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Mechanisms and management of the coagulopathy of trauma and sepsis: trauma-induced coagulopathy, sepsis-induced coagulopathy, and disseminated intravascular coagulation. | LitMetric

Mechanisms and management of the coagulopathy of trauma and sepsis: trauma-induced coagulopathy, sepsis-induced coagulopathy, and disseminated intravascular coagulation.

J Thromb Haemost

Department of Anesthesiology, Critical Care, and Surgery, Duke University School of Medicine, Durham, North Carolina, USA. Electronic address: https://twitter.com/JerroldLevy.

Published: December 2023

AI Article Synopsis

  • Disseminated intravascular coagulation (DIC) often arises from different causes, with sepsis being a common trigger, while trauma-induced coagulopathy (TIC) affects 25% of seriously injured patients upon hospital arrival.
  • TIC begins with impaired hemostasis from extreme blood loss and tissue damage and can evolve into a prothrombotic state, driven by factors like inflammation and endothelial injury, which can also increase mortality rates in sepsis.
  • Although TIC and sepsis-induced coagulopathy (SIC) are distinct in their initial presentations, both share common pathophysiological features and require tailored management strategies, emphasizing the need to address the underlying causes and utilize supportive therapies such as hemostatic

Article Abstract

Disseminated intravascular coagulation can occur due to different causes but commonly following sepsis. Trauma-induced coagulopathy (TIC) occurs on hospital arrival in approximately 25% of seriously injured patients who initially presents with impaired hemostasis and a bleeding phenotype that can later progress to a prothrombotic phase. Following traumatic injury, ineffective hemostasis is driven by massive blood loss, tissue damage, and hyperfibrinolysis. This initial impaired hemostasis continues until surgical or other management strategies not only to stop the causes of hemorrhage but also progresses to a prothrombotic and hypofibrinolytic state, also termed fibrinolytic shutdown. Prothrombotic progression is also promoted by inflammatory mediator release, endothelial injury, and platelet dysregulation, which is commonly seen in sepsis with increased mortality. Unlike TIC, the early phase of sepsis is frequently complicated by multiorgan dysfunction described as sepsis-induced coagulopathy (SIC) that lacks a hemorrhagic phase. The phenotypes of SIC and TIC are different, especially in their initial presentations; however, patients who survive TIC may also develop subsequent infections and potentially sepsis and SIC. Although the pathophysiology of SIC and TIC are different, endothelial injury, dysregulated fibrinolysis, and coagulation abnormalities are common. Management includes treatment of the underlying cause, tissue injury vs infection is critical, and supportive therapies, such as hemostatic resuscitation and circulatory support are essential, and adjunct therapies are recommended in guidelines. Based on clinical studies and certain guidelines, additional therapies include tranexamic acid in the limited timing of initial traumatic injury and anticoagulants, such as antithrombin and recombinant thrombomodulin in disseminated intravascular coagulation.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10873124PMC
http://dx.doi.org/10.1016/j.jtha.2023.05.028DOI Listing

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