Abstract

RationaleExperimental studies suggest that intra-abdominal infection (IAI) induces biological alterations that may affect the risk of lung infection.ObjectivesTo investigate the potential effect of IAI at ICU admission on the subsequent occurrence of ventilator-associated pneumonia (VAP).MethodsWe used data entered into the French prospective multicenter Outcomerea database in 1997–2011. Consecutive patients who had severe sepsis and/or septic shock at ICU admission and required mechanical ventilation for more than 3 days were included. Patients with acute pancreatitis were not included.Measurements and Main ResultsOf 2623 database patients meeting the inclusion criteria, 290 (11.1%) had IAI and 2333 (88.9%) had other infections. The IAI group had fewer patients with VAP (56 [19.3%] vs. 806 [34.5%], P<0.01) and longer time to VAP (5.0 vs.10.5 days; P<0.01). After adjustment on independent risk factors for VAP and previous antimicrobial use, IAI was associated with a decreased risk of VAP (hazard ratio, 0.62; 95% confidence interval, 0.46–0.83; P<0.0017). The pathogens responsible for VAP were not different between the groups with and without IAI (Pseudomonas aeruginosa, 345 [42.8%] and 24 [42.8%]; Enterobacteriaceae, 264 [32.8%] and 19 [34.0%]; and Staphylococcus aureus, 215 [26.7%] and 17 [30.4%], respectively). Crude ICU mortality was not different between the groups with and without IAI (81 [27.9%] and 747 [32.0%], P = 0.16).ConclusionsIn our observational study of mechanically ventilated ICU patients with severe sepsis and/or septic shock, VAP occurred less often and later in the group with IAIs compared to the group with infections at other sites.

Highlights

  • Despite the availability of numerous therapeutic interventions, ventilator-acquired pneumonia (VAP) remains a major public health issue [1]

  • In our observational study of mechanically ventilated intensive care unit (ICU) patients with severe sepsis and/or septic shock, VAP occurred less often and later in the group with intra-abdominal infection (IAI) compared to the group with infections at other sites

  • We modeled the risk of day-30 mortality after VAP using another Cox model in the subgroup with VAP

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Summary

Introduction

Despite the availability of numerous therapeutic interventions, ventilator-acquired pneumonia (VAP) remains a major public health issue [1]. VAP is the leading nosocomial infection in intensive care unit (ICU) patients and is responsible for high morbidity and mortality rates [2]. In ICU patients, acute alterations in innate and adaptative immunity with immunoparalysis characterized by impaired antigen presentation and endotoxin tolerance may play a pivotal role in the occurrence of nosocomial infections [3, 4]. Endotoxin tolerance is due to a substantial decrease in the cytokine response to lipopolysaccharide (LPS) after the first LPS stimulation, as shown in both animal models and humans [5, 6]. The role for endotoxin tolerance in the pathophysiology of nosocomial infections remains unclear. Recent studies suggest that endotoxin tolerance may involve re-programming of immune cells [9] responsible for changes in their behavior without impairments in phagocytic [10], or bactericidal capabilities [10]

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