高氧液治疗急性一氧化碳中毒迟发脑病的临床疗效观察

目的:观察高氧液治疗急性一氧化碳中毒迟发脑病的临床效果。方法:对68例急性一氧化碳中毒迟发脑病患者进行高氧液治疗,分析治疗前、后脑电图变化及临床疗效。结果:高氧液治疗组同治疗前及对照组相比,急性一氧化碳中毒迟发脑病患者脑电图明显好转,临床总有效率显著提高。结论:高氧液对急性一氧化碳中毒迟发脑病患者有显著治疗效果,脑电图可作为诊断病情及观察临床疗效的一个重要的客观指标。     

一氧化碳中毒并发迟发性脑病的护理

急性一氧化碳中毒患者经过及时的积极治疗后,多数可以治愈,但也有部分患者出现迟发性脑病,又称急性一氧化碳中毒后续症、后发症、续发症等,是指急性一氧化碳患者,意识清醒后,经过一段假愈期,突然发生以痴呆、精神症状和锥体外系表现为主的神经系统疾病[1]。该病病程长,恢复慢,并发症多,致残率高,严重危害人们的健康,影响生活质量。我院于2003年12月~2007年2月共收治958例一氧化碳中毒患者,其中并发迟发性脑病患者123例(占12·8%),现将护理体会总结如下。1临床资料123例患者中,男78例,女45例,年龄8~52岁,病因为通风条件不良的室内使用热水器…     

腹腔注射法制备一氧化碳中毒迟发性脑病大鼠模型

目的：建立可靠的急性一氧化碳（CO）中毒迟发性脑病的动物模型。方法：雄性SD大鼠,分次腹腔注射CO染毒制备模型,动态监测尾血碳氧血红蛋白（HbCO）浓度;Morris水迷宫检测大鼠1-5w逃避潜伏期;尼氏染色及TUNEL原位末端凋亡染色检测大脑皮质及海马细胞损伤及凋亡。结果：染毒后,大鼠出现典型的CO重度中毒症状,体内血液HbCO浓度迅速升高,使用分次腹腔注射法,大鼠可维持长时间（〉12h）高HbCO状态（HbCO〉48%）;中毒组大鼠水迷宫检测认知功能较对照组下降,病理学检查显示大鼠出现脑细胞损伤、凋亡明显。结论：本研究建立了一种较为符合迟发性脑病临床特征的动物模型,具有简单、可靠、重复性好的特点,为深入研究急性CO中毒致迟发性脑损伤的机制提供可靠基础。     

腹腔注射法制备一氧化碳中毒迟发性脑病大鼠模型

目的:建立可靠的急性一氧化碳(CO)中毒迟发性脑病的动物模型。方法:雄性SD大鼠,分次腹腔注射CO染毒制备模型,动态监测尾血碳氧血红蛋白(HbCO)浓度;Morris水迷宫检测大鼠1-5w逃避潜伏期;尼氏染色及TUNEL原位末端凋亡染色检测大脑皮质及海马细胞损伤及凋亡。结果:染毒后,大鼠出现典型的CO重度中毒症状,体内血液HbCO浓度迅速升高,使用分次腹腔注射法,大鼠可维持长时间(>12h)高HbCO状态(HbCO>48%);中毒组大鼠水迷宫检测认知功能较对照组下降,病理学检查显示大鼠出现脑细胞损伤、凋亡明显。结论:本研究建立了一种较为符合迟发性脑病临床特征的动物模型,具有简单、可靠、重复性好的特点,为深入研究急性CO中毒致迟发性脑损伤的机制提供可靠基础。     

颈动脉与鞘内注射脐带血干细胞治疗一氧化碳中毒迟发性脑病的临床研究

目的观察脐带血干细胞蛛网膜下腔及颈动脉注射治疗一氧化碳中毒迟发性脑病(DEACMP)的安全性及治疗效果。方法收集沧州市中心医院2012年10月至2015年9月期间因DEACMP入院治疗的患者32例,设立治疗组:对17例DEACMP患者以颈动脉及鞘内进行间充质干细胞(MSC)注射,每次注射MSC为2×10~7,每次间隔7 d,注射4次为1疗程并在治疗前和治疗后与对照组进行影像学和症状体征,治疗副作用及智能精神状态评分(MMSE)和日常生活活动能力(Barthl)评分;对照组:仅给予常规改善脑代谢药物胞二磷胆碱等及维生素类药物治疗。对2个组不能进食者予以补液治疗。各组数据使用重复测量资料的方差分析对结果进行统计分析。结果所有患者在干细胞治疗中均无特殊不适,均未出现治疗不良反应。治疗组患者MMSE评分为94.35±12.56,高于对照组3.24±2.32(t=27.6288,P=0.000);治疗组Barthl评分为93.60±13.36,高于对照组6.39±6.80,差异均有统计学意义(t=22.3845,P=0.000)。治疗组影像检查结果好转率为76.47%,对照组好转率为26.66%两组比较差异有统计学意义(χ~2=4.402,P=0.0359)。结论 MSC颈动脉与鞘内注射治疗DEACMP效果显著。     

