Sepsis and Nutritional Blood Flow

Abstract

Despite the great progress that has been made in intensive care medicine, the incidence of sepsis and its sequelae has not diminished and still carries high mortality [1, 2]. Although the pathogenesis is not completely understood, sepsis is generally known to be caused by the activation of inflammatory cells and the release of endogenous humoral mediators in response to bacterial products, in particular endotoxins [3]. Evidence is slowly accumulating that excessively activated endogenous inflammatory cells and their compounds may be responsible for structural damage and functional deterioration of remote vital organ systems [4]. However, besides the activation of neutrophils and macrophages and the actions of cytokines, arachidonic acid metabolites, complement products, proteolytic enzymes and toxic oxygen radicals, impaired nutritional blood flow has been advocated as a key determinant for the development of organ dysfunction and subsequent multiple organ failure in septic shock [5, 6].