神经节苷脂联合高压氧治疗一氧化碳中毒迟发性脑病疗效分析

目的探讨神经节苷脂联合高压氧治疗急性一氧化碳中毒迟发性脑病的临床疗效。方法将78例急性一氧化碳中毒迟发性脑病患者随机分为两组,治疗组及对照组各39例。对照组给予高压氧等常规治疗措施,治疗组在常规治疗基础上加用神经节苷脂,两组均治疗14d。结果治疗组总有效率为87.18%,对照组总有效率为71.80%,两组疗效比较差异有统计学意义(P<0.05)。结论在常规高压氧治疗基础上加用神经节苷脂,能明显提高疗效,有效改善一氧化碳中毒迟发性脑病患者的预后。     

高压氧综合治疗一氧化碳中毒后迟发性脑病

急性一氧化碳(CO)迟发性脑病系指急性CO中毒患者,经抢救后意识恢复,于数日至数周的间歇期后再次出现以痴呆和锥体外系为主的神经精神症状.根据国内资料表明,其发生率为10.42%.有的学者报告年龄>40岁的CO中毒者,发生迟发性脑病机率最大.为了进一步提高治愈率,预防迟发性脑病的发生,现将我院41例患者的临床情况报告如下:1 临床资料1.1 一般资料:41例患者均为高压氧科住院病人,符合急性CO中毒后迟发性脑病的诊断标准.男23例,女18例,年龄24岁～74岁,平均年龄54.5岁.急性中毒后,当天接受高压氧治疗者8人,中毒后昏迷未及时接受高压氧治疗者33人;发现病     

高压氧联合药物治疗一氧化碳中毒迟发性脑病69例

目的总结一氧化碳中毒后迟发性脑病的临床特征及治疗方法。方法对收治的69例一氧化碳中毒迟发性脑病患者的临床资料进行回顾分析,分析其发病情况、临床表现、检查和治疗方法。结果 69例均有一氧化碳中毒清醒后再出现意识障碍,大部分有精神症状,少数有锥体外系表现,CT或MIR检查64例有异常表现,脑地形图检查均有异常,经高压氧联合药物治疗后取得较好疗效,其中痊愈38例,显效20例,无效9例,死亡2例。结论一氧化碳中毒后出现神经功能障碍,部分病例有锥体系功能障碍,CT、脑电图检查均有异常表现。采用药物联合高压氧治疗可获得满意疗效。     

高压氧综合疗法治疗一氧化碳中毒迟发性脑病

目的观察高压氧综合疗法治疗一氧化碳中毒迟发性脑病的临床疗效。方法对72例一氧化碳中毒迟发性脑病患者给予高压氧治疗，治疗压力为0．25MPa，每次吸氧60min，中间休息10min，每日1次。10次为1疗程，平均为2．2个疗程；并取主穴、配穴针刺治疗，每日1次，10d为1个疗程，共治疗3个疗程；同时配合应用神经细胞营养药物，维生素B1、B6、C、E及改善循环药物。结果高压氧综合疗法治疗一氧化碳中毒迟发性脑病的总有效率为77．8％。结论一氧化碳中毒迟发性脑病一经确诊在无高压氧绝对禁忌证的情况下，应尽早给予高压氧综合治疗。     

高压氧治疗一氧化碳中毒迟发性脑病28例

目的以确立一个在急诊一氧化碳中毒治疗过程中正确应用高压氧的指导原则。方法以记分法对急性一氧化碳(CO)中毒迟发性脑病(DEACMP)治疗前后常见的9项临床症状、体征进行统计学处理。结果28例CO中毒迟发性脑病高压氧与综合治疗后,有效率为80.5%。结论高压氧能有效地治疗DEACMP。     

高压氧联合治疗一氧化碳中毒迟发性脑病临床观察

一氧化碳中毒迟发性脑病（delayed encephalopathy after acute carbon monoxide poisoning,DEACMP）是指在急性一氧化碳中毒（COP）经治疗好转后,经2～60d的＂假愈期＂,又出现     

