European Journal of Cardiovascular Medicine

Mechanical ventilation is a cornerstone of life-support in modern intensive care units (ICUs), providing vital respiratory assistance for patients with acute respiratory failure, profound sedation, or neurological impairment. However, this life-saving intervention carries significant risks, chief among them being Ventilator-Associated Pneumonia (VAP). VAP is defined as a pneumonia that arises more than 48 hours after endotracheal intubation and was not incubating at the time of intubation [1]. It represents the most common and fatal nosocomial infection among critically ill patients receiving invasive mechanical ventilation [2].

The global burden of VAP is substantial. Epidemiological studies indicate that it occurs in 10% to 30% of mechanically ventilated patients, with an incidence density ranging from 5 to 20 cases per 1000 ventilator days [3]. This incidence is even higher in developing countries and specific high-risk populations. The consequences are dire; VAP is independently associated with a marked increase in morbidity, attributing to a crude mortality rate that ranges from 20% to 50%, and even higher when caused by multidrug-resistant (MDR) pathogens [4]. For survivors, VAP leads to a prolonged

duration of mechanical ventilation, an extended ICU and hospital stay—often by an average of 7 to 9 days—and a significant escalation in healthcare costs [5].

The pathogenesis of VAP is multifactorial, primarily involving the colonization of the aerodigestive tract and the subsequent aspiration of contaminated secretions into the lower airways. The endotracheal tube itself plays a pivotal role, acting as a conduit for bacteria by compromising the body's natural cough reflex and mucociliary clearance. Biofilm formation on the inner and outer surfaces of the tube creates a protected reservoir of microorganisms that can be dislodged into the lungs during suctioning or ventilator flow cycles [6]. Host factors, such as immunosuppression, comorbidities (e.g., COPD, diabetes), and severity of critical illness, further increase susceptibility [7].

VAP is typically categorized as either early-onset (occurring within the first 4 days of ventilation) or late-onset (occurring on or after day 5). This distinction has important etiological and therapeutic implications. Early-onset VAP is often caused by antibiotic-sensitive community-acquired organisms like Streptococcus pneumoniae and Haemophilus influenzae. In contrast, late-onset VAP is frequently associated with MDR nosocomial pathogens, such as Pseudomonas aeruginosa, Acinetobacter baumannii, and Methicillin-resistant Staphylococcus aureus (MRSA), making treatment considerably more challenging [3, 8].

Diagnosing VAP remains a complex challenge in clinical practice. There is no single gold-standard test, and diagnosis often relies on a combination of clinical, radiological, and microbiological criteria, such as those established by the Centers for Disease Control and Prevention (CDC) [9]. The clinical pulmonary infection score (CPIS) is another tool used to standardize diagnosis, but its accuracy can be variable. This diagnostic ambiguity can lead to both over-diagnosis and unnecessary antibiotic use, or under-diagnosis and delayed treatment, each with significant consequences.

In response to the high burden of VAP, preventive "care bundles" have been developed and widely promoted. These bundles package a set of evidence-based interventions—such as head-of-bed elevation, daily sedation vacations and spontaneous breathing trials, peptic ulcer prophylaxis, thromboprophylaxis, and daily oral care with chlorhexidine—that, when implemented together, have been shown to reduce VAP rates more effectively than individual measures [10]. However, the consistent application and adherence to these bundles vary widely across institutions.

Despite these advances in understanding and prevention, VAP continues to be a major problem in ICUs worldwide, with its epidemiology and antibiogram constantly evolving. Local data on incidence, causative pathogens, and specific risk factors are crucial for developing effective institutional protocols for prevention and empirical antibiotic therapy. This study was, therefore, undertaken to determine the contemporary incidence and outcomes of VAP in our ICU, to identify the predominant microbial agents and their resistance patterns, and to elucidate the key modifiable risk factors contributing to its development. The findings aim to inform and strengthen local quality improvement initiatives aimed at reducing the burden of this formidable complication.

