preventive benefits of prophylactic antibiotics for VAP have been considerably
lower in ICUs with high endemic levels of antibiotic
resistance.110 116 In this setting, SDD seemed to increase the selective pressure for antibiotic-resistant
microorganisms that are likely to occur in burn patients with high colonization and infection rates.114
Thus, despite positive reviews of the many randomized clinical trials and meta-analyses that have influenced European practice,117 critical care (including
burn) providers in the United States have been reluctant to adopt prophylactic antibiotics for these reasons, arguing that the benefits derived by reducing
early-onset VAP episodes are outweighed by this antibiotic selection pressure. Therefore, although prophylactic antibiotics reduce early-onset VAP, routine
prophylactic use of antibiotics should be discouraged
in hospital settings where there are high levels of antibiotic resistance. Recommendation grade: A.
Decreasing Oropharyngeal Bacterial Colonization.
Chlorhexidine oral rinse has been shown in many studies to be a simple and cost-effective prevention strategy
for VAP in many different patient populations. DiRiso
et als11 prospective, randomized, double-blind trial in
coronary artery bypass graft patients showed a 69% reduction in the incidence of respiratory infections with
no change in antibiotic resistance patterns. Similarly,
Houston et al118 found a 58% reduction in pneumonia
in patients intubated 24 hours. Benefits have also
Mosier and Pham
915
been shown in critically ill medicine patients ventilated 48 hours, with a 65% reduction in VAP.119
Meta-analysis has further supported the finding that oral
antisepsis decreases the incidence of VAP.120 122 On
the other hand, the PIRAD study groups multicenter
double-blind, placebo-controlled study found that although antiseptic decontamination significantly decreased oropharyngeal colonization of aerobic pathogens in ventilated patients, its efficacy was insufficient to
reduce the incidence of respiratory infections caused by
multiresistant bacteria.123 Given that many trials indicate a VAP reduction with this strategy, we recommend
oral chlorhexidine to decrease oropharyngeal colonization as an effective VAP prevention strategy. Recommendation grade: A.
Practice of Restrictive Blood Transfusion.
Postinjury immunosuppression is a recognized complication of severe burn injury, and common therapies used in caring for injured patients, such as blood
transfusion, add to the immune compromised
state.124,125 In a multicenter, prospective observational study of 1518 patients receiving mechanical
ventilation for 48 hours in 284 mixed-ICUs across
the U.S., Shorr et al126 established that transfusion
independently increased the risk for VAP (OR: 1.89;
95% CI: 1.332.68) and that the effect of transfusion
on late-onset VAP (defined as arising 5 days of mechanical ventilation) was more pronounced (OR:
2.16; 95% CI: 1.273.66).
The American Burn Association Burn Multicenter
Trials group has examined the effect of blood transfusion in 666 patients at 21 burn centers with acute
burn injuries 20% TBSA and found a 13% increased
risk of infection with each unit of blood transfused.
VAP occurred in 42% of those transfused and only in
6% of those who did not receive a blood transfusion,
although patients in the latter group were much less
severely ill.127 In addition, a number of retrospective
clinical studies have documented adverse outcome
associations, including higher VAP incidence, with
allogeneic blood transfusion and prolonged storage
times.128 130 Therefore, a restrictive transfusion policy in mechanically ventilated burn patients reduces
infections and should be applied to burn patients.
Recommendation grade: C.
Intensive Insulin Therapy. Intensive insulin therapy to control blood glucose levels (to levels 80 110
mg/dL) reduced mortality in surgical ICU patients
in a landmark trial published in 2001,131 but this
effect was not confirmed in subsequent trials.132,133
These subsequent studies have also raised the issue of
hypoglycemia during intensive insulin therapy, which
may negate its benefit in critically ill patients. Arabi
et als132 study of medical and surgical ICU patients
916 Mosier and Pham
found hypoglycemia occurred more frequently with

intensive insulin therapy (goal of 80 110 mg/dL)
compared with conventional therapy (goal of 180
200 mg/dL) at 28.6 vs 3.1%, with no difference in
any other secondary outcomes. Similarly, Brunkhorst
et als133 study of patients with severe sepsis showed a
significantly higher rate of severe hypoglycemia (40
mg/dL) in the intensive insulin therapy group (17.0
vs 4.1%), with a higher rate of serious adverse events
(10.9 vs 5.2%). There have been few such studies in
burns; however, Hemmila et al recently evaluated
their experience with intensive insulin therapy in burn
patients. Their adoption of an intensive insulin therapy protocol (140 mg/dL) did not have an impact
on mortality, although it did decreased VAP rate.134
The potential benefit of intensive insulin therapy in
burn patients needs to be confirmed in large prospective trials before a formal recommendation can be
made in burn patients. At this time, implementation
of an intensive insulin protocol constitutes an option
in mechanically ventilated burn patients. Recommendation grade: C.
Environmental Infection Control Practices.
The environment, healthcare devices, and staff can all
serve as sources of infection.1,135 Colonization of the
ventilator circuit may also lead to VAP.66 Many prospective, randomized trials have shown that the frequency of ventilator circuit changes does not affect
the incidence of VAP,136,137 but condensate collecting in the circuit can become contaminated from
patient secretions and be introduced into the lower
airway with position changes.138 Passive humidifiers
or heat exchangers decrease ventilator circuit colonization but have not significantly reduced the incidence of VAP.139,140 Recently, the U.S. military has
been able to significantly decrease their incidence of
VAP in Iraq with institution of an aggressive infection
control protocol that has included hand hygiene,
contact barrier precautions, patient and staff cohorting, chlorhexidine oral care, and reducing the duration and spectrum of surgical antimicrobial prophylaxis. Institution of their protocol decreased the
incidence of VAP from a high of 60.6 per 1000 ventilator days to a low of 9.7 per 1000 ventilator
days.141 We recommend the inclusion of infection control measures as part of standard VAP prevention measures in the burn ICU. Recommendation grade: A.
Prevention Protocols (Known as Bundles). The
creation of the Leapfrog group in 2000 aimed to
reduce preventable medical errors and to improve the
quality and affordability of healthcare by encouraging
health providers to publicly report their quality and
outcomes so that consumers and purchasing organizations can make informed healthcare choices. Pres-

ident George W. Bush issued an executive order in

August 2006 to increase healthcare transparency by
encouraging the adoption of health information technology standards, the provision of options that promote quality and efficiency in health, and the pricing
and quality information be made publicly available.
These and other actions have dramatically increased
the pressure to initiate patient safety measures at individual hospitals and to publicly report process of
care and hospital outcomes, including complications.
Given these regulatory pressures and the recognized poor adherence to evidence-based best practice
in the ICU setting, ventilator bundles were developed to reduce associated complications. Bonello et
al142 demonstrated a positive impact with such an
approach, with an increase in ventilator bundle compliance from 50 to 82% by the last 3 months of the
study and a decrease in the incidence of VAP from
11.7 to 6.9 events per 1000 ventilator days, a 41%
reduction. Similarly, a Quality Rounds Checklist
has helped DuBose et al143 to improve their adherence with VAP prevention measures, such as head of
bed elevation 30 degrees, daily interruption of sedation, peptic ulcer disease prophylaxis, and deep venous thrombosis prophylaxis, and to decrease their
incidence of VAP from 16.3 to 8.9 events per 1000
ventilator days.
In contrast, Ogaard et al at Regions Burn Center
examined the impact of ventilator bundles on VAP
incidence over 2 years. The Institute for Healthcare
Improvement ventilator bundle consisted of four elements: elevation of the head of the bed between 30
and 45 degrees, daily sedation vacation and daily assessment of readiness to extubate, peptic ulcer prophylaxis, and deep venous thrombosis prophylaxis.
VAP incidence of 6.3 per 1000 ventilator days in the
first year was reduced to 2.8 per 1000 ventilator days
in the second year. Mean monthly compliance of the
VAP bundle was 59 and 78% for the first and second
years, respectively. Overall compliance for months
with and without VAP was 69%, thus, with the incomplete compliance rate and the already low incidence of VAP, they could not demonstrate an impact
in their VAP rate with the use of the Institute for
Healthcare Improvement VAP bundle.144 However,
their burn center had a lower VAP rate than the
pooled mean of the 12 burn centers nationwide reporting to the National Nosocomial Infections Surveillance System in 2006.
Thus, improved and continued reporting of data
from burn centers nationwide is essential to understand VAP occurrences. Despite enormous regulatory pressures and data from nonburn ICUs indicating its benefits, ventilator bundle implementation has

Volume 30, Number 6
not yet been confirmed of benefit in burn patients. As

such, this strategy of prevention of bundles remains
an option until further data becomes available. Recommendation grade: C.
Diagnosis of VAP
Despite its common occurrence, no clinical gold
standard exists for the diagnosis of VAP. The Canadian Critical Care Society, the American Thoracic Society, and Infectious Disease Society of America have
created guidelines for the prevention and management of VAP145; however, establishing the diagnosis
of VAP can be particularly difficult in the burn patient
where other causes of pulmonary dysfunction (inhalation injury, systemic inflammation, and pulmonary
edema) not only predispose the patient to postinjury
pneumonia but also may obscure its diagnosis. Traditionally, VAP is suspected if the patient has clinical
findings suggesting infection, including fever, purulent sputum, leukocytosis or leukopenia, and decline
in oxygenation along with a new or progressive infiltrate on chest radiograph. Unfortunately, no consensus exists on which combination of findings yields an
accurate diagnosis of VAP,14,146,147 and many patients with the clinical diagnosis of pneumonia may
have noninfectious etiologies for their clinical findings, such that as many as 66% of patients with the
clinical diagnosis of VAP may not meet microbiologic
criteria for infection.148
Efforts to improve our ability to diagnose VAP
have led to scoring systems such as the CDC Criteria
and the Clinical Pulmonary Infection Score (CPIS),
which combine clinical, radiographic, physiologic
(PaO2/FiO2), and microbiologic data, to improve
the specificity of VAP diagnosis.149,150 An initial
score 6 and a persistently elevated CPIS 6 after 3
days of empiric treatment are strongly associated with
VAP in medical and mixed ICU patients.149,150
Application of a clinical strategy such as CPIS to
injured patients is limited by common findings of
fever, leukocytosis, and the presence of ARDS in this
patient population. Two retrospective studies in
trauma and burns have pointed to the presence of
systemic inflammation and coexisting pulmonary dysfunction as potential limitations to the utility of
CPIS,151153 and one larger study from France suggests that a strategy based on the CPIS to decide that
which patients with suspected VAP should receive
prolonged administration of antibiotics would seem
to overprescribe these agents, when compared with a
strategy based on bronchoscopy.154 These studies
highlight the fact that injured patients, whether from
trauma, cutaneous burn, or smoke inhalation, have
numerous reasons for exhibiting an inflammatory re-
Mosier and Pham
917
sponse. The CPIS scale is not able to differentiate

