I. What every physician needs to know.
Ventilator-associated pneumonia (VAP) is defined as pneumonia occurring in patients after forty-eight hours of intubation and mechanical ventilation. It is an important diagnosis because it is the second most common nosocomial infection in critically ill patients, and it carries substantial morbidity and mortality. Clinicians must maintain a high index of suspicion and vigilant monitoring for this condition, and they should be familiar with diagnostic and treatment standards. Moreover, in the era of patient safety, clinicians who provide care for critically ill and injured patients should employ standard preventive measures to limit the incidence in patients who are receiving mechanical ventilation.
II. Diagnostic Confirmation: Are you sure your patient has ventilator-associated pneumonia?
The diagnosis of VAP is challenging, and it requires careful analysis of clinical variables, combined with a culture of lower respiratory tract secretions. The clinical variables used to assess VAP, referred to as the Clinical Physiologic Infection Score, include fever higher than 38 degrees Centigrade, leukocytosis or leukopenia, a change in secretions, a new or progressive infiltrate on chest radiograph, and alteration in oxygenation as noted by a reduction in the PaO2/FiO2 ratio. When combined with microbiologic data, this approach provides reasonable sensitivity and specificity for diagnosing pneumonia and may be best used when there is a clinical re-assessment after three days.
Strategies that employ invasive diagnostic maneuvers, such as bronchoscopy with bronchoalveolar lavage (BAL), can improve the accuracy of the diagnosis and help avoid overuse of antibiotics in the ICU setting, but no survival advantage has been noted with an approach that routinely employs such testing.
The gold standard for diagnosis–autopsy–has little practical value.
A. History Part I: Pattern Recognition:
Patients with VAP are often in the ICU, intubated for at least two days, with an unexpected change in their clinical status. This change may first manifest as fever , hypoxemia on bedside pulse oxymetry monitoring, or a change in secretions. The change in secretions may include an increase in volume, noted by the need for more frequent suctioning or a change in secretion color or odor.
When these changes are noted, simple diagnostic tests–measurement of the white blood cell (WBC) count and a portable upright chest radiograph (CXR)–should be obtained. When a new fever is accompanied by change in secretions, the need to increase the FiO2 to maintain stable oxygen saturations, a newly elevated WBC count, and new or evolving infiltrate on CXR, then the diagnosis can be straightforward. If the first change noted is a new infiltrate, it may be challenging to identify the presence or absence of pneumonia, as other explanations, such as atelectasis, aspiration, or thromboembolic disease, could be relevant.
B. History Part 2: Prevalence:
VAP occurs in a quarter or more of all intubated ICU patients; the primary risk factor is length of time on mechanical ventilation. However, the incidence appears to be decreasing because of broader application of preventive strategies, including efforts to liberate patients from mechanical ventilation at the earliest opportunity. While the incidence of VAP increases with duration of mechanical ventilation, the daily rate is highest early in the ICU course (before day 5) and then diminishes slightly in subsequent days.
C. History Part 3: Competing diagnoses that can ventilator-associated pneumonia.
The differential diagnosis for VAP includes atelectasis, gross aspiration without infection, pulmonary infarction, and non-infectious inflammatory infiltrates that are attributable to lung disease or systemic disorders. Since atelectasis is common, it is important to distinguish it from VAP. The challenge here is apparent because atelectasis can be associated with a low-grade fever and hypoxia. However, atelectasis should not be accompanied by an elevated WBC count or a change in secretions.
Pulmonary embolism (PE) and infarction, which are usually accompanied by hypoxemia, may also be associated with fever. The infiltrate in PE may be “wedge-shaped,” and secretions would not be expected to change.
Aspiration without infection may be the most challenging diagnosis to exclude. Other causes of infiltrates, such as cryptogenic organizing pneumonia, lupus pneumonitis, and other inflammatory disorders, may require biopsy. These conditions may be suspected after a course of antibiotic therapy fails to lead to a response.
D. Physical examination findings.
Fever is generally present, but it may be suppressed by steroids or other medications. On exam, classic findings of consolidation are not seen in the majority of patients, but they may be evident with careful auscultation. Mechanical ventilation can limit the accuracy of the exam, but this issue should not dissuade the provider from using a stethoscope. Secretions will be evident at the bedside and when reviewing the nurses’ observations.
