Abstract
Intensive care unit (ICU) patients suffering from severe illness (e.g., after major surgery, sepsis or trauma) are known to show a wide spectrum of coagulation abnormalities (Fig. 1) [1–3]. Thrombin generation and activation of fibrinolysis are physiologic responses to tissue damage during surgery and trauma [4]. This may result in an imbalance between the procoagulant and inhibitory processes of the coagulation system [1, 5]. In addition to the conventional components of the hemostatic system, other processes are involved in the development of hemostatic disorders in the ICU patient, e.g., activation of the inflammatory cascade may produce either activation or inhibition of the hemostatic process. Coagulation abnormalities in the critically ill are additionally triggered and/or modified by circulatory, respiratory or metabolic disorders [1]. Finally, extensive neuroendocrine response may enhance hemostatic alterations, including decreased fibrinolysis and increased platelet activity [6].
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Boldt, J. (2001). Changes of the Hemostatic Network in the Critically III. In: Vincent, JL. (eds) Yearbook of Intensive Care and Emergency Medicine 2001. Yearbook of Intensive Care and Emergency Medicine 2001, vol 2001. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-59467-0_12
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DOI: https://doi.org/10.1007/978-3-642-59467-0_12
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