丁苯酞联合神经节苷酯治疗一氧化碳中毒迟发性脑病疗效观察

目的探讨丁苯酞联合神经节苷酯治疗一氧化碳中毒迟发性脑病临床疗效。方法回顾分析2010年~2015年我科收治的一氧化碳中毒迟发性脑病患者60例,随机分成对照组和治疗组,每组各30例,对照组应用高压氧及常规治疗,治疗组在高压氧及常规治疗的基础上联合丁苯酞联合神经节苷酯。治疗前及治疗1个月后测定日常生活活动能力量表(BI),痴呆简易筛查量表(BSSD),比较2个量表数值变化,评价临床效果。结果入院时2组患者BI、BSSD评分无显著差异(P>0.05)。治疗1个月后治疗组有效率86 66%,对照组有效率56.66%,治疗组疗效明显优于对照组(P<0.05)。结论丁苯酞联合神经节苷酯治疗一氧化碳中毒迟发性脑病临床疗效显著,值得推广。     

高压氧治疗急性一氧化碳中毒迟发性脑病疗效分析

急性一氧化碳（CO）中毒迟发性脑病是临床常见病,一旦发生,治疗复杂,部分遗留严重神经功能缺失甚至因此而死亡。本文对本院2001年6月收住的急性CO中毒迟发性脑病33例的临床特点、发病机制及治疗进行回顾性分析。1资料与方法1．1一般资料急性CO中毒者33例,其中男14例,女19例,年龄20-82岁,平均55．4岁。患者中毒后均有较长时间的昏迷史,最长5d,最短2h,平均10h左右。患者均出现“假愈期”,其中最长60d,最短2d,大多数在15—20d。     

高压氧治疗一氧化碳中毒迟发性脑病56例临床分析

目的总结高压氧治疗一氧化碳中毒迟发性脑病的效果。方法选择2010年6月-2012年11月本院收治的56例一氧化碳中毒迟发性脑病患者为研究对象,对其进行高压氧治疗,观察治疗前后脑电图变化及临床疗效。结果治愈25例（44．64％）,好转26例（46．43％）,无效5例（8．93％）;治疗后脑电图检查结果明显优于治疗前,差异有统计学意义（P〈0．05）;治疗效果与患者年龄、昏迷时间呈负相关,与假愈期及治疗次数呈正相关,且组间差异有统计学意义（P〈0．05）。结论高压氧治疗在一氧化碳中毒迟发性脑病中的应用效果良好,值得推广使用。     

高压氧预防急性一氧化碳中毒迟发性脑病的临床分析

目的探讨高压氧对预防急性一氧化碳中毒迟发性脑病的可行性。方法对112例中重度急性一氧化碳中毒患者行高压氧治疗者（HBO组）,对比未高压氧舱治疗的96例急性中重度一氧化碳中毒患者经常规治疗者（对照组）,并对临床资料进行分析总结。结果 HBO组总有效率94.64%,对照组总有效率72.92%,两组疗效差异具有显著性（P〈0.05）;迟发性脑病发生率HBO组5.36%,对照组22.92%,两组发生率差异具有显著性（P〈0.05）。结论高压氧治疗急性一氧化碳中毒可明显降低迟发性脑病发生。     

急性一氧化碳中毒致迟发性脑病患者的高压氧疗效观察

自1988年5月至1998年5月,应用高压氧(HBO)治疗急性一氧化碳中毒迟发性脑病(ACMPDE)50例,结果总有效率为86％。疗效与患者年龄、治疗次数及昏迷时间等有关,即年轻者疗效较高,HBO治疗在30次以上者疗效显著,昏迷期越短疗效越好。     

依达拉奉联合高压氧治疗急性一氧化碳中毒迟发性脑病30例分析

目的研究探讨依达拉奉联合高压氧治疗急性一氧化碳中毒只发行脑病的临床效果。方法将我院2013年9月至2015年9月收治的急性一氧化碳中毒迟发性脑病患者60例作为本次研究对象,随机分为对照组和观察组。对照组患者采取常规的治疗措施,观察组在对照组患者治疗的基础上使用依达拉奉联合高压氧进行治疗,比较两组患者临床治疗效果。结果治疗结果显示,观察组治疗有效率为93.3%,对照组患者治疗总有效率为73.3%,数据符合统计学差异(P<0.05)。结论治疗急性一氧化碳中毒迟发性脑病,相对于常规临床经验治疗方法,使用依达拉奉联合高压氧进行治疗,效果更为显著,有助于促进患者康复。     

