1. Clinical presentation and diagnosis of ventilator-associated pneumonia http://www.uptodate.com/contents/clinical-presentation-and-diagnosis-of...
Official reprint from UpToDate® www.uptodate.com
©2011 UpToDate®
Clinical presentation and diagnosis of ventilator-associated
pneumonia
Author Section Editors Deputy Editor
Marin H Kollef, MD Polly E Parsons, MD Kevin C Wilson, MD
John G Bartlett, MD
Last literature review version 19.1: enero 2011 | This topic last updated: enero 27, 2010
INTRODUCTION — Ventilator-associated pneumonia (VAP) is a type of hospital-acquired (or
nosocomial) pneumonia that develops after more than 48 hours of mechanical ventilation. Its
incidence is estimated to be 9 to 27 percent, with a mortality of 25 to 50 percent [1,2]. Early
diagnosis is important because appropriate management can be lifesaving.
The clinical presentation and diagnosis and differential diagnosis of VAP will be reviewed here. The
approach to patients who are suspected of having hospital-acquired pneumonia, but who are not
intubated, is virtually identical.
Risk factors, prevention, and treatment of VAP are discussed elsewhere. (See "Treatment of hospital-
acquired, ventilator-associated, and healthcare-associated pneumonia in adults" and "Risk factors and
prevention of hospital-acquired, ventilator-associated, and healthcare-associated pneumonia in
adults" and "The ventilator circuit and ventilator-associated pneumonia".).
CLINICAL PRESENTATION — Ventilator-associated pneumonia (VAP) is usually suspected when a
patient receiving mechanical ventilation develops a new or progressive pulmonary infiltrate with
fever, leukocytosis, and/or purulent tracheobronchial secretions [3]. Additional signs of possible VAP
include an increased respiratory rate, increased minute ventilation, decreased tidal volume, decreased
oxygenation, and a need for more ventilatory support or inspired oxygen.
DIFFERENTIAL DIAGNOSIS — There are many causes of pulmonary infiltrates and fever, which
can be difficult to distinguish from ventilator-associated pneumonia (VAP). Leukocytosis, purulent
tracheobronchial secretions, or respiratory abnormalities can be associated with most of these causes.
The differential diagnosis of VAP includes the following:
Aspiration pneumonitis (ie, chemical aspiration without infection)
Atelectasis
Pulmonary embolism
Acute respiratory distress syndrome
Pulmonary hemorrhage
Lung contusion
Infiltrative tumor
Radiation pneumonitis
Drug reaction
Cryptogenic organizing pneumonia
DIAGNOSTIC TESTS — Diagnostic testing is required whenever ventilator-associated pneumonia
(VAP) is suspected because the clinical findings alone are nonspecific [4-6]. The purpose of diagnostic
testing is to confirm VAP and identify the likely pathogen. Diagnostic testing involves radiographic
imaging and analysis of lower respiratory tract secretions, including Gram stain and culture. Lung
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biopsy can be diagnostic, but is seldom performed because of its invasiveness.
Imaging — All patients suspected of having VAP should have a chest radiograph [1]. Common
abnormalities include air bronchograms, alveolar infiltrates, and silhouetting of adjacent solid organs.
The chest radiograph can also help determine the severity of the disease (multilobar versus unilobar)
and identify complications, such as pleural effusions or cavitation.
The diagnosis of VAP requires an abnormal chest radiograph, although radiographic abnormalities
alone are insufficient to diagnose VAP because they are nonspecific (ie, they frequently exist in the
absence of VAP) [1,4,7,8]. In an observational study, only 43 percent of patients who had clinical and
radiographic evidence of VAP at the time of their death were confirmed to have VAP by postmortem
examination [8].
Microbiology — All patients suspected of having VAP should undergo lower respiratory tract
sampling, followed by microscopic analysis and culture of the specimen [1].
Sampling methods — There are a variety of methods for sampling material from the airways and
alveoli, including bronchoscopic and nonbronchoscopic (ie, blind) techniques.
