Ventilator Associated Pneumonia (VAP)



(Chest 2006;130(2):597)

New VAP Recs

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103 for Protected Brush, 104 for BAL, 105-106 for tracheal aspirate



Does this pt have VAP (JAMA 2007;297(14):1583)Box. Centers for Disease Control and Prevention (CDC) NationalHealthcare Safety Network Definition for Ventilator-AssociatedPneumonia


Radiology signs

Two or more serial chest radiographs with at least 1 of the following:*

  • New or progressive and persistent infiltrate
  • Consolidation
  • Cavitation

Clinical signs

At least 1 of the following:

  • Fever (temperature >38°C [100.4°F] with no other recognized cause)
  • Leukopenia (<4000 white blood cells/µL) or leukocytosis (12 000 white blood cells/µL)
  • For adults 70 years or older, altered mental status with no other recognized cause

Plus at least 2 of the following:

  • New onset of purulent sputum, or change in character of sputum, or increased respiratory secretions, or increased suctioning requirements
  • New-onset or worsening cough, or dyspnea, or tachypnea
  • Rales or bronchial breath sounds
  • Worsening gas exchange (eg, O2 desaturations [eg, PaO2/FiO2   240], increased oxygen requirements, or increased ventilation demand

Microbiological criteria (optional) At least 1 of the following:        Positive growth in blood culture not related to another source of infection        Positive growth in culture of pleural fluid        Positive quantitative culture from bronchoalveolar lavage (104 colony-forming units/mL) or protected specimen brushing( 103 colony-forming units/mL)        Five percent or more of cells with intracellular bacteria on direct microscopic examination of Gram-stained bronchoalveolar lavage fluid        Histopathological evidence of pneumonia

*In patients without underlying pulmonary or cardiac disease (eg, respiratory distress syndrome, bronchopulmonary dysplasia, pulmonary edema, or chronic obstructive pulmonary disease), 1 definitive chest radiograph is acceptable. first signs are slowly increasing fio2 requirement

Assessment of a chest radiograph is a practical place to begin.The appearance of a new infiltrate suggests that VAP is possible(summary LR, 1.7; 95% CI, 1.1-2.5) and should prompt a secondlook at the patient’s temperature, sputum purulence, and leukocytecount. When 2 or more of these signs are positive, then VAP becomes more likely (summary LR, 2.8; 95% CI, 0.97-7.9). Taking a 9.7% incidence as the prior probability for VAP among ventilated patients, 8 the above combination of findings will increase thelikelihood of VAP to 23% (95% CI, 9.4%-46% after taking thelimits of the LR confidence interval). Expert clinicians tend to also consider impairment of gas exchange as a necessary,albeit nonspecific and insufficient, criterion to diagnose VAP. 24 This intuitive requirement was not formally assessed in theindependent studies included in this review.

In contrast, the absence of new infiltrates substantively lowersthe likelihood of VAP (summary LR, 0.35; 95% CI, 0.14-0.87).The absence of fever, sputum purulence, or an elevated whiteblood cell count does not add information to that gained froma radiograph without infiltrates. If the pretest probabilityof VAP is 9.7%, 8 then routine clinical evaluation includinga stable chest radiograph without new infiltrates can lowerthe probability of VAP to 3.6% (95% CI, 1.5%-8.5%).

Analysis of pulmonary secretions can further refine the likelihoodthat VAP is present or absent. BAL fluid in which less than 50% of the cells are neutrophils argues against the presenceof VAP, with an LR that ranges from 0.05 to 0.10. By contrast,the presence of microorganisms on a Gram stain of pulmonary secretions substantively increases the probability of VAP. The suggestiveness of a positive Gram stain result increases almost exponentially with progressively more invasive diagnostic techniques—thepositive LR for a positive Gram stain result on a blind bronchialaspirate is only 2.1 (95% CI, 0.81-5.5), but this increases to 5.3 (95% CI, 1.3-22) with mini-BAL and up to 18 (95% CI,1.1-302) on BAL fluid gathered via fiberoptic-guided bronchoscopy. Quantitative bacterial cultures of pulmonary secretions canalso help diagnose VAP. Growth of more than 105 colony-formingunits/mL of bacteria from a blind bronchial aspirate is highlysuggestive of VAP (summary LR, 9.6; 95% CI, 2.4-38). A threshold of only 104 colony-forming units/mL on BAL fluid, by contrast,is not definitive. This is likely a reflection of greater potentialfor contaminant organisms to reach this lower growth threshold. Negative quantitative cultures of both bronchial aspirates and BAL fluid only moderately decrease the probability of VAP.

