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Author Notes:

Address correspondence to: Craig M Coopersmith, 101 Woodruff Circle, Suite WMB 5105, Atlanta, GA 30322, Phone: (404) 727-4273, Fax: (404) 727-3660, cmcoop3@emory.edu

We thank the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) and their Office of Science Policy, Analysis and Communications for their support of this Workshop.

Copyright Disclosure Forms: Dr. Coopersmith’s institution received funding from the National Institutes of Health (NIH) and Society of Critical Care Medicine.

He received grant support from the NIH.

He disclosed that he was the president of Society of Critical Care Medicine in 2015.

A stipend was paid to Emory University for his time in this role for part of 2014 (as president-elect) and in 2015 (as president).

Drs. Coopersmith and Lyons received support for article research from the NIH.

Disclaimer: This information or content and conclusions are those of the authors and should not be construed as the official position or policy of, nor should any endorsements be inferred by, the National Institutes of Health, the US Department of Health and Human Services, or the US government.

Subjects:

Research Funding:

This work was supported by funding from the National Institutes of Health (GM072808, GM095442, GM104323, GM109779, GM113228, GM117895)

Keywords:

  • Science & Technology
  • Life Sciences & Biomedicine
  • Critical Care Medicine
  • Pediatrics
  • General & Internal Medicine
  • intestinal barrier
  • microbiome
  • multiple organ dysfunction syndrome
  • pediatrics
  • ORGAN DYSFUNCTION
  • SEPSIS
  • MORTALITY
  • INJURY
  • SHOCK
  • METAANALYSIS
  • PERITONITIS
  • INHIBITION
  • ACTIVATION
  • SURVIVAL

Pathophysiology of the Gut and the Microbiome in the Host Response

Tools:

Journal Title:

Pediatric Critical Care Medicine

Volume:

Volume 18, Number 3 Suppl 1

Publisher:

, Pages S46-S49

Type of Work:

Article | Post-print: After Peer Review

Abstract:

Objective: To describe and summarize the data supporting the gut as the motor driving critical illness and multiple organ dysfunction syndrome presented at the Eunice Kennedy Shriver National Institute of Child Health and Human Development MODS Workshop (March 26-27, 2015). Data Sources: Summary of workshop keynote presentation. Study Selection: Not applicable. Data Extraction: Presented by an expert in the field, the data assessing the role of gastrointestinal dysfunction driving critical illness were described with a focus on identifying knowledge gaps and research priorities. Data Synthesis: Summary of presentation and discussion supported and supplemented by relevant literature. Conclusions: The understanding of gut dysfunction in critical illness has evolved greatly over time, and the gut is now often considered as the "motor" of critical illness. The association of the gut with critical illness is supported by both animal models and clinical studies. Initially, the association between gut dysfunction and critical illness focused primarily on bacterial translocation into the bloodstream. However, that work has evolved to include other gut-derived products causing distant injury via other routes (e.g., lymphatics). Additionally, alterations in the gut epithelium may be associated with critical illness and influence outcomes. Gut epithelial apoptosis, intestinal hyperpermeability, and perturbations in the intestinal mucus layer have all been associated with critical illness. Finally, there is growing evidence that the intestinal microbiome plays a crucial role in mediating pathology in critical illness. Further research is needed to better understand the role of each of these mechanisms and their contribution to multiple organ dysfunction syndrome in children.

Copyright information:

© 2017 by the Society of Critical Care Medicine and the World Federation of Pediatric Intensive and Critical Care Societies.

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