Fibrinolysis

Abstract Fibrinolysis is a natural physiologic process that maintains homeostasis by regulating clot formation and degradation. This balance allows for clot remodeling and prevents diffuse thrombosis formation. Fibrinolysis is largely mediated by tissue plasminogen activator (tPA), which cleaves plasminogen into plasmin, ultimately leading to fibrin degradation and clot dissolution. Fibrinolysis can be measured quantitatively via thromboelastography (TEG) and rotational thromboelastometry (ROTEM). Detection of fibrinolysis via these assays and others allows for directed therapy and potential pharmaceutical inhibition of fibrinolysis. This pharmaceutical inhibition, also termed antifibrinolytic therapy, is most commonly performed with medications such as aprotinin, aminocaproic acid, and tranexamic acid. Antifibrinolytic therapy may be indicated in the setting of significant hemorrhage or excessive fibrinolysis (known as hyperfibrinolysis). Because of this, antifibrinolytic therapy has become commonly used in many clinical settings, including trauma, surgery, and cardiopulmonary bypass. When considering initiation of antifibrinolytic therapy, the benefit of decreased hemorrhage and anti-inflammatory effects must be weighed against the theoretical risk of unchecked thrombus formation.