Bronchoscopic sampling of the lower respiratory tract is performed using either bronchoalveolar
lavage (BAL) or a protected specimen brush (PSB) (see "Flexible bronchoscopy: Indications and
contraindications" and "Flexible bronchoscopy: Equipment, procedure, and complications"):
BAL involves the infusion and aspiration of sterile saline through a flexible fiberoptic
bronchoscope that is wedged in a bronchial segmental orifice. The technique of BAL is discussed
in detail elsewhere. (See "Basic principles and technique of bronchoalveolar lavage".)
A PSB is a brush that is contained within a protective sheath. It is designed to minimize the
likelihood that the brush will be contaminated during bronchoscopy. The procedure involves
placing the bronchoscope tip next to a bronchial segmental orifice, pushing the sheath through
the bronchoscope, and then advancing the brush out of the sheath and into the airway.
Specimens are collected by brushing the airway wall, withdrawing the brush into the sheath,
and then removing the sheath from the bronchoscope.
Nonbronchoscopic lower respiratory tract sampling includes tracheobronchial aspiration or mini-BAL
[9-17]. Tracheobronchial aspiration is performed by advancing a catheter through the endotracheal
tube until resistance is met and then applying suction. Mini-BAL is performed by advancing a catheter
through the endotracheal tube until resistance is met, infusing sterile saline through the catheter,
and then aspirating. A clinician is not necessary to perform or supervise nonbronchoscopic sampling.
This reduces the cost, allows specimens to be obtained quickly, and facilitates serial sampling when
necessary.
Bronchoscopic and nonbronchoscopic sampling for suspected VAP have been compared [18-22]. Taken
together, the evidence indicates that bronchoscopic sampling does not improve mortality, length of
hospital stay, duration of mechanical ventilation, or length of intensive care unit stay [18,20,22].
However, it may lead to a narrower antimicrobial regimen and/or more rapid de-escalation of
antimicrobial therapy [18,19,21,23].
Microscopic analysis — The most common microscopic analysis is the Gram stain of a lower
respiratory specimen (ie, tracheobronchial aspirate, BAL fluid, or mini-BAL fluid). It can be used to
characterize the morphology of bacteria, as well as to semiquantitate polymorphonuclear leukocytes
and other cell types. The presence of abundant neutrophils is consistent with VAP and the bacterial
morphology may suggest a likely pathogen. Gram stain analysis might decrease the incidence of
inappropriate antimicrobial therapy and improve diagnostic accuracy when correlated with culture
results [1].
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A differential cell count is an additional type of microscopic analysis that can be performed following a
BAL. It determines the proportion of total nucleated cells in the spun sediment of BAL fluid that are
neutrophils, lymphocytes, macrophages, eosinophils, basophils, or other nucleated cells. In a
prospective cohort study of 39 patients, VAP was correctly excluded in all patients in whom
neutrophils were fewer than 50 percent of the total nucleated cells [24].
Quantitative culture — Quantitative cultures can be performed on specimens obtained
bronchoscopically or nonbronchoscopically. VAP is supported when an established threshold of
bacterial growth is exceeded. Only bacteria that are pulmonary pathogens should be counted. As an
example, Staphylococcus epidermidis, most gram positive bacilli (except actinomycosis and nocardia),
and enterococci should be not be counted.
Thresholds of 1,000,000 colony forming units (cfu)/mL for samples obtained by tracheobronchial
aspiration, 10,000 cfu/mL for samples obtained by BAL, or 1000 cfu/mL for samples obtained by PSB
are most accurate because they are sufficiently high that patients with tracheobronchial colonization
are unlikely to be mistaken for patients with VAP [1,25,26].
Lower thresholds are reasonable if the risk of a missing a VAP (ie, a false-negative) exceeds the risk
of unnecessary treatment (ie, a false-positive) [27]. According to a prospective cohort study of 122
patients, thresholds between 1000 and 10,000 cfu/mL for BAL specimens and between 100 and 1000
cfu/mL for PSB specimens decrease the likelihood of a false-negative result to a greater degree than
they increase the likelihood of a false-positive result [28].
In general, quantitative cultures derived from nonbronchoscopic specimens tend to have a lower
specificity than quantitative cultures derived from bronchoscopic specimens [11,13]. However, this is
balanced by a higher sensitivity, resulting in comparable diagnostic accuracy. In a prospective cohort
study of 38 patients, the diagnostic accuracy of quantitative cultures was greatest when the sample
was obtained by tracheobronchial aspiration, followed (in order of decreasing accuracy) by BAL,
mini-BAL, and PSB [11].
