Department of Anaesthesiology, University of Heidelberg, Heidelberg, Germany.
Acta Anaesthesiol Scand. 2012 Nov;56(10):1277-90. doi: 10.1111/j.1399-6576.2012.02750.x. Epub 2012 Aug 17.
In the pathogenesis of sepsis, inflammation-induced changes in coagulation play a pivotal role.
In total, 90 patients (30 patients with septic shock, 30 surgical patients following major abdominal surgery and 30 healthy volunteers) were enrolled. Blood samples from patients with septic shock were collected at the time of sepsis diagnosis as well as 24 h, 4 days, 7 days, 14 days and 28 days later. Samples from surgical patients with a post-surgical inflammatory response were collected three times (before surgery, immediately after surgery and 24 h after surgery) and once from healthy volunteers. Thromboelastometry (ROTEM (®) ), as well as whole blood impedance aggregometry (Multiplate(®) ) were performed. Additionally, plasma concentrations of interleukin-6 and tumour necrosis factor-alpha were measured using enzyme-linked immunosorbent assay kits.
Thromboelastometry lysis index was shown to be a reliable biomarker for septic shock. Furthermore, in septic patients with overt disseminated intravascular coagulation, thromboelastometry revealed signs indicating a hypocoagulable status, whereas patients without overt disseminated intravascular coagulation were found to be hypercoagulable. Platelet aggregation capability, as assessed by whole blood impedance aggregometry, was significantly reduced in septic patients with overt disseminated intravascular coagulation, whereas it was comparable with healthy volunteers and in septic patients without overt disseminated intravascular coagulation.
Viscoelastic and aggregometric point-of-care testing was shown to be potentially useful for bedside diagnosis of sepsis. Moreover, viscoelastic and aggregometric point-of-care testing was able to determine the phase of septic coagulopathy (hypercoagulability vs. hypocoagulability) and therefore identified patients at high risk for overt disseminated intravascular coagulation.
在脓毒症的发病机制中，炎症引起的凝血变化起着关键作用。
共纳入 90 例患者（30 例感染性休克患者、30 例腹部大手术后的外科患者和 30 名健康志愿者）。感染性休克患者的血液样本分别在脓毒症诊断时以及 24 小时、4 天、7 天、14 天和 28 天后采集。外科手术后有炎症反应的患者采集了 3 次样本（手术前、手术后即刻和手术后 24 小时），健康志愿者采集了 1 次样本。进行血栓弹性描记法（ROTEM®）和全血阻抗聚集法（Multiplate®）检测。此外，采用酶联免疫吸附试剂盒测量白细胞介素-6 和肿瘤坏死因子-α的血浆浓度。
血栓弹性描记法的纤溶指数被证明是感染性休克的可靠生物标志物。此外，在有显性弥散性血管内凝血的脓毒症患者中，血栓弹性描记法显示出低凝状态的迹象，而无显性弥散性血管内凝血的患者则表现出高凝状态。通过全血阻抗聚集法评估的血小板聚集能力在有显性弥散性血管内凝血的脓毒症患者中显著降低，而与健康志愿者和无显性弥散性血管内凝血的脓毒症患者相当。
基于即时检测的粘弹性和聚集性检测可能对脓毒症的床边诊断有用。此外，基于即时检测的粘弹性和聚集性检测能够确定脓毒症凝血障碍的阶段（高凝状态与低凝状态），从而识别出有显性弥散性血管内凝血高风险的患者。
