AI Article Synopsis

  • This study aimed to explore hypercoagulability characteristics in patients experiencing sepsis and septic shock, particularly during the initial phase of their infection response.
  • Researchers analyzed 24 patients with chemotherapy-related febrile neutropenia by using the thrombin generation test at fever onset and 48 hours later, discovering a decrease in thrombin generation during early sepsis.
  • The findings indicate that despite the decreased thrombin generation, patients with sepsis do not exhibit a clinically significant hypercoagulable state, which could explain the lack of clinical benefits from systemic anticoagulant treatments in sepsis cases.

Article Abstract

Purpose: The purpose was to investigate the presence of hypercoagulability in the very early phase of the host response to an infection in the clinical course of sepsis and septic shock.

Material And Methods: Twenty-four patients with chemotherapy-associated febrile neutropenia were evaluated at baseline, at the time of fever onset, and 48 hours thereafter using the thrombin generation test, a more physiological and global assay of hemostasis.

Results: The rate of thrombin generation was decreased and no signals of systemic hypercoagulability could be observed during the first 48 hours of sepsis. Moreover, patients that evolved to septic shock presented a more significant impairment in thrombin generation than those with noncomplicated sepsis.

Conclusions: Patients with sepsis and febrile neutropenia present an impairment in thrombin generation from very early stages of their disease course. These results suggest that the procoagulant in vitro alterations described during sepsis do not necessarily translate into a clinically relevant systemic hypercoagulable state. These findings could help explain why treatment with systemic anticoagulants did not translate to clinical benefits in human sepsis and highlight the need for a better understanding of the hemostatic alterations in sepsis before new treatments targeting coagulation activation are developed.

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Source
http://dx.doi.org/10.1016/j.jcrc.2013.08.015DOI Listing

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