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Infection Site Foretells Death in Septic Shock

By HospiMedica International staff writers
Posted on 03 Jun 2013
A new study suggests that the anatomical site where septic shock infections originate can predict mortality among patients.

Researchers at the University of British Columbia (Vancouver, Canada) conducted a retrospective, multicenter, cohort study of 7,974 patients admitted between January 1989 and May 2008 to 29 academic and community hospitals in Canada, the United States, and Saudi Arabia. More...
The researchers classified 20 anatomic sources of infection, and logistic regression was used to analyze the effect of infection source on hospital survival, adjusting for predisposing factors and potential mediators, including number of day one organ failures, bacteremia, appropriate antibiotics, and adjunct therapy.

The results showed that overall crude hospital mortality was 52.4%. After adjustment, eight anatomic sites were identified to be significantly associated with higher survival, and four with significantly lower survival. Survival rates were highest for disseminated infections (84.5%), spontaneous bacterial peritonitis (76%), toxic megacolon (68.3%), and other abdominal infections (66.7%). The lowest were for hydronephrosis (21.1%), enterocolitis and diverticulosis (28%), and pyelonephritis (34.5%). Adjusting for timing of initiation of antibiotics had little impact on these relationships. The study was presented at the annual conference of the American Thoracic Society, held during May 2013 in Philadelphia (PA, USA).

“Knowing that the source of infection can affect mortality in ICU patients who have septic shock may help guide treatment in these patients,” said study presenter Prof. Peter Dodek, MD, MHSc. “Further research should examine whether targeted treatment of the anatomic source of infection improves outcomes. In addition, these findings support stratification by anatomic source of infection of patients who are enrolled in clinical trials of sepsis treatments.”

Uncontrolled local infection leads to a systemic inflammatory response; therefore, the anatomical source of infection may influence the clinical outcome of septic shock. Understanding the mortality associated with the source of infection in septic shock may help studies of adjunctive agents that inhibit proinflammatory mediators in patients who are at a higher risk of mortality, as well as a shift from broad to narrower spectrum antimicrobial agents in patients who are at a lower risk of mortality.

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University of British Columbia



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