1. clinical presentation and diagnosis of ventilator-associated pneumonia

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23.7.2014 Clinical presentation and diagnosis of ventilator-associated pneumonia http://www.uptodate.com/contents/clinical-presentation-and-diagnosis-of-ventilator-associated-pneumonia?topicKey=PULM%2F1635&elapsedTimeMs=3&… 1/13 Official reprint from UpToDate www.uptodate.com ©2014 UpToDate Author Marin H Kollef, MD Section Editors Polly E Parsons, MD John G Bartlett, MD Deputy Editor Geraldine Finlay, MD Clinical presentation and diagnosis of ventilator-associated pneumonia All topics are updated as new evidence becomes available and our peer review process is complete. Literature review current through: Jun 2014. | This topic last updated: Mar 19, 2014. INTRODUCTION — Ventilator-associated pneumonia (VAP) is a type of hospital-acquired (ie, nosocomial) pneumonia that develops after more than 48 hours of mechanical ventilation. It is a common and serious problem, with an estimated incidence of 10 to 25 percent and an all-cause mortality of 25 to 50 percent [ 1,2 ]. Early diagnosis is important because prompt, appropriate treatment can be lifesaving. The clinical presentation and diagnosis of VAP are reviewed here. The risk factors for VAP and its prevention and treatment are discussed separately. (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 FEATURES Presentation — VAP typically presents with a new or progressive pulmonary infiltrate and one or more of the following findings: fever, purulent tracheobronchial secretions, leukocytosis, increased respiratory rate, decreased tidal volume, increased minute ventilation, and decreased oxygenation [ 3 ]. These symptoms and signs may develop gradually or suddenly. Medical history — Patients with VAP are typically unable to provide any history because they are either sedated or their ability to communicate is impaired by the endotracheal or tracheostomy tube. Those few patients who are able to convey symptoms are likely to report dyspnea or chest congestion. Physical examination — Fever and an increased volume of purulent tracheobronchial secretions are common among patients with VAP. On auscultation, patients typically have diffuse, asymmetric rhonchi due to the tracheobronchial secretions that the patient is unable to mobilize. The rhonchi are often accompanied by focal findings, such as crackles and decreased breath sounds. In addition, many patients are tachypneic with increased respiratory effort. Bronchospasm (wheezing and increased expiratory time) and hemoptysis are also common. These pulmonary signs may be accompanied by systemic abnormalities, such as encephalopathy or sepsis. (See "Sepsis and the systemic inflammatory response syndrome: Definitions, epidemiology, and prognosis", section on 'Sepsis' .) Ventilator performance — Deterioration in the patient’s respiratory performance, as identified during routine assessment of the mechanical ventilator, may be the initial sign of VAP. This includes an increased respiratory rate, decreased tidal volume, increased minute ventilation, or decreased oxygenation. Many patients will require more ventilatory support or inspired oxygen than they did previously. DIAGNOSTIC EVALUATION — Diagnostic evaluation is required any time that VAP is suspected because clinical features alone are nonspecific [ 4-6 ]. The goal is to confirm VAP and to identify the likely pathogen, so that the appropriate treatment can be initiated. The evaluation begins with a chest radiograph. Patients who have an abnormal chest radiograph should have their respiratory tract sampled and specimens sent for microscopic analysis and culture. These steps are ideally performed prior to the initiation of antibiotic therapy because antibiotic therapy reduces the sensitivity of both the microscopic analysis and culture [ 7,8 ] (similarly, these steps are ideally performed ® ®

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  • 23.7.2014 Clinical presentation and diagnosis of ventilator-associated pneumonia

    http://www.uptodate.com/contents/clinical-presentation-and-diagnosis-of-ventilator-associated-pneumonia?topicKey=PULM%2F1635&elapsedTimeMs=3& 1/13

    Official reprint from UpToDate www.uptodate.com 2014 UpToDate

    AuthorMarin H Kollef, MD

    Section EditorsPolly E Parsons, MDJohn G Bartlett, MD

    Deputy EditorGeraldine Finlay, MD

    Clinical presentation and diagnosis of ventilator-associated pneumonia

    All topics are updated as new evidence becomes available and our peer review process is complete.Literature review current through: Jun 2014. | This topic last updated: Mar 19, 2014.

