Published in:
01-04-2006 | Editorial
Go with the flow—recruit the microcirculation!
Author:
Can Ince
Published in:
Intensive Care Medicine
|
Issue 4/2006
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Excerpt
The origin of the metabolic defect seen in sepsis has long been a source of debate. Although systemic hemodynamic parameters correlate well with metabolic distress in other forms of shock, in resuscitated septic shock, systemic hemodynamic and oxygen derived variables can be in acceptable ranges while clear signs of metabolic distress continue to persist [
1]. Early explanations were that there was an increased oxygen need by the tissue cells which was not being met by systemic oxygen delivery. Attempts at providing supranormal levels of oxygen delivery, however, proved unsuccessful in resolving this defect in oxygen extraction or in improving survival [
2]. Two explanations now presented themselves: either the origin of this defect in sepsis was in the mitochondria of the tissue cells unable to utilize oxygen to produce high-energy phosphates, or there were distributive (micro)vascular abnormalities leading to shunting of microcirculatory units masked from the systemic hemodynamic variables. To what extent promotion of microcirculatory perfusion is associated with the metabolic distress in sepsis has never been addressed in a clinical study. In this issue of
Intensive Care Medicine, Creteur and co-workers [
3] have done so in a study of septic shock patients. Their findings have highlighted the importance of the microcirculation in consolidating the metabolic disorder seen in sepsis. …