SESSION TITLE: Sepsis & Septic Shock
SESSION TYPE: Original Investigation Slide
PRESENTED ON: Sunday, October 26, 2014 at 04:30 PM - 05:30 PM
PURPOSE: Sepsis caused by gram negative rods (GNR) is a major cause of mortality in critically ill patients. Studies have shown that humans exposed to GNR endotoxin have decreased inflammatory responses to subsequent exposures. We hypothesized that adult intensive care unit (ICU) patients admitted with GNR bacteremia who have prior GNR exposure would exhibit more favorable clinical outcomes than those who do not as measured by systemic inflammatory response syndrome (SIRS) criteria, Acute Physiology and Chronic Health Evaluation II (APACHE II) scores, and thirty day mortality rates.
METHODS: We reviewed the electronic medical records all subjects admitted to an academic ICU from January 2002 to December 2011 with GNR bacteremia. Eligible patients belonged to one of three groups: residents of an affiliated long-term care facility with positive GNR culture data within 14 days prior to admission (LTC-EXP, n=86), residents from the same facility with negative culture data (LTC-NON-E, n=47), and community-dwelling patients (COMM, n=96). To address temporal changes in disease patterns and therapy, analyses were adjusted for year of admission.
RESULTS: Mean ± SD age was 57.6 ± 15.6 yr and 55% were male with no significant group differences in these variables. Among LTC-EXP, 42% met SIRS criteria versus 91% in LTC-NON-E and 85% in COMM (p<0.0001 for LTC-EXP vs. either comparator). APACHE II score was 11.5±4.2 in LTC-EXP versus 23.5±6.4 in LTC-NON-E and 23.7±10.1 in COMM (p<0.0001 for LTC-EXP vs. either comparator). Thirty-day mortality was 20% for LTC-EXP compared to 43% for LTC-NON-E and 34% for COMM (p<0.005 for LTC-EXP vs. either comparator). All reported differences were robust to adjustment for comorbidities and prior antibiotic use.
CONCLUSIONS: Patients exposed to gram negative bacteria within 14 days of ICU admission for GNR bacteremia have blunted systemic inflammatory responses, lower APACHE II scores, and decreased mortality rates compared with exposure-naïve patients. These differences are not affected by temporal bias, comorbid conditions, or prior antibiotic use.
CLINICAL IMPLICATIONS: Further investigation is needed to determine the immunologic mechanisms of the diminished inflammatory response and decreased mortality rate associated with GNR exposure. Identification of such underlying processes may provide future therapeutic options for GNR bacteremia and sepsis.
DISCLOSURE: The following authors have nothing to disclose: Jessica Buchner, Andrea Levine, Avelino Verceles, Soren Snitker, Alan Cross, Anthony Harris, Marjan Bahador
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