Brainstem auditory evoked potentials in patients with delayed encephalopathy after acute carbon monoxide poisoning

Objective:To evaluate the changes of brainstem auditory evoked potential (BAEP) in patients with delayed encephalopathy after acute carbon monoxide poisoning. Methods: BAEPs were performed in 32 controls and 40 patients. Wave Ⅰ , Ⅱ , Ⅲ ,Ⅳ, Ⅴ latencies and Ⅰ-Ⅲ , Ⅲ-Ⅴ , Ⅰ-Ⅴ interpeak latencies were measured, respectively. Results: Abnormalities of BAEPs in 13 patients (13/40, 32 ％). Among the13 abnormal BAEPs, 3 displayed prolongation of latency to waves in one side, no potential in another side; 5 displayed a similar abnormality which was bilateral prolongation of latency to waves ;and another 5 displayed unilateral latency delay. Compared wave Ⅰ , Ⅱ , Ⅲ , Ⅳ, Ⅴ latencies and Ⅰ-Ⅲ , Ⅲ-Ⅴ , Ⅰ-Ⅴ interpeak latencies in the patients and the controls, there were no significant differences (P＞0.05). Conclusion: BAEPs can be used for evaluating the diagnostic and prognostic values in the cases of delayed encephalopathy after acute carbon monoxide poisoning.

Multimodality evoked potentials in patients with delayed encephalopathy after acute carbon monoxide poisoning

Objective： To evaluate the diagnostic and prognostic values in patients with delayed encephalopathy after acute carbon monoxide poisoning. Methods： The tibial nerve somatosensory evoked potentials （SEPs）, vision evoked potentials （VEPs）, and brain stem audition evoked potentials（BAEPs） were performed in 32 healthy adults and 43 patients with delayed encephalopathy after acute carbon monoxide poisoning. Results： This paper indicated abnormalities of tibial nerve SEPs in 31 patients （31/43, 72.1%）, VEPs in 17 patients （17/28, 60.7%）, and BAEPs in 14, patients （14/43, 32.6%）. These results showed that the greatest diagnostic value was SEPs, followed by VEPs and, BAEPs with the lowest sensitivity. Conclusion： Multimodality evoked potentials （EPs） can be used for evaluating the diagnostic and prognostic values in cases of delayed encephalopathy after acute carbon monoxide poisoning.

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

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

Influence of mouse nerve growth factor combined with hyperbaric oxygen on serum cytokines and cognitive function in patients with delayed encephalopathy after carbon monoxide poisoning

Objective:To study the influence of mouse nerve growth factor (mNGF) combined with hyperbaric oxygen on serum cytokines and cognitive function in patients with delayed encephalopathy after carbon monoxide poisoning (DEACMP).Methods: 218 patients with DEACMP who were treated in our hospital between June 2012 and September 2016 were chosen as research subjects and retrospectively divided into the control group (n=100) who underwent hyperbaric oxygen treatment and the observation group (n=118) who underwent mouse nerve growth factor combined with hyperbaric oxygen treatment. Serum contents of nerve injury indexes and inflammatory mediators were compared between two groups of patients and cognitive function was assessed.Results:Before treatment, differences in serum levels of nerve injury indexes and inflammatory mediators, total MMSE score and each dimension score were not statistically significant between two groups of patients. After treatment, serum contents of nerve injury indexes creatine kinase-BB (CK-BB), neuron-specific enolase (NSE), S-100β protein (S-100β) and lactate (Lac) in observation group were lower than those in control group;serum contents of inflammatory mediators interleukin-6 (IL-6), interleukin-10 (IL-10), interleukin-18 (IL-18), hypersensitive C-reactive protein (hs-CRP) and tumor necrosis factor (TNF-α) were lower than those in control group;total MMSE score and each dimension score were higher than those of control group.Conclusion:mNGF combined with hyperbaric oxygen treatment of DEACMP is helpful to reduce the nerve injury and systemic inflammatory response, and improve the cognitive function.

