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Aim of the study This observational study was performed to assess the cerebral tissue oxygen saturation during and after therapeutic hypothermia in comatose patients after out-of-hospital cardiac arrest. Methods We performed a prospective observational study on the cerebral tissue oxygen saturation (SctO 2 ) in post-cardiac arrest patients treated with therapeutic hypothermia (TH) between March 2011 and April 2012. SctO 2 (measured by near-infrared spectroscopy) was non-invasively and continuously measured in 28 post-cardiac arrest patients during hypothermia and active rewarming. Results At the start of mechanically induced TH, SctO 2 was 68% (65–72) and PaCO 2 was 47.2mmHg (36.9–51.4). SctO 2 and PaCO 2 significantly decreased to 59% (57–64; p =0.006) and 36.6mmHg (33.9–44.7; p =0.002), respectively, within the first 3h of mechanically induced TH. Cerebral tissue oxygen saturation was significantly lower in non-survivors ( n =10) compared with survivors ( n =18) at 3h after induction of hypothermia ( p =0.02) while the decrease in PaCO 2 was similar in both groups. During TH maintenance, SctO 2 gradually returned to baseline values (69% (63–72)) at 24h, with no differences between survivors and non-survivors ( p =0.65). Carbon dioxide remained within the range of mild hypocapnia (32–38mmHg) throughout the hypothermic period. During rewarming, SctO 2 further increased to 71% (67–78). Conclusions Induction of TH in comatose post-CA patients changes the balance between oxygen delivery and supply. The decrease in SctO 2 was less pronounced in patients surviving to hospital discharge.

Method: We conducted a database study at Cochin hospital in Paris, France. Between December 2006 and January 2010, we included 381 patients who were all resuscitated from an OHCA (excepted those with a primary neurological cause or moribunds). A moderate glycemic control was applied in all patients (aiming to maintain glycemia between 5.1 and 7.7mmol/l). BG was measured every 3h during the first 48h. The median glycemia and the largest delta were assessed. Amultivariate analysis was performed to determine parameters that independently influenced the main outcome (CPC level at ICU discharge). Results: 136/381 patients (36%) had a favorable outcome (CPC 1–2). Median BG level was 7.6mmol/l [6.3–9.8] in patients with a favorable outcome compared to 9.0mmol/l (IQR: 7.1–10.6) for patientswithanunfavorableneurologic outcome (p 8.4mmol/l) was found to be an independent predictor of poor neurological issue (OR=0.43; 95% CI [0.24–0.78], p=0.006). Other predictive factors of poor outcome were an unshockable rhythm, cardiac arrest location, a no flow >4min and a low flow >15min. Finally an increase in median BG was associated with an increase in the proportion of patients with a poor neurological outcome (Fig. 1). Conclusion: Even after adjustment with usual prognostic factors, an increase in glycemia during the first 48h is associated with an unfavorable neurological outcome.