hemostaasia

Hemostasis, sometimes referred to as hemostaasia, is the physiological process that stops bleeding at sites of vascular injury while preserving normal blood flow elsewhere. It involves interactions among blood vessels, platelets, and coagulation factors that rapidly respond to vessel damage to form a stable hemostatic plug.

During primary hemostasis, damaged endothelium exposes subendothelial collagen, promoting platelet adhesion and activation. Platelets change shape, release granules, and aggregate to create a platelet plug, aided by von Willebrand factor. Secondary hemostasis involves a coagulation cascade that activates thrombin, converting fibrinogen to insoluble fibrin, which stabilizes the plug. Clot retraction and wound healing subsequently consolidate the repair. Finally, fibrinolysis dissolves the clot as healing completes, restoring normal blood flow.

Hemostasis is tightly regulated by pro- and anticoagulant pathways. Disturbances can cause excessive bleeding (bleeding disorders such as hemophilia A or von Willebrand disease) or thrombosis (deep vein thrombosis, pulmonary embolism). Laboratory testing includes prothrombin time (PT/INR), activated partial thromboplastin time (aPTT), platelet counts, and specific factor assays. Management varies from vitamin K–dependent factor replacement and desmopressin for deficiencies to antifibrinolytics, platelet transfusions, or anticoagulants for thrombotic risk. Understanding hemostasis is essential in surgery, trauma care, and the management of liver disease and other coagulopathies.