Clinical meaning
Ventilator-associated pneumonia (VAP) develops >= 48 hours after endotracheal intubation, with an incidence of 5-15% of mechanically ventilated patients. Pathogenesis involves aspiration of colonized oropharyngeal or gastric secretions around the ETT cuff into the lower airways. The ETT bypasses upper airway defenses (glottis, cough reflex) and creates a conduit for bacterial migration via biofilm formation on the inner tube surface. Early-onset VAP (< 5 days) is typically caused by community organisms (S. pneumoniae, H. influenzae, MSSA), while late-onset VAP (>= 5 days) involves MDR organisms: MRSA, Pseudomonas aeruginosa, Acinetobacter, Klebsiella (ESBL-producing), Stenotrophomonas. Risk factors include reintubation, supine position, sedation depth, gastric acid suppression, and transport out of ICU. Prevention bundles have reduced VAP incidence by 40-70%.
Diagnosis & workup
Diagnostics & workup: - Clinical suspicion: new or worsening infiltrate on CXR + 2 of: fever > 38°C, leukocytosis > 12,000 or leukopenia < 4,000, purulent tracheal secretions - Clinical Pulmonary Infection Score (CPIS) >= 6 suggests VAP (temperature, WBC, tracheal secretions, oxygenation, CXR, culture) - Quantitative endotracheal aspirate (ETA): > 10⁶ CFU/mL supports VAP diagnosis - BAL or mini-BAL: quantitative culture > 10⁴ CFU/mL; more specific than ETA - Protected specimen brush (PSB): > 10³ CFU/mL - Blood cultures: positive in 8-20% of VAP cases (if positive, associated with higher mortality) - Procalcitonin: > 0.5 mcg/L supports bacterial infection; serial levels guide antibiotic duration - CXR: new or progressive infiltrate (limited specificity in critically ill — may be atelectasis, edema, ARDS)