Quantitative cultures do not appear to improve clinical outcomes. In a meta-analysis of three
randomized trials (1240 patients), quantitative cultures did not alter mortality, days of mechanical
ventilation, or length of ICU stay, compared to semiquantitative culture [29]. Despite the lack of
improvement in clinical outcomes, we believe quantitative cultures are advantageous because they
may lead to more judicious use of antibiotics.
Semiquantitative culture — Semiquantitative cultures can also be performed on specimens
obtained bronchoscopically or nonbronchoscopically. They are typically reported as showing heavy,
moderate, light, or no growth [1]. The amount of growth that suggests VAP has not been firmly
established, but it is reasonable to consider a semiquantitative culture with moderate or heavy growth
to be positive.
Compared to quantitative cultures, semiquantitative cultures are less likely to distinguish patients
whose airways are colonized from those who have VAP [1]. As a result, false-positive results are more
likely, which can lead to inappropriate therapy.
Effect of antibiotics — Lower respiratory tract specimens should be collected prior to initiating
antibiotic therapy because antibiotic therapy reduces the sensitivity of both microscopic analysis and
culture [30,31]. Similarly, specimens should be collected prior to changing the antibiotic regimen of
patients suspected of developing VAP while receiving antibiotics [26,32].
Antibiotic therapy also influences the type of pathogens that cause VAP. In a prospective cohort study
of 135 patients, prior antibiotic use was independently associated with VAP due to an antibiotic-
resistant pathogen, especially if the antibiotic regimen included a third generation cephalosporin,
fluoroquinolone, or imipenem [33].
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Procalcitonin — Biologic markers are sometimes used to try to distinguish between bacterial and
non-bacterial causes of pneumonia. Procalcitonin is one of the most promising biologic markers.
Procalcitonin is the peptide precursor of calcitonin. It is released by parenchymal cells in response to
bacterial toxins, leading to elevated serum levels in patients with bacterial infections.
Procalcitonin is measured by two commercially available tests, the Kryptor assay and the LUMI assay.
The former is generally preferred because it has a higher sensitivity.
The use of serum procalcitonin to facilitate the decision of whether to initiate antibiotics in patients
admitted with suspected pneumonia has been evaluated in randomized trials [34-36]. The trials found
that serum procalcitonin decreased antibiotic exposure without affecting clinical outcomes. However,
most of the trials enrolled patients with suspected community-acquired pneumonia only and not
patients with suspected VAP.
In patients with suspected VAP, it is uncertain if serum procalcitonin levels are a useful guide for the
decision of whether to initiate antibiotics because the evidence is conflicting. This was illustrated by
two prospective cohort studies in which VAP was confirmed in approximately half of the cases. One
study of 20 patients found that a procalcitonin level 3.0 ng/mL diagnosed VAP with a sensitivity and
specificity of 78 and 97, respectively [37]. In contrast, another study of 73 patients reported that a
serum procalcitonin level ≥2 ng/mL diagnosed VAP a sensitivity and specificity of only 41 and 61
percent, respectively [38].
Until higher quality studies resolve the uncertainty, we recommend not using serum procalcitonin
levels routinely to guide the decision of whether to initiate antibiotics in patients with suspected VAP.
However, there are two situations in which procalcitonin may be useful in patients with confirmed
VAP:
Procalcitonin may be helpful in the decision as to whether to discontinue antibiotic therapy. This
was illustrated by a trial that randomly assigned 101 patients with VAP to a conventional
antibiotic discontinuation strategy or a procalcitonin-guided antibiotic discontinuation strategy
[39]. The latter strategy reduced the duration of antibiotic therapy and did not affect clinical
outcomes, such as mortality, hospital length of stay, ventilator-free days, or ICU-free days.
Procalcitonin may be a useful prognostic marker, since progressive increases in serum
procalcitonin have been associated with septic shock and mortality [40-42].