Study Design and Setting This was a combined retrospective and prospective observational study conducted in the Intensive Care Unit of MVJ Medical College and Research Hospital over a period of 24 months. The study was approved by the Institutional Review Board. Study Population A total of 100 patients who received mechanical ventilation for more than 48 hours were included. • Inclusion Criteria: Patients aged >15 years, of either sex, on mechanical ventilation for >48 hours. • Exclusion Criteria: Patients with pre-existing pneumonia at the time of intubation, those with acute respiratory distress syndrome (ARDS), or those who died or were discharged within 48 hours of initiation of ventilation. Data Collection Data were collected using a pre-designed proforma. The collected data included: • Patient demographics and comorbidities. • ICU admission details (APACHE II, SOFA scores). • Mechanical ventilation parameters (mode, duration, re-intubation, tracheostomy). • Criteria for VAP diagnosis as per CDC guidelines (fever, leukocytosis, purulent secretions, radiological findings, microbiological culture). • Risk factors (aspiration, oral care, PPI use, antibiotic use, patient positioning). • Patient outcomes (ICU length of stay, duration of ventilation, mortality). VAP Diagnosis VAP was diagnosed based on the CDC criteria, requiring a new or progressive radiographic infiltrate plus at least two of the following: fever (>38°C), leukocytosis/leukopenia, or purulent tracheal secretions, with microbiological confirmation from endotracheal aspirate or bronchoalveolar lavage (BAL) [1]. Statistical Analysis Data were analyzed using SPSS version 26.0. Categorical variables were expressed as numbers and percentages and compared using the Chi-square test or Fisher's exact test. Continuous variables were expressed as mean ± standard deviation or median (interquartile range) and compared using the student’s t-test or Mann-Whitney U test. A p-value of <0.05 was considered statistically significant.

A total of 100 patients who received mechanical ventilation for more than 48 hours were enrolled in the study. Among these, 22 patients developed VAP, yielding an overall incidence of 22% and an incidence density of 14.5 cases per 1000 ventilator days. The baseline characteristics of the study population are detailed in Table 1. The mean age of the patients was 58.4 ± 12.7 years, with a male predominance (62%). The VAP and non-VAP groups were comparable at baseline, with no statistically significant differences in age, gender distribution, or severity of illness as measured by the APACHE II score (p=0.09). The prevalence of comorbidities such as Diabetes Mellitus, Hypertension, Chronic Kidney Disease, and COPD/Asthma was also similar between the two groups, as were the primary reasons for ICU admission.

Table 1: Baseline Characteristics of the Study Population

Table 2: Microbiological Profile and Classification of VAP Cases (n=22)

The classification and microbiological etiology of the 22 VAP cases are summarized in Table 2. Late-onset VAP, occurring on or after 5 days of mechanical ventilation, was more common, accounting for 14 cases (63.6%). Microbiological analysis of endotracheal aspirate or bronchoalveolar lavage (BAL) samples revealed that Gram-negative bacilli were the predominant pathogens. Acinetobacter baumannii was the most frequently isolated organism (36.4%), followed by Pseudomonas aeruginosa (27.3%) and Klebsiella pneumoniae (18.2%). A concerning finding was the high rate of multidrug resistance (MDR), observed in 72.7% (16 out of 22) of the isolates.

Table 3: Comparison of Risk Factors between VAP and Non-VAP Groups

*Prior to VAP diagnosis for the VAP group, or during the first week of ventilation for the non-VAP group.

A comparative analysis of potential risk factors between the VAP and non-VAP groups is presented in Table 3. The median duration of mechanical ventilation was significantly longer in the VAP group (12 days) compared to the non-VAP group (5 days), with a p-value of <0.001. Furthermore, failure to maintain the head of the bed elevated to more than 30 degrees (supine positioning) was significantly associated with VAP development (54.5% vs. 29.5%, p=0.03). Pharmacologically, the use of Proton Pump Inhibitors (PPIs) or H2 Blockers was also identified as a significant risk factor, with 81.8% of VAP patients receiving them compared to 59.0% in the non-VAP group (p=0.04). Other factors, such as re-intubation, tracheostomy, and the use of broad-spectrum antibiotics prior to diagnosis, were more common in the VAP group but did not reach statistical significance.