inflammation from infection, a differentiation that
can be definitively made by quantitative culture.
In contrast to the clinical strategy, the bacteriologic
approach is used to obtain a lower airway quantitative
culture when VAP is suspected, using broncheoalvolar lavage (BAL), protected specimen brush, or a
nonbronchoscopic technique (so-called mini-BAL).
The advantages of the quantitative strategy are the
increased specificity of diagnosis and the clear-cut
identification of responsible organisms, which may
reduce the extended use of broad-spectrum antimicrobials in the ICU.14,63,145,147,155159 Limitations
include the limited availability of these diagnostic
techniques and the potential for introducing infection into lower airways with an invasive procedure.
Furthermore, some patients may be too severely ill to
tolerate lower airway intubation and sampling because of hypoxemia and shock. An additional point of
disagreement exists as to the appropriate threshold
for positivity in injured patients. Most authors use
104 cfu/mL for BAL and 103 cfu/mL for protected
specimen brush 160 162; however, several studies in
the trauma population have used a BAL threshold of
105 cfu/mL to limit unnessary administration of systemic antibiotics and demonstrated similar rates of VAP
recurrence.153,163,164 BAL should not be thought of as
100% accurate in capturing the offending organisms, as
has been shown on lung biopsy,165 but does show good
correlation,166,167 and many clinicians place a greater
value in their culture results compared to with endotracheal aspirate and are more likely to de-escalate antibiotic therapy.14,147
Comparison of clinical and bacteriologic strategies
in mixed ICU populations has yielded inconsistent
results.146,157 Patients who underwent quantitative
culture in a French multicenter randomized trial had
reduced mortality at day 14 (16.2 and 25.8%, P
.022), decreased sepsis-related organ failure assessment scores at day 3 and day 7, and decreased antibiotic use (P .001).157 In contrast, the Canadian
Critical Care Trials Groups146 study showed similar
outcomes and overall use of antibiotics with quantitative culture vs endotracheal aspirate and nonquantitative culture; however, this study has been criticized for its many limitations that influence its
results.147,156,168
As part of the Inflammation and the Host Response to Injury research program, the investigators
evaluated existing evidence-based data and guidelines
for prevention, diagnosis, and treatment of VAP and
developed a standard operating procedure to unify
management of patients with suspected pneumonia.
The protocol states as follows: clinical findings con-
918 Mosier and Pham
sistent with pneumonia should lead to a quantitative

respiratory specimen culture and a Gram stain. A
chest film should be used to document radiographic
evidence of pneumonia. Empiric therapy may be
started and should be based on local burn center and
patient-specific flora and resistance patterns. Cultures
should be obtained before initiating empiric therapy
if possible. Antibiotics should be adjusted based on
culture-based sensitivity and resistance patterns determined locally.160 We recommend that, when feasible, a bacteriologic strategy using quantitative lower
airway cultures is preferred to confirm VAP diagnosis.
Recommendation grade: B.
Treatment
Early-onset pneumonia, defined as being within the
first 4 days, usually carries a better prognosis and is
more likely to be caused by antibiotic sensitive bacteria. Patients with inhalation injury are at particularly
high risk for early-onset VAP. A recent study by
Mosier et al169 documented that 16% of diagnostic
BAL on admission grew 100,000 cfu/mL of predominantly community-acquired organisms. Streptococcus pneumoniae and Haemophilus influenzae are
more typical of early-onset VAP in patients without
other risk factors. At present, many strains of S.
pneumoniae are penicillin resistant because of altered penicillin-binding proteins. Some such
strains are resistant to cephalosporins, macrolides,
tetracyclines, and clindamycin.170
In contrast, late-onset VAP is most commonly
caused by aerobic Gram-negative bacilli such as
Pseudomonas aeruginosa, E. coli, Klebsiella sp., and
Acinetobacter, as well as MRSA. Carter et al confirmed this finding in burn patients as well; in their
retrospective review, MRSA surveillance culture positivity predicted the occurrence of MRSA VAP. In
addition, all patients who developed MDR VAP did
so after 7 days of mechanical ventilation.171
Significant growth of oropharyngeal flora (Streptococcus viridans, coagulase-negative staphylococci, Neisseria,
and Corynebacterium) from distal bronchial specimens
can be difficult to interpret but can produce infection in
immunocompromised hosts and some immunocompetent patients.172 Rates of polymicrobial infection vary
widely, but seem to be increasing, and are especially
high in patients with ARDS.14,22 P. aeruginosa is the
most common MDR Gram-negative pathogen causing
VAP and has intrinsic resistance to many antimicrobial
agents.173 Klebsiella, Enterobacter, and Serratia are intrinsically resistant to ampicillin and other aminopenicillins and can acquire resistance to cephalosporins and
aztreonam by the production of extended-spectrum
beta-lactamases.174 176

Reviews from individual burn units now identify

Acinetobacter baumannii as a common infectious organism in many burn units worldwide.177 Acinetobacter species, although typically less virulent than P.
aeruginosa, have become problematic pathogens because of increasing antibiotic resistance. Acinetobacter isolates are typically highly multiresistant, with
many distinct strains, and is more common in tropical
warm climates or during summer months. More than
85% of isolates are susceptible to carbapenems, but
resistance is increasing because of either metaloenzymes or carbapenemases. An alternative therapy is
sulbactam, usually used as an enzyme inhibitor, but
with direct antibacterial activity against Acinetobacter
species.176
In the United States, nearly 60% of the ICU infections caused by S. aureus are with MRSA. Patients
with MRSA VAP are often older, have higher disease
severity scores, and have been on mechanical ventilation longer at onset of VAP.178 Many important virulence factors exist with MRSA, including strains
bearing the Panton-Valentine leukocidin gene,179
which is associated with severe necrotizing VAP resulting in tissue destruction, cavitation, hemoptysis,
and increased mortality.180 Although vancomycin intermediate sensitivity and resistance are emerging, all
isolates causing respiratory tract infections have
fortunately been sensitive to linezolid.181,182 Unfortunately, linezolid resistance has also emerged in
S. aureus but is currently rare.183 Successful treatment of MRSA VAP with vancomycin may be low,
ranging from only 35 to 57% as this agent has poor
lung penetration.184
Nosocomial pneumonia caused by fungi such as
Candida and Aspergillus fumigatus, may occur in organ transplant or immunocompromised, neutropenic
patients, but is uncommon in immunocompetent patients. Isolation of Candida albicans and other species from endotracheal aspirates is common, but usually represents colonization of the airways, rather than
pneumonia in immunocompetent patients, and rarely
requires treatment with antifungals.185189 However,
patients with severe burns should be considered immunocompromised, and burn patients have been
cited as being among the highest risk groups for invasive fungal infections. Burn wounds provide an
ideal portal for invasive infection while inducing substantial immune dysfunction. Fungal organisms are
now among the most common causes of burn wound
infection, with increasing risk as burn size increases
and with delay in excision of the burn wound.
Early Initiation of Broad-Spectrum Antibiotic
Coverage. Whether VAP is early or late in onset,
multiple studies have shown that a delay in the initi-

Volume 30, Number 6
ation of appropriate antibiotic therapy for patients

with VAP is associated with increased morbidity, cost
of care, and mortality.159,190 195 Therefore, once a
patient is diagnosed with VAP, broad-spectrum antibiotic therapy should begin immediately targeting
specific likely pathogens based on timing of VAP onset and modified by knowledge of local patterns of
antibiotic resistance.159,196 201 Choice of antibiotics
should not be guided by Gram stain because multiple
studies have shown poor correlation between Gram
stain and final culture results.161,202204 Similarly, tracheal aspirates and sputum cultures do not accurately
reflect presence or absence of infectious organisms in
the lower airways because the upper airway and endotracheal tube are rapidly colonized.14,205210 Importantly, a quantitative culture should be obtained
before initiation of antibiotics, if possible, and diagnostic threshold should be lowered if the culture is
obtained after administration of antibiotics.211214
Thus, we recommend that broad-spectrum antibiotic
therapy begin immediately targeting specific likely
pathogens based on timing of VAP onset and modified by knowledge of local patterns of antibiotic resistance, following attainment of a quantitative culture. Recommendation grade: C.
De-Escalation of Broad-Spectrum Antibiotic
Coverage. If quantitative culture was obtained, narrowing the antimicrobial spectrum using microbiologic results and sensitivities, known as de-escalation
is most appropriate. This is an important concept and
benefit of a quantitative culture approach, because
the incidence of MDR bacteria continues to rise,215,216
whereas our arsenal of antibiotics is limited, and a clinical strategy does not permit safe antibiotic therapy deescalation. Use of an ICU-specific, broad-spectrum,
empiric therapy regimen can lead to a significant
increase in the administration of appropriate antimicrobial treatment, a decrease in the development
of secondary episodes of antibiotic-resistant VAP,
and a significant reduction in the total duration of
antimicrobial treatment.197200,214 In addition, a
recent international consensus conference agreed
that the use of broad-spectrum antibiotics for 48
hours would not induce a significant risk of
MDR.217 Thus, we recommend de-escalation of
broad-spectrum antibiotic coverage once quantitative culture results are known. Recommendation
grade: C.
ICU-Specific Antibiotic Rotation Protocol. Although no study has specifically examined its role in
burns, antibiotic rotation has been evaluated and
adopted by many intensivists. Retrospective evaluations
and three large prospective evaluations in medical, surgical,
and trauma ICU patients have indicated a decreased inci-
Mosier and Pham
919
dence of MDR bacteria and possible mortality benefit with

an antibiotic rotation protocol.199,200,218220 Knowledge
of local antibiotic resistance patterns should be considered
when choosing empiric antibiotics; however, antibiotic
rotation should be considered an option for individual
burn centers to reduce the spread of MDR bacteria until
further burn unit specific data become available. These
strategies should be tailored to the sensitivity and resistance patterns observed in individual burn centers. Recommendation grade: A.
Duration of Antibiotic Treatment. No study has
specifically addressed length of antibiotic treatment
for VAP in burn patients; however, recent data from
other trials suggest that antibiotics can be stopped
once clinical signs of infection have resolved. This
may also decrease the incidence of secondary pneumonias with MDR organisms.
Micek et al221 showed that an antibiotic discontinuation policy based on a predefined clinical response
to antimicrobial therapy was associated with a shorter
duration of antibiotic use and no difference in the
occurrence of secondary VAP episodes when compared with conventional antibiotic management.
Mueller et al have used repeat BAL to guide antibiotic
duration. In their pilot study of 52 patients, antibiotic
therapy was discontinued if bacterial growth dropped
to 10,000 cfu on repeat BAL performed on day 4 of
antibiotic therapy. Their results showed no difference
in pneumonia relapse, ventilator-free ICU days, ICU
days, or mortality, but it did show a significant reduction in the duration of antibiotic therapy at a mean of
9.8 3.8 days vs 16.7 7.4 days, suggesting that
antibiotic duration for VAP can generally be shorter
than 2 weeks.222 Dennesen et al223 have reported that
most of the clinical signs of pneumonia have resolved
by 6 days of therapy, and a recent multicenter randomized trial in France demonstrated no difference
in mortality or recurrent infection in patients treated
with an 8-day course of antibiotics compared with
those treated with a 15-day course. In addition, those
treated with 8 days of antibiotics had a lower incidence of multiresistant pathogens if a recurrent infection developed. Notably, if the original infecting organism was a nonlactose fermenting Gram-negative
bacilli such as P. aeruginosa or Acinetobacter baumanii, those treated with an 8-day course had a higher
pulmonary infection recurrence rate.224 No difference was noted in secondary outcomesmortality at
28 and 60 days, number of organ failure-free days,
number of ventilator-free days, length of ICU stay,
and unfavorable outcome ratein patients with VAP
caused by nonlactose fermenting Gram-negative bacilli treated for 8 vs 15 days. Similar to the increased
virulence of nonlactose fermenting Gram-negative

