Ventilator-associated pneumonia (VAP) is a nosocomial pneumonia that occurs after 48 hours of mechanical ventilation via an endotracheal tube (ETT) or tracheostomy tube.
Clinical pulmonary infection score (CPIS) utilizes clinical, radiographic, physiologic, and microbiologic data. CPIS assigns a numerical score to the presence (or absence) of (1,5):
A new or progressive pulmonary infiltrate on chest radiograph
Fever >38.3°C
Leukocytosis or leukopenia
Purulent tracheobronchial secretions
Evidence exists that a score >6 correlates with VAP.
However, because these findings are non-specific, they can lead to inappropriate antibiotic treatment of non-infectious processes and also correlate poorly with microbiologic cultures.
VAP is the most common nosocomial infection in the ICU, extends ICU length of stay, increases admission cost significantly, and carries a significant morbidity and mortality.
Epidemiology
Incidence
Estimated incidence ranges from 9–28% of all intubated patients (5).
Incidence is greatest early in the course of hospital stay; 50% of all cases occur within the first 4 days of mechanical ventilation (1).
Risk has been found to be 3% per day during the first 5 days of ventilation, 2% per day during Days 5–10, and 1% per day after Day 10 (1,5).
Most common pathogens: Pseudomonas aeruginosa, Escherichia coli, Klebsiella pneumonia, and Acinetobacter species; infections with methicillin-resistant Staphylococcus aureus are becoming more common in the US.
Morbidity
Prolongs ICU stay by an average of 4.3 days; prolongs cost by ~$40,000 (1)
Improved prognosis with early onset (within 96 hours of the start of ventilation); more likely to be infected with antibiotic-sensitive bacteria
Worsened prognosis with late onset (after 96 hours of mechanical ventilation); more likely to be infected with multidrug-resistant bacteria and have greater mortality
Mortality
Overall: 25–50%; influenced by the type of infecting organism (P. aeruginosa and Acinetobacter species), underlying comorbidities (bacteremia), severity of host response, and treatment with ineffective antibiotic therapy (2)
Etiology/Risk Factors
Endotracheal intubation; no difference between oral and nasal intubations (4,5)
Reintubation (particularly following unplanned or failed extubation); likely due to aspiration of infected upper airway secretions while reintubating
Critically ill, APACHE II score >16
Supine position
Nasogastric and enteral feeding tubes; promotes gastroesophageal disease
H2 blocker or antacid therapy
Acute or chronic lung disease, cigarette smoking
Age >60 years
Impaired mental status or excessive sedation
Witnessed aspiration
Paralytic agents
Continuous or over-sedation
Prolonged antibiotic use
Frequent ventilator circuit changes
Impaired swallowing reflex
Physiology/Pathophysiology
In health, the lungs are sterile. There are numerous defense mechanisms in place to protect against infection: Antimicrobial agents in saliva (non-immune), cough reflexes, mucociliary clearance, cell-mediated immunity (alveolar macrophages, neutrophils), and humoral immunity.
Intubated patients have accumulations of contaminated secretions in the subglottic space and above the ETT cuff (from the oropharynx), as well as impaired cough reflexes and mucociliary clearance, combined with injured tracheal epithelial cell.
The mechanism of micro-aspiration can result from increased hydrostatic pressure of subglottic secretions above the ETT cuff as well as aerosolization of bacteria within the respiratory tubing.
Critically ill patients can have dysfunctional or overwhelmed immune systems (impaired neutrophils, structural and functional alveolar changes). Thus, gross or micro-aspiration of oropharyngeal organisms into the distal bronchi can be followed by bacterial proliferation and pneumonia.
Less commonly, sinus and dental organisms or direct contamination from bacteremia can result in VAP.
Stress ulcer prophylaxis, a commonly implemented technique in critically ill patients, alkalinizes gastric fluid and may favor bacterial overgrowth with anaerobic gram-negative bacteria. Gastroesophageal reflux and aspiration around the ETT cuff may therefore contribute to VAP. This is controversial and studies have yielded mixed results.
Oral flora can also shift toward more aerobic gram-negative bacilli and Staphylococcus species in critical illness or secondary to antibiotic exposure
ETTs also serve as a reservoir for microbes by providing them a surface to adhere to by forming a BIOFILM.
