Abstract
The pathophysiologic course of sepsis involves the release of cyto- and chemokines in addition to the activation of endothelial and neutrophil cells, initiating a cascade of cell-surface interactions. Activation of the coagulation system has been characterized by widespread intravascular fibrin deposition and platelet aggregation (disseminated intravascular coagulation, DIC) with subsequent microvascular and tissue injury, ultimately leading to multiple organ failure (MOF) and death. The contributing role of platelets in the pathophysiology of sepsis and related organ dysfunction is not entirely clear, although the degree and duration of thrombocytopenia, as well as the net change in the platelet count, are important determinants for survival [1, 2]. Of note, the involvement of platelets in sepsis-associated coagulopathy was already studied by many groups more than 25 years ago, focusing on the interaction of platelets with endotoxin, and the role of thrombin generation and DIC on platelet function [3, 4]. However, regarding the various pathogenic mechanisms that have recently been implicated in the activation of coagulation in sepsis, a reassessment of the role of platelets is needed.
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Keywords
- Severe Sepsis
- Fresh Freeze Plasma
- Thrombotic Thrombocytopenic Purpura
- Granulocyte Elastase
- Congenital Thrombotic Thrombocytopenic Purpura
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References
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Claus, R.A., Reinhart, K., Brunkhorst, F.M. (2006). Altered Functionality of von Willebrand Factor in Sepsis and Thrombocytopenia — Potential Role of the vWF Cleaving Protease ADAMTS-13. In: Vincent, JL. (eds) Intensive Care Medicine. Springer, New York, NY. https://doi.org/10.1007/0-387-35096-9_21
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