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
Summary
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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