920 Mosier and Pham
bacilli, MRSA pneumonias (particularly with the

Panton-Valentine leukocidin gene and difficulties
in achieving appropriate antibiotic treatment) are
often quite virulent, with demands for longer ventilator and ICU support.179,180,225227 Therefore, we
recommend limiting antibiotic treatment to 8 days
for VAP, unless caused by MRSA or nonlactose fermenting Gram-negative rods, in which case we recommend treatment be continued for 15 days. Recommendation grade: A.
Areas of Uncertainty and Investigation

Protocolized Management of Inhalation Injury.
The significant pulmonary dysfunction that accompanies inhalation injury has led to multiple approaches to mechanical ventilation. Volume control,
synchronized intermittent mandatory ventilation and
pressure support, pressure control to reverse inspiratory to expiratory ratios, permissive hypercapnia, and
high-frequency ventilation are all currently practiced.
Despite all these options, well-controlled clinical trials defining the optimal mode of ventilation for adults
with inhalation injury have yet to be performed. Alternative modes of mechanical ventilation have been
explored, and their benefits also need to be tested in
rigorous trials. One method that has been studied in
several studies is high-frequency percussive ventilation (HFV). Cioffi et al228 reported a 20% decreased
incidence of pneumonia compared with that in historical controls, indicating the importance of small
airway patency in the pathogenesis of inhalation injury sequelae and supporting further use and evaluation of HFV. Correlative evaluation of HFV in
baboons indicated that the prophylactic use of highfrequency ventilation significantly reduces ventilatorinduced pulmonary damage and may explain the decreased mortality in inhalation injury patients treated
with HFV.229
Role of Tracheostomy in VAP Prevention. Another unanswered question is the role of tracheostomy in burn patients. Multiple studies have tried to
answer the question of whether early tracheostomy is
beneficial to patients. Saffle et als230 randomized trial
of 44 adult patients showed no difference in ventilator support, incidence of pneumonia, or survival with
early tracheostomy. Similarly, Barret et als231 review

of 290 children revealed no difference in the incidence of pneumonia in patients with tracheostomies
vs endotracheal tubes. The debate over tracheostomy
compared with translaryngeal intubation remains unresolved. For any benefit of tracheostomy to be realized, this procedure should be done early in the patients course. However, predictors of successful
ventilator weaning are often inaccurate, and tracheostomy can be a morbid procedure in the setting of
massive tissue edema. Recently, percutaneous tracheostomy has been demonstrated as a safe alternative
procedure and may have a lower incidence of pneumonia and complications, when compared with open
tracheostomy.232
Promising Diagnostic Approaches. A number of
biomarkers have been evaluated with the hope to better identify patients with VAP. Promising earlier observational studies with procalcitonin led investigators
to study procalcitonin and C-reactive protein levels in
serum and BAL fluid to try to predict or assist in the
diagnosis of VAP with disappointing results at this
point.233,234 Gibot et als small study evaluating medical
patients with sepsis of pulmonary (VAP) or extrapulmonary origin combined the use of serum procalcitonin
and BAL lavage fluid soluble triggering receptor expressed on myeloid cells-1 showed a good correlation
with elevated values and assisted in determination of
pulmonary or extrapulmonary source.235 Procalcitonin
may be more helpful as a prognostic marker for whether
a patient will have a favorable or unfavorable outcome
when they have already been diagnosed with VAP,
where persistently elevated levels have shown to correlate with an unfavorable outcome.236,237
Modes of Antimicrobial Delivery. Aerosolization
may enhance antibiotic delivery to the lower respiratory
tract. Agents most studied in this fashion have been
aminoglycosides and polymyxin B. The following studies have been on general ICU patients and, thus, are not
specific to burns, yet provide some interesting findings.
Brown et al238 performed a small prospective randomized study of tobramycin vs intravenous therapy in VAP,
which failed to show an improvement in clinical outcome, although patients receiving aerosolized tobramycin had higher microbiologic eradication rates. Palmer
Table 4. Recommendations for diagnosis of ventilator-associated pneumonia

Strategy
Clinical findings consistent with pneumonia should
lead to a quantitative respiratory specimen culture
and a Gram stain
Level of
Evidence
Study Population
Sources
Class II

and burns
References
14, 63, 145148, 151160

Volume 30, Number 6
Mosier and Pham
921
Table 5. Recommendations for treatment of ventilator-associated pneumonia

Strategy
Level of
Evidence
Study Population
Sources
Early initiation of broad-spectrum antibiotic coverage
Class II
De-escalation of broad-spectrum antibiotic coverage

Intensive care unit specific antibiotic rotation
protocol
Duration of antibiotics: 8 days, unless non-lactose
fermenting Gram negatives, methicillin-resistant
Staphylococcus aureus, or recurrent ventilatorassociated pneumonia, in which case, 15 days is
recommended
Class II
Class I

and burns
and burns
Class I
et al conducted a more recent double-blind, randomized, placebo-controlled study of aerosolized vancomycin and gentamycin for ventilator-associated tracheobronchitis in 43 ICU patients. The aerosolized
antibiotic group had reduced signs of respiratory infection by CDC and CPIS criteria, lower white blood cell
count at day 14, reduced bacterial resistance, reduced
use of systemic antibiotics, and improved ventilator
weaning.239 Claridge et al investigated aerosolized
antibiotics as prophylaxis against VAP in a singleinstitution, double-blind, randomized trial comparing a 7-day course of aerosolized ceftazidime
with placebo. In the 105 patients evaluated, they
found no difference in the incidence of VAP, MDR
VAP, or other infectious complications in the two
groups.240 The authors concluded that the prophylactic use of aerosolized antibiotics for prophylaxis
cannot be recommended.
Another mode of antibiotic delivery to be further
investigated is that of continuous vancomycin infusion. Several authors have proposed the use of continuous infusion of vancomycin for MRSA VAP. This
strategy would involve adjusting the dose of infusion
to maintain a serum vancomycin plateau concentration between 20 to 30 mg/L.241243 This is attractive
because vancomycin has poor lung penetration, but
the ability to obtain bacterial killing is concentration
dependent, and intermittent dosing often results in
suboptimal serum vancomycin concentrations.
Whether continuous infusion of vancomycin leads to
superior results in the treatment of burn patients with
MRSA VAP remains to be investigated.
SUMMARY
VAP is common in mechanically ventilated burn patients, and inhalation injury is a unique risk factor in
this patient population. As such, strategies for preven-
References
159, 190204, 211214
197200, 214216
199, 200, 218220
179, 180, 221227
tion, accurate diagnosis, and treatment of VAP are

important components of the care of the mechanically ventilated burn patient. The recommendations
in these guidelines are derived from review of the
available general critical care and burn literature. Although most of the data were obtained by study of
medical, surgical, and trauma patients and not burn
patients, these important findings are also applicable
to the mechanically ventilated, critically ill burn patient (Tables 35). Nevertheless, future studies that
directly focus on the critically ill burn population
would help to validate many of the findings from the
critical care literature and strengthen their application
in our patients.
REFERENCES
1. Centers for Disease Control and Prevention. Guidelines for
preventing health-careassociated pneumonia, 2003: recommendations of CDC and the Healthcare Infection Control
Practices Advisory Committee. MMWR Recomm Rep 2004;
53:136.
2. Centers for Disease Control and Prevention. The National
Healthcare Safety Network (NHSN) manual: patient safety
component protocol 2007; available from: http://
www.cdc.gov/ncidod/dhqp/pdf/nhsn/NHSN_
Manual_PatientSafetyProtocol_CURRENT.pdf; Internet;
accessed December 14, 2008.
3. Safdar N, Dezfulian C, Collard HR, Saint S. Clinical and
economic consequnces of ventilator-associated pneumonia: a
systematic review. Crit Care Med 2005;33:2184 93.
4. Rello J, Ollendorf D, Oster G, et al; VAP Outcomes Scientific Advisory Group. Epidemiology and outcomes of
ventilator-associated pneumonia in a large US database.
Chest 2002;122:211521.
5. Santucci S, Gobara S, Santos C, Fontana C, Levin AS. Infections in a burn intensive care unit: experience of seven years.
J Hosp Infect 2003;53:6 13.
6. Wibbenmeyer L, Danks R, Faucher L, et al. Prospective analysis of nosocomial infection rates, antibiotic use, and patterns
of resistance in a burn population. J Burn Car Res 2006;27:
152 60.
7. Lazarus H, Fox J, Lloyd J, et al. A six-year descriptive study of
hospital-associated infection in trauma patients: demograph-

922 Mosier and Pham
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
20.
21.
22.
23.
24.
25.
26.
ics, injury features, and infection patterns. Surg Infect

