[Sepsis-induced coagulopathy]

Sepsis-induced coagulopathy (SIC) represents a frequent and prognostically highly relevant complication of sepsis, characterized by a dysregulated interaction between inflammation, endothelial activation and coagulation. Pathophysiologically, the excessive host immune response to pathogen-associated molecular patterns (PAMP) and damage-associated molecular patterns (DAMP), activation of the complement cascade, formation of neutrophil extracellular traps (NET) and disruption of the endothelial glycocalyx collectively promote a prothrombotic and antifibrinolytic microenvironment, resulting in microvascular thrombosis, organ dysfunction and increased mortality. Approximately 20-25% of critically ill patients with sepsis fulfil the diagnostic criteria for SIC. Current diagnostic approaches rely on scoring systems such as the International Society on Thrombosis and Hemostasis (ISTH)-SIC, ISTH overt-disseminated intravascular coagulation (DIC) and Japanese Society on Thrombosis and Hemostasis (JSTH)-DIC scores; however, their clinical utility remains limited as they predominantly collate hemorrhagic parameters even though sepsis is typically characterized by a thrombotically dominated phenotype. Viscoelastic point-of-care assays enable dynamic bedside assessment of coagulation and fibrinolysis, including the frequently occurring hypofibrinolysis or fibrinolytic shutdown, which is associated with an unfavorable outcome; however, for this specific purpose, these methods have not yet been sufficiently validated or established as a diagnostic standard. Data and recommendations on specific therapeutic options are limited. A consistent pharmacological thromboprophylaxis remains the cornerstone in patients with sepsis, with low-molecular weight heparins demonstrating advantages over unfractionated heparin regarding venous thromboembolic complications. Coagulation modulating treatment, such as antithrombin, recombinant thrombomodulin or activated protein C, have thus far failed to demonstrate consistent survival benefits in large randomized clinical trials. Experimental approaches targeting NET formation, complement activation or fibrinolytic modulation appear mechanistically promising but require further clinical validation. Overall, SIC necessitates an individualized, pathophysiology-driven diagnostic and therapeutic approach integrating inflammatory, endothelial, thrombotic and fibrinolytic alterations.