    INTRODUCTION Ventilator-associated pneumonia (VAP) is a type of hospital-acquired (ie, nosocomial)

    pneumonia that develops after more than 48 hours of mechanical ventilation. It is a common and serious

    problem, with an estimated incidence of 10 to 25 percent and an all-cause mortality of 25 to 50 percent [1,2].

    Early diagnosis is important because prompt, appropriate treatment can be lifesaving.

    The clinical presentation and diagnosis of VAP are reviewed here. The risk factors for VAP and its prevention

    and treatment are discussed separately. (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 FEATURES

    Presentation VAP typically presents with a new or progressive pulmonary infiltrate and one or more of the

    following findings: fever, purulent tracheobronchial secretions, leukocytosis, increased respiratory rate,

    decreased tidal volume, increased minute ventilation, and decreased oxygenation [3]. These symptoms and

    signs may develop gradually or suddenly.

    Medical history Patients with VAP are typically unable to provide any history because they are either

    sedated or their ability to communicate is impaired by the endotracheal or tracheostomy tube. Those few

    patients who are able to convey symptoms are likely to report dyspnea or chest congestion.

    Physical examination Fever and an increased volume of purulent tracheobronchial secretions are common

    among patients with VAP. On auscultation, patients typically have diffuse, asymmetric rhonchi due to the

    tracheobronchial secretions that the patient is unable to mobilize. The rhonchi are often accompanied by focal

    findings, such as crackles and decreased breath sounds. In addition, many patients are tachypneic with

    increased respiratory effort. Bronchospasm (wheezing and increased expiratory time) and hemoptysis are also

    common. These pulmonary signs may be accompanied by systemic abnormalities, such as encephalopathy or

    sepsis. (See "Sepsis and the systemic inflammatory response syndrome: Definitions, epidemiology, and

    prognosis", section on 'Sepsis'.)

    Ventilator performance Deterioration in the patients respiratory performance, as identified during routine

    assessment of the mechanical ventilator, may be the initial sign of VAP. This includes an increased respiratory

    rate, decreased tidal volume, increased minute ventilation, or decreased oxygenation. Many patients will require

    more ventilatory support or inspired oxygen than they did previously.

    DIAGNOSTIC EVALUATION Diagnostic evaluation is required any time that VAP is suspected because

    clinical features alone are nonspecific [4-6]. The goal is to confirm VAP and to identify the likely pathogen, so

    that the appropriate treatment can be initiated. The evaluation begins with a chest radiograph. Patients who have

    an abnormal chest radiograph should have their respiratory tract sampled and specimens sent for microscopic

    analysis and culture.

    These steps are ideally performed prior to the initiation of antibiotic therapy because antibiotic therapy reduces

    the sensitivity of both the microscopic analysis and culture [7,8] (similarly, these steps are ideally performed

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    prior to changing the antibiotic regimen of patients suspected of developing VAP while receiving antibiotics

    [9,10]). Once the respiratory specimens have been obtained, empiric antibiotic therapy is indicated for all cases

    of suspected VAP, unless the clinical suspicion is low and the microscopic analysis of lower respiratory tract

    samples is negative (ie, few neutrophils). Occasionally, the severity of illness or delays in sampling requires that

    empiric antibiotic therapy be initiated prior to diagnostic sampling. (See "Treatment of hospital-acquired,

    ventilator-associated, and healthcare-associated pneumonia in adults", section on 'Empiric treatment'.)

    Chest imaging A chest radiograph should be performed on all patients with suspected VAP [1]. A normal

    chest radiograph excludes VAP, while an abnormal radiograph should prompt the collection of respiratory tract

    secretions. Common radiographic abnormalities in VAP include alveolar infiltrates, air bronchograms, and

    silhouetting of adjacent solid organs.

    While an abnormal chest radiograph is required to diagnose VAP, it is not sufficient. The reason that

    radiographic abnormalities alone are insufficient to diagnose VAP is that they are nonspecific (ie, they frequently

    exist in the absence of VAP) [1,4,11,12]. This was illustrated by an observational study in which only 43 percent

    of patients who had clinical and radiographic evidence of VAP at the time of their death were subsequently

    confirmed to have VAP by postmortem examination [12].

    Additional benefits of the chest radiograph are that it can help determine the severity of the disease (multilobar

    versus unilobar) and identify complications, such as pleural effusions or cavitation.