(Larchmt) 2007;8:46373.
Tablan OC, Anderson LJ, Besser R, Bridges C, Hajjeh R;
CDC; Healthcare Infection Control Practices Advisory Committee. Guidelines for preventing health-care-associated
pneumonia, 2003: recommendations of the CDC and the
Healthcare Infection Control Practices Advisory Committee.
MMWR Recomm Rep 2004;53:136.
Cook D, Walter S, Cook R, et al. Incidence of and risk factors
for ventilator-associated pneumonia in critically ill patients.
Ann Intern Med 1998;129:433 40.
Bahrani-Mougeot F, Paster B, Coleman S, et al. Molecular
analysis of oral and respiratory bacterial species associated
with ventilator-associated pneumonia. J Clin Microbiol
2007;45:1588 93.
DeRiso AJ II, Ladowski JS, Dillon TA, Justice JW, Peterson
AC. Chlorhexidine gluconate 0.12% oral rinse reduces the
incidence of total nosocomial respiratory infection and nonprophylactic systemic antibiotic use in patients undergoing
heart surgery. Chest 1996;109:1556 61.
Seguin P, Tanguy M, Laviolle B, Tirel O, Malledant Y. Effect
of oropharyngeal decontamination by povidone-iodine on
ventilator-associated pneumonia in patients with head
trauma. Crit Care Med 2006;34:1514 9.
Bonten MJ, Gaillard CA, de Leeuw PW, Stobberingh EE.
Role of colonization of the upper intestinal tract in the pathogenesis of ventilator-associated pneumonia. Clin Infect Dis
1997;24:309 19.
Chastre J, Fagon JY. Ventilator-associated pneumonia. Am J
Respir Crit Care Med 2002;165:867903.
Fagon JY, Chastre J, Hance AJ, Montravers P, Novara A,
Gibert C. Nosocomial pneumonia in ventilated patients: a
cohort study evaluating attributable mortality and hospital
stay. Am J Med 1993;94:281 8.
Richards MJ, Edwards JR, Culver DH, Gaynes RP. Nosocomial infections in medical ICUs in the United States: National Nosocomial Infections Surveillance System. Crit Care
Med 1999;27:88792.
Trouillet JL, Chastre J, Vuagnat A, et al. Ventilatorassociated pneumonia caused by potentially drug-resistant
bacteria. Am J Respir Crit Care Med 1998;157:5319.
Eckert M, Davis K, Reed RL II, et al. Ventilator-associated
pneumonia, like real estate: location really matters. J Trauma
2006;60:104 10; discussion 110.
Brochard L, Mancebo J, Wysocki M, et al. Noninvasive ventilation for acute exacerbations of chronic obstructive pulmonary disease. N Engl J Med 1995;333:81722.
Antonelli M, Conti G, Rocco M, et al. A comparison of
noninvasive positive-pressure ventilation and conventional
mechanical ventilation in patients with acute respiratory failure. N Engl J Med 1998;339:429 35.
Hilbert G, Gruson D, Vargas F, et al. Noninvasive ventilation
in immunosuppressed patients with pulmonary infiltrates, fever, and acute respiratory failure. N Engl J Med 2001;344:
81722.
Celis R, Torres A, Gatell JM, Almela M, Rodrguez-Roisin R,
Agust-Vidal A. Nosocomial pneumonia. A multivariate analysis of risk and prognosis. Chest 1988;93:318 24.
Pham TN, Cho K, Adamson LK, et al. Burn injury induces an
inhibitory signal in the lung Smad pathway. Cytokine 2004;
27:66 73.
Patel PJ, Faunce DE, Gregory MS, Duffner LA, Kovacs EJ.
Elevation in pulmonary neutrophils and prolonged production of pulmonary macrophage inflammatory protein-2 after
burn injury with prior alcohol exposure. Am J Respir Crit
Care Med 1999;20:1229 37.
Harms BA, Bodai BI, Kramer GC, Demling RH. Microvascular fluid and protein flux in pulmonary and systemic circulations after thermal injury. Microvasc Res 1982;23:77 86.
Carajal HF, Linares HA, Brouhard BH. Relationship of burn
27.
28.
29.
30.
31.
32.
33.
34.
35.
36.
37.
38.
39.
40.
41.
42.
43.
44.
45.
46.
47.
48.
49.
size to vascular permeability changes in rats. Surg Gynecol

Obstet 1979;149:193202.
Ward PA, Till GO. Pathophysiologic events related to thermal injury of skin. J Trauma 1990;30:S759.
Rodriguez JL, Miller CG, Garner WL, et al. Correlation of
the local and systemic cytokine response with clinical outcome following thermal injury. J Trauma 1993;34:684 94;
discussion 694 5.
Edelman DA, Khan N, Kempf K, White MT. Pneumonia
after inhalation injury. J Burn Car Rehabil 2007;28:241 6.
Smith DL, Cairns BA, Ramdan F, et al. Effect of inhalation
injury, burn size, and age on mortality: a study of 1447 consecutive burn patients. J Trauma 1994;37:6559.
Shirani KZ, Pruitt B Jr, Mason AD Jr. The influence of inhalation injury and pneumonia on burn mortality. Ann Surg
1987;205:827.
Sellersk BJ, Davis BL, Larkin PW, Morris SE, Saffle JR. Early
prediction of prolonged ventilator dependence in thermally
injured patients. J Trauma 1997;43:899 903.
Tredget EE, Shankowsky HA, Taerum TV, Moysa GL, Alton
JD. The role of inhalation injury in burn trauma. A Canadian
experience. Ann Surg 1990;212:720 7.
Kimura R, Traber LD, Herndon DN, Linares HA, Lubbesmeyer HJ, Traber DL. Increasing duration of smoke exposure induces more severe lung injury in sheep. J Appl
Physiol 1988;64:110713.
Haponik E. Clinical smoke inhalation injury: pulmonary effects. Occup Med 1993;8:430 68.
Abdi S, Evans MJ, Cox RA, Lubbesmeyer H, Herndon DN,
Traber DL. Inhalation injury to tracheal epithelium in an
ovine mofel of cotton smoke exposure. Early phase (30 minutes). Am Rev Respir Dis 1990;142:1436 9.
Linares HA, Herndon DN, Traber DL. Sequence of morphologic events in experimental smoke inhalation. J Burn Car
Rehabil 1989;10:2737.
Stothert JC Jr, Ashley KD, Kramer GC, et al. Intrapulmonary
distribution of bronchial blood flow after moderate smoke
inhalation. J Appl Physiol 1990;69:1734 9.
Abdi S, Herndon DN, McGuire J, Traber L, Traber DL.
Time course of alterations in lung lymph and bronchial blood
flows after inhalation injury. J Burn Car Rehabil 1990;11:
510 5.
Ramzy PI, Barret JP, Herndon DN. Thermal injury. Crit
Care Clin 1999;15:33352.
Soejima K, Schmalstieg FC, Sakurai H, Traber LD, Traber
DL. Pathophysiological analysis of combined burn and
smoke inhalation injuries in sheep. Am J Physiol Lung Cell
Mol Physiol 2001;280:L1233 41.
Cox RA, Burke AS, Soejima K, et al. Airway obstruction in
sheep with burn and smoke inhalation injuries. Am J Respir
Cell Mol Biol 2003;29:295302.
Herndon DN, Traber LD, Linares H, et al. Etiology of the
pulmonary pathophysiology associated with inhalation injury. Resuscitation 1986;14:4359.
Traber DL, Herndon DN, Stein MD, Traber LD, Flynn JT,
Niehaus GD. The pulmonary lesion of smoke inhalation in an
ovine model. Circ Shock 1986;18:31123.
Hales CA, Barkin P, Jung W, Quinn D, Lamborghini D,
Burke J. Bronchial artery ligation modifies pulmonary edema
after exposure to smoke with acrolein. J Appl Physiol 1989;
67:1001 6.
Kraneveld AD, Nijkamp FP. Tachykinins and neuro-immune
interactions in asthma. Int Immunopharmacol 2001;1:
1629 50.
Virag L. Poly (ADP-ribosyl)ation in asthma and other lung
diseases. Pharmacol Res 2005;52:8392.
Soejima K, Traber LD, Schmalstieg FC, et al. Role of nitric
oxide in vascular permeability after combined burns and
smoke inhalation injury. Am J Respir Crit Care Med 2001;
163:74552.
Traber DL, Schlag G, Redl H, Traber LD. Pulmonary edema

Volume 30, Number 6
50.
51.
52.
53.
54.
55.
56.
57.
58.
59.
60.
61.
62.
63.
64.
65.
66.
67.
68.
and compliance changes following smoke inhalation. J Burn

Car Rehabil 1985;6:490 4.
Youn YK, LaLonde C, Demling R. Oxidants and the pathophysiology of burn and smoke inhalation injury. Free Radic
Biol Med 1992;12:409 15.
Niehaus GD, Kimura R, Traber LD, Herndon DN, Flynn JT,
Traber DL. Administration of a synthetic antiprotease reduces smoke-induced lung injury. J Appl Physiol 1990;69:
694 9.
Nieman GF, Clark WR Jr. Effects of wood and cotton smoke
on the surface properties of pulmonary surfactant. Respir
Physiol 1994;97:112.
Wright MJ, Murphy JT. Smoke inhalation enhances early
alveolar leukocyte responsiveness to endotoxin. J Trauma
2005;59:64 70.
Klein MB, Hayden D, Elson C, et al. The association between
fluid administration and outcome following major burn: a
multicenter study. Ann Surg 2007;245:622 8.
Chastre J, Trouillet JL, Vaugnat A, et al. Nosocomial pneumonia in patients with acute respiratory distress syndrome.
Am J Respir Crit Care Med 1998;157:116572.
Wunderink RG, Waterer GW. Pneumonia complicating the
acute respiratory distress syndrome. Semin Respir Crit Care
Med 2002;23:443 8.
Iregui M, Kollef M. Ventilator-associated pneumonia complicating the acute respiratory distress syndrome. Semin Respir Crit Care Med 2001;22:31726.
Delclaux C, Roupie E, Blot F, Brochard L, Lemaire F,
Brun-Buisson C. Lower respiratory tract colonization and
infection during severe acute respiratory distress syndrome. Incidence and diagnosis. Am J Respir Crit Care
Med 1997;156:1092 8.
Meduri GU, Reddy RC, Stanley T, El-Zeky F. Pneumonia in
acute respiratory distress syndrome: a prospective evaluation
of bilateral bronchoscopic sampling. Am J Respir Crit Care
Med 1998;158:870 5.
Sutherland KR, Steinberg KP, Maunder RJ, Milberg JA,
Allen DL, Hudson LD. Pulmonary infection during the acute
respiratory distress syndrome. Am J Respir Crit Care Med
1995;152:550 6.
Bell RC, Coalson JJ, Smith JD, Johanson WG Jr. Multiple
organ system failure and infection in adult respiratory distress
syndrome. Ann Intern Med 1983;99:293 8.
Markowicz P, Wolff M, Djedaini K, et al. Multicenter prospective study of ventilator-associated pneumonia during
acute respiratory distress syndrome. Incidence, prognosis,
and risk factors. ARDS Study Group. Am J Respir Crit Care
Med 2000;161:1942 8.
Fagon JY, Chastre J. Diagnosis and treatment of nosocomial
pneumonia in ALI/ARDS patients. Eur Respir J Suppl 2003;
42:77s 83.
Horan TC, Culver DH, Gaynes RP, Jarvis WR, Edwards JR,
Reid CR. Nosocomial infections in surgical patients in the
United States, January 1986 June1992. National Nosocomial Infections Surveillance (NNIS) System. Infect Control
Hosp Epidemiol 1993;14:73 80.
Torres A, Gatell JM, Aznar E, et al. Re-intubation increases
the risk of nosocomial pneumonia in patients needing mechanical ventilation. Am J Respir Crit Care Med 1995;152:
137 41.
Cook D, De Jonghe B, Brochard L, Brun-Buisson C. Influence of airway management on ventilator-associated
pneumonia: evidence from randomized trials. JAMA 1998;
279:7817.
De Bast Y, De Baker D, Moraine JJ, Lemaire M, Vandenborght C, Vincent JL. The cuff leak test to predict failure of
tracheal extubation for laryngeal edema. Intensive Care Med
2002;28:126772.
Sandhu RS, Pasquale MD, Miller K, Wasser TE. Measurement of endotracheal tube cuff leak to predict post extubation
Mosier and Pham
69.
70.
71.
72.
73.
74.
75.
76.
77.
78.
79.
80.
81.
82.
83.
84.
85.
86.
87.
88.
923
stridor and need for reintubation. J Am Coll Surg 2000;190:

