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Thoracic duct in patients with multiple organ failure: no major route of bacterial translocation

L C Lemaire1, J B van Lanschot, C P Stoutenbeek

  • 1Department of Surgery, Academic Medical Center, Amsterdam, The Netherlands.

Annals of Surgery
|January 29, 1999
PubMed
Abstract

Insights

Bacterial translocation into the thoracic duct occurs in multiple organ failure (MOF), but it is not the primary route. Endotoxin translocation was observed, but in small quantities, suggesting other pathways are more significant in MOF development.

Area of Science:

  • Gastroenterology
  • Critical Care Medicine
  • Immunology

Background:

  • Bacterial and endotoxin translocation are hypothesized causes of multiple organ failure (MOF).
  • Lymphatic translocation via the thoracic duct is proposed as a major route, yet rarely demonstrated.
  • Previous research primarily focused on the hematogenic translocation pathway.

Purpose of the Study:

  • To investigate bacterial and endotoxin translocation into the thoracic duct in patients with MOF.
  • To assess the role of the thoracic duct as a route for translocation in MOF.
  • To measure endotoxin and cytokine levels in thoracic duct lymph and blood.

Main Methods:

  • Thoracic duct drainage for 5 days in MOF patients (n=8) and controls (n=transthoracic esophageal resection).
  • Measurement of endotoxin, proinflammatory cytokines, and anti-inflammatory cytokines in lymph and blood.
  • Comparison of translocation markers between MOF patients and controls.

Main Results:

  • Endotoxin levels in lymph and blood were similar between MOF patients and controls.
  • The quantity of endotoxin translocated via the thoracic duct was minimal.
  • MOF patients exhibited low proinflammatory cytokine and high anti-inflammatory cytokine antagonist levels.

Conclusions:

  • Evidence suggests endotoxin translocation into the thoracic duct occurs in MOF.
  • The thoracic duct is unlikely to be a major route for bacterial translocation in MOF.
  • Findings indicate a complex interplay of inflammatory and anti-inflammatory responses in MOF.

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