Association between Source of Infection and Hospital Mortality in Patients Who Have Septic Shock

  • Aleksandra Leligdowicz
    Department of Internal Medicine and
  • Peter M. Dodek
    Division of Critical Care Medicine and
  • Monica Norena
    Center for Health Evaluation and Outcome Sciences, St. Paul's Hospital and University of British Columbia, Vancouver, British Columbia, Canada
  • Hubert Wong
    Center for Health Evaluation and Outcome Sciences, St. Paul's Hospital and University of British Columbia, Vancouver, British Columbia, Canada
  • Aseem Kumar
    Biomolecular Sciences Program, Department of Chemistry and Biochemistry, Laurentian University, Sudbury, Ontario, Canada; and
  • Anand Kumar
    Section of Critical Care Medicine, Health Sciences Centre, St. Boniface Hospital, University of Manitoba, Winnipeg, Manitoba, Canada the Co-operative Antimicrobial Therapy of Septic Shock Database Research Group

書誌事項

公開日
2014-05
権利情報
  • https://academic.oup.com/pages/standard-publication-reuse-rights
DOI
  • 10.1164/rccm.201310-1875oc
公開者
Oxford University Press (OUP)

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説明

<jats:title>Abstract</jats:title> <jats:sec> <jats:title>Rationale</jats:title> <jats:p>Mortality caused by septic shock may be determined by a systemic inflammatory response, independent of the inciting infection, but it may also be influenced by the anatomic source of infection.</jats:p> </jats:sec> <jats:sec> <jats:title>Objectives</jats:title> <jats:p>To determine the association between the anatomic source of infection and hospital mortality in critically ill patients who have septic shock.</jats:p> </jats:sec> <jats:sec> <jats:title>Methods</jats:title> <jats:p>This was a retrospective, multicenter cohort study of 7,974 patients who had septic shock in 29 academic and community intensive care units in Canada, the United States, and Saudi Arabia from January 1989 to May 2008.</jats:p> </jats:sec> <jats:sec> <jats:title>Measurements and Main Results</jats:title> <jats:p>Subjects were assigned 1 of 20 anatomic sources of infection based on clinical diagnosis and/or isolation of pathogens. The primary outcome was hospital mortality. Overall crude hospital mortality was 52% (21–85% across sources of infection). Variation in mortality remained after adjusting for year of admission, geographic source of admission, age, sex, comorbidities, community- versus hospital-acquired infection, and organism type. The source of infection with the highest standardized hospital mortality was ischemic bowel (75%); the lowest was obstructive uropathy–associated urinary tract infection (26%). Residual variation in adjusted hospital mortality was not explained by Acute Physiology and Chronic Health Evaluation II score, number of Day 1 organ failures, bacteremia, appropriateness of empiric antimicrobials, or adjunct therapies. In patients who received appropriate antimicrobials after onset of hypotension, source of infection was associated with death after adjustment for both predisposing and downstream factors.</jats:p> </jats:sec> <jats:sec> <jats:title>Conclusions</jats:title> <jats:p>Anatomic source of infection should be considered in future trial designs and analyses, and in development of prognostic scoring systems.</jats:p> </jats:sec>

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