Venous Thromboembolism in Sepsis: From Bench to Bedside

Abstract

Septic patients were commonly affected by coagulation disorders; thus, they are at high risk of thrombotic complications. In the last decades, novel knowledge has emerged about the interconnected and reciprocal influence of immune and coagulation systems. This phenomenon is called immunothrombosis, and it indicates an effective response whereby immune cells and the coagulation cascade cooperate to limit pathogen invasion and endothelial damage. When this network becomes dysregulated due to a systemic inflammatory activation, as occurs during sepsis, it can result in pathological thrombosis. Endothelium, platelets and neutrophils are the main characters involved in this process, together with the TF and coagulation cascade, playing a critical role in both the host defense and in thrombogenesis. A deeper understanding of this relationship may allow us to answer the growing need for clinical instruments to establish the thrombotic risk and treatments that consider more the connection between coagulation and inflammation. Heparin remains the principal therapeutical response to this phenomenon, although not sufficiently effective. To date, no other significant alternatives have been found yet. In this review, we discuss the role of sepsis-related inflammation in the development and resolution of venous thromboembolism and its clinical implications, from bench to bedside.