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脓毒症诱导的凝血病:病理生理学、生物标志物及现行指南的最新进展

Sepsis-Induced Coagulopathy: An Update on Pathophysiology, Biomarkers, and Current Guidelines.

作者信息

Tsantes Andreas G, Parastatidou Stavroula, Tsantes Emmanuel A, Bonova Elli, Tsante Konstantina A, Mantzios Petros G, Vaiopoulos Aristeidis G, Tsalas Stavros, Konstantinidi Aikaterini, Houhoula Dimitra, Iacovidou Nicoletta, Piovani Daniele, Nikolopoulos Georgios K, Sokou Rozeta

机构信息

Laboratory of Haematology and Blood Bank Unit, "Attiko" Hospital, School of Medicine, National and Kapodistrian University of Athens, 12462 Athens, Greece.

Microbiology Department, "Saint Savvas" Oncology Hospital, 11522 Athens, Greece.

出版信息

Life (Basel). 2023 Jan 28;13(2):350. doi: 10.3390/life13020350.

DOI:10.3390/life13020350
PMID:36836706
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9961497/
Abstract

Significant cross talk occurs between inflammation and coagulation. Thus, coagulopathy is common in sepsis, potentially aggravating the prognosis. Initially, septic patients tend to exhibit a prothrombotic state through extrinsic pathway activation, cytokine-induced coagulation amplification, anticoagulant pathways suppression, and fibrinolysis impairment. In late sepsis stages, with the establishment of disseminated intravascular coagulation (DIC), hypocoagulability ensues. Traditional laboratory findings of sepsis, including thrombocytopenia, increased prothrombin time (PT) and fibrin degradation products (FDPs), and decreased fibrinogen, only present late in the course of sepsis. A recently introduced definition of sepsis-induced coagulopathy (SIC) aims to identify patients at an earlier stage when changes to coagulation status are still reversible. Nonconventional assays, such as the measurement of anticoagulant proteins and nuclear material levels, and viscoelastic studies, have shown promising sensitivity and specificity in detecting patients at risk for DIC, allowing for timely therapeutic interventions. This review outlines current insights into the pathophysiological mechanisms and diagnostic options of SIC.

摘要

炎症与凝血之间存在显著的相互作用。因此,凝血病在脓毒症中很常见,可能会加重预后。最初,脓毒症患者往往通过外源性途径激活、细胞因子诱导的凝血放大、抗凝途径抑制和纤维蛋白溶解受损而呈现血栓前状态。在脓毒症晚期,随着弥散性血管内凝血(DIC)的发生,会出现低凝状态。脓毒症的传统实验室检查结果,包括血小板减少、凝血酶原时间(PT)和纤维蛋白降解产物(FDPs)增加以及纤维蛋白原减少,仅在脓毒症病程后期出现。最近引入的脓毒症诱导的凝血病(SIC)定义旨在在凝血状态变化仍可逆转的早期阶段识别患者。非常规检测方法,如抗凝蛋白和核物质水平的测量以及粘弹性研究,在检测有DIC风险的患者方面显示出有前景的敏感性和特异性,从而能够及时进行治疗干预。这篇综述概述了目前对SIC病理生理机制和诊断方法的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b974/9961497/b179d3f173dc/life-13-00350-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b974/9961497/847b5c1586ca/life-13-00350-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b974/9961497/3e2f9ea212de/life-13-00350-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b974/9961497/b179d3f173dc/life-13-00350-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b974/9961497/847b5c1586ca/life-13-00350-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b974/9961497/3e2f9ea212de/life-13-00350-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b974/9961497/b179d3f173dc/life-13-00350-g003.jpg

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