Table 4: Clinical Outcomes Comparison

The impact of VAP on patient outcomes was substantial, as detailed in Table 4. Patients who developed VAP had a significantly prolonged median ICU length of stay (18 days vs. 8 days, p<0.001) and total hospital length of stay (28 days vs. 16 days, p<0.001). The mortality rate in the VAP group was 36.4%, which was significantly higher than the 12.8% mortality rate observed in the non-VAP group (p=0.01). Additionally, escalation of therapy—such as the need for higher-tier antibiotics or extracorporeal membrane oxygenation (ECMO)—was required significantly more often in VAP patients (31.8% vs. 5.1%, p<0.001).

This observational study provides a contemporary analysis of the burden and impact of Ventilator-Associated Pneumonia in a tertiary care ICU. Our principal findings reveal a VAP incidence of 22%, a predominance of multidrug-resistant Gram-negative pathogens, identifiable modifiable risk factors, and a significant associated increase in mortality, length of stay, and healthcare resource utilization.

The observed incidence of 22% aligns with the widely cited global range of 10-30% for VAP [3]. However, it falls on the higher end of this spectrum, reflecting the challenging environment of the ICU and potentially indicating gaps in the consistent application of preventive measures. This incidence is notably higher than the 12.5% reported in a large multi-center study by Papazian et al. (2020), which reviewed data from well-resourced ICUs with established VAP prevention protocols [3]. The disparity underscores the variability in VAP rates across different healthcare settings and highlights the critical need for local epidemiological data to drive quality improvement initiatives, rather than relying solely on international benchmarks.

The microbiological profile uncovered in our study is consistent with the modern paradigm of late-onset VAP. The predominance of Acinetobacter baumannii (36.4%) and Pseudomonas aeruginosa (27.3%), with a startling 72.7% rate of multidrug resistance, paints a picture of a difficult-to-treat infection. This pattern is alarmingly similar to findings from a study by Chen et al. (2018), which also reported a high prevalence of MDR Acinetobacter and Pseudomonas in their VAP cases, complicating treatment regimens and leading to poorer outcomes [4]. The high MDR burden in our ICU signals an urgent need for robust antimicrobial stewardship programs and regular updates to institutional empirical antibiotic guidelines based on local antibiogram data.

Our analysis successfully identified several key modifiable risk factors. The most potent was the duration of mechanical ventilation, which is a well-established and almost universal predictor of VAP risk. More notably, we found that supine positioning and the use of acid-suppressive therapy (PPIs/H2 Blockers) were significantly associated with VAP. The link between supine positioning and VAP provides strong local validation for a cornerstone of the VAP prevention bundle. This finding reinforces the results of a randomized controlled trial by Reignier et al. (2013), which demonstrated that strategies minimizing aspiration risk, including head-of-bed elevation, are crucial in VAP prevention [5]. The association with PPI use adds to the growing body of evidence questioning the routine use of stress ulcer prophylaxis in all critically ill patients. By reducing gastric acidity, these drugs may facilitate gastric colonization and subsequent pulmonary aspiration of pathogens, thereby increasing VAP risk.

The clinical consequences of VAP in our cohort were severe and unequivocal. Patients with VAP experienced a more than two-fold increase in median ICU stay and a significantly higher mortality rate (36.4% vs. 12.8%). These figures starkly illustrate the human and economic toll of this complication. Our findings on mortality corroborate those of an earlier seminal study which concluded that nosocomial pneumonia is an independent contributor to mortality in ICU patients, separate from the severity of the underlying illness [6]. The prolonged ventilator dependence and frequent need for therapy escalation we observed further strain ICU resources and underscore that preventing a single case of VAP can save lives and reduce significant costs.

In conclusion, this study confirms that VAP remains a formidable and costly problem in our ICU, driven by multidrug-resistant organisms and influenced by specific, modifiable clinical practices. The findings compellingly argue for a renewed and rigorous focus on a multi-faceted prevention strategy. We recommend a strict, audited adherence to the VAP care bundle, with particular emphasis on maintaining head-of-bed elevation, conducting daily spontaneous breathing trials to reduce ventilator days, and implementing judicious protocols for the use of sedatives and acid-suppressive drugs. Furthermore, the local microbiological data provided here should be used to inform and regularly update empirical antibiotic policies. Future efforts should focus on the implementation science of embedding these evidence-based practices into daily routine, ensuring that our preventive measures are as resilient as the pathogens we aim to thwartarman.

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