    Respiratory sampling Lower respiratory tract sampling is indicated for all patients who are suspected of

    having VAP and have an abnormal chest radiograph [1]. There are a variety of methods available to sample

    material from the airways and alveoli, including nonbronchoscopic (ie, blind) and bronchoscopic techniques.

    Nonbronchoscopic lower respiratory tract sampling includes tracheobronchial aspiration or mini-BAL [13-21]:

    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 sampling 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"):

    Bronchoscopic sampling and nonbronchoscopic sampling have been compared in the setting of suspected VAP

    [22-26]. 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 [22,24,26,27]. However, it minimizes

    airway contamination of the alveolar samples and provides an accurate assessment of the alveolar cell

    population. Bronchoscopic sampling may lead to a narrower antimicrobial regimen and more rapid de-escalation

    of antimicrobial therapy [22,23,25,28], which presumably reduces antibiotic resistance.

    The decision about whether to perform nonbronchoscopic or bronchoscopic sampling ultimately depends upon a

    case-by-case determination of the benefits of a narrow antibiotic regimen versus the risks of bronchoscopy. In

    patients for whom the risk of bronchoscopy is low, we frequently perform bronchoscopic BAL [29].

    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.

    BAL involves the infusion and aspiration of sterile saline through a flexible bronchoscope that is wedged in

    a bronchial segmental orifice. The technique of BAL is discussed in detail separately. (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.

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    Microscopic analysis The lower respiratory specimens should be sent for microscopic analysis. The most

    common microscopic analysis is the Gram stain. It can be used to semi-quantitate polymorphonuclear

    leukocytes and other cell types, as well as to characterize the morphology of bacteria. The presence of

    abundant neutrophils is consistent with VAP and the bacterial morphology may suggest a likely pathogen.

    Gram stain analysis may decrease the incidence of inappropriate antimicrobial therapy and improve diagnostic

    accuracy when correlated with culture results [1].

    A differential cell count can also be performed by microscopic analysis 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 [30].

    Respiratory culture The lower respiratory specimens should also be sent for culture. Quantitative or

    semiquantitative cultures are both acceptable, with the choice depending largely upon availability.

    Quantitative culture Quantitative cultures can be performed on bronchoscopic or nonbronchoscopic

    specimens. VAP is supported when an established threshold of bacterial growth is exceeded. Only bacteria that

    are pulmonary pathogens should be counted. As examples, Staphylococcus epidermidis, enterococci, and

    most gram positive bacilli (except actinomycosis and nocardia) should 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 [1,9,31]. Lower thresholds are reasonable if the risk of a missing a VAP (ie, a false-negative

    result) exceeds the risk of unnecessary treatment (ie, a false-positive result) [32]. 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 [33].

    Generally speaking, quantitative cultures derived from nonbronchoscopic specimens tend to have a lower

    specificity than quantitative cultures derived from bronchoscopic specimens [15,17]. However, this is balanced

    by a higher sensitivity, resulting in comparable diagnostic accuracy. In a prospective cohort study of 38

    patients, the 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 [15].

    Quantitative cultures do not appear to improve clinical outcomes, compared with semiquantitative cultures. This

    was illustrated by a meta-analysis of three randomized trials (1240 patients), which found that quantitative

    cultures did not alter mortality, days of mechanical ventilation, or length of ICU stay, compared with

    semiquantitative cultures [27]. Despite the lack of improvement in clinical outcomes, many clinicians believe

    that quantitative cultures are advantageous because they may lead to more judicious use of antibiotics [29].

    Semiquantitative culture Semiquantitative cultures can also be performed on bronchoscopic or

    nonbronchoscopic samples. 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 with 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.

    Other diagnostic tests Procalcitonin, the clinical pulmonary infection score, and lung biopsy are additional

    diagnostic tests that are often discussed; however, they have little role in the evaluation of suspected VAP.

    Biological markers Biologic markers are sometimes used to try to distinguish between bacterial and

    non-bacterial causes of pneumonia.

    Procalcitonin is a promising biologic marker. The use of serum procalcitonin to facilitate the decision about

    whether or not to initiate antibiotics in patients admitted with suspected community-acquired pneumonia

    was evaluated in several randomized trials that found that serum procalcitonin decreased antibiotic

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    DIAGNOSTIC CRITERIA The diagnosis of VAP is made when a patient who has been mechanically

    ventilated for 48 hours develops a new or progressive infiltrate and the respiratory specimens are positive (ie,

    increased neutrophils are seen in the microscopic analysis and growth of a pathogen in culture exceeds a

    predefined threshold).

