Abstract
Coagulopathy commonly occurs in sepsis as a critical host response to infection that can progress to disseminated intravascular coagulation (DIC) with an increased mortality. Recent studies have further defined factors responsible for the thromboinflammatory response and intravascular thrombosis, including neutrophil extracellular traps, extracellular vesicles, damage-associated molecular patterns, and endothelial glycocalyx shedding. Diagnosing DIC facilitates sepsis management, and is associated with improved outcomes. Although the International Society on Thrombosis and Haemostasis (ISTH) has proposed criteria for diagnosing overt DIC, these criteria are not suitable for early detection. Accordingly, the ISTH DIC Scientific Standardization Committee has proposed a new category termed “sepsis-induced coagulopathy (SIC)” to facilitate earlier diagnosis of DIC and potentially more rapid interventions in these critically ill patients. Therapy of SIC includes both treatment of the underlying infection and correcting the coagulopathy, with most therapeutic approaches focusing on anticoagulant therapy. Recently, a phase III trial of recombinant thrombomodulin was performed in coagulopathic patients. Although the 28-day mortality was improved by 2.6% (absolute difference), it did not reach statistical significance. However, in patients who met entry criteria for SIC at baseline, the mortality difference was approximately 5% without increased risk of bleeding. In this review, we discuss current advances in managing SIC and DIC.
Highlights
Activation of coagulation in sepsis is recognized as a host immune response against infection [1], over-activation of coagulation may be detrimental to the host [2]
In 2001, the International Society on Thrombosis and Haemostasis (ISTH) defined Disseminated intravascular coagulation (DIC) as “an acquired syndrome characterized by intravascular activation of coagulation with loss of localization arising from different causes that can originate from and cause damage to the microvasculature, which if sufficiently severe, can produce organ dysfunction” [4]
The concept of “sepsis-induced coagulopathy (SIC)” has been advocated by the ISTH DIC Standardization Subcommittee (SSC) [58]. According to this definition of SIC, evidence of organ dysfunction is assessed according to the SOFA scoring that includes respiratory, cardiovascular, hepatic, and renal dysfunction, as well as coagulopathy based on thrombocytopenia and a prolonged prothrombin time ratio (Table 1)
Summary
Activation of coagulation in sepsis is recognized as a host immune response against infection [1], over-activation of coagulation may be detrimental to the host [2]. In 2001, the International Society on Thrombosis and Haemostasis (ISTH) defined DIC as “an acquired syndrome characterized by intravascular activation of coagulation with loss of localization arising from different causes that can originate from and cause damage to the microvasculature, which if sufficiently severe, can produce organ dysfunction” [4]. This important definition better characterizes both the bleeding and the organ dysfunction that occurs. Antithro m b in heparin, heparinoids fib rin m onom er fib rin polym er FDP plasminogen activator inhibitor 1 plasmin plasminogen activator plasminogen
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