E. What diagnostic tests should be performed?
Culture of respiratory secretions (either tracheal aspirate or a protected specimen from the lower respiratory tract such as BAL)
1. What laboratory studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?
Caution is advised in interpreting the results of tracheal aspirates, as colonization of the tracheobronchial tree is common in intubated ICU patients, and the simple presence of a pathogen does not imply pneumonia. All culture results must be analyzed through the prism of the patient’s clinical condition. Similarly, a new infiltrate might be due to atelectasis and simply serve as a starting point for an analysis of the specific etiology. Since a rise in WBC may be from an alternate source, this, too, lacks specificity when viewed in isolation. Therefore, the diagnosis requires both a high index of suspicion and broad application of clinical skills.
2. What imaging studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?
Chest radiograph remains the most important imaging study for this diagnosis. The differentiation of atelectasis from pneumonia can be challenging and may not be possible based upon the CXR alone. Pneumonia does not lead to “volume loss,” a reduction in lung volume from collapse of alveoli that, when substantial enough, leads to shifting of intrathoracic structurestoward the sideof the atelectasis. For example, left lower lobe atelectasis (seen not infrequently in ventilated patients because of the preference that suction catheters enter the right endobronchial tree) may be associated with a shift of the heart or trachea to the left.
Computerized tomography (CT) scan offers great clarity for viewing the lung fields but cannot definitively identify infection as the cause of an infiltrate. Basilar atelectasis may still be challenging to differentiate from pneumonia.
F. Over-utilized or “wasted” diagnostic tests associated with this diagnosis.
Avoid sending tracheal aspirate for culture when pneumonia is not suspected. The results will simply lead to confusion or over-treatment. Cultures should be obtained only when infection is suspected.
There is currently a controversy as to whether daily CXR should be routinely ordered on intubated patients. However, all experts agree that a CXR should be ordered for any change in the patient’s cardiopulmonary status.
III. Default Management.
When VAP is suspected:
Obtain lower respiratory tract (protected or not) for gram stain and routine culture.
If suspicion is high or the patient has a significant change in clinical condition, begin empiric antibiotics.
Use standardized antibiotics guided by local microbiological data.
Assess culture results and adjust or discontinue therapy based upon results.
If cultures are positive and the patient responds, consider de-escalation of antibiotics.
Some pathogens can be treated for 7-8 days, while others require longer duration of therapy.
A. Immediate management.
Since patients with VAP are already receiving supportive care in an ICU setting, the principle focus of immediate treatment is prompt antibiotics.
B. Physical examination tips to guide management.
Fever response and chest findings should be monitored daily.
C. Laboratory tests to monitor response to and adjustments in management.
WBC should be monitored daily, and culture results should be reviewed as they become available.
The CXR may not show rapid change even if treatment is effective.
D. Long-term management.
Antibiotic duration can be 7-8 days if the patient responds and the pathogen is notPseudomonas aeruginosa or Acinetobacter. Pseudomonas aeruginosarequires longer duration of therapy – up to two weeks in some cases.
E. Common pitfalls and side effects of management
Consider stopping anti-infective therapy if cultures are negative, and seek alternative explanations for changes in the patient’s condition.
In patients with early onset disease and low risk for resistant pathogens, options include*ceftriaxone, a quinolone, ampicillin/sulbactam, and carbepenem.
In patients with early or late onset disease and high risk for resistant pathogens, options include*an antipseudomonal cephalosporin, such as cefipime or ceftazidime, OR an anti-pseudomonal extended spectrum penicillin (piperacillin/tazobactam), OR an anti-pseudomonal carbepenem PLUS an anti-pseudomonal fluoroquinolone or an aminoglycoside PLUS Linezolid or vancomycin.
IV. Management with co-morbidities
Antibiotic dosing must take into account relative organ function and applicable pharmacological principles.
A. Renal insufficiency.
Alteration in dosage of antibiotics and monitoring drug levels of aminoglycosides and vancomycin are mandated.
B. Liver insufficiency.
Linezolid is metabolized through the hepatic route, but no dosage adjustment is necessary for mild to moderate liver disease (Child’s class A or B). There is limited data for patients with severe liver disease, so caution is advised in these patients. In addition, that liver toxicity has been reported with Linezolid must be considered in the context of any change in liver function studies during therapy.
C. Systolic and diastolic heart failure
No change in therapy.
D. Coronary artery disease or peripheral vascular disease
No change in therapy.
E. Diabetes or other endocrine issues
No change in therapy.
No change in therapy.
G. Immunosuppression (HIV, chronic steroids, etc).
No change in therapy.
H. Primary lung disease (COPD, asthma, ILD)
No change in therapy, but consider resistant pathogens even for early VAP of low severity.
I. Gastrointestinal or nutrition issues
No change in therapy.
J. Hematologic or coagulation issues
Linezolid can lead to thrombocytopenia. Caution is advised in the setting of pre-existing thrombocytopenia.
K. Dementia or psychiatric illness/treatment
No change in therapy.