6827.
Fisher MM, Raper RF. The cuff-leak test for extubation.
Anaesthesia 1992;47:10 2.
Kriner EJ, Shafazand S, Colice GL. The endotracheal tube
cuff-leak test as a predictor for postextubation stridor. Respir
Care 2005;50:1632 8.
Craven DE, Steger KA. Nosocomial pneumonia in mechanically ventilated adult patients: epidemiology and prevention
in 1996. Semin Respir Infect 1996;11:3253.
Weinstein R. Epidemiology and control of nosocomial infections in adult intensive care units. Am J Med 1991;91:
179S 84.
Ely EW, Baker AM, Dunagan DP, et al. Effect on the duration of mechanical ventilation of identifying patients capable
of breathing spontaneously. N Engl J Med 1996;335:
1864 9.
Kollef MH, Shapiro SD, Silver P, et al. A randomized, controlled trial of protocol-directed versus physician-directed
weaning from mechanical ventilation. Crit Care Med 1997;
25:56774.
Kress JP, Pohlman AS, OConnor MF, Hall JB. Daily interruption of sedative infusions in critically ill patients undergoing mechanical ventilation. N Engl J Med 2000;342:14717.
Robertson TE, Sona C, Schallom L, et al. Improved extubation rates and earlier liberation from mechanical ventilation
with implementation of a daily spontaneous-breathing trial
protocol. J Am Coll Surg 2008;206:489 95.
Girard TD, Kress JP, Fuchs BD, et al. Efficacy and safety of a
paired sedation and ventilator weaning protocol for mechanically ventilated patients in intensive care (Awakening and
Breathing Controlled trial): a randomised controlled trial.
Lancet 2008;371:126 34.
Esteban A, Alia I, Tobin MJ, et al. Effect of spontaneous
breathing trial duration on outcome of attempts to discontinue mechanical ventilation. Spanish Lung Failure Collaborative Group. Am J Respir Crit Care Med 1999;159:512 8.
Valles J, Artigas A, Rello J, et al. Continuous aspiration of
subglottic secretions in preventing ventilator-associated
pneumonia. Ann Intern Med 1995;179 86.
Mahul P, Auboyer C, Jospe R, et al. Prevention of nosocomial
pneumonia in intubated patients: respective role of mechanical subglottic secretions drainage and stress ulcer prophylaxis. Intensive Care Med 1992;18:20 5.
Kollef MH, Skubas N, Sundt TM. A randomized clinical trial
of continuous aspiration of subglottic secretions in cardiac
surgery patients. Chest 1999;116:1339 46.
Pneumatikos I, Koulouras V, Nathanail C, Goe D, Nakos G.
Selective decontamination of subglottic area in mechanically
ventilated patients with multiple trauma. Intensive Care Med
2002;28:4327.
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 7.
Smulders K, van der Hoeven H, Weers-Pothoff I, VandenbrouckeGrauls C. A randomized clinical trial of intermittent subglottic secretion drainage in patients receiving mechanical ventilation.
Chest 2002;121:858 62.
Petering HG. Pharmacology and toxicology of heavy metals:
silver. Pharmacol Ther 1976;1:12730.
Ahearn DG, Grace DT, Jennings MJ, et al. Effects of hydrogel/silver coatings on in vitro adhesion to catheters of bacteria associated with urinary tract infections. Curr Microbiol
2000;41:120 5.
Gabriel MM, Sawant AD, Simmons RB, Ahearn DG. Effects
of silver on adherence of bacteria to urinary catheters in vitro
studies. Curr Microbiol 1995;30:1722.
Berra L, De Marchi L, Yu ZX, Laquerriere P, Baccarelli A,
Kolobow T. Endotracheal tubes coated with antiseptics decrease bacterial colonization of the ventilator circuits, lungs,
and endotracheal tube. Anesthesiology 2004;100:1446 56.
924 Mosier and Pham
89. Kollef MH, Afessa B, Anzueto A, et al. Silver-coated endotracheal tubes and incidence of ventilator-associtated pneumonia, The NASCENT randomized trial. JAMA 2008;300:
80513.
90. Drakulovic MB, Torres A, Bauer TT, Nicolas JM, Nogue S,
Ferrer M. Supine body position as a risk factor for nosocomial
pneumonia in mechanically ventilated patients: a randomised
trial. Lancet 1999;354:1851 8.
91. 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;
80:82732.
92. Davis K Jr, Johannigman JA, Campbell RS, et al. The acute
effects of body position strategies and respiratory therapy in
paralyzed patients with acute lung injury. Crit Care 2001;5:
817.
93. Orozco-Levi M, Torres A, Ferrer M, et al. Semirecumbent
position protects from pulmonary aspiration but not completely from gastroesophageal relux in mechanically ventilated patients. Am J Respir Crit Care Med 1995;152:
138790.
94. Torres A, Serra-Batlles J, Ros E, et al. Pulmonary aspiration of
gastric contents in patients receiving mechanical ventilation:
the effect of body position. Ann Intern Med 1992;116:
540 3.
95. Prodhom G, Leuenberger P, Koerfer J, et al. Nosocomial
pneumonia in mechanically ventilated patients receiving antacid, ranitidine, or sucralfate as prophylaxis for stress ulcer: a
randomized controlled trial. Ann Intern Med 1994;120:
653 62.
96. Bonten MJ, Gaillard CA, van der Geest S, et al. The role of
intragastric acidity and stress ulcer prophylaxis on colonization and infection in mechanically ventilated ICU patients. A
stratified, randomized, double-blind study of sucralfate versus antacids. Am J Respir Crit Care Med 1995;152:182534.
97. Cook D, Guyatt G, Marshall J, et al. A comparison of sucralfate and ranitidine for the prevention of upper gastrointestinal
bleeding in patients requiring mechanical ventilation. Canadian Critical Care Trials Group. N Engl J Med 1998;338:
7917.
98. Dissanaike S, Pham T, Shalhub S, et al. Effect of immediate
enteral feeding on trauma patients with an open abdomen:
protection from nosocomial infections. JACS 2008;207:
690 7.
99. Heyland DK, Drover GW, MacDonald S, Novak F, Lam M.
Effect of postpyloric feeding on gastroesophageal regurgitation and pulmonary microaspiration: results of a randomized
controlled trial. Crit Care Med 2001;29:1495501.
100. Ho KM, Dobb GJ, Webb SA. A comparison of early gastric
and post-pyloric feeding in critically ill patients: a metaanalysis. Intensive Care Med 2006;32:639 49.
101. Abele-Horn M, Dauber A, Bauernfeind A, et al. Decrease in
nosocomial pneumonia in ventilated patients by selective oropharyngeal decontamination (SOD). Intensive Care Med
1997;23:18795.
102. Bergmans DC, Bonten MJ, Gaillard CA, et al. Prevention of
ventilator-associated pneumonia by oral decontamination: a
prospective, randomized, double-blind, placebo-controlled
study. Am J Respir Crit Care Med 2001;164:382 8.
103. Pugin J, Auckenthaler R, Lew DP, Suter PM. Oropharyngeal
decontamination decreases incidence of ventilator-associated
pneumonia: a randomized, placebo controlled, double-blind
clinical trial. JAMA 1991;265:2704 10.
104. Rodriguez-Roldan JM, Altuna-Cyesta A, Lopez A, et al. Prevention of nosocomial lung infection in ventilated patients:
use of an antimicrobial pharyngeal nonabsorbable paste. Crit
Care Med 1990;18:1239 42.
105. Silvestri L, van Saene HK, Thomann C, Peric M. Selective
decontamination of the digestive tract reduces pneumonia
and mortality without resistance emerging. Am J Infect Control 2007;35:354 7.

106. Liberati A, DAmico R, Pifferi S, Torri V, Brazzi L. Antibiotic

prophylaxis to reduce respiratory tract infections and mortality in adults receiving intensive care. Cochrane Database Syst
Rev 2004:CD000022.
107. Barret JP, Jeschke MD, Herndon DN. Selective decontamination of the digestive tract in severely burned pediatric patients. Burns 2001;27:439 45.
108. de la Cal MA, Cerda E, Garcia-Hierro P, et al. Survival benefit
in critically ill burned patients receiving selective decontamination of the digestive tract: a randomized, placebocontrolled, double-blind trial. Ann Surg 2005;241:424 30.
109. Kimura A, Mochizuki T, Nishizawa K, Mashiko K,
Yamamoto Y, Otsuka T. Trimethoprim-sulfamethoxazole for
the prevention of methicillin-resistant Staphylococcus aureus
pneumonia in severely burned patients. J Trauma 1998;45:
3837.
110. Gastinne H, Wolff M, Delatour F, Faurisson F, Chevret S. A
controlled trial in intensive care units of selective decontamination of the digestive tract with nonabsorbable antibiotics.
The French Study Group on Selective Decontamination of
the Digestive Tract. N Engl J Med 1992;326:594 9.
111. Hammond JMJ, Potgieter PD, Saunders GL, Forder AA.
Double-blind study of selective decontamination of the digestive tract in intensive care. Lancet 1992;340:59.
112. Wiener J, Itozaku G, Nathan C, Kabins SA, Weinstein RA. A
randomized, double-blind placebo-controlled trial of selective decontamination in a medical-surgical intensive care unit.
Clin Infect Dis 1995;20:8617.
113. Lingnau W, Berger J, Javorsky F, Fille M, Allerberger F,
Benzer H. Changing bacterial ecology during a five year period of selective intestinal decontamination. J Hosp Infect
1998;39:195206.
114. Verwaest C, Verhaegen J, Ferdinande P, et al. Randomized,
controlled trial of selective digestive decontamination in 600
mechanically ventilated patients in a multidisciplinary intensive care unit. Crit Care Med 1997;25:6371.
115. Misset B, Kitzis M, Mahe P, et al. Bacteriological side effects
of gut decontamination with polymixen E, gentamycin, and
amphotericin B. Infect Control Hosp Epidemiol 1993;13:
62 4.
116. Misset B, Kitzis M, Conscience G, Goldstein F, Fourrier A,
Carlet J. Mechanisms of failure to decontaminate the gut with
polymixen E, gentamycin, and amphotericin B in patients in
intensive care. Eur J Clin Microbiol Infect Dis 1994;13:
16570.
117. van Saene HK, Petros AJ, Ramsay G, Baxby D. All great
truths are iconoclastic: selective decontamination of the digestive tract moves from heresy to level 1 truth. Intensive
Care Med 2003;29:67790.
118. Houston S, Hougland P, Anderson JJ, LaRocco M, Kennedy
V, Gentry LO. Effectiveness of 0.12% cholhexidine gluconate
oral rinse in reducing prevalence of nosocomial pneumonia in
patients undergoing heart surgery. Am J Crit Care 2002;11:
56770.
119. Koeman M, van der Ven AJ, Hak E, et al. Oral decontamination
with chlorhexadine reduces the incidence of ventilatorassociated pneumonia. Am J Respir Crit Care Med 2006;173:
1348 55.
120. Chan EY, Ruest A, Meade MO, Cook DJ. Oral decontamination for prevention of pneumonia in mechanically ventilated adults: systematic review and meta-analysis. BMJ 2007;
334:889.
121. Chlebicki MP, Safdar N. Topical chlorhexidine for prevention of ventilator-associated pneumonia: a meta-analysis. Crit
Care Med 2007;35:595 602.
122. Kola A, Gastmeier P. Efficacy of oral chlorhexadine in preventing lower respiratory tract infections. Meta-analysis of
randomized controlled trials. J Hosp Infect 2007;66:
20716.
123. Fourrier F, Dubois D, Pronnier P, et al. Effect of gingival and
dental plaque antiseptic decontamination on nosocomial in-

