早期目标导向镇静下镇静药物对谵妄和炎症因子的影响
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摘要
目的:研究在早期目标导向镇静策略下,右美托咪定、咪达唑仑、丙泊酚三种药物对谵妄发生和炎症因子的影响。方法:选取川北医学院附属医院重症医学科需要接受镇静治疗的患者100例(2016年1月至2017年6月),随机分配接受右美托咪定(A组)、咪达唑仑(B组)、丙泊酚(C组)镇静治疗。躁动镇静评分量表评估各组镇静的水平,以达到躁动镇静评分-2～+1分镇静目标。用重症监护病房意识模糊评估法评估患者是否发生谵妄及持续时间。监测患者第1、3、7 d以及谵妄发生时炎症因子PCT、IL-6、CRP。结果:谵妄总体发生率为19.56%。A组谵妄发生率12.5%,明显低于B组34.8%(P=0.01)和C组20.7%(P=0.03)。A组CRP在第7 d显著低于与另两组(52.64±68.13 mg/L vs 92.65±68.53 mg/L vs 123.14±97.51 mg/L,P=0.013)。除C组CRP变化无统计学差异外,其余三组三种炎症因子均随时间显著下降,A组下降时间趋势更明显。在谵妄和非谵妄组中比较,IL-6(P=0.012)和CRP(P=0.021)具有统计学差异。多因素logistic回归分析,CRP(OR=1.011,95%CI:1.001～1.021,P=0.036)为炎症因子中影响谵妄发生的独立危险因素。结论:在早期目标导向镇静策略下,使用右美托咪定谵妄发生率更低、持续时间更短。右美托咪定对炎症因子的抑制作用最突出,右美托咪定减少谵妄发生机制与降低炎症反应有关。
Objective:To study the effect of dexmedetomidine, midazolam, and propofol on the occurrence of delirium and inflammatory factors under the strategy of early goal-directed sedation.Methods:A total of 100 patients who were hospitalized in the Department of Critical Care Medicine, The Affiliated Hospital of North Sichuan Medical College, from January 2016 to June 2017 were enrolled and randomly assigned to receive dexmedetomidine(group A), midazolam(group B), or propofol(group C) for sedation. The level of sedation in each group was assessed using the Richmond Agitation and Sedation Scale(RASS) with RASS score-2 to +1 as the target score. Occurrence of delirium and its duration were assessed by the Confusion Assessment Method used in the intensive care unit. Procalcitonin, interleukin-6(IL-6), and C-reactive protein(CRP) were monitored on days 1, 3, and 7, as well as during the occurrence of delirium.Results:The overall incidence of delirium was 19.56%. The incidence of delirium in group A was 12.5%, which was significantly lower than that in group B(34.8%, P = 0.01) and group C(20.7%, P = 0.03).The level of CRP was significantly lower in group A than in the other two groups on day 7(52.64 ± 68.13 mg/L vs92.65 ± 68.53 mg/L and 123.14 ± 97.51 mg/L, P = 0.013). All the three inflammatory factors in the three groups(except for CRP in group C) decreased significantly with time, with the greatest decrease observed in group A. There were significant differences in IL-6 and CRP between delirium and non-delirium groups(P = 0.012 and 0.021, respectively). A multivariate logistic regression analysis showed that CRP was an independent risk factor for delirium among the inflammatory factors(odds ratio = 1.011, 95% confidence interval: 1.001 ～ 1.021, P = 0.036).Conclusion:Under the strategy of early goal-directed sedation, dexmedetomidine results in a lower incidence of delirium with a shorter duration of delirium. Dexmedetomidine has the most prominent inhibitory effect on inflammatory factors, and the mechanism of reducing delirium by dexmedetomidine is related to the reduction of inflammatory response.