Hyperbaric Oxygen for Carbon Monoxide Poisoning

Poisoning with carbon monoxide (CO) is an important cause of unintentional and intentional injury worldwide. Hyperbaric oxygen (HBO) enhances CO elimination and has been postulated to reduce the incidence of neurological sequelae. These observations have led some clinicians to use HBO for selected patients with CO poisoning, although there is considerable variability in clinical practice. This article assesses the effectiveness of HBO compared with normobaric oxygen (NBO) for the prevention of neurological sequelae in patients with acute CO poisoning. The following databases were searched: MEDLINE (1966 to present), EMBASE (1980 to present), and the Controlled Trials Register of the Cochrane Collaboration, supplemented by a manual review of bibliographies of identified articles and discussion with recognised content experts. All randomised controlled trials involving people acutely poisoned with CO, regardless of severity, were examined. The primary analysis included all trials from which data could be extracted. Sensitivity analysis examined trials with better validity (defined using the validated instrument of Jadad) and those enrolling more severely poisoned patients. Two reviewers independently extracted from each trial, including information on the number of randomised patients, types of participants, the dose and duration of the intervention, and the prevalence of neurological sequelae at follow-up. A pooled odds ratio (OR) for the presence of neurological symptoms at 1-month follow-up was calculated using a random effects model. Bayesian models were also investigated to illustrate the degree of certainty about clinical effectiveness. Eight randomised controlled trials were identified. Two had no evaluable data and were excluded. The remaining trials were of varying quality and two have been published only as abstracts. The severity of CO poisoning varied among trials. At 1-month follow-up after treatment, sequelae possibly related to CO poisoning were present in 242 of 761 patients (36.1%) treated with NBO, compared with 259 of 718 patients (31.8%) treated with HBO. Restricting the analysis to the trials with the highest quality scores or those that enrolled all patients regardless of severity did not change the lack of statistical significance in the outcome of the pooled analysis. We found empiric evidence of multiple biases that operated to inflate the benefit of HBO in two positive trials. In contrast, the interpretation of negative trials was hampered by low rates of follow-up, unusual interventions for control patients and inclusion of less severely poisoned patients. Collectively, these limitations may have led negative trials to overlook a real and substantial benefit of HBO (type II error). There is conflicting evidence regarding the efficacy of HBO treatment for patients with CO poisoning. Methodological shortcomings are evident in all published trials, with empiric evidence of bias in some, particularly those that suggest a benefit of HBO. Bayesian analysis further illustrates the uncertainty about a meaningful clinical benefit. Consequently, firm guidelines regarding the use of HBO for patients with CO poisoning cannot be established. Further research is needed to better define the role of HBO, if any, in the treatment of CO poisoning. Such research should not exclude patients with severe poisoning, have a primary outcome that is clinically meaningful and have oversight from an independent data monitoring and ethics committee.     

After Treatment with Methylene Blue is Effective against Delayed Encephalopathy after Acute Carbon Monoxide Poisoning

Delayed encephalopathy after acute carbon monoxide (CO) poisoning (DEACMP) is the most severe and clinically intractable complication that occurs following acute CO poisoning. Unfortunately, the mechanism of DEACMP is still vague. Growing evidence indicates that delayed cerebral damage after CO poisoning is related to oxidative stress, abnormal neuro‐inflammation, apoptosis and immune‐mediated injury. Our recent report indicated that methylene blue (MB) may be a promising therapeutic agent in the prevention of neuronal cell death and cognitive deficits after transient global cerebral ischaemia (GCI). In this study, we aimed to investigate the potential of MB therapy to ameliorate the signs and symptoms of DEACMP. Rats were exposed to 1000 ppm CO for 40 min. in the first step; CO was then increased to 3000 ppm, which was maintained for another 20 min. The rats were implanted with 7‐day release Alzet osmotic mini‐pumps subcutaneously under the back skin, which provided MB at a dose of 0.5 mg/kg/day 1 hr after CO exposure. The results showed that MB significantly suppressed oxidative damage and expression of pro‐inflammatory factors, including tumour necrosis factor‐α and interleukin (IL)‐1β. MB treatment also suitably modulated mitochondrial fission and fusion, which is helpful in the preservation of mitochondrial function. Furthermore, MB dramatically attenuated apoptosis and neuronal death. Lastly, behavioural studies revealed that MB treatment preserved spatial learning and memory in the Barnes maze test. Our findings indicated that MB may have protective effects against DEACMP.     

