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Related Experiment Videos

Multiple-organ failure. Generalized autodestructive inflammation?

R J Goris, T P te Boekhorst, J K Nuytinck

    Archives of Surgery (Chicago, Ill. : 1960)
    |October 1, 1985
    PubMed
    Summary
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    Bacterial sepsis is not the primary cause of multiple-organ failure (MOF). Severe trauma or intra-abdominal sepsis may trigger inflammatory responses leading to MOF, independent of bacterial infection.

    Area of Science:

    • Critical Care Medicine
    • Sepsis Pathophysiology
    • Trauma Management

    Background:

    • Multiple-organ failure (MOF) is a common complication in critically ill patients.
    • Bacterial sepsis is often considered a leading cause of MOF.
    • The specific role of bacterial sepsis versus other triggers in MOF requires further clarification.

    Purpose of the Study:

    • To retrospectively evaluate the association between bacterial sepsis and MOF in trauma and intra-abdominal sepsis patients.
    • To compare the incidence, severity, and mortality of MOF in patients with and without bacterial sepsis.
    • To explore alternative hypotheses for MOF development in severe trauma and intra-abdominal sepsis.

    Main Methods:

    • Retrospective analysis of 55 trauma patients and 37 intra-abdominal sepsis patients with MOF.

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  • Grading the severity of MOF and analyzing the day of onset, incidence, severity, sequence, and mortality of organ failures.
  • Assessing the presence of bacterial sepsis in both patient groups.

    • Main Results:

    • No significant differences were found in the sequence, severity, or mortality of organ failures between trauma and intra-abdominal sepsis groups.
    • Bacterial sepsis was identified in 65% of intra-abdominal sepsis patients compared to 33% of trauma patients.
    • These findings suggest bacterial sepsis may not be the essential cause of MOF.

    Conclusions:

    • Sepsis is likely not the essential cause of multiple-organ failure (MOF).
    • Severe tissue trauma or intra-abdominal sepsis may induce MOF through massive inflammatory mediator activation.
    • This inflammatory cascade can lead to endothelial damage, edema, and impaired mitochondrial oxygen availability, irrespective of bacterial infection.