Volume 30, Number 6
fections acquired in the intensive care unit: a double-blind

placebo-controlled multicenter study. Crit Care Med 2005;
33:1728 35.
124. Alexander J. Mechanism of immunologic suppression in burn
injury. J Trauma 1990;30:S70 5.
125. Munster A. Alterations of the host defense mechanism in
burns. Surg Clin North Am 1970;50:121725.
126. Shorr A, Duh M, Kelly K, Kollef MH; CRIT Study Group.
Red blood cell transfusion and ventilator-associated
pneumonia: a potential link? Crit Care Med 2004;32:
666 74.
127. Palmieri TL, Caruso DM, Foster KN, et al; American Burn
Association Burn Multicenter Trials Group. Effect of blood
transfusion on outcome after major burn injury: a multicenter
study. Crit Care Med 2006;34:16027.
128. Leal-Noval SR, Rincon-Ferrari MD, Gaarcia-Curiel A, et al.
Transfusion of blood components and postoperative infection in patients undergoing cardiac surgery. Chest 2001;
2001:1461 8.
129. Purdy FR, Tweeddale MG, Merrick PM. Association of mortality with age of blood transfused in septic ICU patients. Can
J Anaesth 1997;44:1256 61.
130. Basran S, Frumento RJ, Cohen A, et al. The association between duration of storage of transfused red blood cells and
morbidity and mortality after reoperative cardiac surgery.
Anesth Analg 2006;103:1520.
131. van den Berghe G, Wouters P, Weekers F, et al. Intensive
insulin therapy in the critically ill patients. N Engl J Med
2001;345:1359 67.
132. Arabi YM, Dabbagh OC, Tamim HM, et al. Intensive versus
conventional insulin therapy: a randomized controlled trial in
medical and surgical critically ill patients. Crit Care Med
2008;36:3190 7.
133. Brunkhorst FM, Engel C, Bloos F, et al; German Competence Network Sepsis (SepNet). Intensive insulin therapy and
pentastarch resuscitation in severe sepsis. N Engl J Med 2008;
358:12539.
134. Hemmila MR, Taddonio MA, Arbabi S, Maggio PM, Wahl
WL. Intensive insulin therapy is associated with reduced infectious complications in burn patients. Surgery 2008;144:
629 35.
135. Pittet D, Hugonnet S, Harbarth S, et al. Effectiveness of a
hospital-wide programme to improve compliance with hand
hygiene. Infection Control Programme. Lancet 2000;356:
130712.
136. 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 74.
137. Dreyfus 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 43.
138. Craven DE, Goularte TA, Make BJ. Contaminated condensate in mechanical ventilator circuits: a risk factor for nosocomial pneumonia? Am Rev Respir Dis 1984;129:625 8.
139. Hess D. Prolonged use of heat and moisture exchangers: why
do we keep changing things? Crit Care Med 2000;28:
1667 8.
140. Kollef MH, Shapiro SD, Boyd V, et al. A randomized clinical
trial comparing an extended-use hygroscopic condenser humidifier with heated-water humidification in mechanically
ventilated patients. Chest 1998;113:759 67.
141. Landrum ML, Murray CK. Ventilator associated pneumonia
in a military deployed setting: the impact of an aggressive
infection control program. J Trauma 2008;64:S1237.
142. Bonello RS, Fletcher CE, Becker WK, et al. An intensive care
unit quality improvement collaborative in nine Department
of Veterans Affairs hospitals: reducing ventilator-associated
pneumonia and catheter-related bloodstream infection rates.
Jt Comm J Qual Patient Saf 2008;34:639 45.
Mosier and Pham
925
143. DuBose JJ, Inaba K, Shiflett A, et al. Measurable outcomes of

quality improvement in the trauma intensive care unit: the
impact of a daily quality rounding checklist. J Trauma 2008;
64:227.
144. Ogaard JL, Johnston MJ, Cain T, et al. Ventilator-associated
pneumonia in the burn center population does bundle
compliance make a difference? J Burn Car Res 2008;29:S99.
145. American Thoracic Society, Infectious Diseases Society of
America. Guidelines for the management of adults with
hospital-acquired, ventilator-associated, and healthcareassociated pneumonia. Am J Respir Crit Care Med 2005;
171:388 416.
146. The Canadian Critical Care Trials Group. A randomized trial
of diagnostic techniques for ventilator-associated pneumonia. N Engl J Med 2006;335:2619 30.
147. Kollef M. Diagnosis of ventilator-associated pneumonia.
N Engl J Med 2006;355:26912.
148. Fagon JY, Chastre J, Hance AJ, et al. Detection of nosocomial lung infection in ventilated patients: use of a protected
specimen brush and quantitative culture techniques in 147
patients. Am Rev Respir Dis 1988;138:110 6.
149. Pugin J, Auckenthaler R, Mili N, Janssens JP, Lew PD, Suter
PM. Diagnosis of ventilator-associated pneumonia by bacteriologic analysis of bronchoscopic and nonbronchoscopic
blind bronchoalveolar lavage fluid. Am Rev Respir Dis
1991;143:11219.
150. Singh N, Falestiny MN, Rogers P, et al. Pulmonary infiltrates
in the surgical ICU. Prospective assessment of predictors of
etiology and mortality. Chest 2000;114:1129 36.
151. Croce M, Swanson J, Magnotti L, et al. The futility of the
clinical pulmonary infection score in trauma patients.
J Trauma 2006;60:5237; discussion 527 8.
152. Pham T, Neff M, Simmons J, Gibran NS, Heimbach DM,
Klein MB. The clinical pulmonary infection score poorly predicts pneumonia in patients with burns. J Burn Care Res
2007;28:76 9.
153. Croce M, Fabian T, Schurr M, et al. Using bronchoalveolar
lavage to distinguish nosocomial pneumonia from systemic
inflammatory response syndrome: a prospective analysis.
J Trauma 1995;39:1134 9, discussion 1139 40.
154. Luyt CE, Chastre J, Fagon JY. Value of the clinical pulmonary infection score for the identification and management
of ventilator-associated pneumonia. Intensive Care Med
2004;30:844 52.
155. Chastre J, Fagon JY. Invasive diagnostic testing should be
routinely used to manage ventilated patients with suspected
pneumonia. Am J Respir Crit Care Med 1994;150:570 4.
156. Chastre J, Fagon JY. Diagnosis of ventilator-associated pneumonia. N Engl J Med 2007;356:1469 70.
157. Fagon JY, Chastre J, Wolff M, et al. Invasive and noninvasive
strategies for management of suspected ventilator-associated
pneumonia: a randomized trial. Ann Intern Med 2000;132:
62130.
158. Wahl W, Ahrns K, Brandt M, Rowe SA, Hemmila MR,
Arbabi S. Bronchoalveolar lavage in diagnosis of ventilatorassociated pneumonia in patients with burns. J Burn Care
Rehabil 2005;26:57 61.
159. Kollef MH, Ward S. The influence of Mini-BAL cultures on
patient outcomes: implications for the antibiotic management of ventilator-associated pneumonia. Chest 1998;113:
41220.
160. Silver G, Klein M, Herndon D, et al; Inflammation and the
Host Response to Trauma, Collaborative Research Program.
Standard operating procedures for the clinical management
of patients enrolled in a prospective study of Inflammation
and the Host Response to Thermal Injury. J Burn Care Res
2007;28:22230.
161. Croce M, Fabian T, Mueller E, et al. The appropriate diagnostic threshold for ventilator-associated pneumonia using
quantitative cultures. J Trauma 2004;56:931 4; discussion
934 6.
926 Mosier and Pham
162. Minei JP, Nathans AB, West M, et al; Inflammation and the
Host Response to Injury Large Scale Collaborative Research
Program Investigators. Inflammation and the host response
to injury, a large-scale collaborative project: patient-oriented
research corestandard operating procedures for clinical
care. II. Guidelines for prevention, diagnosis and treatment
of ventilator-associated pneumonia (VAP) in the trauma patient. J Trauma 2006;60:1106 13.
163. Croce MA, Fabian TC, Mueller EW, et al. The appropriate
diagnostic threshold for ventilator-associated pneumonia using quantitative culture. J Trauma 2004;56:931 4.
164. Miller P, Meredith J, Chang M. Optimal threshold for diagnosis of ventilator-associated pneumonia using bronchoalveolar lavage. J Trauma 2003;55:2637; discussion 267 8.
165. Barret JP, Ramzy PI, Wolf SE, Herndon DN. Sensitivity and
specificity of bronchoalveolar lavage and protected bronchial
brush in the diagnosis of pneumonia in pediatric burn patients. Arch Surg 1999;134:12437.
166. Chastre J, Fagon JY, Bornet-Lesco M, et al. Evaluation of
bronchoscopic techniques for the diagnosis of nosocomial
167. Johanson WG Jr, Seidenfeld JJ, Gomez P, de los Santos R,
Coalson JJ. Bacteriologic diagnosis of nosocomial pneumonia following prolonged mechanical ventilation. Am Rev Respir Dis 1998;137:259 64.
168. Marik PE, Baram M. Diagnosis of ventilator-associated pneumonia. N Engl J Med 2007;356:1470.
169. Mosier M, Gamelli R, Halerz M, Silver G. Microbial contamination in burn patients undergoing urgent intubation as part
of their early airway management. J Burn Care Res 2008;29:
304 10.
170. Low D. Resistance issues and treatment implications: Pneumococcus, Staphylococcus aureus, and Gram-negative rods. Infect Dis Clin North Am 1998;12:61330.
171. Carter JE, Miller PR III, Holmes JH IV. An epidemiologic
study of ventilator-associated pneumonia (VAP) in burn patients. J Burn Care Res 2008;29:S98.
172. Cabello H, Torres A, Celiss R, et al. Bacterial colonization of
distal airways in healthy subjects and chronic lung diseases: a
bronchoscopic study. Eur Respir J 1997;10:1137 44.
173. Van Eldere J. Multicentre surveillance of Pseudomonas
aeruginosa susceptibility patterns in nosocomial infections.
J Antimicrob Chemother 2003;51:247352.
174. Bradford P. Extended-spectrum beta-lactamases in the 21st
century: characterization, epidemiology, and detection of this
important resistant threat. Clin Microbiol Rev 2001;14:
93351.
175. Nordmann P, Poirel L. Emerging carbapenemases in Gramnegative aerobes. Clin Microbiol Infect 2002;8:32131.
176. Wood G, Hanes S, Croce M, Fabian TC, Boucher BA. Comparison of ampicillin-sulbactam and imipenem-cilastatin for
the treatment of acinetobacter ventilator-associated pneumonia. Clin Infect Dis 2002;34:142530.
177. Chim H, Tan B, Song C. Five-year review of infections in a
burn intensive care unit: high incidence of Acinetobacter baumannii in a tropical climate. Burns 2007;33:1008 14.
178. Combes A, Luyt CE, Fagon JY, et al; PNEUMA Trial Group.
Impact of methicillin resistance on outcome of Staphylococcus
aureus ventilator-associated pneumonia. Am J Respir Crit
Care Med 2004;170:786 92.
179. Vandenesch F, Naimi T, Enright MC, et al. Communityacquired methicillin-resistant Staphylococcus aureus carrying
Panton-Valentine leukocidin genes: worldwide emergence.
Emerg Infect Dis 2003;9:978 84.
180. Gillet Y, Issartel B, Vanhems P, et al. Association between
Staphylococcus aureus strains carrying gene for PantonValentine leukocidin and highly lethal necrotizing pneumonia in young immunocompetent patients. Lancet 2002;359:
7539.
181. Fridkin SK, Hageman J, McDougal LK, et al; VancomycinIntermediate Staphylococcus aureus Epidemiology Study

