Physiologically, haemostasis at its simplest involves vascular spasm, platelet plug formation, and clotting, with subsequent limitation of acute haemorrhage. Vascular spasm, triggered by damage to a vessel, is insufficient by itself to arrest blood loss. Platelets, which circulate freely in the blood, are exposed to the tissue collagen of the damaged vessel wall and not only stick to the breach, but also to each other.
Simultaneously platelets release a number of chemical mediators, such as, adenine diphosphate (ADP) and products of arachidonic acid metabolism, such as thromboxane A2. This further contributes to platelet stickiness, resulting in the formation of a platelet plug, occluding the opening in the vessel wall. Platelet plugs are inherently insecure structures that are subsequently anchored in place by the formation of a fibrin clot. Clotting is dependant on a group of plasma proteins called clotting factors, most of which are synthesised in the liver by Vitamin K-dependant reactions. They are normally present as inactive pro-enzymes, which when activated, proceed down a pro-teolytic cleavage pathway (intrinsic or extrinsic clotting pathways) resulting in the conversion of prothrombin to thrombin.
Thrombin catalyses the conversion of fibrinogen to fibrin monomers and their subsequent polymerisation into cross-linked fibrin strands. The resulting clot traps erythrocytes and bridges the opening in the vessel, securing the platelets in position. In time, clot retraction pulls the damaged edges of the blood vessel together.3
Any technique that augments a part of this pathway, whether it takes a mechanical, electrical, or chemical form will assist in the control of haemostasis. In the authors' experience however, there is no substitute for meticulous surgical technique. In this chapter we aim to cover both novel and well-established techniques of haemostasis used in endocrine surgery.
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