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Biologic Hemostatic Agents in Obstetrics and Gynecology
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Biologic Hemostatic Agents in Obstetrics and Gynecology
In Obstetrics and Gynecology, the practice of biologic hemostatic agents in the field are generally used to augment the basic tenets of hemostasis to decrease the morbidity and mortality of such procedures. These hemostatic agents work along with the body’s physiology to rapidly aid in platelet plug formation, activation of the clotting cascade, the creation of fibrin, and to form a stable clot. The four main sub-categories of hemostatic agents include mechanical, biological, flowable, and fibrin sealants. Mechanical agents act as scaffolding for platelet aggregation to form a platelet plug. Biological agents activate clotting factors in the coagulation cascade to aid in hemostasis. Flowable agents combine biologic with mechanical agents to stabilize clot formation while also providing mechanical tamponade. Fibrin sealants combine high levels of fibrin and thrombin that when combined, form a fibrin clot at an accelerated speed. Hemostatic agents in obstetrics are often used in the setting of postpartum hemorrhage, cesarean delivery and postpartum hysterectomy to decrease the rate of morbidity most commonly seen with abnormal placentation and uterine atony. With gynecologic surgery, hemostatic agents are more commonly used then in obstetrics. They aid in hemostasis with common gynecologic procedures including hysterectomies, ovarian cystectomies, myomectomies, endometriosis cases, incontinence procedures and malignant debulking procedures. Also, with the increase in minimally invasive surgical techniques, topical hemostasis can aid in fewer transfusions, improved visualization in the surgical field decreased operative time and reduction in the risk of conversion to laparotomy.To get more news about IFAK kit, you can visit rusuntacmed.com official website.
Intraoperative hemostasis is primarily achieved through knowledge of anatomy and good surgical technique. Technology has augmented the basic tenets of surgical hemostasis since 1926 and has continued to evolve. In addition to applying pressure and using suture, there are now a wide variety of hemostatic options available to gynecologic surgeons including monopolar/bipolar cautery, harmonic technology, hemoclips, laser, argon beam coagulation, tacks, and topical hemostatic agents. Like any other trade, it is important to have the right tool for the job. If there is bleeding in a sensitive anatomic location in the pelvis, mechanical and thermal techniques may not be practical given the risk to adjacent tissues. Topical hemostatic agents have been available since the mid 20th century and can act as an adjunct to provide both active and passive hemostasis in situations where bleeding is difficult or impractical to be controlled by conventional methods. Topical hemostatic agents work by augmenting specific parts of physiologic hemostasis. Of the four phases of hemostasis [1, 2], topical hemostatic agents primarily affect formation of the platelet plug and propagation of the coagulation cascade. Topical hemostatic agent use is common practice in many surgical procedures, and has been utilized across all surgical specialties [3]. Likely due to marketing, usage of topical hemostatic agents has increased by 10–21% since 2000 [4]. This chapter will focus on use of topical hemostatic agents in obstetrics/gynecological surgeries with a focus on postpartum hemorrhage, myomectomy, hysterectomy, endometriosis surgery, oncologic debulking, and ovarian cystectomy.In order to understand the mechanism of action of topical hemostatic agents, it is important to understand the basic physiology of hemostasis. There are four main phases of hemostasis: endothelial injury and platelet plug formation, activation of the clotting cascade, termination of the clotting, and fibrinolysis [3]. Hemostasis represents a delicate and regulated balance between thrombosis and thrombolysis. Formation of a stable hemostatic clot relies on a complex interaction between vasoconstriction, circulating clotting factors, and platelet factors. In a surgical patient, the inciting event is endothelial damage from trauma. Injury to the endothelium exposes blood to subendothelial elements that promote platelet adhesion and activation. Endothelial injury also activates both the extrinsic and intrinsic coagulation pathways through increased expression of tissue factor and exposure to negatively charged surfaces respectively.
After vessel injury, there is temporary vasoconstriction which facilitates platelet adhesion and subsequent activation. This forms a fragile platelet plug which requires stabilization during secondary hemostasis to form a clot. Initiation of the coagulation cascade occurs through both extrinsic and intrinsic pathways. This involves multiple plasma proteins, calcium ions, and platelets. At the end of the cascade, thrombin ultimately converts fibrinogen to fibrin leading to a stable clot [5]. This is critical as thrombin can be applied alone or in combination with other hemostatic agents, bypassing the intrinsic and extrinsic pathways as long as there is adequate circulating fibrinogen present.