    VAP cannot be confirmed or excluded until the culture results are complete, which generally takes two to three

    days. At that time, the patient should be reevaluated to determine if additional diagnostic evaluation or changes

    in management are warranted. These decisions are based upon the culture results and response to empiric

    therapy (algorithm 1):

    Antimicrobial therapy for VAP is discussed separately. (See "Treatment of hospital-acquired, ventilator-

    associated, and healthcare-associated pneumonia in adults".)

    DIFFERENTIAL DIAGNOSIS There are many causes of pulmonary infiltrates, fever, respiratory

    exposure without affecting clinical outcomes [34-36]. In suspected VAP, however, it is unknown if serum

    procalcitonin levels are a useful guide for the decision about whether to initiate antibiotics because the

    evidence is conflicting [37,38]. Until higher quality studies resolve the uncertainty, we believe that serum

    procalcitonin levels should not be used for this purpose. However, there are two situations in which

    procalcitonin may be useful in patients with confirmed VAP. First, procalcitonin may be helpful in the

    decision of whether to discontinue antibiotic therapy [39]. Second, procalcitonin may be a useful

    prognostic marker, since progressive increases in serum procalcitonin have been associated with septic

    shock and mortality [40-42].

    Other biomarkers, such as C-reactive protein (CRP) and soluble triggering receptor expressed on myeloid

    cells-1 (sTREM-1), were initially considered promising markers for improving diagnostic strategies for VAP.

    However, more recent studies suggest that the measurement of such biomarkers in BAL fluid has minimal

    diagnostic value for VAP [43-45].

    Clinical Pulmonary Infection Score (CPIS) The 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 six correlated with VAP [46]. However, subsequent studies failed to confirm this. In one prospective

    cohort study, the CPIS identified VAP with a sensitivity and specificity of only 60 and 59 percent,

    respectively [47].

    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 a lack of standardized histologic criteria to define VAP. In a

    prospective cohort study, 39 patients who died while receiving mechanical ventilation underwent post

    mortem open lung biopsy [48]. 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.

    Laboratory tests Patients with VAP usually develop leukocytosis with a neutrophil predominance.

    However, there are no laboratory findings that are specific for VAP.

    Patients with negative cultures who have not improved may not have VAP; therefore, 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.

    Patients with positive cultures who have not improved probably have VAP, but they may be receiving

    inappropriate antimicrobial therapy, have a complication of the VAP (eg, abscess, empyema), have a

    second source of infection, or have a second diagnosis. The antimicrobial regimen should be adjusted and

    then potential causes for failing to improve clinically should be sought.

    Patients with positive cultures who have improved probably have VAP, which has responded to

    antimicrobial therapy; the antimicrobial therapy should be narrowed according to the culture results.

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    abnormalities, and leukocytosis other than VAP. The following conditions can present with this constellation of

    findings:

    VENTILATOR ASSOCIATED EVENTS The CDC National Healthcare Safety Network implemented ventilator-

    associated events (VAE) surveillance in January 2013 [49]. This is a three-tier surveillance definition algorithm.

    This algorithm uses objective, readily available data elements to identify a broad range of conditions and

    Aspiration pneumonitis Aspiration pneumonitis refers to chemical aspiration without infection; it is

    distinguished from VAP by history (ie, witnessed aspiration), microscopic analysis and culture of

    respiratory secretions (ie, negative), and clinical course (ie, self-limited). (See "Aspiration pneumonia in

    adults".)

    Pulmonary embolism with infarction Pulmonary embolism can mimic VAP if it causes pulmonary

    infarction; it is distinguished from VAP when computed tomography pulmonary angiography (CT-PA),

    ventilation-perfusion (V/Q) scanning, or conventional pulmonary angiography reveals pulmonary embolism.

    (See "Diagnosis of acute pulmonary embolism".)

    Acute respiratory distress syndrome Acute respiratory distress syndrome (ARDS) is characterized by

    an acute onset of bilateral pulmonary infiltrates and severe hypoxemia in the absence of an elevated left

    atrial pressure; it is distinguished from VAP by history (ie, risk factors for ARDS may be present) and the

    microscopic analysis and culture of respiratory secretions (ie, negative). (See "Acute respiratory distress

    syndrome: Clinical features and diagnosis in adults".)

