• Claudio Sandroni, Daniele Natalini, and Jerry P Nolan.
• Università Cattolica del Sacro Cuore, Largo Francesco Vito 1, 00168, Rome, Italy. claudio.sandroni@policlinicogemelli.it.
• Crit Care. 2022 Nov 24; 26 (1): 361361.

AbstractMost of the patients who die after cardiac arrest do so because of hypoxic-ischemic brain injury (HIBI). Experimental evidence shows that temperature control targeted at hypothermia mitigates HIBI. In 2002, one randomized trial and one quasi-randomized trial showed that temperature control targeted at 32-34 °C improved neurological outcome and mortality in patients who are comatose after cardiac arrest. However, following the publication of these trials, other studies have questioned the neuroprotective effects of hypothermia. In 2021, the largest study conducted so far on temperature control (the TTM-2 trial) including 1900 adults comatose after resuscitation showed no effect of temperature control targeted at 33 °C compared with normothermia or fever control. A systematic review of 32 trials published between 2001 and 2021 concluded that temperature control with a target of 32-34 °C compared with fever prevention did not result in an improvement in survival (RR 1.08; 95% CI 0.89-1.30) or favorable functional outcome (RR 1.21; 95% CI 0.91-1.61) at 90-180 days after resuscitation. There was substantial heterogeneity across the trials, and the certainty of the evidence was low. Based on these results, the International Liaison Committee on Resuscitation currently recommends monitoring core temperature and actively preventing fever (37.7 °C) for at least 72 h in patients who are comatose after resuscitation from cardiac arrest. Future studies are needed to identify potential patient subgroups who may benefit from temperature control aimed at hypothermia. There are no trials comparing normothermia or fever control with no temperature control after cardiac arrest.© 2022. The Author(s).

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