Acute carbon monoxide poisoning and delayed neurological sequelae: a potential neuroprotection bundle therapy

Currently, there is no known optimal therapy for carbon monoxide （CO） poisoning and CO-associated delayed neu- rological sequelae. Hyperbaric oxygen therapy （HBOT） is a well-known treatment method, but its use for CO poison- ing patients is controversial to use due to lack of evidences regarding its efficacy. Thus, it is unlikely that HBOT alone will be accepted as the standard treatment method. In this article, current and potential treatment methods of CO poi- soning are presented as well as the tentative multi-factorial pathophysiology. A series of treatments are suggested for use as a bundle therapy, with targeted temperature management as the base treatment method. Such a therapy holds a great potential, especially for the cases where HBOT is not readily available. We suggest further investigations for elucidating the effects of these suggested treatments and their roles in terms of the complex pathophysiology of CO poisoning. Future ac- ceptance of this therapy based on the improved scientific and clinical knowledge may result in injury prevention and mini- mization of the signs and the symptoms in CO poisoning.

Early Biomarkers in 1H Nuclear Magnetic Resonance Spectroscopy of Striatal Pathological Mechanisms after Acute Carbon Monoxide Poisoning in Rats

Objective In vivo Proton Magnetic Resonance Spectroscopy （1H-MRS） can be used to evaluate the levels of specific neurochemical biomarkers of pathological mechanisms in the brain. Methods We conducted T2-Weighted Magnetic Resonance Imaging （MRI） and 1H-MRS with a 3.0-Tesla animal MRI system to investigate the early microstructural and metabolic profiles in vivo in the striatum of rats following carbon monoxide （CO） poisoning. Results Compared to baseline, we found significant cortical surface deformation, cerebral edema changes, which were indicated by the unclear gray/white matter border, and lateral ventricular volume changes in the brain. A significant reduction in the metabolite to total creatine （Cr） ratios of N-acetylaspartate （NAA） was observed as early as 1 h after the last CO administration, while the lactate （Lac） levels increased marginally. Both the Lac/Cr and NAA/Cr ratios leveled off at 6 h and showed no subsequent significant changes. In addition, compared to the control, the choline （Cho）/Cr ratio was slightly reduced in the early stages and significantly increased after 6 h. In addition, a pathological examination revealed mild cerebral edema on cessation of the insult and more severe cerebral injury after additional CO poisoning. Conclusion The present study demonstrated that 1H-MRS of the brain identified early metabolic changes after CO poisoning. Notably, the relationship between the increased Cho/Cr ratio in the striatum and delayed neuropsychologic sequelae requires further research.

Massive subdural hematoma misdiagnosed as delayed encephalopathy of carbon monoxide poisoning: a case report and literature review

Subdural hematoma is often secondary to brain trauma and other diseases.The onset is hidden and the condition is critical.Timely detection and early treatment are particularly important.The patient denied a history of trauma,but had a history of consciousness loss after charcoal burning.The clinical symptoms were progressive cognitive impairment.The initial diagnosis was delayed encephalopathy caused by carbon monoxide poisoning.However,computed tomography(CT)scan of the brain showed a large area of subdural hematoma on the left side and the formation of a cerebral hernia,which was life-threatening.The patienfs symptoms gradually improved after an emergency operation.

Effects of intravascular laser phototherapy on delayed neurological sequelae after carbon monoxide intoxication as evaluated by brain perfusion imaging:A case report and review of the literature

BACKGROUND Delayed neurological sequelae(DNS)caused by carbon monoxide(CO)intoxication poses considerable treatment challenges for clinical practitioners.In this report,we used nuclear medicine imaging and the Mini-Mental State Examination(MMSE)to evaluate the effectiveness of intravascular laser irradiation of blood(ILIB)therapy for the management of DNS.CASE SUMMARY A 51-year-old woman presented to our medical center experiencing progressive bradykinesia,rigidity of limbs,gait disturbance,and cognitive impairment.Based on her neurological deficits,laboratory tests and imaging findings,the patient was diagnosed with delayed neurological sequelae of CO intoxication.She received intensive rehabilitation and ILIB therapy during 30 sessions over 2 mo after diagnosis.Brain single-photon emission computed tomography was performed both prior to and after ILIB therapy.The original hypoperfusion area in bilateral striata,bilateral frontal lobe,right parietal lobe,and bilateral cerebellum showed considerable improvement after completion of therapy.The patient’s MMSE score also increased markedly from 6/30 to 25/30.Symptoms of DNS became barely detectable,and the woman was able to carry out her daily living activities independently.CONCLUSION ILIB therapy could facilitate recovery from delayed neurological sequelae in patients with CO intoxication,as demonstrated by improved cerebral blood flow and functional outcomes in our patient.

