Thrombosis & Haemostasis Research Unit, Department of Clinical Biochemistry, Aarhus University Hospital, Denmark.
Department of Anaesthesiology and Intensive Care Medicine, Aarhus University Hospital, Denmark.
Thromb Res. 2020 Jan;185:33-42. doi: 10.1016/j.thromres.2019.11.011. Epub 2019 Nov 14.
Platelet function during sepsis-related disseminated intravascular coagulation (DIC) is only sparsely investigated. We aimed to determine 1) platelet aggregation, independently of platelet count, and platelet activation among septic shock patients and 2) whether platelet aggregation or platelet activation differed among patients with and without DIC.
We included 38 septic shock patients at the Intensive Care Unit, Aarhus University Hospital, Denmark. Blood samples were obtained within 24 h of admission and the two consecutive days. Platelet aggregation was measured by impedance aggregometry including a model defining expected platelet aggregation relative to platelet count. Platelet activation was measured employing flow cytometry.
Platelet aggregation was significantly lower in septic shock patients than in healthy controls (p < .0001) and was lower in patients with DIC than in patients without DIC (p < .05). However, patients with septic shock, regardless of DIC-status, had platelet aggregation as expected for their platelet counts and were within the 95% prediction interval calculated from healthy controls. Platelet activation was significantly higher in septic shock patients than in healthy controls indicated by higher platelet surface-bound fibrinogen and CD63 (p < .05). Surface-bound P-selectin was significantly lower among septic shock patients than in healthy controls (p < .001), but plasma soluble P-selectin was significantly higher among septic shock patients than in healthy controls (p < .0001).
Patients with septic shock displayed no impairment of platelet aggregation when interpreted relative to platelet count. Platelet activation, measured with flow cytometry, was increased among septic shock patients compared with healthy controls.
脓毒症相关弥散性血管内凝血 (DIC) 期间的血小板功能研究甚少。我们旨在确定 1)脓毒性休克患者血小板聚集(独立于血小板计数)和血小板活化的情况,以及 2)是否在有或无 DIC 的患者之间,血小板聚集或血小板活化存在差异。
我们纳入了丹麦奥胡斯大学医院重症监护病房的 38 例脓毒性休克患者。在入院后 24 小时内和连续两天采集血样。通过阻抗聚集法测量血小板聚集,包括一个相对于血小板计数定义预期血小板聚集的模型。通过流式细胞术测量血小板活化。
与健康对照组相比,脓毒性休克患者的血小板聚集显著降低(p<0.0001),且 DIC 患者的血小板聚集显著低于非 DIC 患者(p<0.05)。然而,无论 DIC 状态如何,脓毒性休克患者的血小板聚集均与预期的血小板计数相符,且在根据健康对照组计算的 95%预测区间内。与健康对照组相比,脓毒性休克患者的血小板活化明显升高,表现为血小板表面结合的纤维蛋白原和 CD63 更高(p<0.05)。与健康对照组相比,脓毒性休克患者的血小板表面结合的 P-选择素显著降低(p<0.001),但血浆可溶性 P-选择素显著升高(p<0.0001)。
当相对于血小板计数进行解释时,脓毒性休克患者的血小板聚集并未受损。与健康对照组相比,流式细胞术测量的血小板活化在脓毒性休克患者中增加。