Clinical score — The Clinical Pulmonary Infection Score (CPIS) combines clinical, radiographic,
physiologic, and microbiologic data into a numerical result (table 1). Initial validation of the CPIS
found that a score greater than 6 correlated with VAP [43]. However, subsequent studies failed to
confirm this. In a prospective cohort study, the CPIS identified VAP with a sensitivity and specificity of
only 60 and 59 percent, respectively [44].
Lung biopsy — Histologic examination of lung tissue obtained by biopsy is an imperfect and seldom
used method of diagnosing VAP. In addition to requiring an invasive procedure, its reliability and
reproducibility are uncertain. This is probably due to lack of standardized histologic criteria to define
VAP.
In a prospective cohort study, 39 patients who died while receiving mechanical ventilation underwent
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5. Clinical presentation and diagnosis of ventilator-associated pneumonia http://www.uptodate.com/contents/clinical-presentation-and-diagnosis-of...
post mortem open lung biopsy [45]. The histology was reviewed separately by four pathologists who
reported a prevalence of VAP ranging from 18 to 38 percent. One pathologist reinterpreted the
histology six months later and reclassified the VAP status of two patients.
DIAGNOSTIC APPROACH — Ventilator-associated pneumonia (VAP) should be considered in any
mechanically ventilated patient who develops new or increased fever, alveolar infiltrate, respiratory
secretions, leukocytosis, or respiratory abnormalities. The latter may include an increased respiratory
rate, increased minute ventilation, decreased tidal volume, decreased oxygenation, or a need for
more ventilatory support or inspired oxygen.
All patients with suspected VAP should have a chest radiograph (figure 1). A normal chest radiograph
excludes VAP, although ventilator-associated tracheobronchitis may exist. (See "Endotracheal tube
management and complications", section on 'Tracheobronchitis'.)
Patients with suspected VAP and an abnormal chest radiography should have their lower respiratory
tract secretions collected for microscopic analysis and culture. This can be done bronchoscopically or
nonbronchoscopically. The bronchoscopic approach probably leads to narrower antibiotic coverage,
earlier de-escalation of antimicrobial therapy, and, presumably, less antibiotic resistance. However, it
is invasive, less readily available, and does not appear to improve mortality, duration of mechanical
ventilation, or length of stay.
Sampling of the lower respiratory tract is ideally performed prior to initiating antibiotic therapy (or
prior to changing the antibiotic regimen if the patient is suspected of developing VAP while receiving
antibiotics). Quantitative or semiquantitative cultures are both acceptable, with the choice depending
largely on availability.
Sampling should not delay the initiation of necessary antibiotic therapy. Empiric antimicrobial therapy
can be withheld if the clinical suspicion for VAP is low and microscopic analysis of lower respiratory
tract samples is negative (ie, few neutrophils). Otherwise, empiric broad-spectrum antimicrobial
therapy should be initiated, as described separately. (See "Treatment of hospital-acquired, ventilator-
associated, and healthcare-associated pneumonia in adults", section on 'Empiric treatment'.)
Culture results should be available within two to three days. The decision on subsequent antibiotic
therapy should take into account the culture results and the patient's response to empiric therapy
(figure 1):
Patients with negative cultures who have not improved may not have VAP. Other diagnoses or
sites of infection should be sought.
Patients with negative cultures who have improved may not have VAP. Antimicrobial therapy
should be discontinued, unless it is indicated for an infection other than VAP.
Patients with positive cultures who have not improved probably have VAP. However, they may
be receiving inappropriate antimicrobial therapy, have a complication of the VAP, have a second
source of infection, or have a second diagnosis. The antimicrobial regimen should be adjusted
and then complications, other sites of infection, and other pathogens should be sought.
Patients with positive cultures who have improved probably have VAP, which has responded to
antimicrobial therapy. Antimicrobial therapy should be narrowed according to the culture
results.
The treatment of VAP is discussed separately. (See "Treatment of hospital-acquired, ventilator-
associated, and healthcare-associated pneumonia in adults".)
SUMMARY AND RECOMMENDATIONS
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6. Clinical presentation and diagnosis of ventilator-associated pneumonia http://www.uptodate.com/contents/clinical-presentation-and-diagnosis-of...