Group. Epidemiological and microbiological characterization of infections caused by Staphylococcus aureus with reduced susceptibility to vancomycin, United States
19972001. Clin Infect Dis 2003;36:429 39.
182. Chang S, Sievert DM, Hageman JC, et al; Vancomycinresistant Staphylococcus aureus Investigative Team. Infection
with vancomycin-resistant Staphylococcus aureus containing
the vanA resistance gene. N Engl J Med 2003;348:13427.
183. Tsiodras S, Gold HS, Sakoulas G, et al. Linezolid resistance in
a clinical isolate of Staphylococcus aureus. Lancet 2001;358:
207 8.
184. Lam AP, Wunderink RG. Methicillin-resistant S. aureus
ventilator-associated pneumonia: strategies to prevent and
treat. Semin Respir Crit Care Med 2006;27:92103.
185. El-Ebiary M, Torres A, Fabregas N, et al. Significance of the
isolation of Candida species from respiratory samples in critically ill, non-neutropenic patients. Am J Respir Crit Care
Med 1997;156:58390.
186. Krasinski K, Holzman RS, Hanna B, Greco MA, Graff M,
Bhogal M. Nosocomial fungal infection during hospital renovation. Infect Control 1985;6:278 82.
187. Lentino JR, Rosenkranz MA, Michaels JA, Kurup VP, Rose
HD, Rytel MW. Nosocomial aspergillosis: a retrospective review of airborne disease secondary to road construction and
contaminated air conditioners. Am J Epidemiol 1982;116:
430 7.
188. Sarubbi FA Jr, Kopf HB, Wilson MB, McGinnis MR, Rutala
WA. Increased recovery of Aspergillus flavus from respiratory
specimens during hospital construction. Am J Rev Respir Dis
1982;125:33 8.
189. Gage AA, Dean DC, Schimert G, Minsley N. Aspergillus infection after cardiac surgery. Arch Surg 1970;101:384 7.
190. Iregui M, Ward S, Sherman G, Fraser VJ, Kollef MH. Clinical
importance of delays in the initiation of appropriate antibiotic
treatment for ventilator-associated pneumonia. Chest 2002;
122:262 8.
191. Garnacho-Montero J, Garcia-Garmendia JL, BarreroAlmodovar A, et al. Impact of the outcome of adequate empirical antibiotherapy in patients admitted to the ICU for
sepsis. Crit Care Med 2003;31:274251.
192. Leone M, Burgoin A, Cambon S, Dubuc M, Albane`se J,
Martin C. Empirical antimicrobial therapy of septic shock
patients: adequacy and impact on the outcome. Crit Care
Med 2003;31:4627.
193. Luna CM, Vujacich P, Niederman MS, et al. Impact of BAL
data on the therapy and outcome of ventilator-associated
pneumonia. Chest 1997;111:676 85.
194. Rello J, Gallego M, Mariscal D, Son
ora R, Valles J. The value
of routine microbial investigation in ventilator-associated
195. Dupont H, Mentec H, Sollet JP, Bleichner G. Impact of
appropriateness of initial antibiotic therapy on the outcome
of ventilator-associated pneumonia. Intensive Care Med
2001;27:355 62.
196. Alvarez-Lerma F. Modification of empiric antibiotic treatment in patients with pneumonia acquired in the intensive
care unit. ICU-acquired Pneumonia Study Group. Intensive
Care Med 1996;22:38794.
197. Ibrahim EH, Ward S, Sherman G, Schaiff R, Fraser VJ, Kollef
MH. Experience with a clinical guideline for the treatment of
ventilator-associated pneumonia. Crit Care Med 2001;29:
1109 15.
198. Namias N, Samiian L, Nino D, et al. Incidence and susceptibility of pathogenic bacteria vary between intensive care units
within a single hospital: implications for empiric antibiotic
strategies. J Trauma 2000;49:638 45.
199. Gruson D, Hilbert G, Vargas F, et al. Rotation and restricted
use of antibiotics in a medical intensive care unit: impact on
the incidence of ventilator-associated pneumonia caused by
antibiotic-resistant Gram-negative bacteria. Am J Respir Crit
Care Med 2000;162:837 43.

Volume 30, Number 6
200. Dellit TH, Chan DJ, Skerrett SJ, Nathens AB. Development
of a guideline for the management of ventilator associated
pneumonia based on local microbiolgic findings and impact
of the guideline on antimicrobial use practices. Infect Control
Hosp Epidemiol 2008;29:52533.
201. Kumar A, Roberts D, Wood KE, et al. Duration of hypotension before initiation of effective antimicrobial therapy is the
critical determinant of survival in human septic shock. Crit
Care Med 2006;34:1589 96.
202. Croce MA, Fabian T, Waddle-Smith L, et al. Utility of
Grams stain and efficacy of quantitative cultures for posttraumatic pneumonia: a prospective study. Ann Surg 1998;227:
74351.
203. Allaouchiche B, Jaumain H, Chassard D, Bouletreau P. Gram
stain of bronchoalveolar lavage fluid in the early diagnosis of
ventilator-associated pneumonia. Br J Anaesth 1999;83:
8459.
204. Davis KA, Eckert MJ, Reed RL II, et al. Ventilator-associated
pneumonia in injured patients: do you trust your Grams
stain? J Trauma 2005;58:462 6; discussion 466 7.
205. Feldman C, Kassel M, Cantrell J, et al. The presence and
sequence of endotracheal tube colonization in patients undergoing mechanical ventilation. Eur Respir J 1999;13:
546 51.
206. Adair CG, Gorman S, Feron BM, et al. Implications of endotracheal tube biofilm for ventilator-associated pneumonia.
Intensive Care Med 1999;25:1072 6.
207. Kollef M. Epidemiology and risk factors for nosocomial
pneumonia. Emphasis on prevention. Clin Chest Med 1999;
20:65370.
208. Olson ME, Harmon BG, Kollef MH. Silver-coated endotracheal tubes associated with reduced bacterial burden in the
lungs of mechanically ventilated dogs. Chest 2002;12:
86370.
209. Rello J, Kollef M, Diaz E, et al. Reduced burden of bacterial
airway colonization with a novel silver-coated endotracheal
tube in a randomized multiple-center feasibility study. Crit
Care Med 2006;34:2766 72.
210. Craven DE. Ventilator-associated tracheobronchitis (VAT):
questions, answers, and a new paradigm? Crit Care 2008;12:
157.
211. Prats E, Dorca J, Pujol M, et al. Effects of antibiotics on
protected specimen brush sampling in ventilator-associated
pneumonia. Eur Respir J 2002;19:944 51.
212. Montravers P, Fagon JY, Chastre J, et al. Follow-up protected
specimen brushes to assess treatment in nosocomial pneumonia. Am Rev Respir Dis 1993;147:38 44.
213. Souweine B, Veber B, Bedos JP, et al. Diagnostic accuracy of
protected specimen brush and bronchoalveolar lavage in nosocomial pneumonia: impact of previous antimicrobial treatments. Crit Care Med 1998;26:236 44.
214. Hubmayr RD, Burchardi H, Elliot M, et al; American Thoracic Society Assembly on Critical Care; European Respiratory Society; European Society of Intensive Care Medicine;
Societe de Reanimation de Langue Francaise. Statement of
the 4th International Consensus Conference in Critical Care
on ICU-acquired pneumoniaChicago, Illinois, May 2002.
Intensive Care Med 2002;28:152136.
215. Berenholtz SM, Pronovost PJ, Ngo K, et al; Core Sepsis
Measurement Team. Developing quality measures for sepsis
care in the ICU. Jt Comm J Qual Patient Saf 2007;33:
559 68.
216. Pieracci FM, Barie PS. Strategies in the prevention and management of ventilator-associated pneumonia. Am Surg 2007;
73:419 32.
217. Rello J, Paiva JA, Baraibar J, et al. International conference
for the development of consensus on the diagnosis and treatment of ventilator-associated pneumonia. Chest 2001;120:
95570.
218. Kollef MH, Vlasnik J, Sharpless L, Pasque C, Murphy D,
Fraser V. Scheduled change of antibiotic classes. A strategy to
Mosier and Pham
927
decrease the incidence of ventilator-associated pneumonia.