The finding that analysis of both blind bronchial aspirate and BAL can contribute useful information but that neither is definitiveis consistent with a recent randomized clinical trial showingno difference in 28-day mortality regardless of which of these2 diagnostic strategies was initially used. 51 Patients wereselected to be included in that study if they manifested theclassic clinical features of VAP analyzed in this review. Allpatients were given broad-spectrum antibiotics immediately after diagnostic sampling. Approximately 40% of the patients in bothgroups of the trial, however, were not cured by the end of thestudy, raising the possibility that their clinical syndromewas not caused by true, histological VAP but by some other etiology.This again bespeaks the imperfect accuracy of clinical signsfor VAP. The trial teaches that obtaining blind bronchial aspirates might be a reasonable starting procedure for the majority ofpatients, but patients who do not improve with antibiotics guidedby this strategy merit further diagnostic workup. This could include bronchoscopy to further evaluate whether VAP is present,as well as other specialized studies to assess for noninfectiouscauses of pulmonary disease.

The findings of this review support the consensus opinions publishedby the Infectious Diseases Society of America and the AmericanThoracic Society. 24 Their guidelines acknowledge the lack ofa definitive gold standard to diagnose VAP and the practicaldifficulty of making the diagnosis at the bedside. Both societies recommend a combination of clinical signs and quantitative microbiologicaldata to diagnose and manage VAP, while emphasizing the importanceof constant reevaluation of the diagnosis over time. Clinicians should suspect VAP when chest radiography reveals the presenceof a new or progressive infiltrate and the patient has at least2 of fever, abnormal white blood cell count, or purulent secretions. As soon as VAP is suspected, clinicians are urged to immediatelyobtain a lower respiratory tract specimen for microscopy andculture (quantitative or semiquantitative). Because of the uncertainty in diagnosis when a patient is initially examined, antibioticsare typically started unless the pretest probability for VAPis very low. After 48 to 72 hours of antibiotic therapy, clinical response should be assessed by reevaluating the patient’s temperature,white blood cell count, oxygenation, and results of chest radiography,pulmonary secretion microscopy, and secretion culture. Absence of improvement should prompt a search for an alternative diagnosisor a reason for therapeutic failure.

The findings of this review are tempered by limitations of the source data. Many of the conclusions were based on a limited number of small studies that differed in both their methodsand their findings. Moreover, even a histological gold standardis not without controversy. First, series limited to patients ultimately undergoing autopsy are inherently biased toward the sickest patients. Second, pulmonary biopsies risk missing the isolated patchy lesions that are characteristic of VAP. Third, interobserver agreement between pathologists has been reportedto be only moderately good ( = 0.45). 10 Finally, the interpretation of pulmonary pathology is complicated by delay between the initial clinical development of pneumonia and the subsequent autopsy, during which interim healing and antibiotic exposure can complicate the histological picture.

The best available evidence suggests that clinical examination can be used to alert physicians to the possibility of VAP but that examination alone is insufficient to establish a definitive diagnosis. Examination of pulmonary secretions can help refine physicians’ clinical suspicions. The presence of bacteria onGram stain or bacterial growth above a quantitative thresholdfavors the diagnosis, while less than 50% neutrophils in a pulmonary specimen makes VAP less likely. The absence of a new infiltrate on chest radiograph also makes disease unlikely. Clinicians caring for ventilated patients with a clinical syndrome consistentwith VAP should be ready to consider additional diagnoses andfurther investigations, particularly when an empirical trial of antibiotics does not lead to improvement within 48 to 72hours.



VAP>48 hours on vent


New analysis seems to indicate no benefit from head of bed up (An evidence-based recommendation on bed head elevation for mechanically ventilated patients Critical Care 2011, 15:R111)


In trauma patients, low dose steroids may reduce VAP

Roquilly A, Mahe PJ, Seguin P, et al. Hydrocortisone therapy for patients with multiple trauma: the randomized controlled HYPOLYTE study. JAMA. 2011 Mar 23;305(12):1201-9. (Original) PMID: 21427372


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