Hemostasis

Hemostasis is the set of responses that halts the loss of blood from an injured vessel while keeping blood fluid everywhere else. It proceeds in three overlapping steps. First, smooth muscle in the injured wall contracts (vascular spasm), narrowing the vessel and slowing flow. Second, platelets stick to collagen exposed in the torn wall, with help from von Willebrand factor, then become activated, change shape and release substances such as ADP that draw in more platelets to build a temporary plug.

Third, coagulation turns the plug into a firm clot. A cascade of clotting factors, mostly made in the liver and several of them dependent on vitamin K, is started by tissue factor from damaged tissue (the extrinsic pathway) or by contact activation within the blood (the intrinsic pathway). Both routes meet at factor X, which drives the conversion of prothrombin into thrombin, and thrombin turns soluble fibrinogen into strands of fibrin that bind the clot together. Natural anticoagulants such as antithrombin confine the clot to the injury, and later the enzyme plasmin dissolves it as the vessel heals, a process called fibrinolysis.

Too little hemostasis causes bleeding disorders such as hemophilia; clotting inside intact vessels causes thrombosis. In surgery, the word also means deliberately controlling bleeding with pressure, clamps, ties, cautery or hemostatic agents.