Am J Respir Crit Care Med 1997;156:1040 8.
219. Raymond DP, Pelletier SJ, Crabtree TD, et al. Impact of
rotating empiric antibiotic schedule on infectious mortality in
an intensive care unit. Crit Care Med 2001;29:1101 8.
220. Gruson D, Hilbert G, Vargas F, et al. Strategy of antibiotic
rotation: long-term effect on incidence and susceptibilities of
Gram-negative bacilli responsible for ventilator-associated
pneumonia. Crit Care Med 2003;31:1908 14.
221. Micek ST, Ward S, Fraser VJ, Kollef MH. A randomized
controlled trial of an antibiotic discontinuation policy for
clinically suspected ventilator-associated pneumonia. Chest
2004;125:17919.
222. Mueller E, Croce M, Boucher B, et al. Repeat bronchoalveolar lavage to guide antibiotic duration for ventilatorassociated pneumonia. J Trauma 2007;63:1329 37; discussion 1337.
223. Dennesen PJ, Van der Ven AJ, Kessels AG, Ramsay G,
Bonten MJ. Resolution of infectious parameters after microbial therapy in patients with ventilator-associated pneumonia.
Am J Respir Crit Care Med 2001;163:13715.
224. Chastre J, Wolff M, Fagon JY, et al; PneumA Trial Group. Comparison of 8 vs 15 days of antibiotic therapy for ventilatorassociated pneumonia in adults: a randomized trial. JAMA
2003;290:2588 98.
225. Balis E, Diacaki C, Tselioti P, et al. Community-acquired
pneumonia and bacteremia due to methicillin-resistant Staphylococcus aureus carrying Panton-Valentine leukocidin gene in
Greece: two case reports and literature review. J Chemother
2007;19:703 8.
226. Chastre J. Evolving problems with resistant pathogens. Clin
Microbiol Infect 2008;14:314.
227. Vidaur L, Planas K, Sierra R, et al. Ventilator-associated
pneumonia: impact of organisms on clinical resolution and
medical resources utilization. Chest 2008;133:62532.
228. Cioffi WG Jr, Rue LW III, Graves TA, McManus WF, Mason
AD Jr, Pruitt BA Jr. Prophylactic use of high-frequency percussive ventilation in patients with inhalation injury. Ann
Surg 1991;213:575 80.
229. Cioffi WG, deLemos RA, Coalson JJ, Gerstmann DA, Pruitt
BA Jr. Decreased pulmonary damage in primates with inhalation injury treated with high-frequency ventilation. Ann
Surg 1993;218:328 35.
230. Saffle JR, Morris SE, Edelman L. Early tracheostomy does
not improve outcome in burn patients. J Burn Car Rehabil
2002;23:431 8.
231. Barret JP, Desai MH, Herndon DN. Effects of tracheostomies on infection and airway complications in pediatric burn
patients. Burns 2000;26:190 3.
232. Gravvanis AI, Tsoutsos DA, Iconomou TG, Papadopoulos
SG. Percutaneous versus conventional tracheostomy in
burned patients with inhalation injury. World J Surg 2005;
29:15715.
233. Linssen CF, Bekers O, Drent M, Jacobs JA. C-reactive protein and procalcitonin concentrations in bronchoalveolar lavage fluid as a predictor of ventilator-associated pneumonia.
Ann Clin Biochem 2008;45:293 8.
234. Luyt CE, Combes A, Raynaud C, et al. Usefulness of procalcitonin for the diagnosis of ventilator-associated pneumonia.
235. Gibot S, Cravoisy A, Dupays R, et al. Combined measurement of procalcitonin and soluble TREM-1 in the diagnosis
of nosocomial sepsis. Scand J Infect Dis 2007;39:604 8.
236. Luyt CE, Guerin V, Combes A, et al. Procalcitonin kinetics as
a prognostic marker of ventilator-associated pneumonia.
Am J Respir Crit Care Med 2005;171:48 53.
237. Duflo F, Debon R, Monneret G, Bienvenu J, Chassard D,
Allaouchiche B. Alveolar and serum procalcitonin: diagnostic
and prognostic value in ventilator-associated pneumonia. Anesthesiology 2002;96:74 9.
238. Brown RB, Kruse JA, Counts GW, Russell JA, Christou NV,
928 Mosier and Pham
Sands ML. Double-blind study of endotracheal tobramycin

in the treatment of gram-negative bacterial pneumonia. The
Endotracheal Tobramycin Study Group. Antimicrob Agents
Chemother 1990;34:269 72.
239. Palmer LB, Smaldone GC, Chen JJ, et al. Aerosolized antibiotics and ventilator-associated tracheobronchitis in the intensive care unit. Crit Care Med 2008;36:2008 13.
240. Claridge J, Edwards N, Swanson J, et al. Aerosolized ceftazidime prophylaxis against ventilator-associated pneumonia in
high-risk trauma patients: results of a double-blind randomized study. Surg Infect (Larchmt) 2007;8:8390.
241. Bodi M, Diaz E, Rello J. Appropriate antibiotic treatment for
pneumonia. Clin Infect Dis 2000;31:1313 4.
242. Wysocki M, Thomas F, Wolff MA, Pean Y, Ravaud Y,
Herman B. Comparison of continuous with discontinuous
intravenous infusion of vancomycin in severe MRSA infections. J Antimicrob Chemother 1995;35:352 4.
243. Rubenstein E, Cammarata S, Oliphant T, Wunderink R; Linezolid Nosocomial Pneumonia Study Group. Linezolid (PNU100766) versus vancomycin in the treatment of hospitalized
patients with nosocomial pneumonia: a randomized doubleblind multicenter study. Clin Infect Dis 2001;32:40212.
244. Kollef M. The prevention of ventilator-associated pneumonia. N Engl J Med 1999;340:62734.
245. Fourrier F, Cau-Pottier E, Boutigny H, Roussel-Delvallez M,
Jourdain M, Chopin C. Effects of dental plaque antiseptic
decontamination on bacterial colonization and nosocomial
infections in critically ill patients. Intensive Care Med 2000;
26:1239 47.
246. Rouby JJ, Laurent P, Gosnach M, et al. Risk factors and
clinical relevance of nosocomial maxillary sinusitis in the critically ill. Am J Respir Crit Care Med 1994;150:776 83.
247. Bach A, Boehrer H, Schmidt H, Geiss HK. Nosocomial sinusitis in ventilated patients. Nasotracheal versus orotracheal
intubation. Anaesthesia 1992;47:3359.
248. Salord F, Lopez F, Gaussorgues P, et al. Nosocomial maxillary sinusitis during mechanical ventilation: a prospective
comparison of orotracheal versus the nasotracheal route for
intubation. Intensive Care Med 1990;16:390 3.

249. Heyland DK, Dhaliwal R, Drover JW, et al; Canadian Critical

Care Clinical Practice Guidelines Committee. Canadian clinical practice guidelines for nutrition support in mechanically
ventilated, critically ill adult patients. JPEN J Perenter Enteral
Nutr 2003;27:35573.
250. Chevret S, Hemmer M, Carlet J, Langer M. Incidence and
risk factors of pneumonia acquired in intensive care units.
Results from a multicenter prospective study on 996 patients.
European Cooperative Group on nosocomial pneumonia.
251. Rello J, Ausina V, Ricart M, Castella J, Prats G. Impact of
previous antimicrobial therapy on the etiology and outcome
of ventilator-associated pneumonia. Chest 1993;104:
1230 5.
252. Baker AM, Meredith JW, Haponik EF. Pneumonia in intubated trauma patients. Microbiology and outcomes. Am J
Respir Crit Care Med 1996;153:3439.
253. Torres A, Aznar R, Gatell JM, et al. Incidence, risk, and
prognosis factors of nosocomial pneumonia in mechanically
ventilated patients. Am Rev Respir Dis 1990;142:523 8.
254. 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 6.
255. Joshi N, Localio A, Hamory BH. A predictive risk index for
nosocomial pneumonia in the intensive care unit. Am J Med
1992;93:135 42.
256. Antonelli M, Moro ML, Capelli O, et al. Risk factors for early
onset pneumonia in trauma patients. Chest 1994;105:
224 8.
257. Cunnion KM, Weber DJ, Broadhead WE, Hanson LC,
Pieper CF, Rutala WA. Risk factors for nosocomial
pneumonia: comparing adult critical-care populations. Am J
Respir Crit Care Med 1996;153:158 62.
258. Daschner F, Kappstein I, Engels I, et al. Stess ulcer prophylaxis and ventilation pneumonia: prevention by antibacterial
cytoprotective agents? Infect Control Hosp Epidemiol 1988;
9:59 65.

Guias Americanas de Ventilación Mecánica en QUEMADOS

Caricato da

Informazioni sul documento

Copyright

Formati disponibili

Condividi questo documento

Condividi o incorpora il documento

Opzioni di condivisione

Hai trovato utile questo documento?

Questo contenuto è inappropriato?

Copyright:

Formati disponibili

Guias Americanas de Ventilación Mecánica en QUEMADOS

Caricato da

Copyright:

Formati disponibili

PRACTICE GUIDELINES

American Burn Association Practice Guidelines

From the University of Washington Burn Center and Department

when available, is the preferable method to confirm the diagnosis of VAP.

Journal of Burn Care & Research

traditionally defined as an infection occurring 48

Mosier and Pham

Class III: retrospective

A Medline search of the English-language literature was

Journal of Burn Care & Research

912 Mosier and Pham

admission, or subsequently acquired in the ICU, this

Table 2. Identified independent factors for ventilatorassociated pneumonia9,22,244 252

physiology and predict subsequent nosocomial lung

Journal of Burn Care & Research

matory response destroys the lung parenchyma and

VAP Prevention Strategies

Mosier and Pham

Necessity and Duration of Mechanical Ventilation.

Table 3. Recommended ventilator-associated pneumonia prevention strategies

Avoid unnecessary intubation and re-intubation

1, 18, 22, 65, 66, 253

Heat-moisture exchangers to reduce tubing condensate,

Medical, surgical, and trauma

Medical, surgical, trauma,

1, 72, 135, 140, 253

66, 136, 138140

914 Mosier and Pham

patients who need prolonged mechanical ventilation.

Journal of Burn Care & Research

Journal of Burn Care & Research

ity with SDD.107 In contrast, a much larger Spanish

Mosier and Pham

916 Mosier and Pham

found hypoglycemia occurred more frequently with

Journal of Burn Care & Research

ident George W. Bush issued an executive order in

Journal of Burn Care & Research

not yet been confirmed of benefit in burn patients. As

Mosier and Pham

sponse. The CPIS scale is not able to differentiate

918 Mosier and Pham

sistent with pneumonia should lead to a quantitative

Journal of Burn Care & Research

Reviews from individual burn units now identify

Journal of Burn Care & Research

ation of appropriate antibiotic therapy for patients

Mosier and Pham

dence of MDR bacteria and possible mortality benefit with

Journal of Burn Care & Research

920 Mosier and Pham

bacilli, MRSA pneumonias (particularly with the

Areas of Uncertainty and Investigation

early tracheostomy. Similarly, Barret et als231 review

Table 4. Recommendations for diagnosis of ventilator-associated pneumonia

Medical, surgical, trauma,

Journal of Burn Care & Research

Mosier and Pham

Table 5. Recommendations for treatment of ventilator-associated pneumonia

Early initiation of broad-spectrum antibiotic coverage

De-escalation of broad-spectrum antibiotic coverage

Medical, surgical, trauma,

tion, accurate diagnosis, and treatment of VAP are

Journal of Burn Care & Research