hemostasia

Hemostasis, known as hemostasia in some languages, is the physiological process that stops bleeding at injured sites while preserving overall blood flow. It involves vascular, cellular, and plasma components and is tightly regulated to balance bleeding and clotting.

The process consists of three overlapping phases. First, vascular spasm reduces blood flow by constricting the injured vessel. Second, platelets adhere to exposed subendothelial matrix via von Willebrand factor, become activated, and recruit additional platelets to form a loose platelet plug (primary hemostasis). Third, a coagulation cascade activates thrombin, which converts fibrinogen to fibrin, stabilizing the plug into a stable clot (secondary hemostasis).

Stabilization and repair continue with clot retraction and endothelial healing, followed by fibrinolysis to remove the clot once the vessel is repaired. Regulation relies on procoagulant and anticoagulant forces, including natural inhibitors such as antithrombin and the protein C–protein S system, and on the fibrinolytic system that degrades fibrin via plasmin.

Disorders of hemostasis can cause excessive bleeding, as seen in platelet dysfunction or coagulation-factor deficiencies (for example, hemophilia or von Willebrand disease), or excessive clotting, as in thrombophilia or disseminated intravascular coagulation. Diagnosis typically involves platelet counts and coagulation tests such as PT/INR, aPTT, fibrinogen levels, and sometimes viscoelastic testing. Treatment targets the underlying cause and may include antifibrinolytics, vitamin K, plasma or factor concentrates, platelets, or anticoagulants when thrombosis risk is present.