The primary goal of any surgical procedure is the safe alteration or repair of tissue, which requires the immediate and effective control of bleeding, a process known as hemostasis. Uncontrolled blood loss compromises physiological stability, obscures the surgical field, and increases operative time and the risk of complications. Surgical hemostasis employs a selected array of techniques to stop blood flow from injured vessels, ensuring the patient maintains adequate circulating blood volume. The method chosen depends on the vessel size, the type of tissue involved, and the speed required to address the hemorrhage.
Mechanical Methods: Clamping, Tying, and Suturing
Mechanical methods are the most fundamental and direct approach to surgical hemostasis, relying on physical force to occlude the vessel. The initial response to a bleeding vessel is often to temporarily grasp it with a specialized instrument like a hemostat or artery forceps. This clamping action physically crushes the vessel walls, providing momentary control while the surgeon prepares for a permanent solution.
Ligation is the definitive technique following clamping, where a thread or suture material is tied tightly around the severed end of the vessel to physically seal it. Sutures are categorized into absorbable and non-absorbable types, chosen based on expected healing time and tissue location. Absorbable sutures, such as polyglactin or polydioxanone, break down over time through hydrolysis or enzymatic action, making them suitable for internal tissues that quickly regain strength.
Non-absorbable sutures, including materials like polypropylene or silk, are used in areas requiring long-term structural support, such as cardiovascular repairs, or for skin closures where manual removal is necessary. For rapid closure, particularly in minimally invasive procedures, small metal or polymer surgical clips can be applied across the vessel. These clips provide a secure, permanent physical barrier to blood flow, offering a faster alternative to tying a knot.
Applying Energy: Electrosurgery and Thermal Devices
Energy-based devices use heat to coagulate proteins within the blood vessel walls, effectively sealing them shut. Electrosurgery, which uses a high-frequency alternating electrical current, generates heat within the tissue itself. This heat causes cellular water to vaporize and proteins to denature, forming a seal of coagulated tissue.
Monopolar electrosurgery uses a single active electrode, requiring the current to pass through the patient’s body to a distant return pad to complete the circuit. This technique is versatile for cutting and coagulating large areas but carries a risk of burns if return pad contact is inadequate. In contrast, bipolar electrosurgery confines the electrical current entirely between the two tips of a forceps-like instrument, limiting the flow to a small, isolated area. This localized current makes bipolar devices safer for use near delicate structures like nerves, as there is minimal thermal spread.
Other energy modalities offer specialized coagulation effects, such as the Harmonic Scalpel, which uses high-frequency ultrasonic vibration. The mechanical energy from the vibrating blade denatures tissue proteins at a lower temperature than electrosurgery, resulting in less smoke and charring. For broad, superficial bleeding, Argon Beam Coagulation directs a jet of ionized argon gas to conduct electrical current to the tissue in a non-contact fashion. This technique creates a uniform, shallow layer of coagulation over large raw surfaces, such as the liver or spleen.
Topical Agents and Biological Sealants
When vessels are too numerous or small to be sealed individually, topical agents are applied directly to the oozing surface. These materials work either by providing a physical scaffold for clotting or by actively triggering the body’s natural coagulation cascade. Passive hemostatic agents, such as oxidized regenerated cellulose or gelatin sponges, are inert materials that absorb blood and provide a matrix. This physical matrix concentrates platelets and clotting factors, accelerating the formation of a natural clot.
Active hemostatic agents introduce biological components, like purified thrombin, which directly convert the body’s fibrinogen into fibrin. This immediate chemical reaction bypasses the initial steps of the clotting cascade, rapidly forming a fibrin clot at the application site. Fibrin sealants, often called surgical glues, combine fibrinogen and thrombin to mimic the final stage of natural clotting, creating a strong, localized biological seal.
These sealants are valuable for preventing leaks in delicate areas or on highly vascular organs. A specialized agent, bone wax, is a soft, malleable mixture used to manage bleeding from cut bone surfaces. Bone wax achieves hemostasis by physically plugging the small vascular channels in cancellous bone.
Maintaining Patient Stability: Systemic Hemostasis
While local techniques control bleeding at the surgical site, the overall management of the patient’s internal environment, known as systemic hemostasis, is equally important. The anesthesia and surgical teams closely monitor and manage the patient’s circulating blood volume and blood pressure through careful fluid administration. Maintaining adequate pressure is necessary to ensure organs are perfused, but excessive fluid can dilute the patient’s own clotting factors.
If significant blood loss occurs, transfusion protocols are immediately activated to replace lost components in a balanced manner. This replacement includes packed red blood cells to carry oxygen, fresh frozen plasma to supply clotting factors, and platelets to aid in clot formation. Furthermore, the team must be prepared to correct coagulopathy, which is a generalized impairment of the clotting system.
This may involve administering concentrated clotting factors or specific reversal agents for patients who were taking blood thinners before surgery. Medications like tranexamic acid may also be given intravenously to slow the breakdown of existing blood clots, supporting the body’s intrinsic hemostatic efforts.