Ventilator-associated pneumonia (VAP) is a type of hospital-acquired (or nosocomial)
pneumonia that develops after more than 48 hours of mechanical ventilation. (See
'Introduction' above.)
VAP is usually suspected when a patient receiving mechanical ventilation develops a new or
progressive pulmonary infiltrate accompanied by fever, leukocytosis, purulent tracheobronchial
secretions, and/or new respiratory abnormalities. (See 'Clinical presentation' above.)
All patients with suspected VAP should have a chest radiograph performed. A normal chest
radiograph excludes VAP. (See 'Diagnostic approach' above.)
Patients with suspected VAP and an abnormal chest radiograph should have a sample of their
lower respiratory tract secretions collected for microscopic analysis and culture. (See 'Diagnostic
approach' above.)
Empiric antimicrobial therapy can be withheld if the clinical suspicion for VAP is low and
microscopic analysis of lower respiratory tract samples is negative (ie, few neutrophils).
Otherwise, empiric broad-spectrum antimicrobial therapy should be initiated. (See "Treatment
of hospital-acquired, ventilator-associated, and healthcare-associated pneumonia in adults",
section on 'Empiric treatment'.)
Two to three days after lower respiratory tract sampling and the initiation of empiric
antimicrobial therapy, the culture results should be checked and the patient's response to
antimicrobial therapy assessed. VAP is diagnosed on the basis of this assessment (see
'Diagnostic approach' above):
Patients with positive cultures who have not improved probably have VAP. However, they
may be receiving inappropriate antimicrobial therapy, have a complication of the VAP, have
a second source of infection, or have a second diagnosis.
Patients with positive cultures who have improved probably have VAP that has responded
appropriately to antimicrobial therapy.
Patients with negative cultures may not have VAP.
A diagnostic algorithm for VAP is shown in the figure (figure 1) (see 'Diagnostic
approach' above).
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GRAPHICS
Clinical Pulmonary Infection Score (CPIS)
Temperature
≥36.5 or ≤38.4 = 0 point
≥38.5 or ≤38.9 = 1 point
≥39 or <36.5 = 2 points
Blood leukocytes, microL
≥4000 or ≤11,000 = 0 points
<4000 or >11,000 = 1 point
Band forms ≥50 percent = add 1 point
Tracheal secretions
Absence of tracheal secretions = 0 point
Presence of non-purulent tracheal secretions = 1 point
Presence of purulent tracheal secretions = 2 points
Oxygenation
PaO2/FIO2, mmHg >240 or ARDS (defined as PaO2/FIO2 ≤200, PAWP ≤18 mmHg and acute
bilateral infiltrates) = 0 points
PaO2/FIO2 ≤240 and no ARDS = 2 points
Pulmonary radiography
No infiltrate = 0 point
Diffuse (patchy) infiltrate = 1 point
Localized infiltrate = 2 points
Progression of pulmonary infiltrate
No radiographic progression = 0 point
Radiographic progression (after HF and ARDS excluded) = 2 points
Culture of tracheal aspirate
Pathogenic bacteria cultured in rare or few quantities or no growth = 0 point
Pathogenic bacteria cultured in moderate or heavy quantity = 1 point
Same pathogenic bacteria seen on Gram's stain, add 1 point
Total (a score of >6 was considered suggestive of pneumonia)
ARDS: acute respiratory distress syndrome; HF: heart failure; PAWP: pulmonary arterial wedge pressure.
An initial score is based upon the first five variables. The last two variables are assessed on day 2 or 3.
Adapted with permission from: Singh, N, Rogers, P, Atwood, CW, et al. Short-course empiric antibiotic therapy
for patients with pulmonary infiltrates in the intensive care unit: a proposed solution for indiscriminate
antibiotic prescription. Am J Respir Crit Care Med 2000; 162:505. Copyright © 2002 American Thoracic
Society.
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Diagnostic algorithm for hospital-acquired, ventilator
associated pneumonia
WBC: white blood cell. Reproduced with permission from: American Thoracic Society
and the Infectious Diseases Society of America. Guidelines for the management of
adults with hospital-acquired, ventilator associated, and healthcare-associated
pneumonia. Am J Respir Crit Care Med 2005; 171:388. Copyright © 2002 American
Thoracic Society.
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