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Minerva Medica 2021 December;112(6):701-12

DOI: 10.23736/S0026-4806.21.07469-3


language: English

Therapeutic strategies in patients with coagulopathy and disseminated intravascular coagulation: awareness of the phase-dependent characteristics

Toshiaki IBA 1 , Theodore E. WARKENTIN 2, 3, Jean M. CONNORS 4, Jerrold H. LEVY 5

1 Department of Emergency and Disaster Medicine, Juntendo University Graduate School of Medicine, Tokyo, Japan; 2 Department of Pathology and Molecular Medicine, McMaster University, Hamilton, ON, Canada; 3 Department of Medicine, McMaster University, Hamilton, ON, Canada; 4 Division of Hematology, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, USA; 5 Department of Anesthesiology, Critical Care and Surgery, Duke University School of Medicine, Durham, NC, USA

INTRODUCTION: Disseminated intravascular coagulation (DIC) has long been understood as a condition where both thrombotic and hemostatic abnormalities coexist. DIC is a difficult complication for clinicians to manage as it is due to multiple underlying complications of pathophysiologic abnormalities in diverse disease states. Ongoing research continues to define the meaning of DIC, evaluate therapeutic options, and how it presents with the complex paradigm of systemic activation of coagulation. In this review we introduce the current topics regarding this difficult situation.
EVIDENCE ACQUISITION: Online search of published medical literature through MEDLINE and Web of Science using the term “disseminated intravascular coagulation,” “coagulopathy,” “coagulation disorder,” “hemostasis,” “fibrinolysis,” “thrombus” and “anticoagulants.”
EVIDENCE SYNTHESIS: Articles were chosen for inclusion based on their relevance to disseminated intravascular coagulation, coagulopathy, hemostasis and thrombosis in sepsis, COVID-19, trauma, and obstetrics. Reference lists were reviewed to identify additional relevant articles.
CONCLUSIONS: DIC is recognized as a pathologically triggered and dysregulated systemic activation of coagulation in response to various noxious stimuli. DIC’s phenotype and clinical manifestations can vary from prothrombotic to hemorrhagic, depending on the underlying diseases. However, the fundamental mechanisms of systemic and vascular endothelial dysfunction can be explained as different phases of the acute response, with an initial prothrombotic phase that can commonly change to hemostatic insufficiency. Thrombin is the key initiator of the pathophysiologic process along with endothelial injury and initially fibrinolysis activation followed by fibrinolysis suppression. There is no established approach for managing DIC beyond initially treating the underlying disease and replacement therapy for the management of coagulopathy. Targeting anticoagulation therapy with antithrombin concentrates and recombinant thrombomodulin for the prevention of microthrombus formation, and antifibrinolytic therapy using tranexamic acid for the coagulopathy after massive bleeding, continue to be studied as therapeutic options.

KEY WORDS: Disseminated intravascular coagulation; Blood coagulation disorders; Fibrinolysis; Thrombin; Endothelial cells

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