Fibrinolysis shutdown and venous thromboembolism

Abstract

Fibrinolysis is a normal physiologic process that is essential to maintain microvascular patency by removing extraneous fibrin clot [1]. The extremes of fibrinolysis, termed hyperfibrinolysis (excessive breakdown of clot) and fibrinolysis shutdown (resistance to clot breakdown), are associated with increased mortality [1, 2]. The mechanisms and clinical implications of these pathologic extremes and their temporal trends have been detailed in the previous chapter on fibrinolytic derangements following trauma (Chap. 11. While pharmacologic therapies, such as tranexamic acid (TXA), to attenuate hyperfibrinolysis have been studied extensively in trauma, studies to identify effective strategies to treat fibrinolysis shutdown are limited.