SCIENTIFIC BACKGROUND – Haemostasis is an essential process in the prevention of blood loss. It facilitates undisturbed blood flow in the vasculature, resulting in the arrest of bleeding in response to injury of a blood vessel. The hemostatic process consists of multiple components, including platelets, endothelial cells, and plasma proteins that together facilitate the coagulation cascade and are therefore vital in the prevention of bleeding.
In the healthy vessel, platelets circulate in blood in a resting state. They are kept dormant through release of platelet inhibitors by the endothelial cell. While circulating, platelets continuously monitor the vascular wall for breaches and respond rapidly when they encounter a defect. Upon such a vascular injury, sub-endothelial layers containing collagen fibres are exposed to the blood that together with the plasma protein Von Willebrand Factor forms an adhesive surface to which platelets will adhere.
The result is a monolayer of activated platelets that supports the adhesion and activation of additional platelets. Agonists like thrombin, ADP and thromboxane A2 play an important role herein, and induce intracellular platelet signaling, causing the release of granule content as well as activation of integrin αIIbβ3 enabling cohesion between platelets (aggregation). The net result is a hemostatic plug consisting of activated platelets within a fibrin mesh.
This structure is stable enough to withstand the forces of the flowing blood in the circulation, and will effectively seal the injury to stop the bleeding from the injured vessel and prevent excessive blood loss. When platelets are unable to form an adequate platelet plug, e.g. due to inherited or acquired deficiencies causing an inability to respond to a stimulus, this will lead to an increased risk of bleeding.
Injured vessel wall – Platelet adhesion.
Injured vessel wall – Platelet aggregation.
Injured vessel wall – Arrest of bleeding.