    Pulmonary hemorrhage Both pulmonary hemorrhage and VAP may cause hemoptysis in addition to the

    constellation of findings described above. Pulmonary hemorrhage tends to present with frank bleeding

    while VAP often appears as blood mixed with purulent secretions, but this distinction is imperfect.

    Definitively distinguishing pulmonary hemorrhage from VAP requires that the cause of the hemoptysis be

    identified. (See "Etiology and evaluation of hemoptysis in adults".)

    Lung contusion Pulmonary contusion is due to trauma, but it may be difficult to distinguish from VAP

    because the clinical and radiographic manifestations are similar and often delayed following the trauma.

    Pulmonary contusion is distinguished from VAP by history (ie, recent trauma) and the microscopic

    analysis and culture of respiratory secretions (ie, negative). (See "Overview of inpatient management in the

    adult trauma patient", section on 'Pulmonary contusion'.)

    Infiltrative tumor The lung is a common site of primary or metastatic cancer and the manifestations of a

    diffuse infiltrative cancer are similar to VAP. Diffuse infiltrative cancer is distinguished from VAP by history

    (ie, history of malignancy), as well as both culture (ie, negative) and microscopic analysis (ie, negative for

    neutrophils and bacteria, but positive for malignant cells) of respiratory secretions.

    Radiation pneumonitis Radiation-induced lung injury may cause acute pneumonitis or chronic fibrosis.

    The former develops approximately four to twelve weeks after irradiation, with symptoms and signs that

    mimic VAP; it is distinguished from VAP by history (ie, prior irradiation) and the microscopic analysis and

    culture of respiratory secretions (ie, negative). (See "Radiation-induced lung injury".)

    Drug reaction Pulmonary drug toxicity can result from many different drugs, most notably antineoplastic

    agents (eg, cyclophosphamide, methotrexate). The clinical manifestations of pulmonary drug toxicity can

    be identical to VAP and the timing of the onset of symptoms and signs is highly variable (ie, days to

    months after receiving the medication). Pulmonary drug toxicity is distinguished from VAP by history (ie,

    received a potentially toxic agent within the past months) and the microscopic analysis and culture of

    respiratory secretions (ie, negative). (See "Pulmonary toxicity associated with systemic antineoplastic

    therapy: Clinical presentation, diagnosis, and treatment".)

    Cryptogenic organizing pneumonia Cryptogenic organizing pneumonia (COP) is an idiopathic form of

    organizing pneumonia. Its clinical features may be identical to VAP; it is distinguished from VAP by

    history (ie, risk factors for COP may be present, such as a recent viral infection) and the microscopic

    analysis and culture of respiratory secretions (ie, negative). Definitive diagnosis of COP requires lung

    biopsy. (See "Cryptogenic organizing pneumonia".)

    http://www.cdc.gov/nhsn/acute-care-hospital/vae/http://www.uptodate.com/contents/clinical-presentation-and-diagnosis-of-ventilator-associated-pneumonia/abstract/49http://www.uptodate.com/contents/aspiration-pneumonia-in-adults?source=see_linkhttp://www.uptodate.com/contents/diagnosis-of-acute-pulmonary-embolism?source=see_linkhttp://www.uptodate.com/contents/acute-respiratory-distress-syndrome-clinical-features-and-diagnosis-in-adults?source=see_linkhttp://www.uptodate.com/contents/etiology-and-evaluation-of-hemoptysis-in-adults?source=see_linkhttp://www.uptodate.com/contents/overview-of-inpatient-management-in-the-adult-trauma-patient?source=see_link&anchor=H9#H9http://www.uptodate.com/contents/radiation-induced-lung-injury?source=see_linkhttp://www.uptodate.com/contents/cyclophosphamide-drug-information?source=see_linkhttp://www.uptodate.com/contents/methotrexate-drug-information?source=see_linkhttp://www.uptodate.com/contents/pulmonary-toxicity-associated-with-systemic-antineoplastic-therapy-clinical-presentation-diagnosis-and-treatment?source=see_linkhttp://www.uptodate.com/contents/cryptogenic-organizing-pneumonia?source=see_link

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    complications occurring in mechanically ventilated adult patients. These include, but are not limited to VAP. The

    first tier definition, ventilator-associated condition (VAC), identifies patients with a period of sustained respiratory

    deterioration following a sustained period of stability or improvement on the ventilator (changes in PEEP or

    FiO ). The second tier definition, infection-related ventilator-associated complication (IVAC), requires that

    patients with VAC also have an abnormal temperature or white blood cell count, and be started on a new

    antimicrobial agent. The third tier definitions, possible and probable VAP, require that patients with IVAC also

    have laboratory and/or microbiological evidence of respiratory infection [50]. The effect of implementing this

    surveillance system and of VAP bundles on the prevention of VACs is unknown.

