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Related Experiment Videos

Translocation. Incidental phenomenon or true pathology?

A M Munster1, M Smith-Meek, C Dickerson

  • 1Department of Surgery, Johns Hopkins University, Baltimore, Maryland.

Annals of Surgery
|September 1, 1993
PubMed
Summary

Reducing early postburn endotoxemia with polymyxin B did not impact the cytokine cascade, sepsis development, or mortality rates in burn patients. The inflammatory response is primarily driven by the injury itself.

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Area of Science:

  • Burn injury research
  • Immunology
  • Critical care medicine

Background:

  • Translocational endotoxemia is a known complication following burns in both animal models and human patients.
  • Endotoxin plays a critical role in initiating the cytokine cascade, which subsequently leads to the clinical symptoms of sepsis.
  • The potential impact of reducing postburn endotoxemia on cytokine induction remained uninvestigated.

Purpose of the Study:

  • To investigate whether mitigating early postburn endotoxemia affects the cytokine cascade.
  • To determine the influence of endotoxemia reduction on clinical sepsis manifestations.
  • To assess the impact on overall mortality rates in burn patients.

Main Methods:

  • A prospective, randomized study involving 76 burn patients.

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  • Patients received intravenous polymyxin B for one week postburn, aiming to neutralize circulating endotoxemia, or served as control subjects.

    • Main Results:

    • A statistically significant decrease in plasma endotoxin concentration was observed in the polymyxin B group.
    • No significant reduction was found in sepsis scores or interleukin-6 (IL-6) levels.
    • There were no discernible differences in mortality rates between the treatment and control groups.

    Conclusions:

    • Early postburn translocational endotoxemia is treatable with anti-endotoxin agents like polymyxin B.
    • However, this intervention does not alter the cytokine cascade or reduce mortality rates.
    • The systemic inflammatory response syndrome (SIRS) in burn patients is primarily induced by the injury itself and is not significantly affected by reducing plasma endotoxin levels.