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

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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.

Original languageEnglish
JournalActa Anaesthesiologica Scandinavica
Volume67
Issue number7
Pages (from-to)909-917
Number of pages9
ISSN0001-5172
DOIs
Publication statusPublished - 2023

Bibliographical note

Funding Information:
The authors would like to extend our gratitude to Pär Johansson, Randa Zo El-Ghina, Tina Olsen, Marianne Røndbjerg, and Anja Skaaning the Blood Bank of Region Hovedstaden for their assistance in ascertaining coagulation test results. The CASS study and this sub-study was funded by Trygfonden (application no. 7-10-1301), Lundbeckfonden (application no. R54-A5342) and Danish National Research Foundation (Grant number DNRF126), and The Research Foundation for the Capital Region of Denmark (A6052). The authors declare no conflict of interest.

Funding Information:
The authors would like to extend our gratitude to Pär Johansson, Randa Zo El‐Ghina, Tina Olsen, Marianne Røndbjerg, and Anja Skaaning the Blood Bank of Region Hovedstaden for their assistance in ascertaining coagulation test results. The CASS study and this sub‐study was funded by Trygfonden (application no. 7‐10‐1301), Lundbeckfonden (application no. R54‐A5342) and Danish National Research Foundation (Grant number DNRF126), and The Research Foundation for the Capital Region of Denmark (A6052). The authors declare no conflict of interest.

Publisher Copyright:
© 2023 The Authors. Acta Anaesthesiologica Scandinavica published by John Wiley & Sons Ltd on behalf of Acta Anaesthesiologica Scandinavica Foundation.

    Research areas

  • coagulopathy, sepsis, septic shock, therapeutic hypothermia

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