丹红注射液联合大剂量纳洛酮在治疗急性一氧化碳中毒所致迟发性脑病中的作用

目的 观察丹红注射液联合大剂量纳洛酮在治疗急性一氧化碳（CO）中毒所致迟发性脑病的临床效果.方法 将2011年4月-2013年4月收治的150例随机分为3组,每组50例,均给予常规治疗,综合组加用丹红注射液联合大剂量纳洛酮,丹红组加用丹红注射液,纳洛酮组加用纳洛酮,并对3组总有效率及AAMD和MMSE评分进行比较.结果 综合组总有效率、AAMD和MMSE评分明显分别高于丹红组和纳洛酮组（P＜0.05）,丹红组总有效率、AAMD和MMSE评分高于纳洛酮组（P＜0.05）.结论 在常规治疗的基础上应用丹红注射液联合大剂量纳洛酮治疗急性CO中毒致迟发性脑病效果显著.     

弥散张量成像对急性一氧化碳中毒迟发性脑病的临床应用研究

目的探讨磁共振弥散扩散张量成像(DTI)对急性一氧化碳中毒迟发性脑病(DEACMP)的临床应用价值。方法选取2012年12月至2015年2月我院确住院治疗的DEACMP患者30例,采用高压氧联合甲强龙治疗,治疗前后分别行MMSE智能量表、ADL生活能力量表评定和DTI扫描。结果治疗前后患者MMSE、Barthel评分、DTI参数ADC和FA值均有显著改善(P<0.05)。治疗前患者的MMSE评分与治疗前ADC值显著相关(r=0.38,P<0.05),治疗后MMSE评分也与治疗前ADC值显著相关(r=0.40,P<0.05)。结论DTI成像对DEACMP的病情进展、预后评估及临床治疗均具有重要意义。     

鼠神经生长因子治疗急性一氧化碳中毒迟发性脑病临床观察

目的 探讨鼠神经生长因子(mNGF)治疗急性一氧化碳中毒迟发性脑病的临床效果.方法 随机将诊断为急性一氧化碳中毒迟发性脑病的87例分为mNGF组及对照组,对照组给予常规药物、高压氧治疗,mNGF组在对照组治疗基础上每天加用mNGF 30 μg肌内注射,治疗前、后分别对患者进行症状观察、脑电图检查及长谷川痴呆量表评分,评定临床疗效.结果 mNGF组显效率为81.4%,对照组显效率为47.7%,两组比较差异有统计学意义(P＜0.05).结论 鼠神经生长因子对急性一氧化碳中毒迟发性脑病有明显疗效.     

鼠神经生长因子治疗急性一氧化碳中毒迟发性脑病临床观察

目的探讨鼠神经生长因子（mNGF）治疗急性一氧化碳中毒迟发性脑病的临床效果。方法随机将诊断为急性一氧化碳中毒迟发性脑病的87例分为mNGF组及对照组,对照组给予常规药物、高压氧治疗,mNGF组在对照组治疗基础上每天加用mNGF30μg肌内注射,治疗前、后分别对患者进行症状观察、脑电图检查及长谷川痴呆量表评分,评定临床疗效。结果 mNGF组显效率为81.4%,对照组显效率为47.7%,两组比较差异有统计学意义（P〈0.05）。结论鼠神经生长因子对急性一氧化碳中毒迟发性脑病有明显疗效。