Changshin Kang1, Yong Nam In2, Jung Soo Park3, Yeonho You1, Jin Hong Min4, Insool Yoo4, Yong Chul Cho1, Wonjoon Jeong1, Hong Joon Ahn1, Seung Ryu1, Jinwoong Lee1, Seung Whan Kim1, Sung Uk Cho1, Se Kwang Oh1, Byung Kook Lee5, Chan Kang6. 1. Department of Emergency Medicine, Chungnam National University Hospital, 282, Munhwa-ro, Jung-gu, Daejeon, Republic of Korea. 2. Department of Emergency Medicine, Hanyang University Hanmaeum Changwon Hospital, 21, Woni-daero, Seongsan-gu, Changwon, Republic of Korea. 3. Department of Emergency Medicine, Chungnam National University Hospital, 282, Munhwa-ro, Jung-gu, Daejeon, Republic of Korea; Department of Emergency Medicine, College of Medicine, Chungnam National University, 282, Mokdong-ro, Jung-gu, Daejeon, Republic of Korea. Electronic address: cpcr@cnu.ac.kr. 4. Department of Emergency Medicine, Chungnam National University Hospital, 282, Munhwa-ro, Jung-gu, Daejeon, Republic of Korea; Department of Emergency Medicine, College of Medicine, Chungnam National University, 282, Mokdong-ro, Jung-gu, Daejeon, Republic of Korea. 5. Department of Emergency Medicine, Chonnam National University Medical School, Gwangju 61469, Republic of Korea. 6. Department of Orthopaedic Surgery, Chungnam National University School of Medicine, Daejeon, Repubilic of Korea.
Abstract
AIM: In a previous study, low and high-normal arterial carbon dioxide tension (PaCO2) were not associated with serum neuron-specific enolase (NSE) in cardiac arrest survivors. We assessed the effect of PaCO2 on NSE in cerebrospinal fluid (CSF) and serum. METHODS: This was a retrospective study. PaCO2 for the first 24 h was analysed in four means, qualitative exposure state (qES), time-weighted average (TWA), median, and minimum-maximum (Min-Max). These subgroups were divided into low (LCO2) and high PaCO2 (HCO2) groups defined as PaCO2 ≤ 35.3 and PaCO2 > 43.5 mmHg, respectively. NSE was measured at 24, 48, and 72 h (sNSE24,48,72 and cNSE24,48,72) from return of spontaneous circulation (ROSC). The primary outcome was the association between PaCO2 and the NSE measured at 24 h after ROSC. RESULTS: Forty-two subjects (male, 33; 78.6%) were included in total cohort. PaCO2 in TWA subgroup was associated with cNSE24,48,72, while PaCO2 in the other subgroup were only associated with cNSE24. PaCO2 and cNSE in qES subgroup showed good correlation (r = -0.61; p < 0.01), and in TWA, median, and Min-Max subgroup showed moderate correlations (r = -0.57, r = -0.48, and r = -0.60; p < 0.01). Contrastively, sNSE was not associated and correlated with PaCO2 in all analysis. Poor neurological outcome in LCO2 was significantly higher than HCO2 in qES, TWA, and median subgroups (p < 0.01, p < 0.01, and p = 0.02). CONCLUSION: Association was found between NSE and PaCO2 using CSF, despite including normocapnic ranges; TWA of PaCO2 may be most strongly associated with CSF NSE levels. A prospective, multi-centre study is required to confirm our results.
AIM: In a previous study, low and high-normal arterial carbon dioxide tension (PaCO2) were not associated with serum neuron-specific enolase (NSE) in cardiac arrest survivors. We assessed the effect of PaCO2 on NSE in cerebrospinal fluid (CSF) and serum. METHODS: This was a retrospective study. PaCO2 for the first 24 h was analysed in four means, qualitative exposure state (qES), time-weighted average (TWA), median, and minimum-maximum (Min-Max). These subgroups were divided into low (LCO2) and high PaCO2 (HCO2) groups defined as PaCO2 ≤ 35.3 and PaCO2 > 43.5 mmHg, respectively. NSE was measured at 24, 48, and 72 h (sNSE24,48,72 and cNSE24,48,72) from return of spontaneous circulation (ROSC). The primary outcome was the association between PaCO2 and the NSE measured at 24 h after ROSC. RESULTS: Forty-two subjects (male, 33; 78.6%) were included in total cohort. PaCO2 in TWA subgroup was associated with cNSE24,48,72, while PaCO2 in the other subgroup were only associated with cNSE24. PaCO2 and cNSE in qES subgroup showed good correlation (r = -0.61; p < 0.01), and in TWA, median, and Min-Max subgroup showed moderate correlations (r = -0.57, r = -0.48, and r = -0.60; p < 0.01). Contrastively, sNSE was not associated and correlated with PaCO2 in all analysis. Poor neurological outcome in LCO2 was significantly higher than HCO2 in qES, TWA, and median subgroups (p < 0.01, p < 0.01, and p = 0.02). CONCLUSION: Association was found between NSE and PaCO2 using CSF, despite including normocapnic ranges; TWA of PaCO2 may be most strongly associated with CSF NSE levels. A prospective, multi-centre study is required to confirm our results.
Authors: Seung Ha Son; Yong Nam In; Jung Soo Park; Yeonho You; Jin Hong Min; Insool Yoo; Yong Chul Cho; Wonjoon Jeong; Hong Joon Ahn; Changshin Kang; Byung Kook Lee Journal: Neurocrit Care Date: 2021-01-11 Impact factor: 3.210