Digit and letter alexia in carbon monoxide poisoning

This study examined a 24-year-old patient with delayed encephalopathy, who was admitted to hospital with complaints of headache and visual impairment 1 week after acute carbon monoxide poisoning. The results of a visual field assessment, electroencephalography and head magnetic resonance imaging indicated damage to the cerebral cortex. After a 2-week treatment period, the patient had recovered from the visual impairment, but exhibited digit- and letter-reading difficulty. The Chinese aphasia battery and the number and letter battery supplement were conducted. The results revealed that the patient exhibited digit and letter alexia, while the ability to read Chinese characters was preserved. In contrast, the patient exhibited a deficit in Chinese character writing, while number and letter writing remained intact. Following treatment, reading and writing ability was improved and electroencephalographic abnormalities were ameliorated. Overall, our experimental findings demonstrated that delayed encephalopathy following acute carbon monoxide poisoning was characterized by digit and letter alexia.

MHR和SII早期联合检测对急性一氧化碳中毒患者病情及预后的评估

目的分析单核细胞与高密度脂蛋白胆固醇比值(MHR)、系统性免疫炎症指数(SII)在急性一氧化碳中毒(ACOP)患者中变化,探讨其早期联合检测对ACOP患者的病情及预后的评估。方法选取2019年1月—2023年1月在河北医科大学哈励逊国际和平医院急救医学部收治的ACOP患者120例,根据患者病情严重程度将其分为轻度中毒组30例、中度中毒组35例和重度中毒组55例;根据患者是否发生急性一氧化碳中毒迟发性脑病(DEACMP)情况分为DEACMP组17例和预后良好组103例;同期健康体检者30例作为对照组。所有患者均在入院时,对照组于体检时,检测MHR、SII、白细胞介素-18(IL-18)和C反应蛋白(CRP)的变化,记录患者60 d内DEACMP发生情况。通过Logistic回归分析ACOP发生DEACMP的独立危险因素。绘制受试者工作特征(ROC)曲线,计算曲线下面积(AUC),评估MHR和SII对ACOP患者发生DEACMP的预测价值。结果入院时,不同中毒程度患者MHR、SII、IL-18和CRP水平均高于对照组,中度高于轻度,重度高于中度、轻度,均有统计学差异(P<0.05)。3组患者DEACMP发生率分别为0,5.71%和27.27%,有统计学差异(χ^(2)=14.777,P=0.001)。相关分析结果显示,ACOP患者中毒程度与DEACMP发生率呈正相关(r=0.648,P=0.000)。Logistic回归分析结果显示,MHR、SII水平升高均是ACOP患者发生DEACMP的危险因素(OR=7.757、5.169,均P<0.01)。入院时MHR、SII、IL-18、CRP及MHR+SII预测发生DEACMP的AUC分别为0.840、0.862、0.771、0.706和0.899,MHR和SII联合应用预测能力优于MHR、SII、IL-18和CRP(P<0.05)。结论MHR和SII是ACOP患者发生DEACMP的独立危险因素,MHR和SII早期联合检测有助于ACOP患者病情和预后的评估。

依达拉奉联合甲泼尼龙治疗一氧化碳中毒迟发性脑病病人的疗效及对血清钙结合蛋白S100B、胱天蛋白酶-3水平的影响

目的 探讨依达拉奉联合甲泼尼龙治疗一氧化碳中毒迟发性脑病(DEACMP)病人的疗效及对血清钙结合蛋白S100B(S100B)、胱天蛋白酶-3(caspase-3)的影响。方法 回顾性分析2019年7月至2022年8月在保定市第二医院治疗的102例DEACMP病人的临床资料,将2019年7月至2021年2月的50例病人设为激素组,将2021年3月至2022年8月的52例病人设为联合组,均按方便抽样法抽取。所有病人均采取常规用药+高压氧治疗,激素组在此基础上应用甲泼尼龙治疗,联合组在激素组基础上采用依达拉奉治疗。比较两组疗效、治疗前后蒙特利尔认知评估量表(MoCA)评分、长谷川痴呆量表(HDS)评分、血清S100B、caspase-3水平及脑电图。结果 联合组总有效率92.31%明显高于激素组的74.00%(P<0.05);主体间效应检验显示治疗前MoCA、HDS评分、血清S100B、caspase-3水平高于治疗后1个月,两组治疗后1个月MoCA、HDS评分、血清S100B、caspase-3水平差异有统计学意义(P<0.05);联合组治疗后1个月脑电图明显优于激素组(P<0.05)。结论 对DEACMP病人实施依达拉奉联合甲泼尼龙治疗的效果确切,可有效下调血清S100B、caspase-3水平,明显减轻痴呆症状及认知障碍,显著改善脑电图。

