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血乳酸清除率、红细胞分布宽度联合神经元特异性烯醇酶对急性一氧化碳中毒患者迟发性脑病的预测研究

Prediction research of blood lactate clearance rate,red blood cell distribution width combined with neuron specific enolase on delayed encephalopathy in patients with acute carbon monoxide poisoning
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摘要 目的探讨血乳酸清除率、红细胞分布宽度(RDW)联合神经元特异性烯醇酶(NSE)对急性一氧化碳(CO)中毒患者迟发性脑病的预测价值。方法收集138例急性CO中毒患者的一般临床资料,并检测患者入院时的血乳酸清除率、RDW、NSE水平。随访3个月,根据有无发生迟发性脑病将患者分为迟发性脑病组和无迟发性脑病组,比较两组的临床资料。采用Logistic回归分析急性CO中毒患者发生迟发性脑病的影响因素,并采用ROC曲线评价血乳酸清除率、RDW联合NSE对急性CO中毒患者发生迟发性脑病的预测价值。结果随访3个月,138例急性CO中毒患者有106例未发生迟发性脑病,有32例发生迟发性脑病,发生率为23.19%。与无迟发性脑病组比较,迟发性脑病组脑血管疾病和重度中毒比率、年龄、中毒时长、昏迷时间、RDW水平、NSE水平均显著升高,早期进行高压氧治疗比率、高压氧疗程及血乳酸清除率均显著降低(P<0.05~0.01)。多因素Logistic回归分析显示,年龄大、合并脑血管疾病、中毒时间长、昏迷时间长、重度中毒及RDW、NSE高水平均是急性CO中毒患者发生迟发性脑病的危险因素(均P<0.05),早期进行高压氧治疗、高压氧疗程及血乳酸清除率是急性CO中毒患者发生迟发性脑病的保护因素(均P<0.05)。血乳酸清除率、RDW联合NSE预测急性CO中毒患者发生迟发性脑病的灵敏度及曲线下面积(AUC)均高于单独预测(均P<0.05),特异度均与单独预测差异无统计学意义(均P>0.05)。结论发生迟发性脑病的急性CO中毒患者RDW、NSE水平呈高表达,而血乳酸清除率呈低表达。三者水平均与急性CO中毒患者发生迟发性脑病有着密切的关系,对于预测迟发性脑病均有一定的效能,但上述指标联合预测效能更佳,值得临床推广。 Objective To investigate the predictive value of blood lactate clearance rate,red blood cell distribution width(RDW)combined with neuron specific enolase(NSE)on delayed encephalopathy in patients with acute carbon monoxide(CO)poisoning.Methods The general clinical data of 138 patients with acute CO poisoning were collected,and all patients were examined for blood lactate clearance,RDW and NSE levels at admission.Followed up for 3 months,the patients were divided into occurrence group and non occurrence group according to whether there was delayed encephalopath,and the clinical data of the two groups were compared.Logistic regression was used to analyze the influencing factors of delayed encephalopathy in patients with acute CO poisoning,and the ROC curve was used to evaluate the predictive value of blood lactate clearance,RDW combined NSE in patients with acute CO poisoning.Results Following up for 3 months,106 of 138 patients with acute CO poisoning did not occured delayed encephalopathy,and 32 patients occured delayed encephalopathy,with an incidence of 23.19%.Compared with those in non occurrence group,the proportion of complicated with cerebrovascular diseases and severe poisoning,age,the length of poisoning,coma time,RDW level and NSE level in the occurrence group were significantly higher,and the rate of early hyperbaric oxygen treatment,the course of hyperbaric oxygen and blood lactate clearance rate were significantly lower(P<0.05-0.01).Multivariate Logistic regression analysis showed that old,complicated with cardiovascular and cerebrovascular diseases,long poisoning time,long coma time,severe poisoning and high expression of RDW and NSE were the risk factors of delayed encephalopathy in patients with acute CO poisoning(all P<0.05),and early hyperbaric oxygen treatment,the course of hyperbaric oxygen and blood lactate clearance rate were the protective factors(all P<0.05).The sensitivity and area under curve(AUC)of blood lactate clearance,RDW combined with NSE in predicting the occurrence of delayed encephalopathy in patients with acute CO poisoning were higher than those predicted alone(all P<0.05),and the specificity were not significantly different from those predicted alone(all P>0.05).Conclusions The levels of RDW and NSE in patients with acute CO poisoning with delayed encephalopathy are highly expressed,while the blood lactate clearance rate is low expressed.The levels of the three are closely related to the occurrence of delayed encephalopathy in patients with acute CO poisoning,and they have a certain effect on the prediction of delayed encephalopathy,but the combine prediction effect of the above indicators is better,which is worthy of clinical promotion.
作者 宋丹 李海红 SONG Dan;LI Haihong(Department of Emergency,Lianyungang First People’s Hospital(First Affiliated Hospital of Kangda College of Nanjing Medical University),Lianyungang 222000,China)
出处 《临床神经病学杂志》 CAS 2023年第4期274-278,共5页 Journal of Clinical Neurology
关键词 血乳酸清除率 红细胞分布宽度 神经元特异性烯醇酶 一氧化碳中毒 迟发性脑病 blood lactate clearance rate red blood cell distribution width neuron specific enolase carbon monoxide poisoning delayed encephalopathy
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