The pathogenesis of human sepsis involves a complex interplay between the infecting organism and the host response, with the consequent multiple organ dysfunction. Sepsis is the systemic inflammatory response to severe microbial infection which initiates important alterations in immune, metabolic, and hemodynamic function that in their most dramatic forms are recognized as sepsis and septic shock. The sepsis syndrome occurs commonly in response to lipopolysaccharide membrane (LPS) from gram-negative bacteria. LPS is a major constituent of gram-negative bacteria cell walls and is essential for membrane integrity. Injured cells releases preformed mediators and synthesize proinflammatory substances, including eicosanoids and the cytokines and tumor necrosis factor [TNF]. These mediators are responsible for the initiation of a nonspecific inflammatory response. The treatment of sepsis is multifaceted and typically requires multidisciplinary competencies. Successful treatment requires great attention to detail in the management of all aspects of the disease, including antibiotic therapy, choice of vasopressors, ventilator management, tight glucose control, and deep venous thrombosis and stress ulcer prophylaxis. Effective anti-ET (Endotoxin) or antimediator treatment such as anticytokine or other anti-proinflammatory mediator strategies need to be directed at a wide spectrum of host inflammatory mediators. Activated protein C decreases inflammation by inhibiting platelet activation, neutrophil recruitment and mast cell degeneration. Recombinant human activated protein C (drotrecogin alfa [activated]) is the first anti-inflammatory agent that has proved effective in the treatment of sepsis.
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