| Abstract | dc.description.abstract | Sepsis with secondary multisystem organ dysfunction syndrome is the leading cause of death
in the pediatric intensive care unit. Increased reactive oxygen species may influence circulating and
endothelial cells, contributing to inflammatory tissue injury and explaining the tissue hypoxia paradigm
based on microvascular dysfunction. An impaired mitochondrial cellular oxygen utilization, rather than
inadequate oxygen delivery, was claimed to play a more important role in the development of
multisystem organ dysfunction syndrome. Anyway, it seems plausible that reactive oxygen species can
mediate the pathophysiologic processes occurring in sepsis. However, the consensus guidelines for the
management of patients with these conditions do not include the enhancement of antioxidant potential.
Therefore, further investigation is needed to support interventions aimed to attenuate the severity of the
systemic compromise by abrogating the mechanism of oxidative damage. Antioxidant supplementation
currently in use lacks a mechanistic support. Specific pharmacologic targets, such as mitochondria or
Nicotinamide Adenine Dinucleotide Phospate-Oxidase (NADPH) oxidase system, need to be explored.
Furthermore, the early recognition of oxidative damage in these seriously ill patients and the usefulness
of oxidative stress biomarkers to define a cut point for more successful therapeutic antioxidant
interventions to be instituted would offer a new strategy to improve the outcome of critically ill children. | es_CL |
