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Ventilator-Associated Pneumonia

By

Sanjay Sethi

, MD, University at Buffalo SUNY

Last full review/revision Mar 2019| Content last modified Mar 2019
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Topic Resources

Ventilator-associated pneumonia (VAP) develops at least 48 hours after endotracheal intubation. The most common pathogens are gram-negative bacilli and Staphylococcus aureus; antibiotic-resistant organisms are an important concern. In ventilated patients, pneumonia usually manifests as fever, increase in white blood cell count, worsening oxygenation, and increased tracheal secretions that may be purulent. Diagnosis is suspected on the basis of clinical presentation and chest x-ray and is sometimes confirmed by a positive blood culture for the same pathogen found in respiratory secretions or bronchoscopic sampling of the lower respiratory tract with quantitative Gram stain and cultures. Treatment is with antibiotics. Overall prognosis is poor, due in part to comorbidities.

(See also Overview of Pneumonia.)

Ventilator-associated pneumonia is pneumonia that develops at least 48 hours after endotracheal intubation. This is distinct from hospital-acquired pneumonia, which is pneumonia that develops at least 48 hours after hospital admission in inpatients who are not receiving mechanical ventilation.

Etiology

The most common cause of ventilator-associated pneumonia is microaspiration of bacteria that colonize the oropharynx and upper airways in seriously ill patients.

Risk factors

Endotracheal  intubation is the major risk factor for ventilator-associated pneumonia. Endotracheal intubation breaches airway defenses, impairs cough and mucociliary clearance, and facilitates microaspiration of bacteria-laden secretions that pool above the inflated endotracheal tube cuff. In addition, bacteria form a biofilm on and within the endotracheal tube that protects them from antibiotics and host defenses. The highest risk of VAP occurs during the first 10 days after intubation. Ventilator-associated pneumonia occurs in 9 to 27% of mechanically ventilated patients.

Major risk factors for postoperative pneumonia are

  • Age > 70

  • Abdominal or thoracic surgery

  • Functional debilitation

Pathogens

Pathogens and antibiotic resistance patterns vary significantly among institutions and can vary within institutions over short periods (eg, month to month). Local antibiograms at the institutional level that are updated on a regular basis are essential in determining appropriate empiric antibiotic therapy. In general, the most important pathogens are Pseudomonas aeruginosa, methicillin-sensitive Staphylococcus aureus, and methicillin-resistant S. aureus (MRSA).

Other important pathogens include enteric gram-negative bacteria (mainly Enterobacter species, Klebsiella pneumoniae, Escherichia coli, Serratia marcescens, Proteus species, and Acinetobacter species).

Methicillin-sensitive S. aureus, Streptococcus pneumoniae, and Haemophilus influenzae are most commonly implicated when pneumonia develops within 4 to 7 days of hospitalization, whereas P. aeruginosa, MRSA, and enteric gram-negative organisms become more common with increasing duration of intubation or hospitalization.

Prior IV antibiotic treatment (within the previous 90 days) greatly increases the likelihood of antibiotic-resistant organisms, particularly MRSA and Pseudomonas infection in VAP (1). Infection with a resistant organism markedly increases mortality and morbidity. Other risk factors for antibiotic-resistant organisms specific to VAP include

  • Septic shock at time of VAP

  • Acute respiratory distress syndrome (ARDS) preceding VAP

  • Hospitalization for ≥ 5 days prior to the occurrence of VAP

  • Acute renal replacement therapy prior to VAP onset

High-dose corticosteroids increase the risk of Legionella and Pseudomonas infections. Chronic suppurative lung diseases such as cystic fibrosis and bronchiectasis increase the risk of gram-negative pathogens, including antibiotic-resistant strains.

Etiology reference

  • 1. Kalil AC, Metersky ML, Klompas M, et al: Management of adults with hospital-acquired and ventilator-associated pneumonia: 2016 clinical practice guidelines by the Infectious Diseases Society of America and the American Thoracic Society. Clinical Infectious Diseases 63(5):e61–111, 2016.

Symptoms and Signs

Pneumonia in critically ill, mechanically ventilated patients more typically causes fever and increased respiratory rate or heart rate or changes in respiratory parameters, such as an increase in purulent secretions or worsening hypoxemia.

Diagnosis

  • Chest x-ray and clinical criteria (limited accuracy)

  • Sometimes bronchoscopy or blood cultures

Diagnosis is imperfect. In practice, ventilator-associated pneumonia is often suspected on the basis of the appearance of a new infiltrate on a chest x-ray that is taken for evaluation of new symptoms or signs (eg, fever, increased secretions, worsening hypoxemia) or of leukocytosis. However, no symptom, sign, or x-ray finding is sensitive or specific for the diagnosis, because all can be caused by atelectasis, pulmonary embolism, or pulmonary edema and may be part of the clinical findings in acute respiratory distress syndrome.

Gram stain and semiquantitive cultures of endotracheal aspirates, though not definitive for identifying infection, are recommended for guiding treatment in VAP. Bronchoscopic sampling of lower airway secretions for quantitative culture yields more reliable specimens that can differentiate colonization from infection. Information gained from bronchoscopic sampling reduces antibiotic use and assists in switching from broader to narrower antibiotic coverage. However, it has not been shown to improve outcomes.

