Anticoagulation in the ICU: a future for contact pathway inhibition?

Bleeding and thrombotic complications are the main cause of morbidity and mortality in critically ill patients on the intensive care unit (ICU), receiving short-term percutaneous mechanical circulatory support (pMCS) by extracorporeal membrane oxygenation (ECMO), balloon pumps or microaxial flow pumps [1]. This is due to a bidirectional interplay of various factors influencing the haemostatic balance, including coagulopathy during critical illness, sepsis/inflammation, platelet consumption, hyperfibrinolysis, shear-induced acquired von Willebrand syndrome and direct contact pathway activation by the artificial surface of the pMCS device [2]. To prevent thrombotic complications and device-induced localised intravascular coagulopathy (LIC), anticoagulation is indicated. Unfortunately, all currently available anticoagulants carry an increased bleeding risk, further jeopardising patients’ outcomes [3]. Therefore, the search for safer anticoagulants continues: the holy grail for the treatment of patients on pMCS and by extension, all patients on anticoagulation is to prevent thrombosis without affecting haemostasis, thus lowering the bleeding risk