Management of bleeding is fundamentally important in any surgical procedure. Historically, surgeons applied boiling oil solution and soothing balms to detoxify and cauterize wounds. It was in the sixteenth century that the French surgeon, Ambroise Paré, revolutionized the practice of surgery by introducing the use of vascular ligatures to control bleeding in amputations, sucking chest wounds and chronic ulcers.1 The fields of medicine and surgery have undergone significant transformation since then. Dermatologic surgeons have become more cognizant of hemostasis because they now perform invasive office-based procedures, often on patients with complicated medical histories. Adequate control of bleeding during these procedures is vital to achieving optimal outcomes. The overall safety of dermatologic surgery is well established, but complications do arise and are often attributable to bleeding.
This chapter will review the principles of hemostasis as they relate to cutaneous surgery. Normal hemostasis, as well as disorders, medications, and supplements that affect hemostasis will be discussed. Various surgical approaches and relevant hemostatic agents used to control bleeding during procedures will be presented.
BIOLOGY OF NORMAL HEMOSTASIS
Understanding the principles behind hemostasis can lead to better utilization of the various tools available to achieve hemostasis during dermatologic surgery. It is also important to understand the mechanisms behind the medications that alter coagulation. The hemostatic process can be divided into four physiologic events that are intimately linked and occur in conjunction with each other – vasoconstriction, platelet plug formation, fibrin clot formation, and fibrinolysis. A schematic of normal hemostasis is shown on Figure 13-1, and is discussed in detail below.
Schematic of the four interrelated physiologic processes of hemostasis. vWF, von Willebrand factor; ADP, adenosine diphosphate; Ca2+, calcium)
Damage to blood vessels during surgery precipitates the process of hemostasis. Vascular constriction is the initial response to this injury and is dependent on local contraction of smooth muscle. This process is closely linked to platelet plug formation. When platelets adhere and aggregate at the site of injury, they induce factors that further potentiate vasoconstriction. Thromboxane A2, made from arachidonic acid on platelet membranes; endothelin, released from the injured endothelium; and serotonin, released from activated platelets, are all powerful vasoconstrictors. Bradykinin and fibrinopeptides, both involved in the coagulation scheme, are also capable of contracting vascular smooth muscle.2
There are three steps necessary for effective platelet plug formation – platelet adhesion, granule release, and platelet aggregation. Injury to the intima of a vessel wall exposes collagen fibrils in the subendothelium, leading to platelet adherence. This process requires von Willebrand factor (vWF), a subendothelial protein that cements platelet adhesion by binding to glycoprotein receptors on the platelet membrane.3