General Medical Information

Coagulation Phase

David J. Terris

Injury causes hemorrhage with exposure of platelets to the thrombogenic subendothelial connective tissue. This activates the platelets, resulting in an almost immediate release of numerous vasoactive substances that cause vasoconstriction (serotonin via S2 receptors and catecholamines). The transient (5 to 10 minutes) vasoconstriction helps to control bleeding and is followed by the formation of a primary hemostatic plug as the platelets aggregate. The remaining vasoactive substances (serotonin via S1 receptors, bradykinin, and histamine) cause vasodilation of small vessels (predominantly venules), leading to the transit of plasma proteins, red blood cells, and leukocytes into the wound.

Platelets are critical elements of this early response, not only because of their hemostatic function but also because of the concurrent release of numerous cytokines that are necessary to initiate the cascade of events that follow. The clotting cascade depends heavily on the activation of platelets, which causes the release of stored products, initiating both the intrinsic coagulation pathway (via contact activation of factor XII, or Hageman factor) and the extrinsic coagulation pathway (via activation of factor VII by tissue factor). The fibrin that is produced not only contributes to hemostasis but also forms a matrix across which fibroblasts, leukocytes, and keratinocytes subsequently migrate.