hemostasis

Hemostasis is the physiological process that stops bleeding at sites of vascular injury and preserves blood in a fluid state within intact vessels. It involves interactions among the vascular wall, platelets, coagulation factors, and the fibrinolytic system to achieve rapid cessation of blood loss and subsequent wound repair.

Primary hemostasis begins with vascular constriction and platelet adhesion to exposed subendothelial collagen, mediated by von Willebrand factor. Activated platelets release granules containing adenosine diphosphate, thromboxane A2, and other mediators, recruit additional platelets, and form a loose platelet plug that temporarily seals the injury.

Secondary hemostasis reinforces the plug through a coagulation cascade that generates thrombin and converts fibrinogen into fibrin. The intrinsic and extrinsic pathways converge on the common pathway, producing a stable fibrin mesh that reinforces the platelet plug. This phase involves multiple coagulation factors synthesized by the liver and regulated by natural anticoagulants.

Regulation of hemostasis ensures balance between bleeding and thrombosis. Endothelial cells provide antithrombotic signals such as prostacyclin and nitric oxide, while thrombomodulin and protein C–S pathways limit coagulation. The fibrinolytic system dissolves clots when repair is underway, primarily via plasmin.

Disorders of hemostasis include bleeding diatheses such as hemophilia A or B and von Willebrand disease, as well as thrombotic conditions. Diagnostic tests include platelet counts, prothrombin time and activated partial thromboplastin time, and more dynamic tests like thromboelastography. Treatments range from local hemostasis and antifibrinolytics to targeted factor replacement, desmopressin for certain deficiencies, vitamin K for deficiency, and platelet transfusion when needed.