老年急性一氧化碳中毒迟发性脑病的临床特征及预后影响因素

目的观察老年急性一氧化碳中毒迟发性脑病(DEACMP)的临床特征及高压氧等综合治疗的效果,分析可能影响预后的相关因素。方法分层整群抽样,回顾分析100例DEACMP患者临床资料,仔细阅览患者病例资料,记录其一般人口学资料,包括性别、年龄、职业等,同时记录患者发病情况与治疗情况,包括病情程度、临床表现、头颅磁共振成像(MRI)或CT影像学征象、脑电图结果等。全部患者接受高压氧、降颅压、营养神经等综合治疗。根据治疗效果分为预后良好组及预后不良组,对比两组一般资料及治疗情况,经单因素与多因素分析找出可能影响患者预后的相关因素。结果老年DEACMP患者多表现出智力下降、肌张力升高、精神行为异常、运动障碍、震颤等帕金森症状,病情多为中重度;头颅MRI或CT检查结果显示,患者皮质下白质区、双侧额叶、基底节区、侧脑室旁脑白质对称性低密度,长T1、T2及脱髓鞘改变;脑电图检查均有不同程度慢波变化。经高压氧等综合治疗后,100例患者中预后良好者90例,预后不良者10例;经单因素与多因素分析结果显示,年龄、脱离中毒环境至接受治疗时间、脑血管病危险因素、病情严重程度均是影响老年DEACMP患者预后的相关因素。结论老年DEACMP患者大脑皮质及基底节区神经功能损害情况严重,表现出不同程度的智力下降、精神行为异常等帕金森症状,高压氧等综合治疗能改善患者预后,但患者预后的好坏仍受年龄、病情严重程度等因素的影响,发病后越早接受治疗、患者中毒程度越轻,预后越好。     

急性一氧化碳中毒迟发性脑病102例临床分析

目的 提高急性一氧化碳（CO）中毒迟发性脑病（DEACMP）的诊治水平。方法 回顾性分析102例急性DEACMP患者的临床特点。结果 DEACMP好发于中老年人,主要临床表现为智能障碍;首发症状多为行为、精神异常;脑电图异常主要表现为广泛不规则慢波,持续性出现;综合治疗加高压氧治疗效果好。结论 DEACMP临床表现多样,脑电图动态监测有助于早期诊断,足疗程高压氧治疗可明显改善预后。     

老年人急性一氧化碳中毒迟发性脑病的脑CT表现

老年人急性一氧化碳中毒迟发性脑病的脑ＣＴ表现方燕敏海军机关门诊部（１００８４１）迟发性脑病是急性一氧化碳中毒神经系统严重的续发病，且无有效的治疗方法，严重影响病人的生活质量。本文研究老年人迟发性脑病的ＣＴ表现，以期达到早期防治。现将我院（海军总医院）...     

急性CO中毒迟发性脑病相关因素分析

为探讨急性ＣＯ中毒发生迟发性脑病的危险因素，我们对５６例急性一氧化碳中毒住院患者进行随访，现报告如下。１临床资料１．１一般资料本组男２５例，女３１例，年龄１３～７７岁，平均４６±９岁。出现迟发性脑病者２３例，男６例，女１７例。有高血压病史１８例，糖尿...     

急性一氧化碳中毒后迟发性脑病40例分析

探讨急性一氧化碳中毒迟发性脑病的影响因素及其防治，对40例病人进行临床观察治疗回顾性分析。     

急性一氧化碳中毒后迟发性脑病的临床与磁共振改变

急性一氧化碳中毒后迟发性脑病 (ＤＥＡＣＭＰ)国内仅有个别磁共振成像 (ＭＲＩ)的文献[1] 。我院 1997年 1月至 2 0 0 0年6月收治 12例ＤＥＡＣＭＰ病人 ,报道如下。一、资料与方法12例均为临床确诊病例 ,诊断符合蒋雯巍等[2 ] 提出的诊断标准。男 10例 ,女 2例。年龄 12～ 71岁 ,平均年龄 41 5岁。急性期均有昏迷 ,时间 6ｈ～ 18ｄ。 11例昏迷清醒后距迟发脑病发病时间为 2～ 30ｄ ,平均 16ｄ ,1例无明显间歇期。4例行腰穿脑脊液检查 ,压力均正常 ,除 1例ＩｇＧ稍增高外 ,余患者脑脊液常规、生化及其他项目检查均正常。 5例行头部ＣＴ ,除…     

急性一氧化碳中毒致迟发性脑病的研究进展

急性一氧化碳中毒后迟发性脑病系指一氧化碳中毒患者经急性中毒症状的抢救恢复后,经数日或数周表现正常或接近正常的“假愈期”后再次出现以急性痴呆为主的一组神经精神症状,是急性一氧化碳中毒最严重的并发症。本文就一氧化碳中毒致迟发性脑病的发病机制、临床表现、治疗方法及影响预后的相关因素分析综述如下。     