丁苯酞序贯疗法联合高压氧疗及糖皮质激素对急性一氧化碳中毒迟发性脑病的临床疗效研究

目的 评估丁苯酞序贯疗法(BST)辅助治疗对急性一氧化碳中毒迟发性脑病(DEACMP)的临床疗效。方法 选取延安市人民医院神经内科2018年1月至2023年6月就诊的DEACMP患者为研究对象。采用随机数字表法,将DEACMP患者随机分为高压氧治疗(HBOT)组、糖皮质激素(GC)组(GC联合HBOT)、BST组(HBOT、GC联合BST),均持续治疗30 d。观察并比较3组DEACMP治疗期间不良反应发生情况及治疗后临床疗效。比较3组治疗前后炎症指标、神经损伤指标、认知功能、神经功能和日常生活能力。结果 研究共纳入患者120例,每组各40例。治疗期间,3组患者均未观察到严重不良反应事件,无1例患者因不良反应而终止治疗。BST组治疗总有效率显著高于GC组和HBOT组,而GC组高于HBOT组(P<0.05)。治疗前,3组炎症指标、神经损伤指标、认知功能、神经功能和日常生活功能评分差异均无统计学意义(P> 0.05)。治疗后,3组血清脂蛋白磷脂酶(LP-PLA2)、全身炎症反应指数(SIRI)、肿瘤坏死因子-α(TNF-α)、中枢神经特异蛋白(S100-β)、神经元特异性烯醇化酶(NSE)水平均较治疗前下降(P<0.05),且BST组低于HBOT组和GC组,GC组低于HBOT组(P<0.05)。治疗后,3组简易智力状态检查量表(MMSE)、蒙特利尔认知评估量表(MoCA)、和Barthel指数(BI)评分均较治疗前升高(P<0.05),但美国国立卫生研究院卒中量表(NIHSS)评分下降(P<0.05)。此外,BST组MMSE、MoCA、和BI评分高于HBOT组和GC组(P<0.05),NIHSS评分低于HBOT组和GC组(P<0.05);GC组MMSE、MoCA、BI评分高于HBOT组,NIHSS评分低于HBOT组(P<0.05)。结论 与HBOT治疗和HBOT联合GC治疗比较,BST辅助治疗可提升DECAMP患者临床疗效,改善炎症状态、认知功能和日常生活能力。

急性一氧化碳中毒发生迟发性脑病的相关因素分析

目的分析急性一氧化碳(CO)中毒患者发生迟发性脑病的相关因素分析。方法选取2020年1月至2022年8月葫芦岛地区177例符合急性CO中毒诊断的住院患者,回顾性分析纳入病例的临床资料,应用Spearman相关性分析与CO中毒迟发性脑病相关的影响因素。结果177例患者中男性91例(51.41%),发病年龄集中在60岁以上,共86例(48.59%);发病时间集中在凌晨4~8点,共42例(23.73%);地域主要集中在农村,共139例(78.53%);文化程度主要集中在初中及以下,共113例(63.84%);中毒方式以取暖方式不当为主,共107例(60.45%);中毒场所主要在家中,共132例(74.58%)。177例患者中死亡2例,发生一氧化碳中毒迟发性脑病患者18例(10.17%)。既往合并基础病(心血管病,高血压,糖尿病,脑梗死)、就诊时间、昏迷时间及早期出现脏器损害(包括急性肝损伤,急性肾损伤)与一氧化碳中毒迟发性脑病呈正相关,GCS评分与一氧化碳中毒迟发性脑病呈负相关。结论急性一氧化碳中毒主要集中在农村的老年人群,中毒原因主要由家中取暖方式错误,其中合并基础疾病(心血管病,高血压,糖尿病,脑梗死)、就诊时间及昏迷时间长,GCS评分低,早期出现脏器损害均与发生迟发性脑病相关,应早期识别迟发性脑病的高危患者,对其尽早进行干预治疗,提高治愈率,降低并发症。

