CHIP/PERSIMUNE, Department of infectious diseases, Rigshospitalet, Copenhagen University Hospital - Rigshospitalet, Copenhagen, Denmark.
Department of Anesthesiology, Copenhagen University Hospital - Bispebjerg, Copenhagen, Denmark.
Acta Anaesthesiol Scand. 2023 Aug;67(7):909-917. doi: 10.1111/aas.14254. Epub 2023 May 2.
Coagulation abnormalities and microthrombi contribute to septic shock, but the impact of body temperature regulation on coagulation in patients with sepsis is unknown. We tested the hypothesis that mild induced hypothermia reduces coagulation and platelet aggregation in patients with septic shock. Secondary analysis of randomized controlled trial. Adult patients with septic shock who required mechanical ventilation from eight intensive care units in Denmark were randomly assigned to mild induced hypothermia for 24 h or routine thermal management. Viscoelastography and platelet aggregation were assessed at trial inclusion, after 12 h of thermal management, and 24 h after inclusion. A total of 326 patients were randomized to mild induced hypothermia (n = 163) or routine thermal management (n = 163). Mild induced hypothermia slightly prolonged activated partial thromboplastin time and thrombus initiation time (R time 8.0 min [interquartile range, IQR 6.6-11.1] vs. 7.2 min [IQR 5.8-9.2]; p = .004) and marginally inhibited thrombus propagation (angle 68° [IQR 59-73] vs. 71° [IQR 63-75]; p = .014). The effect was also present after 24 h. Clot strength remained unaffected (MA 71 mm [IQR 66-76] with mild induced hypothermia vs. 72 mm (65-77) with routine thermal management, p = .9). The proportion of patients with hyperfibrinolysis was not affected (0.7% vs. 3.3%; p = .19), but the proportion of patients with no fibrinolysis was high in the mild hypothermia group (8.8% vs. 40.4%; p < .001). The mild induced hypothermia group had lower platelet aggregation: ASPI 85U (IQR 50-113) versus 109U (IQR 74-148, p < .001), ADP 61U (IQR 40-83) versus 79 U (IQR 54-101, p < .001), TRAP 108 (IQR 83-154) versus 119 (IQR 94-146, p = .042) and COL 50U (IQR 34-66) versus 67U (IQR 46-92, p < .001). In patients with septic shock, mild induced hypothermia slightly impaired clot initiation, but did not change clot strength. Platelet aggregation was slightly impaired. The effect of mild induced hypothermia on viscoelastography and platelet aggregation was however not in a range that would have clinical implications. We did observe a substantial reduction in fibrinolysis.
凝血异常和微血栓形成与感染性休克有关，但体温调节对感染性休克患者凝血的影响尚不清楚。我们检验了这样一个假设，即轻度诱导性低温可降低感染性休克患者的凝血和血小板聚集。
这是一项来自丹麦 8 个重症监护病房的成年感染性休克患者的随机对照试验的二次分析。患者被随机分配至接受 24 小时轻度诱导性低温或常规体温管理。在试验纳入时、接受 12 小时体温管理后以及纳入后 24 小时评估血流变仪和血小板聚集。共有 326 名患者被随机分配至轻度诱导性低温组（n = 163）或常规体温管理组（n = 163）。
轻度诱导性低温组患者的活化部分凝血活酶时间和血栓起始时间（R 时间 8.0 分钟 [四分位距，IQR 6.6-11.1] 与 7.2 分钟 [IQR 5.8-9.2]；p =.004）略有延长，血栓延伸率（角度 68° [IQR 59-73] 与 71° [IQR 63-75]；p =.014）也略有抑制。24 小时后也观察到了这种效果。血栓强度保持不变（MA 71 毫米 [IQR 66-76] 与常规体温管理的 72 毫米 [IQR 65-77]，p =.9）。纤溶亢进的患者比例没有受到影响（0.7% vs. 3.3%；p =.19），但低温组无纤溶的患者比例较高（8.8% vs. 40.4%；p <.001）。
ASPI 85U（IQR 50-113）与 109U（IQR 74-148，p <.001），ADP 61U（IQR 40-83）与 79U（IQR 54-101，p <.001），TRAP 108（IQR 83-154）与 119（IQR 94-146，p =.042）和 COL 50U（IQR 34-66）与 67U（IQR 46-92，p <.001）。
在感染性休克患者中，轻度诱导性低温轻度损害血栓形成起始，但不改变血栓强度。血小板聚集轻度受损。然而，轻度诱导性低温对血流变仪和血小板聚集的影响并未达到具有临床意义的范围。我们确实观察到纤溶的大量减少。