一氧化碳中毒后迟发性脑病36例临床分析

目的探讨一氧化碳中毒后迟发性脑病(DEACMP)影像学及临床特点。方法对36例DEACMP病人的急性期、假愈期、恢复期的头部CT/磁共振成像(MRI)、脑电图(EEG)及临床表现进行回顾性分析。结果本组病例,假愈期为(11.2±4.6)d,经治疗30d内基本痊愈13例(36.11%),显著好转15例,总有效率77.78%。结论DEACMP的影像学改变与病情轻重及预后相关,EEG对进一步的治疗有指导价值,及时综合治疗可明显改善预后。     

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（carbon monoxide,CO）为一种无色、无味的气体,是工业生产和日常生活中常见的容易导致吸人性中毒的有害气体,通常为含碳物质不完全燃烧时产生,冬季为一氧化碳中毒发病高峰期。CO由呼吸道经气体交换人血后即迅速与血红蛋白结合形成碳氧血红蛋白,由于CO与血红蛋白的亲和力远大于0,与血红蛋白的结合力,而解离速度又远慢于氧合血红蛋白的解离,故而直接导致组织和细胞的缺氧。由于脑是对缺氧最敏感的器官,因此,CO中毒导致的一系列反应主要以脑部症状表现为主,轻者可致头晕、头痛,重者可导致死亡,部分患者即使经抢救成功存活,     

急性CO中毒迟发性脑病相关因素分析

对比分析28例急性CO中毒迟发性脑病(DEACMP)患者和99例未发生DEACMP的急性CO中毒患者的临床资料.结果 显示,与未发生DEACMP者相比,发生DEACMP者年龄较大、昏迷时间较长、合并症较多、接受高压氧治疗较晚、高压氧及综合治疗时间较短,且恢复期多受到精神刺激.认为DEACMP好发于高龄重症急性CO中毒患者;早期、足量高压氧治疗可减少DEACMP发生.     

急性一氧化碳中毒迟发性脑病的临床表现及预后相关因素

目的通过对15例急性一氧化碳中毒迟发性脑病的临床资料分析,探讨其发病及预后的相关因素。方法回顾性分析我院2006年6月~2014年1月收治的一氧化碳中毒迟发性脑病15例患者的临床资料,根据临床表现分为轻度、中度和重度。结果患者临床主要表现为智能下降、精神行为异常,肌张力增高、震颤、运动障碍等帕金森样症状。头颅CT或MRI检查示,双侧额叶、皮质下脑白质,侧脑室旁脑白质及基底节区对称性低密度、长T1、长T2及脱髓鞘改变。脑电图有不同程度的慢波改变。一氧化碳暴露时间≥4h的5例中,3例重度,2例中度;暴露时间<4h的10例中,中度5例,轻度5例。有脑血管病危险因素的7例中,3例重度,4例中度。经高压氧等综合治疗,1例85岁重度患者无效,14例临床症状均有不同程度改善。轻度5例中,痊愈4例、好转1例;中度7例均好转;重度3例中,好转2例、无效1例。结论一氧化碳中毒迟发性脑病患者大脑皮质和基底节区神经功能损害明显。高压氧等综合治疗可改善预后。年龄越大、病情越重,预后越差。     

Value of early-stage cerebral oxygen utilization coefficient in predicting delayed encephalopathy after acute carbon monoxide poisoning

正Objective To investigate the dynamic change in cerebral oxygen utilization coefficient(O2UCc)in the early stage of acute severe carbon monoxide poisoning(ASCMP)and its value in predicting delayed encephalopathy after acute carbon monoxide poisoning(DEACMP).Methods A prospective observational study was conducted for patients with ASCMP who were admitted to our hospital from November 2013 to March 2016,and their     

Effects of Ginaton on nitric oxide and nitric oxide synthase in patients with delayed encephalopathy after carbon monoxide poisoning

正Objective To observe the effects of Ginaton on blood nitric oxide(NO)and nitric oxide synthase(NOS)in patients with delayed encephalopathy after acute carbon monoxide poisoning(DEACMP).Methods A total of116 patients with DEACMP who were treated in Emergency Department of Harrison International Peace Hospi-     

高压氧治疗对一氧化碳中毒后迟发性脑病大鼠海马组织中炎症因子表达的影响

目的 研究高压氧(HBO)治疗对一氧化碳中毒(COP)后迟发性脑病(DEACMP)大鼠海马组织中炎症因子表达的影响.方法 将60只雄性SD大鼠随机分为空白对照组(NC组)、迟发性脑病组(DEACMP组)、高压氧治疗组(HBO组),每组16只,另12只备用补充.Morris水迷宫检测各组大鼠学习记忆能力;HE染色法观察各...     

