Li Tatyana, Zhailauova Azhar, Kuanyshbek Aidyn, Wachruschew Iwan, Tulegenov Shaimurat, Sazonov Vitaliy, Kapyshev Timur
Department of Anaesthesia and Intensive Care, Heart Center CF "University Medical Center", Astana 010000, Kazakhstan.
Department of Surgery, Nazarbayev University School of Medicine, Astana 010000, Kazakhstan.
J Clin Med. 2024 Dec 14;13(24):7633. doi: 10.3390/jcm13247633.
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.
接受体外膜肺氧合（ECMO）治疗的患者出现肝素抵抗（HR）会加剧出血和血栓形成。到目前为止，对于这种情况的具体内涵尚无统一的定义，也没有评估肝素在ECMO患者中疗效的统一策略。在定义HR时，最常见的差异在于报告的剂量不同：每天单位数（U/d）或每千克每小时单位数（U/kg/h）。在测量普通肝素（UFH）疗效的各种方法方面也存在分歧。由于从启动ECMO开始就有众多过程，包括在回路表面形成蛋白质层、免疫细胞募集、补体和接触激活系统激活以及血小板激活等，评估单纯抗凝血酶消耗情况很复杂。此外，有一种由丝氨酸蛋白酶抑制剂肝素辅因子II执行的替代抗凝程序，这也可能导致肝素消耗。考虑到ECMO中与人工表面接触后同时启动的炎症和血栓形成过程，我们列出了导致额外抗凝血酶消耗的可能机制。还描述了血流对血小板激活和血管性血友病因子（vWF）组装的影响。我们检索了PubMed和Embase上的科学文献，以确定儿科和成人队列中ECMO治疗期间肝素抵抗的可能定义。我们识别出13条描述评估HR不同方法的记录，并阐述了我们对ECMO上HR界定的看法。
