Вентилятор-асоційована пневмонія

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

Pneumonia in critically ill, mechanically ventilated patients 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.

• 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 semiquantitative 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.

The mortality in 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 bacteria worsens prognosis.

• 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. The current, 2016 recommendations (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.

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 (BPAP) prevents the breach in airway defense that occurs with endotracheal intubation and eliminates the need for intubation in some patients, and has been associated with a reduced incidence of ventilator associated pneumonia.

Continuous aspiration of subglottic secretions using a specially designed endotracheal tube attached to a suction device reduces the risk of microaspiration and the incidence of VAP; however, overall clinical outcomes are not altered. Silver coated endotracheal tubes reduce biofilm formation and the incidence of VAP, however, overall clinical outcomes are not altered.

Selective decontamination of the oropharynx (using topical gentamicin, colistin, chlorhexidine, vancomycin cream, or a combination) or of the entire gastrointestinal 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.