    SUMMARY AND RECOMMENDATIONS

    Use of UpToDate is subject to the Subscription and License Agreement.

    REFERENCES

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    2

    Ventilator-associated pneumonia (VAP) is a type of hospital-acquired (ie, nosocomial) pneumonia that

    develops after more than 48 hours of mechanical ventilation. (See 'Introduction' above.)

    VAP typically presents with the gradual or sudden onset of a new or progressive pulmonary infiltrate and

    one or more of the following findings: fever, purulent tracheobronchial secretions, leukocytosis, increased

    respiratory rate, decreased tidal volume, increased minute ventilation, and decreased oxygenation. (See

    'Clinical features' above.)

    A diagnostic evaluation is required whenever VAP is suspected because clinical features alone are

    nonspecific. The goal of the diagnostic evaluation is to confirm VAP and identify the likely pathogen. A

    typical evaluation begins with a chest radiograph. For patients with an abnormal chest radiograph, the

    respiratory tract is sampled and the specimens are sent for microscopic analysis and culture. (See

    'Diagnostic evaluation' above.)

    These steps are ideally performed prior to the initiation of antibiotic therapy because antibiotic therapy

    reduces the sensitivity of both the microscopic analysis and culture (similarly, these steps are ideally

    performed prior to changing the antibiotic regimen of patients suspected of developing VAP while receiving

    antibiotics). Once the respiratory specimens have been obtained, empiric antibiotic therapy is indicated for

    all cases of suspected VAP, unless the clinical suspicion is low and the microscopic analysis of lower

    respiratory tract samples is negative (ie, few neutrophils). Occasionally, the severity of illness or delays in

    sampling requires that empiric antibiotic therapy be initiated prior to diagnostic sampling. (See 'Diagnostic

    evaluation' above.)

    The diagnosis of VAP is made when a patient who has been mechanically ventilated for at least 48 hours

    develops a new or progressive pulmonary infiltrate and cultures of the respiratory specimens are positive

    (ie, increased neutrophils are seen in the microscopic analysis and growth of a pathogen in culture

    exceeds a predefined threshold). (See 'Diagnostic criteria' above.)

    There are many causes of pulmonary infiltrates, fever, respiratory abnormalities, and leukocytosis other

    than VAP. These include aspiration pneumonitis, pulmonary embolism with infarction, acute respiratory

    distress syndrome, pulmonary hemorrhage, pulmonary contusion, infiltrative tumor, radiation pneumonitis,

    pulmonary drug toxicity, and cryptogenic organizing pneumonia. (See 'Differential diagnosis' above.)

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    Topic 1635 Version 9.0

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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 240 or ARDS (defined as PaO /FIO 200, PAWP 18 mmHg and

    acute bilateral infiltrates) = 0 points

    PaO /FIO 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 stain, add 1 point

    Total (a score of >6 was considered suggestive of pneumonia)

    An initial score is based upon the first five variables. The last two variables are assessed

    on day 2 or 3.

    ARDS: acute respiratory distress syndrome; HF: heart failure; PAWP: pulmonary arterial wedge

    pressure.

    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.

    2 2 2 2

    2 2

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    Graphic 77054 Version 4.0

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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.

    Graphic 76508 Version 2.0

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    Disclosures: Marin H Kollef, MD Nothing to disclose. Polly E Parsons, MD Nothing to disclose. John G Bartlett, MD Nothing todisclose. Geraldine Finlay, MD Employee of UpToDate, Inc.

    Contributor disclosures are review ed for conflicts of interest by the editorial group. When found, these are addressed by vettingthrough a multi-level review process, and through requirements for references to be provided to support the content. Appropriatelyreferenced content is required of all authors and must conform to UpToDate standards of evidence.

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