Salmon J, Cardigan R, Mackie I, Cohen S L, Machin S, Singer M
Bloomsbury Institute of Intensive Care Medicine, Department of Medicine, University College London Medical School, UK.
Intensive Care Med. 1997 Jan;23(1):38-43. doi: 10.1007/s001340050288.
To investigate whether continuous venovenous haemofiltration using polyacrylonitrile filters causes activation of the contact system and intrinsic coagulation pathways and if this, and/or low plasma levels of endogenous anticoagulants, influences filter lifespan.
Observational study.
University Teaching Hospital Intensive Care Unit.
Twelve critically ill patients with acute renal failure receiving continuous venovenous haemofiltration.
Blood samples were taken before starting haemofiltration, at 15 min, 1 h, 3-4 h, 8-12 h, 24 h and at 24-h intervals thereafter until filter blockage occurred. Measurement was made of the contact and intrinsic coagulation system proteins factor XII, activated factor XII and prekallikrein and the protease inhibitors antithrombin III, heparin co-factor II, alpha 2-macroglobulin and C1-esterase inhibitor. Thrombin-antithrombin complex levels were measured to provide evidence of thrombin generation.
(i) Factor XII, prekallikrein and contact system inhibitors were subnormal in 10/12 and activated factor XII raised in 11/12 patients at baseline, implying pre-existing contact pathway activation. (ii) No change occurred during haemofiltration in the intrinsic coagulation pathway factor or inhibitor levels. (iii) Clotting of the filter circuit within the first 24 h occurred in 5/12 and was associated with low baseline levels of antithrombin III and heparin co-factor II. Only in these patients did thrombin-antithrombin complex levels rise significantly.
The contact system was not activated further by continuous venovenous haemofiltration using polyacrylonitrile filters in critically ill patients. Premature clotting of the haemofilter circuit was more common in patients with very low levels of antithrombin III and heparin co-factor II; although this was related to thrombin generation, the intrinsic coagulation pathway does not appear to be implicated.
研究使用聚丙烯腈滤器的持续静脉-静脉血液滤过是否会激活接触系统和内源性凝血途径,以及这一点和/或内源性抗凝剂的低血浆水平是否会影响滤器使用寿命。
观察性研究。
大学教学医院重症监护病房。
12例接受持续静脉-静脉血液滤过的急性肾衰竭危重症患者。
在血液滤过开始前、15分钟、1小时、3 - 4小时、8 - 12小时、24小时以及此后每隔24小时采集血样,直至滤器堵塞。检测接触系统和内源性凝血系统蛋白因子XII、活化因子XII和前激肽释放酶以及蛋白酶抑制剂抗凝血酶III、肝素辅因子II、α2-巨球蛋白和C1酯酶抑制剂。检测凝血酶-抗凝血酶复合物水平以提供凝血酶生成的证据。
(i)12例患者中有10例在基线时因子XII、前激肽释放酶和接触系统抑制剂低于正常水平,11例患者的活化因子XII升高,这意味着接触途径已预先激活。(ii)血液滤过期间内源性凝血途径因子或抑制剂水平无变化。(iii)12例患者中有5例在最初24小时内滤器回路发生凝血,这与抗凝血酶III和肝素辅因子II的低基线水平相关。仅在这些患者中,凝血酶-抗凝血酶复合物水平显著升高。
在危重症患者中,使用聚丙烯腈滤器进行持续静脉-静脉血液滤过不会进一步激活接触系统。抗凝血酶III和肝素辅因子II水平极低的患者中,血液滤过器回路过早凝血更为常见;尽管这与凝血酶生成有关,但内源性凝血途径似乎并未涉及。