Hippocampus hypoxia-inducible factor-1 alpha and heme oxygenase-1 expression in the delayed encephalopathy after acute carbon monoxide poisoning rat model

正Objective To research the expression of hypoxia-inducible factor-1 alpha(HIF-1α)and heme oxygenase-1(HO-1)in hippocampus of rats with delayed encephalopathy after acute carbon monoxide poisoning(DEACMP)and its functions.Methods One hundred and fiftysix rats were selected and randomly divided into several     

The occurrence of delayed neuropsychologic sequelae in acute carbon monoxide poisoning patients after treatment with hyperbaric or normobaric oxygen therapy

This study aimed at assessing which one of the 2 therapies is better for treating carbon monoxide (CO) poisoning from the perspective of reducing delayed neuropsychologic sequelae (DNS).We used Taiwan''s National Health Insurance Research Database (NHIRD) to conduct a nationwide population-based cohort study to assess which therapy is better for CO poisoning patients. To accurately identify patients with DNS, the definition of DNS is included neurological sequelae, and cognitive and psychological sequele. The independent variable was therapy and the dependent variable was DNS occurred within 1 year after discharge from a medical institution. The control variables were age, gender, the severity of CO poisoning, and comorbidities present before CO poisoning admission.The risk of developing DNS in patients treated with Hyperbaric Oxygen (HBO) was 1.87-fold (P < .001) than normobaric oxygen (NBO) therapy. The severity of CO poisoning and comorbidities were also found to have significant influences on the risk of developing DNS.HBO may be a risk therapy for treating CO poisoning.     

Echocardiographic findings after acute carbon monoxide poisoning.

Myocardial lesions are frequently seen at necropsy after fatal carbon monoxide poisoning. Clinically, while there have been numerous reports of chest pain and electrocardiographic changes associated with acute carbon monoxide poisoning, other evidence for left ventricular abnormality has not been reported. The echocardiographic findings in five cases of non-fatal poisoning are presented here. Abnormal left ventricular wall motion was shown by echocardiography in 3 cases. Motion returned to normal in 2 of the 3 in follow-up tracings. Echocardiograms on 3 of the 5 patients showed mitral valve prolapse. Though the mitral valve prolapse may have been present before the poisoning, the reported high incidence of papillary muscle lesions in fatal cases suggests a possible relation of the prolapse to the effects of the carbon monoxide poisoning.     

108例急性一氧化碳中毒患者并发心肌损害分析

目的分析急性一氧化碳中毒(acute carbon monoxide poisoning,ACOP)时临床心电图表现、心肌酶及肌钙蛋白(cTNT)的改变对心肌损害的临床意义。方法对我院2008年11月～2012年12月收治的108例ACOP患者进行心电图、心肌酶及cTNT定量临床观察,并做回顾性分析。结果 108例ACOP患者均有不同程度意识障碍,昏迷82例,占75.9%;心电图异常80例,占74.1%,其中ST-T改变69例,占63.9%;心肌酶活性升高69例,占63.9%;cTNT活性升高25例,占27.8%。心电图的改变及心肌酶、cTNT的活性升高与年龄呈正比,与中毒程度呈正相关,差异有统计学意义,中、重度中毒与轻度中毒者,重度中毒与中度中毒者比较,差异均有统计学意义(P<0.01)。经治疗,101例患者康复出院,5例因中毒时间长合并多脏器功能衰竭死亡,2例发生一氧化碳中毒迟发性脑病。结论 ACOP可以造成心肌不同程度的损害,需要积极进行相应治疗。     

Early subcortical ischemic infarction and delayed leucoencephalopathy after carbon monoxide poisoning

Controversy still exists about uric acid as a potential prognosticrisk factor for outcomes in patients with acute myocardial infarction. We prospectively assessed, in 856 patients with ST-elevation myocardial infarction (STMI) consecutively admitted to our Intensive Cardiac Care Unit after primary percutaneous coronary intervention (PCI) whether uric acid (UA) levels are associated with in-hospital mortality and complications. Killip classes III-–IV were more frequent in the 3° UA tertile that was associated with the highest values of peak Tn I (p = 0.005), NT-proBNP (p < 0.001), and fibrinogen (p = 0.036). Uric acid was associated with mortality (crude OR: 1.24; 95% CI 1.03–1.51; p = 0.025), but, when adjusted for Tn I and renal failure (as inferred by eGFR <60 ml/min/1.73 m²), uric acid lost its statistical significance, while Tn I (100 pg/ml step OR: 1.002; 95% CI 1.000–1.003; p = 0.007) and renal failure (OR 9.16; 95% CI 3.60–23.32; p < 0.001) were independent predictors for in-ICCU mortality. Uric acid remained as independent predictor for in-ICCU complications (1 mg/dl step OR: 1.11; 95% CI 1.01–1.21; p = 0.030) together with admission glycemia (1 g/dl step OR: 1.50; 95% CI 1.19–1.91; p < 0.001) and renal failure (OR: 1.46; 95% CI 0.99–2.16; p < 0.001). In STEMI patients submitted to PCI, increased uric acid levels identify a subgroup more prone to in-ICCU complications, probably because hyperuricemia stems from several complex mechanisms ranging from pre-existing risk factors to the degree of myocardial ischemia (as indicated by Killip class, ejection fraction) and to the acute metabolic response (as inferred by glucose levels). Hyperuricemia is not independently associated with early mortality when adjusted for renal function and the degree of myocardial damage.