Biomarkers of sepsis-induced coagulopathy: diagnostic insights and potential therapeutic implications

Fig. 1. Biomarkers for coagulation disorder in sepsis. Coagulation activation is initiated by tissue factor (TF) and phosphatidylserine expression on monocytes. Other cells, such as platelets, endothelial cells, and granulocytes, also contribute by expressing procoagulant factors. Prothrombin time (PT) and activated partial thromboplastin time (aPTT) tests are commonly used to assess the extrinsic and intrinsic pathways of coagulation. Fibrin, the final coagulation product, is dissolved by plasmin into fibrin/fibrinogen degradation products and D-dimer. Thrombin, a key mediator of intravascular inflammation, is neutralized by antithrombin and converted into an antithrombotic agent by activated protein C. The thrombin generated can be measured as thrombin-antithrombin complex (TAT). Intravascular inflammation promotes interactions between cells, leading to the release of adhesion molecules such as intracellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) into the plasma. Additionally, increased levels of plasminogen activator inhibitor-1 (PAI-1), angiopoietin-2 (Ang-2), and von Willebrand factor are known to reflect endothelial damage in sepsis

Fig. 2. Two step approach to diagnose disseminated intravascular coagulation in sepsis. Coagulation activation is a nearly universal event in sepsis. To screen for coagulation disorders, platelet count and prothrombin time-international normalized ratio (PT-INR) should be measured in all septic patients. If the patient meets the sepsis-induced coagulopathy (SIC) criteria, anticoagulant therapy may be considered. Additionally, fibrinogen and D-dimer levels should be assessed to determine if overt disseminated intravascular coagulation (DIC) is present