高压氧在急性一氧化碳中毒救治中的应用

目的研讨高压氧在急性一氧化碳中毒(AcMP)救治中的应用。方法选取2020年5月~2022年10月我院急诊救治的AcMP患者68例。随机分为两组,每组34例。对照组予以常规治疗,观察组在对照组的基础上增加高压氧治疗。全部患者均治疗10天,比较两组治疗前后的动脉血气指标[血氧分压(PaO_(2))、二氧化碳分压(PaCO_(2))]、意识复常时间、住院时间以及并发症发生率。结果治疗后:观察组PaO_(2)高于对照组,PaCO_(2)低于对照组(P<0.05);观察组意识复常时间、住院时间短于对照组(P<0.05);观察组并发症发生率(5.88%),对照组(23.53%),差异(P<0.05)。结论高压氧能够辅助改善AcMP患者的动脉血气,减少并发症发生,有利于患者病情恢复。

IP3R2及RYR2介导Ca^(2+)信号在急性一氧化碳中毒迟发性脑病小鼠模型中的表达

背景:研究发现星形胶质细胞中Ca^(2+)的表达与认知功能密切相关,目前由1,4,5-三磷酸肌醇受体(Inositol 1,4,5-trisphosphate receptors,IP3Rs)2、兰尼碱受体(ryanodine receptors,RYRs)2受体及其调控的Ca^(2+)信号通路已经成为认知障碍相关疾病研究的热点。目的:研究急性一氧化碳中毒迟发性脑病动物模型中,海马组织内星形胶质细胞和IP3R2、RYR2介导的Ca^(2+)信号的表达情况,探索急性一氧化碳中毒迟发性脑病可能的发病机制。方法:Morris水迷宫实验筛选认知功能合格的C57BL小鼠随机分为对照组、实验组,实验组小鼠采用静态吸入一氧化碳建立急性一氧化碳中毒迟发性脑病模型,对照组小鼠吸入等量空气。造模后第21天,利用Morris水迷宫、苏木精-伊红染色、Western blot、免疫荧光双标法、Ca^(2+)荧光探针检测中毒小鼠行为学及神经元改变、星形胶质细胞特异性标记物胶质纤维酸性蛋白及IP3R2、RYR2受体、星形胶质细胞内Ca^(2+)浓度变化。结果与结论:①Morris水迷宫实验发现与对照组相比,实验组小鼠逃避潜伏期明显延长(P<0.05);②苏木精-伊红染色表明实验组小鼠海马锥体细胞数减少、细胞结构紊乱、细胞核碎裂伴溶解;③免疫荧光检测表明海马区IP3R2、RYR2分别和胶质纤维酸性蛋白存在共表达,且实验组海马区IP3R2、RYR2和胶质纤维酸性蛋白表达均上调(P<0.05);④Western blot检测显示实验组海马区IP3R2、RYR2及胶质纤维酸性蛋白的蛋白表达均增多(P<0.05);⑤Ca^(2+)荧光探针法检测表明实验组小鼠海马区星形胶质细胞内Ca^(2+)浓度明显升高(P<0.05);⑥结果说明,星形胶质细胞可能通过介导IP3R2、RYR2受体影响Ca^(2+)信号,进而使一氧化碳中毒的小鼠认知功能受损,最终导致急性一氧化碳中毒迟发性脑病发生。

急性一氧化碳中毒迟发性脑病预测方法的现状及进展

急性一氧化碳中毒迟发性脑病(delayed encephalopathy after acute carbon monoxide poisoning,DEACMP)发病隐匿、病程较长、致残率高,主要表现为精神意识的障碍。尽管早期预测DEACMP的发生有助于改善预后、减少后遗症的发生,但如何对DEACMP进行准确的预测一直是临床上急需解决的难点问题。近年来,对DEACMP的预测从临床表现、实验室指标、神经电生理检查、影像学检查及遗传易感性等方面均取得了一定的进展,临床医生需要综合研判,预测迟发性脑病的发生,及时进行干预。

