Overview
sepsis is defined as a systemic inflammatory
response initiated by a source of infection. The incidence,
hospitalization rates, and mortality of sepsis
remains one of the leading causes of morbidity and
mortality worldwide.2-5 In sepsis, stimulation of the
innate immune system, activation of white blood cells,
and response of endothelial cells can lead to the
release of a number of mediators or cytokines. This
activation causes a variety of physiological changes
including vasodilation, enhanced expression of adhesion molecules, increased capillary permeability,
increased clot formation, and decreased fibrinolysis.
Although the immune system response is
protective in nature, aimed at combating infection
in sepsis, overactivity of mediators has been cited
as a causal factor contributing to endothelial cell
damage, microcapillary permeability changes, capillary
leak, and profound vasodilation and hypotension.
6,7 These responses play a role in the progression
of severe sepsis and influence the development of
multiple organ system dysfunction. Importantly,
early recognition and treatment of
sepsis is crucial for clinicians to
improve outcomes and decrease sepsis-
related mortality.8