Measurement of inflammatory mediators in bronchoalveolar lavage fluid or serum has not been shown to be reliable in deciding on initiation of antibiotics. The only finding that reliably identifies both pneumonia and the responsible organism is a pleural fluid culture (obtained via thoracentesis in a patient with pleural effusion) that is positive for a respiratory pathogen.

Blood cultures are also relatively specific if a respiratory pathogen is identified but are insensitive.

Prognosis

The mortality associated with ventilator-associated pneumonia is high despite the availability of effective antibiotics. However, not all mortality is attributable to the pneumonia itself; many of the deaths are related to the patient's underlying illness. Adequacy of initial antimicrobial therapy clearly improves prognosis. Infection with antibiotic-resistant gram-negative or gram-positive bacteria worsens prognosis.

Treatment

  • Empirically chosen antibiotics active against resistant organisms

If ventilator-associated pneumonia is suspected, treatment is with antibiotics that are chosen empirically based on

  • Local sensitivity patterns

  • Patient risk factors for antibiotic-resistant pathogens

In the 2007 guidelines, the Infectious Diseases Society of America and the American Thoracic Society used very broad criteria for defining the population at risk of infection with antibiotic-resistant pathogens, which resulted in the majority of patients with VAP requiring broad-spectrum antibiotic therapy for MRSA and resistant Pseudomonas. New recommendations in 2016 (1) emphasize use of a narrower spectrum of empiric antibiotics when possible. Empiric therapy for VAP without risk factors for antibiotic-resistant organisms and high mortality (mechanical ventilation for pneumonia or septic shock), in an institution where MRSA incidence is < 10% to 20% (of S. aureus isolates) and P. aeruginosa resistance is < 10% for commonly used empiric antipseudomonal antibiotics, could include any one of the following:

  • Piperacillin/tazobactam

  • Cefepime

  • Levofloxacin

  • Imipenem

  • Meropenem

Doses depend on renal function (see table Usual Doses of Commonly Prescribed Antibiotics).

In treatment settings where MRSA rates are > 10% to 20%, vancomycin or linezolid should be added. In patients who are at high risk for mortality or who have risk factors for antibiotic-resistant organisms, or in the absence of reliable local antibiograms, recommendations include triple therapy using 2 drugs with activity against Pseudomonas and 1 drug with activity against MRSA:

  • An antipseudomonal cephalosporin (cefepime or ceftazidime) or an antipseudomonal carbapenem (imipenem, meropenem) or a beta-lactam/beta-lactamase inhibitor (piperacillin/tazobactam)

  • An antipseudomonal fluoroquinolone (ciprofloxacin or levofloxacin) or an aminoglycoside (amikacin, gentamicin, tobramycin)

  • Linezolid or vancomycin

While indiscriminate use of antibiotics is a major contributor to development of antimicrobial resistance, adequacy of initial empiric antibiotics is a major determinant of a favorable outcome. Therefore, treatment must begin with initial use of broad-spectrum drugs, which are then changed to the narrowest regimen possible based on clinical response and the results of cultures and antibiotic susceptibility testing.

Treatment reference

  • 1. Kalil AC, Metersky ML, Klompas M, et al: Management of adults with hospital-acquired and ventilator-associated pneumonia: 2016 clinical practice guidelines by the Infectious Diseases Society of America and the American Thoracic Society. Clinical Infectious Diseases 63(5):e61–111, 2016.

Prevention

There are a number of measures that can help prevent ventilator-associated pneumonia. Semiupright or upright positioning reduces risk of aspiration and pneumonia compared with recumbent positioning and is the simplest and most effective preventive method. Noninvasive ventilation using continuous positive airway pressure (CPAP) or bilevel positive airway pressure (BiPAP) prevents the breach in airway defense that occurs with endotracheal intubation and eliminates the need for intubation in some patients.

Continuous aspiration of subglottic secretions using a specially designed endotracheal tube attached to a suction device seems to reduce the risk of microaspiration and the incidence of VAP.

Selective decontamination of the oropharynx (using topical gentamicin, colistin, chlorhexidine, vancomycin cream, or a combination) or of the entire GI tract (using polymyxin, an aminoglycoside or quinolone, and either nystatin or amphotericin B) is controversial because of concerns about resistant strains and because decontamination, although it decreases incidence of VAP, has not been shown to decrease mortality.

Surveillance cultures and routinely changing ventilator circuits or endotracheal tubes have not been shown to decrease VAP.

Key Points

  • Ventilator-associated pneumonia (VAP) is pneumonia that develops at least 48 hours after endotracheal intubation.

  • Likely pathogens differ from those causing community-acquired pneumonia and often require initial empiric antibiotic therapy that is active against antibiotic-resistant organisms.

  • Diagnosis is difficult, with culture of a potential pathogen from pleural fluid or blood being the most specific finding.

  • Reassess patients 2 to 3 days after initiation of treatment, and change antibiotics based on available culture and clinical data.

Drugs Mentioned In This Article

Drug Name Select Trade
ZOSYN
CILOXAN, CIPRO
IQUIX, LEVAQUIN, QUIXIN
FORTAZ, TAZICEF
TOBI, TOBREX
GENOPTIC
VANCOCIN
MERREM
ZYVOX
NYSTOP
MAXIPIME
No US brand name
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