Mild induced hypothermia and coagulation and platelet function in patients with septic shock: Secondary outcome of a randomized trial

• Published in: Acta anaesthesiologica Scandinavica 2023-08, Vol.67 (7), p.909-917
• Main Authors: Itenov, Theis S., Kromann, Maria E., Ostrowski, Sisse R., Bestle, Morten H., Mohr, Thomas, Gyldensted, Louise, Lindhardt, Anne, Thormar, Katrin, Sessler, Daniel I., Juffermans, Nicole P., Lundgren, Jens D., Jensen, Jens‐Ulrik
• Format: Article
• Language: English
• Subjects: Abnormalities; Adult; Blood clots; Blood Coagulation; Blood Coagulation Disorders - complications; Blood Coagulation Tests; Body temperature; Coagulation; coagulopathy; Fibrinolysis; Hospitals; Humans; Hypothermia; Hypothermia, Induced; Intensive care units; Mechanical ventilation; Platelet aggregation; Platelets; Secondary analysis; Sepsis; Septic shock; Shock, Septic - complications; Shock, Septic - therapy; therapeutic hypothermia; Thermoregulation; Thromboplastin; Thrombosis
• ISSN: 0001-5172; 1399-6576
• DOI: 10.1111/aas.14254

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