Abstract

Purpose of the study: Cardiac arrest (CA) is an important cause of death and disability. With the standardized use of target temperature management and on going sedation for 48–72h, early prognostication after CA is a challenge. The pathophysiology of post CA syndrome is a systemic ischemia/reperfusion response called sepsis-like syndrome.1 Early serum lactate clearance (LC) and lower serum lactate levels have been shown to be associated with decreased mortality in a diverse set of critical illnesses2: why don’t use LC as a prognostic factor of neurological outcome? We analysed the reliability of serum LC as a predictor in patients treated with therapeutic hypothermia after out of hospital CA. Material and methods: through a retrospective analysis of 60 patients admitted to our ICU, we analysed the lactate-level (mg/dl) at ICU admission and after 24h, thenweevaluated the lactate clearance. The LC was calculated as follows: 24-h LC (%) = (0h lactate−24h lactate)/0h lactate×100. Neurological outcome has been evaluated at 6 month using the Pittsburgh Cerebral Performance Category Scale (CPC). Results: themedian value of lactate at T0was26.35 (15.9–65.1); the median value of lactate at T24 was 17.3 (10.15–24.6). 32 patients had a good neurological outcome (CPC 1–2). 28 patients had a bad neurological outcome (CPC 3–5). In the CPC1-2 group the median LC was 73% (−10% to 179%), in the CPC3-5 group the median LCwas 74% (17%–114%). The comparison of LC between the two group showed a p-value of 0.7 Conclusions: there is no correlation for LC in the first 24h after CA between both groups. This conclusion is in contrast with current evidence based in literature.3 Despite Lactacidemia is a sign of microcirculatory damage, our study shows that LC cannot be used to predict the neurological outcome.

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