急性一氧化碳中毒大鼠海马组织NaPi-IIb 蛋白表达的研究

目的:研究急性一氧化碳中毒后大鼠海马组织NaPi-IIb蛋白的表达情况。方法:选取雄性Sprague-Dawley(SD)大鼠48只,随机分为正常对照组(NC组)14只、缺氧组(IB组)17只、急性CO中毒组(CO-P组)17只。利用简易密闭容器建立缺氧模型;利用多次追加腹腔注射CO气体染毒的方法建立急性一氧化碳中毒模型。观察各组大鼠在建模过程中呼吸、活动改变情况。大鼠于建模24 h-26 h后取脑组织制作石蜡切片,选取海马组织平面利用免疫组织化学染色(IHC)观察组织形态及海马组织中NaPi-IIb蛋白的表达情况。同时,分离各组大鼠海马组织,利用蛋白质免疫印迹技术(Western Blot,WB)检测海马组织中NaPi-IIb蛋白的表达情况。结果:IHC、WB结果表明海马组织中NaPi-IIb蛋白的表达在CO-P组中明显高于NC组、IB组(P0.05)。NC组、IB组比较,NaPi-IIb蛋白的表达无明显差异(P0.05)。结论:在本研究中,CO暴露后,大鼠海马组织NaPi-IIb蛋白表达的增高与CO相关。NaPi-IIb蛋白可能成为CO中毒稳定、可靠的诊断标志物。     

高氧液临床应用疗效观察

我院自引进高氧液以来,现已应用于临床650例,涉及病种10余个,现将疗效观察报告如下。     

急性一氧化碳中毒迟发性脑病发病机制的研究进展

一氧化碳(CO)中毒是我国冬春季节常见的窒息性气体中毒。CO中毒迟发性脑病是CO中毒后的严重神经系统后遗症,其发病机制复杂,目前仍未十分明确。本文对近年来CO中毒迟发性脑病发病机制的研究结果作一综述,为临床诊疗工作提供帮助。     

高压氧治疗急性一氧化碳中毒的护理

我科自2003年12月至2009年12月,对330例急性一氧化碳中毒患者采用高压氧治疗,取得较好疗效,现将护理体会报告如下。     

急性一氧化碳中毒131例临床分析

目的：探讨急性一氧化碳中毒（ACOP）患者的发病特点、临床表现及其对预后的影响。方法：回顾性分析2006年1月一2011年12月我院收治的131例ACOP患者,将其按病情的严重程度分为轻、中、重度3组,比较各组的发病原因和临床表现。结果：接触时间、基础疾病、血清肌酸激酶（CK）、昏迷时间在3组间差异有显著性（P〈0．01）,年龄、性别、中毒原因方面3组间差异无显著性（P〉0．05）。迟发性脑病组和无迟发性脑病组在年龄、基础疾病、并发症、接触时间、昏迷时间、CK方面差异有显著性（P〈0．01）;而在性别、中毒原因方面差异无显著性（P〉0．05）。结论：对于ACOP患者而言,接触时间长、伴有基础疾病、昏迷时间长、CK高不仅提示病情的严重程度,更是迟发性脑病的易患因素。而高压氧治疗是ACOP的首选及有效的治疗方法。     

高压氧治疗急性一氧化碳中毒合并迟发脑病330例临床分析

目的:分析总结高压氧治疗急性一氧化碳中毒并发迟发脑病的临床表现,治疗特点及影响因素.方法:回顾性分析我院1996年1月-至2007年12月收治的330例急性一氧化碳中毒合并迟发脑病患者的临床资料.结果:330例患者中痊愈298例,占90.30%,有效32例,占9.70%.结论:治疗时间越早,临床恢复越好;治疗时间越长,效果越好.     

DNA Pooling Base Genome-Wide Association Study Identifies Variants at NRXN3 Associated with Delayed Encephalopathy after Acute Carbon Monoxide Poisoning

Delayed encephalopathy after acute carbon monoxide poisoning (DEACMP) is more characteristic of anoxic encephalopathy than of other types of anoxia. Those who have the same poisoning degree and are of similar age and gender have a greater risk of getting DEACMP. This has made it clear that there are obvious personal differences. Genetic factors may play a very important role. The authors performed a genome-wide association study involving pooling of DNA obtained from 175 patients and 244 matched acute carbon monoxide poisoning without delayed encephalopathy controls. The Illumina HumanHap 660 Chip array was used for DNA pools. Allele frequencies of all SNPs were compared between delayed encephalopathy after acute carbon monoxide poisoning and control groups and ranked. A total of 123 SNPs gave an OR >1.4. Of these, 46 mapped in or close to known genes. Forty-eight SNPs located in 19 genes were associated with DEACMP after correction for 5% FDR in the genome-wide association of pooled DNA. Two SNPs (rs11845632 and rs2196447) locate in the Neurexin 3 gene were selected for individual genotyping in all samples and another cohort consisted of 234 and 271 controls. There were significant differences in the genotype and allele frequencies of rs11845632 and rs2196447 between the DEACMP group and controls group (all P-values <0.05). This study describes a positive association between Neurexin 3 and controls in the Han Chinese population, and provides genetic evidence to support the susceptibility of DEACMP, which may be the resulting interaction of environmental and genetic factors.     

