Abstract
Heparin resistance (HR) in patients on extracorporeal membrane oxygenation (ECMO) exacerbates bleeding and thrombogenesis. Thus far, there is no universal definition of what this condition entails and no unified strategy for assessing heparin's efficacy in ECMO patients. The most frequent discrepancy when it comes to defining HR is the difference in the reported doses: units per day (U/d) or per kilogram per hour (U/kg/h). Another disagreement arises with regard to the various methods of measuring unfractionated heparin (UFH) efficacy. Due to numerous processes that begin with ECMO initiation, including protein layer formation on the surface of circuits, the recruitment of immune cells, the activation of complement and contact activation systems, and platelets, assessing pure antithrombin consumption is complicated. Moreover, there is an alternative anticoagulation procedure performed by a serine protease inhibitor named heparin cofactor II, which could also contribute to heparin consumption. Considering simultaneously launched processes of inflammation and thrombogenesis in response to contact with artificial surfaces on ECMO, we listed the possible mechanisms contributing to additional antithrombin consumption. The effect of the flow on the platelets' activation and von Willebrand factor (vWF) assembly was also described. We reviewed the scientific literature from PubMed and Embase to identify possible definitions of heparin resistance during ECMO treatment among pediatric and adult cohorts. We identified 13 records describing different approaches to assessing HR and described our vision of delineating HR on ECMO.