Haemostasis

Haemostasis is the physiological process that stops bleeding at sites of vascular injury while preserving overall blood fluidity. It involves coordinated interactions between blood vessels, platelets, coagulation factors, and the fibrinolytic system to form a stable hemostatic plug and restore vessel integrity. Haemostasis is traditionally described as primary haemostasis, which governs initial platelet responses, and secondary haemostasis, which establishes a fibrin clot through the coagulation cascade, followed by fibrinolysis to remove the clot when healing occurs.

During primary haemostasis, vascular injury causes vasoconstriction and exposure of subendothelial matrix rich in collagen and von Willebrand factor. Platelets adhere via surface receptors (GPIb-IX-V, GPVI) and become activated, releasing ADP, thromboxane A2, and thrombin. Platelets recruit and aggregate through formation of the GPIIb/IIIa-fibrinogen bridge, forming a temporary platelet plug that limits blood loss.

Secondary haemostasis involves the coagulation cascade, with the intrinsic and extrinsic pathways converging on the activation of factor X and thrombin generation. Thrombin converts fibrinogen to insoluble fibrin, which stabilizes the plug; factor XIII crosslinks fibrin to form a stable clot. Anticoagulant pathways (protein C and S, antithrombin) and fibrinolysis (plasmin) regulate clot formation and breakdown to prevent excessive thrombosis.

Disorders of haemostasis include bleeding diatheses such as haemophilia A and B and von Willebrand disease, as well as thrombotic conditions like deep vein thrombosis and pulmonary embolism. Diagnosis uses tests of platelet function and coagulation (platelet count, bleeding time, PT/INR, aPTT, thrombin time, fibrinogen). Management is condition-specific and may involve desmopressin, antifibrinolytics, transfusion of platelets or clotting factors, vitamin K, or anticoagulants and thrombolytics for thrombosis.