Prevantative Measures
VAP can be somewhat difficult to diagnose and also carries a significant increase in morbidity and mortality; therefore, preventive measures are key. They consist of techniques and measures as well as technology and equipment.
Maintain the patient in a semi-upright position (30–45°), particularly when receiving enteral nutrition. There is some data to support the lateral position to eliminate gravitational forces (2,3).
Daily sedation interruption to screen for patient readiness for extubation (2).
Risk assessment for stress ulcer prophylaxis; should not be automatically instituted. If necessary, consider sucralfate, as there is some evidence to suggest a reduced incidence of VAP (2).
Decontamination of the oropharynx by oral antiseptics (chlorhexidine) may reduce incidence. Oral application of antibiotics has not shown success (2,3).
Digestive decontamination may be considered in the presence of multidrug-resistant pathogens (2,3).
Hand disinfection by the healthcare team (2,3).
Continuous aspiration of subglottic secretions (CASS) can decrease bacterial colonization and requires a specialized ETT (2,3).
Noninvasive ventilation avoids intubation and mechanical ventilation (2,3).
Silver-coated ETT provides a highly effective antimicrobial substance that can prevent BIOFILM formation and subsequent infection (2,3).
Ultrathin cuffs (high volume, low pressure cuff) can prevent formation of folds, provide better sealing, and reduce VAP (2,3).
Early tracheostomy (<7 days after translaryngeal intubation) in VAP prevention remains controversial (2,3).
The CDC recommends that ventilator circuits be changed no more than every 48 hours.
Diagnosis⬆⬇
History, symptoms, signs, physical examination
The non-specific nature of signs and symptoms of VAP makes diagnosis difficult.
Increased respiratory rate, FiO2 demand, hypoxia.
Temperature: >38.3°C
Diagnostic procedures
Chest radiograph: The presence of a new or progressive pulmonary infiltrate
White blood cell count: Leukocytosis
PaO2: Decreases
Microbial sputum smear/Gram stain
Cultures: Sputum, tracheal, or lower respiratory tract samples. Much controversy exists over whether sputum and tracheal aspirates or invasive lower respiratory tract samples improve diagnostic and therapeutic methods. Sputum and tracheal aspirates may yield colonizing organisms from the trachea and ETT and are associated with higher antibiotic use. However, invasive methods have risk, require special equipment, and increase cost but may not improve outcome or reduce mortality. Quantitative cultures may help differentiate colonization from infectious bacterial agents.
Triggering receptor expressed on myeloid cells (TREM-1) is a member of the immunoglobulin superfamily and is involved in the acute inflammatory response. Neutrophils express high levels of TREM-1 on exposure to infected tissues. Shown to have a sensitivity of 98% and specificity of 90%.
Differential Diagnosis
Aspiration pneumonitis
Atelectasis
Pulmonary embolism
ARDS
Drug reaction
Pulmonary hemorrhage
Lung contusion
Radiation pneumonitis
Infiltrative tumor
Treatment⬆⬇
Prompt and appropriate antibiotic treatment significantly improves survival in patients with VAP. Since culture results can be delayed for several days, the Gram stain and clinical suspicion (common organisms in the hospital) may need to guide initial therapy (4).
Empirical therapy for patients suspected of having multidrug-resistant pathogens should include coverage for gram-negative bacilli and Pseudomonas until sputum culture sensitivity data is available. Therapy can be narrowed once culture results arrive (4).
Evidence-based data supports limiting the total duration of antibiotics therapy to 7 days in responders.
Follow-Up⬆⬇
Some evidence to suggest that serial quantitative microbial cultures aid in assessing newer airway colonization.
References⬆⬇
EfratiS, DeutschI.Ventilator associated pneumonia: Current status and future recommendations. J Clin Monit Comput. 2010;24:161–168.
Guidelines for the management of adults with hospital-acquired, ventilator-associated, and healthcare-associated pneumonia: Official statement of ATS and IDSA 2004. Am J Respir Crit Care Med. 2005;171:388–416.
VAP is a nosocomial pneumonia that develops after more than 48 hours of mechanical ventilation.
Currently there are no consensus guidelines for the diagnosis of VAP. The CPIS score combines clinical, radiographical, laboratory, and microbiologic information to aid in diagnosis and treatment and is commonly used.
Preventive measures should be a cornerstone of therapy.