Ventilator-associated pneumonia (VAP) is the second most common nosocomial infection (after CAUTI) and accounts for 15–20% of the total HAIs.

- It is the most common cause of death among HAIs, with a mortality rate of up to 40% and is the primary cause of death in ICUs

- T he VAP rate varies from 1.0 to 46.0 per 1000 mechanical ventilation (MV) days, depending up on the ICU facility and the hospital.

Microbiology

 VAP can be divided into early- and late-onset.

- Early-onset VAP: It occurs during the first 4 days of mechanical ventilation. It is caused by typical community organisms such as pneumococcus, H. influenzae, methicillin susceptible S. aureus (MSSA), etc.

- Late-onset VAP: It develops ≥5 days after mechanical ventilation and is commonly caused by typical multidrug resistant hospital pathogens—P. aeruginosa, Acinetobacter baumannii, E.coli, Klebsiella and methicillin resistant S. aureus (MRSA). It is associated with high attributable mortality. Here, the source of infection may be:

* Endogenous, i.e. patient’s own oropharyngeal microbial flora transmitted to lungs by aspiration

* Exogenous, e.g. hospital environmental sources like air, water, reusable equipment, nebulized medication, etc. contaminated with environmental organisms.

Pathogenesis and risk factors

The pathogenesis of VAP involves a complex interplay between various risk factors (Table 1).

- Colonization: Following hospitalization of critically-ill patients, the normal oropharyngeal flora (e.g. viridans streptococci, Haemophilus, anaerobes) rapidly shifts toward “hospital-associated” pathogens such as Pseudomonas, Acinetobacter species, etc.

- Endotracheal (ET) intubation is the most important risk factor. It disrupts normal ciliary clearance of bronchial secretions, inhibits the cough reflex, damages the respiratory epithelium, and helps oropharyngeal bacteria to gain access directly into the lower respiratory tract

- Biofilm: The organism begins to form biofilm both inside and outside the endotracheal tube within a day of placement, which acts as a reservoir of infection, preventing the entry of antimicrobials and the host immune system

- Subglottic secretions: Secretions pool on and above the ET tube cuff and intermittently seep (microaspiration) to the lower respiratory tract, particularly if the cuff is underinflated or gets shifted during patient movement (Fig. 1). This can be prevented by:

* Maintaining the cuff pressure at 20–30 cm of H2O

* Subglottic suctioning should be done regularly to remove the pooling of secretion above the cuff.

- Sedation: Sedation, coma or unconsciousness inhibits the natural ability to clear secretions and thereby increases the risk of aspiration

- Supine position facilitates microaspiration. Therefore, patients should be put on a semi-recumbent position (30–45˚)

- Nasogastric tubes: Ventilated patients are very often kept on nasogastric tubes, which disrupt the lower esophageal sphincter and increase the risk of aspiration of gastric contents

- Critical illness with comorbidities, poor nutrition and immobilization may increase patients’ susceptibility to infection

- Stress ulcer prophylaxis: Intubated patients are at high-risk for stress ulcers, which may lead to upper gastrointestinal hemorrhage. Therefore, stress ulcer prophylaxis is a common practice in ventilated patients. However, this itself is a risk factor for aspiration pneumonia. The only acceptable prophylaxis is by sucralfate, which is associated with lower risk of VAP.

Table1. risk factors for the development of Vap.

Fig1. Endotracheal (ET) tube with suction.

Diagnosis

 The diagnosis of VAP is based on a combination of clinical, radiological, and microbiological criteria.

Till date, there is no gold standard criteria available which can define VAP accurately. The most popular and widely used criteria is CPIS system.

Clinical pulmonary infection score (CPIS) system is a scoring system, based on six parameters (clinical, radiological and microbiological) with each parameter given a score scale ranging from 0 to 2 (Table 2).

- The maximum score that can be obtained is 12 and a score >6 is diagnostic of VAP

- CPIS score is prone to significant inter-observer variability, mainly in the interpretation of the tracheal secretions and the chest X-ray.

Table2. Modified Clinical pulmonary Infection Score (CPIS) used for ventilator-associated pneumonia.

Microbiological Criteria

The specimens for VAP include endotracheal aspirate (most common), bronchoalveolar lavage (BAL), protected specimen brush (PSB) or lung biopsy. Specimens should be processed immediately. Delay of no more than 2 hours is permissible.

- Gram staining: Gram stain should be performed from the mucopurulent part. The diagnosis of VAP is likely if Gram staining demonstrates—higher numbers of bacteria, intracellular bacteria or presence of fibrin strands. A negative Gram stain result suggests that VAP is unlikely

- Culture: The specimens are subjected to either quantitative or semi-quantitative culture

* Quantitative culture: Considered significant if the colony count exceeds ≥ 10⁵ CFU/mL for endotracheal aspirate, ≥10⁴ CFU/mL for BAL and ≥10³/mL for PSB

* Semi quantitative culture: Moderate to heavy growth is suggestive of colony count of ≥10⁵ CFU/mL.

Radiological Criteria

 Radiological diagnosis of VAP is highly subjective as many other clinical conditions may show similar findings. In general, the most accepted radiological criteria is chest X-ray or CT scan showing one of the following—infiltrate, consolidation or cavitation, in the absence of underlying pulmonary or cardiac disease.

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