Pneumonia, Ventilator-Associated

Incidence of VAP is 1.2–8.5:1000 ventilator days; occurs in 9–27% of intubated mechanically ventilated pts

Risk greatest in the first 5 d of mechanical ventilation

Increased risk: Male sex; admission for trauma; underlying disease severity; surgery; previous antibiotic exposure

Intraop decrease in FRC can worsen the severity of hypoxemia.

Preop high levels of PEEP can lead to decreased preload and hypotension.

Atelectasis and derecruitment of alveoli

Hypoxemia

Mucus plugging of main or intermediate bronchi

VAP is defined as pneumonia occurring in mechanically ventilated pts 48–72 h after endotracheal intubation.

Implications of ETT placement:

• Suppression of cough reflex leading to microaspiration around ETT cuff.

• Pooling of secretions around cuff.

• Biofilm coating ETT, including gram-negative and fungal organisms.

• Impaired mucociliary clearance of secretions.

Microbiology:

• Early VAP (≤4 d on ventilator): Organisms usually sensitive to antibiotics.

• Late VAP (≥5 d on ventilator): Increased risk of organisms resistant to antibiotics.

Early VAP bacteria:

• Streptococcus pneumoniae

• Haemophilus influenzae

• MSSA

• Antibiotic-sensitive enteric gram-negative bacilli: Escherichia coli, Klebsiella pneumoniae, Enterobacter spp., Proteus spp., Serratia marcescens

Late VAP bacteria:

• MDR bacteria: MRSA, Acinetobacter, Pseudomonas aeruginosa, ESBL

• Oropharyngeal bacteria: Streptococcus viridans, Corynebacterium, coagulase-negative Staphylococcus , Neisseria spp.

• Polymicrobial infection

• Fungal infection

VAP pathogen incidence:

• P. aeruginosa (24.4%)

• S. aureus (20.4%; half MSSA and half MRSA)

• Enterobacteriaceae (14.1%): Klebsiella. E. coli , Proteus spp., Enterobacter spp., Serratia spp., Citrobacter spp.

• Streptococcus spp. (12.1%)

• Haemophilus spp. (9.8%)

• Acinetobacter spp. (7.9%)

• Neisseria spp. (2.6%)

• Stenotrophomonas maltophilia (1.7%)

• Others (4.7%): Corynebacterium, Moraxella, Enterococcus, fungi

MDR organisms’ potential mechanisms:

• Pseudomonas

  • Upregulation of efflux pumps (pump antibiotic out).

  • Lower expression of outer membrane porin channel (antibiotic cannot get in).

  • Beta-lactamases (break beta-lactam ring on beta-lactam antibiotics, rendering antibiotic inactive).

• S. aureus: Lower affinity for beta-lactam antibiotics by production of penicillin-binding protein.

• Enterobacteriaceae: Plasmid mediated production of beta-lactamases that destroy extended-spectrum beta-lactam drugs (ESBLs). ESBLs can also cause crossover resistance to aminoglycosides in addition to extended-spectrum beta-lactams.