Neuroprotective Effects of Erythropoietin in Patients with Carbon Monoxide Poisoning

The purpose of this study was to evaluate the efficacy of erythropoietin (EPO) for treating patients with carbon monoxide (CO) poisoning. We conducted a randomized, prospective study of 103 patients with CO poisoning in two groups: an EPO group (n = 54; patients received EPO) and a placebo group (n = 49; patients received normal saline). The study endpoints were the functional outcome at day 30 (the Barthel index and neurologic sequelae), National Institutes of Health Stroke Scale (NIHSS) score, and the levels of S‐100β. At 18 days, the NIHSS score improved significantly and S‐100β levels significantly decreased in patients in the EPO group. At 30 days, patients in the EPO group had a superior Barthel index and fewer patients had delayed neurologic sequelae (DNS). This study demonstrated that early administration of EPO to patients with CO poisoning improved neurological outcomes and reduced the incidence of DNS. © 2013 Wiley Periodicals, Inc. J BiochemMol Toxicol 27:266‐271, 2013; View this article online at wileyonlinelibrary.com . DOI 10.1002/jbt.21484     

Morbidity from Acute Carbon Monoxide Poisoning at Three-year Follow-up

Seventy-four survivors of acute carbon monoxide poisoning were followed up for an average of three years. In eight patients gross neuropsychiatric damage was directly attributable to the poisoning. Three patients had committed suicide and eight had died from other causes. Morbidity and mortality in those deliberately and accidentally poisoned was approximately equal.Of 63 patients alive at follow-up eight showed an improvement and 21 (33.3%) a deterioration of personality after poisoning, and 27 (43%) reported a subsequent impairment of memory. Deterioration of personality and memory impairment were highly correlated. The level of consciousness on admission to hospital in the acute phase of poisoning correlated significantly with the development of gross neuropsychiatric sequelae. These findings emphasize the importance of prompt and efficient treatment of carbon monoxide poisoning and the need to follow-up all cases in the anticipation of a relapsing course or the development of sequelae.     

Outcome of Patients with Carbon Monoxide Poisoning at a Far-East Poison Center

Introduction

Many cases of carbon monoxide poisoning in Taiwan are due to burning charcoal. Nevertheless, few reports have analyzed the mortality rate of these patients who survive to reach a hospital and die despite intensive treatment. Therefore, this study examined the clinical features, physiological markers, and outcomes after carbon monoxide poisoning and the associations between these findings.

Methods

We analyzed the records of 261 patients who were referred for management of carbon monoxide intoxication between 2000 and 2010. Patients were grouped according to status at discharge as alive (survivor, n = 242) or dead (non-survivor, n = 19). Demographic, clinical, laboratory, and mortality data were obtained for analysis.

Results

Approximately half of the cases (49.4%) attempted suicide by burning charcoal. Most of the patients were middle-aged adults (33±19 years), and were referred to our hospital in a relatively short period of time (6±10 hours). Carbon monoxide produced many serious complications after exposure: fever (26.1%), hypothermia (9.6%), respiratory failure (34.1%), shock (8.4%), myocardial infarction (8.0%), gastrointestinal upset (34.9%), hepatitis (18.4%), renal failure (25.3%), coma (18.0%) and rhabdomyolysis (21.8%). Furthermore, the non-survivors suffered greater incidences of hypothermia (P<0.001), respiratory failure (P<0.001), shock (P<0.001), hepatitis ((P=0.016), renal failure (P=0.003), coma (P<0.001) than survivors. All patients were treated with high concentration of oxygen therapy using non-rebreather mask. However, hyperbaric oxygen therapy was only used in 18.8% of the patients. In a multivariate-Cox-regression model, it was revealed that shock status was a significant predictor for mortality after carbon monoxide poisoning (OR 8.696, 95% CI 2.053-37.370, P=0.003). Finally, Kaplan-Meier analysis confirmed that patients with shock suffered greater cumulative mortality than without shock (Log-rank test, Chi-square 147.404, P<0.001).

Conclusion

The mortality rate for medically treated carbon monoxide-poisoned patients at our center was 7.3%. Furthermore, the analysis indicates that shock was most strongly associated with higher risk of mortality.     

七叶皂苷钠对一氧化碳中毒迟发性脑病大鼠模型细胞凋亡 及调控凋亡基因表达的影响

目的:探讨七叶皂苷钠对一氧化碳中毒迟发性脑病大鼠模型细胞凋亡及Caspase-3表达的影响。方法:将30只大鼠随机分为正常对照组、一氧化碳中毒迟发性脑病大鼠模型对照组和七叶皂苷钠治疗组,原位末端标记法(TUNEL)检测细胞凋亡,免疫组化法检测Caspase-3的表达。结果:治疗组大鼠脑细胞凋亡率及Caspase-3表达较迟发性脑病对照组显著降低(P<0.01)。结论:七叶皂苷钠对一氧化碳中毒迟发性脑病的脑保护作用机制可能与干预脑细胞凋亡相关基因表达并减少神经细胞凋亡有关。