INTRODUCTION

Physiological haemostasis involves complex interactions between endothelial cells, platelets and coagulation proteins, that result in a prompt platelet plug and then localised thrombus formation at the site of a break in vascular integrity. Numerous regulatory processes prevent widespread activation of coagulation, ensuring that blood remains fluid in the absence of vascular injury or other pathology. All components of the haemostatic process can be disturbed resulting in either a pro-thrombotic or bleeding tendency, and drugs that modify the haemostatic process are commonly used, particularly in patients with vascular disease. An understanding of normal haemostasis is therefore important for all clinicians that deal with this patient group.

PRIMARY HAEMOSTASIS

Primary haemostasis is the initial response of the body to vascular injury, and involves interaction between platelets, adhesive proteins located in the subendothelial matrix (including collagen and von Willebrand factor), and circulating fibrinogen. The end result of primary haemostasis is the formation of a stable platelet plug around which a fibrin network can then be built. This same process is responsible for the pathogenic thrombus formation in patients with arterial disease. Disorders of primary haemostasis tend to manifest in the main as mucosal bleeding, including epistaxis, oral bleeding and menorrhagia, and often immediate difficulty with haemostasis in the post-operative setting.

Platelets

Platelets are small fragments of megakaryocyte cytoplasm that in the resting state are small discoid structures. The normal range for circulating platelet count in adults is between 150 to 400 × 109/L.