Ninivaggi M, Feijge M A H, Baaten C C F M J, Kuiper G J A J M, Marcus M A E, Ten Cate H, Lancé M D, Heemskerk J W M, van der Meijden P E J
J. W. M. Heemskerk, Department of Biochemistry (CARIM), Maastricht University, P.O. Box 616, 6200 MD Maastricht, The Netherlands, Tel. +31 43 3881671, Fax: +31 43 3884159, E-mail:
P. E. J. van der Meijden, Department of Biochemistry (CARIM), Maastricht University, P.O. Box 616, 6200 MD Maastricht, The Netherlands, Tel. +31 43 3881671, Fax: +31 43 3884159, E-mail:
Thromb Haemost. 2014 Mar 3;111(3):447-57. doi: 10.1160/TH13-06-0493. Epub 2013 Nov 21.
Blood dilution after transfusion fluids leads to diminished coagulant activity monitored by rotational thromboelastometry, assessing elastic fibrin clot formation, or by thrombin generation testing. We aimed to determine the contributions of blood cells (platelets, red blood cells) and plasma factors (fibrinogen, prothrombin complex concentrate) to fibrin clot formation under conditions of haemodilution in vitro or in vivo.Whole blood or plasma diluted in vitro was supplemented with platelets, red cells, fibrinogen or prothrombin complex concentrate (PCC). Thromboelastometry was measured in whole blood as well as plasma; thrombin generation was determined in parallel. Similar tests were performed with blood from 48 patients, obtained before and after massive fluid infusion during cardiothoracic surgery.Addition of platelets or fibrinogen, in additive and independent ways, reversed the impaired fibrin clot formation (thromboelastometry) in diluted whole blood. In contrast, supplementation of red blood cells or prothrombin complex concentrate was ineffective. Platelets and fibrinogen independently restored clot formation in diluted plasma, resulting in thromboelastometry curves approaching those in whole blood. In whole blood from patients undergoing dilution during surgery, elastic clot formation was determined by both the platelet count and the fibrinogen level. Thrombin generation in diluted (patient) plasma was not changed by fibrinogen, but improved markedly by prothrombin complex concentrate. In conclusion, in dilutional coagulopathy, platelets and fibrinogen, but not red blood cells or vitamin K-dependent coagulation factors, independently determine thromboelastometry parameters measured in whole blood and plasma. Clinical decisions for transfusion based on thromboelastometry should take into account the platelet concentration.
输注液体后的血液稀释会导致通过旋转血栓弹力图法（评估弹性纤维蛋白凝块形成）或凝血酶生成测试监测的凝血活性降低。我们旨在确定血细胞（血小板、红细胞）和血浆因子（纤维蛋白原、凝血酶原复合物浓缩物）在体外或体内血液稀释条件下对纤维蛋白凝块形成的作用。体外稀释的全血或血浆补充了血小板、红细胞、纤维蛋白原或凝血酶原复合物浓缩物（PCC）。在全血和血浆中均测量了血栓弹力图；同时测定了凝血酶生成情况。对48例患者在心胸外科手术大量输液前后采集的血液进行了类似测试。以相加和独立的方式添加血小板或纤维蛋白原可逆转稀释全血中受损的纤维蛋白凝块形成（血栓弹力图）。相比之下，补充红细胞或凝血酶原复合物浓缩物无效。血小板和纤维蛋白原可独立恢复稀释血浆中的凝块形成，使血栓弹力图曲线接近全血中的曲线。在手术中经历稀释的患者的全血中，弹性凝块形成由血小板计数和纤维蛋白原水平共同决定。稀释（患者）血浆中的凝血酶生成不受纤维蛋白原影响，但凝血酶原复合物浓缩物可使其显著改善。总之，在稀释性凝血病中，血小板和纤维蛋白原而非红细胞或维生素K依赖的凝血因子独立决定在全血和血浆中测量的血栓弹力图参数。基于血栓弹力图的输血临床决策应考虑血小板浓度。