V. Transitions of Care
A. Sign-out considerations while hospitalized.
Monitor ventilator status carefully, and anticipate the need to augment settings or the fraction of inspired oxygen early in the disease, as the patient’s ventilatory status may decline.
B. Anticipated length of stay.
VAP will increase a patient’s length of stay, but every effort to wean the patient from mechanical ventilation should be pursued.
C. When is the patient ready for discharge?
The patient who responds to antibiotic therapy will show a decline in fever, a decrease in secretions, and an improvement in gas exchange. This improvement will enable the patient to be liberated from mechanical ventilation and discharged from the ICU. Generally, patients who are stable for twenty-four hours after extubation can be transferred out of intensive care if there are no other critical-care concerns.
D. Arranging for clinic follow-up
Follow-up is based upon the conditions that led to the initial hospitalization.
1. When should clinic follow up be arranged and with whom?
Follow-up can be with the patient’s primary care physician or surgeon upon discharge.
2. What tests should be conducted prior to discharge to enable the best clinic first visit?
3. What tests should be ordered as an outpatient prior to, or on the day of, the clinic visit?
E. Placement considerations.
Some patients may require isolation or precautions, depending on culture results.
F. Prognosis and patient counseling.
VAP worsens the prognosis across the broad range of diagnoses that initially account for hospitalization and the need for mechanical ventilation.
VI. Patient Safety and Quality Measures
A. Core indicator standards and documentation.
The JCAHO quality measures to reduce VAP focus on prevention strategies.
Routine changes of the ventilator circuits are not recommended.
Elevate the head of the bed 30-45 degrees unless contra-indicated.
Perform regular oral hygiene with an anti-septic agent, not necessarily chlorhexadine, to reduce colonization of the posterior pharynx.
Perform subglottic suctioning, preferably with an endotracheal tube that has a suction port above the cuff.
Use oral endotracheal tubes inserted through the mouth, rather than nasotracheal intubation, whenever possible.
B. Appropriate prophylaxis and other measures to prevent readmission.
The etiology of VAP is related to aspiration of contaminated secretions along the endotracheal tube and down to the lower airways, where droplets of secretions can transfer bacteria to the lung and lead to pneumonia. Preventive strategies focus on breaking this mechanism of infection. Oral decontamination, suctioning through a port above the endotracheal air cuff, and elevation of the head of the bed are specifically targeted to reduce the incidence of aspirating droplets of secretions that harbor pathogenic bacteria.
What is the evidence?
Minei, JP. “Guidelines for the prevention, diagnosis, and treatment of VAP in the trauma patient”. J Trauma. vol. 60. 2006. pp. 1106-113.
Am J Respir Crit Care Med. vol. 171. 2005. pp. 388-416.
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- I. What every physician needs to know.
- II. Diagnostic Confirmation: Are you sure your patient has ventilator-associated pneumonia?
- A. History Part I: Pattern Recognition:
- B. History Part 2: Prevalence:
- C. History Part 3: Competing diagnoses that can ventilator-associated pneumonia.
- D. Physical examination findings.
- E. What diagnostic tests should be performed?
- 1. What laboratory studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?
- 2. What imaging studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?
- F. Over-utilized or “wasted” diagnostic tests associated with this diagnosis.
- III. Default Management.
- A. Immediate management.
- B. Physical examination tips to guide management.
- C. Laboratory tests to monitor response to and adjustments in management.
- D. Long-term management.
- E. Common pitfalls and side effects of management
- IV. Management with co-morbidities
- A. Renal insufficiency.
- B. Liver insufficiency.
- C. Systolic and diastolic heart failure
- D. Coronary artery disease or peripheral vascular disease
- E. Diabetes or other endocrine issues
- F. Malignancy
- G. Immunosuppression (HIV, chronic steroids, etc).
- H. Primary lung disease (COPD, asthma, ILD)
- I. Gastrointestinal or nutrition issues
- J. Hematologic or coagulation issues
- K. Dementia or psychiatric illness/treatment
- V. Transitions of Care
- A. Sign-out considerations while hospitalized.
- B. Anticipated length of stay.
- C. When is the patient ready for discharge?
- D. Arranging for clinic follow-up
- 1. When should clinic follow up be arranged and with whom?
- 2. What tests should be conducted prior to discharge to enable the best clinic first visit?
- 3. What tests should be ordered as an outpatient prior to, or on the day of, the clinic visit?
- E. Placement considerations.
- F. Prognosis and patient counseling.
- VI. Patient Safety and Quality Measures
- A. Core indicator standards and documentation.
- B. Appropriate prophylaxis and other measures to prevent readmission.
- What is the evidence?