Objective:To study the effect of dexmedetomidine, midazolam, and propofol on the occurrence of delirium and inflammatory factors under the strategy of early goal-directed sedation.Methods:A total of 100 patients who were hospitalized in the Department of Critical Care Medicine, The Affiliated Hospital of North Sichuan Medical College, from January 2016 to June 2017 were enrolled and randomly assigned to receive dexmedetomidine(group A), midazolam(group B), or propofol(group C) for sedation. The level of sedation in each group was assessed using the Richmond Agitation and Sedation Scale(RASS) with RASS score-2 to +1 as the target score. Occurrence of delirium and its duration were assessed by the Confusion Assessment Method used in the intensive care unit. Procalcitonin, interleukin-6(IL-6), and C-reactive protein(CRP) were monitored on days 1, 3, and 7, as well as during the occurrence of delirium.Results:The overall incidence of delirium was 19.56%. The incidence of delirium in group A was 12.5%, which was significantly lower than that in group B(34.8%, P = 0.01) and group C(20.7%, P = 0.03).The level of CRP was significantly lower in group A than in the other two groups on day 7(52.64 ± 68.13 mg/L vs92.65 ± 68.53 mg/L and 123.14 ± 97.51 mg/L, P = 0.013). All the three inflammatory factors in the three groups(except for CRP in group C) decreased significantly with time, with the greatest decrease observed in group A. There were significant differences in IL-6 and CRP between delirium and non-delirium groups(P = 0.012 and 0.021, respectively). A multivariate logistic regression analysis showed that CRP was an independent risk factor for delirium among the inflammatory factors(odds ratio = 1.011, 95% confidence interval: 1.001 ～ 1.021, P = 0.036).Conclusion:Under the strategy of early goal-directed sedation, dexmedetomidine results in a lower incidence of delirium with a shorter duration of delirium. Dexmedetomidine has the most prominent inhibitory effect on inflammatory factors, and the mechanism of reducing delirium by dexmedetomidine is related to the reduction of inflammatory response.
引文
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7.莫伟胜,卜会驹,郭发良.相同镇静深度下右美托咪定与咪达唑仑、丙泊酚对危重症患者炎性反应因子水平的影响研究[J].吉林医学,2014,35(13):2 854-2 855.
8.Peng M,Ye JS,Wang YL,et al.Posttreatment with propofol attenuates lipopolysaccharide-induced up-regulation of inflammatory molecules in primary microglia[J].Inflammation Research,2014,63(5):411-418.
9.Eckenhoff RG,Laudansky KF.Anesthesia,surgery,illness and Alzheimer's disease[J].Progress in Neuro-Psychopharmacology and Biological Psychiatry,2013,47:162-166.
10.de Rooij SE,van Munster BC,Korevaar JC,et al.Cytokines and acute phase response in delirium[J].Journal of Psychosomatic Research,2007,62(5):521-525.
11.Boogaard MVD,Kox M,Quinn KL,et al.Biomarkers associated with delirium in critically ill patients and their relation with long-term subjective cognitive dysfunction;indications for different pathways governing delirium in inflamed and noninflamed patients[J].Critical Care,2011,15(6):1-9.
2.Alain R,Hülya B,Daniela B,et al.Intra-operative events during cardiac surgery are risk factors for the development of delirium in the ICU[J].Critical Care,2016,20(1):264-272.
3.Inouye SK,Robinson T,Blaum C,et al.American geriatrics society abstracted clinical practice guideline for postoperative delirium in older adults[J].Journal of the American Geriatrics Society,2015,63(1):142-150.
4.Silverstein JH,Deiner SG.Perioperative delirium and its relationship to dementia[J].Progress in Neuro-PsychopharMacology&Biological Psychiatry,2013,43(24):108-115.
5.Tanyong P,Kaweesak C,Onuma C,et al.Incidence and risk factors of delirium in multi-center Thai surgical intensive care units:a prospective cohort study[J].Journal of Intensive Care,2015,3(1):53-61.
6.Shehabi Y,Bellomo R,Reade MC,et al.Early goal-directed sedation versus standard sedation in mechanically ventilated critically ill patients:a pilot study[J].Critical Care Medicine,2013,41(8):1 983-1 991.
7.莫伟胜,卜会驹,郭发良.相同镇静深度下右美托咪定与咪达唑仑、丙泊酚对危重症患者炎性反应因子水平的影响研究[J].吉林医学,2014,35(13):2 854-2 855.
8.Peng M,Ye JS,Wang YL,et al.Posttreatment with propofol attenuates lipopolysaccharide-induced up-regulation of inflammatory molecules in primary microglia[J].Inflammation Research,2014,63(5):411-418.
9.Eckenhoff RG,Laudansky KF.Anesthesia,surgery,illness and Alzheimer's disease[J].Progress in Neuro-Psychopharmacology and Biological Psychiatry,2013,47:162-166.
10.de Rooij SE,van Munster BC,Korevaar JC,et al.Cytokines and acute phase response in delirium[J].Journal of Psychosomatic Research,2007,62(5):521-525.
11.Boogaard MVD,Kox M,Quinn KL,et al.Biomarkers associated with delirium in critically ill patients and their relation with long-term subjective cognitive dysfunction;indications for different pathways governing delirium in inflamed and noninflamed patients[J].Critical Care,2011,15(6):1-9.