基于度中心度和格兰杰因果分析研究急性一氧化碳中毒患者脑网络有效连接变化

目的:采用度中心度(DC)和格兰杰因果分析(GCA)方法研究急性一氧化碳中毒(ACMP)患者脑功能网络有效连接变化,探索其与认知功能障碍之间的相关性。方法:对54例ACMP患者(ACMP组)及37名健康对照组(HC组)行静息态功能磁共振成像扫描,在两组间DC值具有显著差异的脑区中,选取左侧颞下回作为种子点,进行全脑体素GCA分析;提取组间具有显著差异的脑区DC值和GCA有效连接值,分析它们与MMSE、MoCA评分之间的相关性。结果:与HC组比较,ACMP组左侧颞下回、左侧海马、左侧海马旁回、左侧额上回、左侧额下回的DC值增高,右侧辅助运动区、右侧小脑Crus1区及Crus2区的DC值减低(P<0.05,FWE校正);左侧颞下回与双侧楔前叶、右侧颞下回及左侧中央旁小叶的双向有效连接效应均存在异常,另外左侧颞下回至右侧顶上回和双侧小脑Crus1区有效连接增强,至双侧扣带回、左侧额上回、左侧额中回有效连接减弱,而右侧中央旁小叶至左侧颞下回的有效连接减弱(P<0.05,GRF校正);相关分析显示,网络有效连接的变化与MoCA、MMSE评分有相关性(P<0.05)。结论:ACMP患者在脑网络中表现出异常程度的度中心性,主要在默认网络、中央执行网络、感觉运动网络间出现有效功能连接异常,提示患者在早期即存在全脑多功能网络损伤。

高压氧联合亚低温治疗急性一氧化碳中毒的临床效果

目的探讨高压氧联合亚低温治疗急性一氧化碳中毒(ACOP)的临床效果。方法86例ACOP患者随机分为两组。在常规治疗基础上,对照组给予高压氧治疗,研究组给予高压氧联合亚低温治疗。比较两组的临床疗效、认知功能、抗氧化物水平。结果研究组的治疗总有效率为93.02%,明显高于对照组的76.74%(P<0.05)。治疗后,两组的MoCA评分均明显高于治疗前,且研究组的MoCA评分明显高于对照组(P<0.05)。治疗后,两组的CAT、LPO水平均明显低于治疗前,且研究组的CAT、LPO水平均明显低于对照组(P<0.05)。结论高压氧联合亚低温治疗ACOP的效果显著,可改善患者的认知功能,降低抗氧化物水平。

天智颗粒联合高压氧治疗急性一氧化碳中毒迟发型脑病的临床研究

目的:探讨天智颗粒联合高压氧治疗急性一氧化碳中毒迟发型脑病(DEACMP)的临床效果及对活化蛋白(AP)-1、核因子-κB(NF-κB)、炎症因子的影响。方法:选取2018年10月—2022年9月通辽市医院神经内科收治的DEACMP患者60例,随机分为高压氧组和联合组,各30例。高压氧组予高压氧及常规治疗,联合组在高压氧组治疗基础上予天智颗粒口服治疗,两组均持续治疗3个月。观察两组临床疗效、脑电图恢复时间及神经症状、体征消失时间情况;比较治疗前后简易精神状态检查量表(MMSE)评分、蒙特利尔认知评估量表(MoCA)评分、日常生活活动能力量表(ADL)评分,血清干扰素(IFN)-γ、白细胞介素(IL)-8、IL-10含量及外周血单个核细胞中活化蛋白(AP)-1、核因子-κB(NF-κB)相对表达水平。结果:与高压氧组相比,联合组总有效率明显提高,电图恢复时间及症状体征消失时间均缩短,差异均有统计学意义(P<0.05)。与治疗前相比,两组治疗后MMSE、MoCA、ADL评分均升高,血清IFN-γ、IL-8均降低,IL-10升高,外周血单个核细胞AP-1、NF-κB相对表达量均降低,差异均有统计学意义(P<0.05);与高压氧组治疗后相比,联合组MMSE、MoCA、ADL评分均升高,血清IFN-γ、IL-8均降低,IL-10升高,外周血单个核细胞AP-1、NF-κB相对表达量均降低,差异均有统计学意义(P<0.05)。结论:天智颗粒联合高压氧治疗DEACMP有良好的临床效果,其机制可能与抑制炎症反应有关。

急性一氧化碳中毒患者使用不同剂量纳洛酮联合高压氧治疗的预后情况观察

目的观察急性一氧化碳中毒患者使用不同剂量纳洛酮联合高压氧治疗的预后情况。方法在本院2020年2月—2022年2月收治的急性一氧化碳中毒患者中选取90例,按照随机数字表法分为两组,研究组(45例)给予大剂量纳洛酮[0.04 mg/(kg·min),总剂量不超过4.0 mg]联合高压氧治疗,对照组(45例)给予常规剂量纳洛酮[0.01 mg/(kg·min)]联合高压氧治疗,比较两组疗效、临床指标[催醒时间,住院时间,简易智力状态检查量表(MMSE)]、血清酶指标[心肌激酶(CK),乳酸脱氢酶(LDH),丙氨酸转氨酶(ALT),天氡氨酸转氨酶(AST)]、不良反应、预后(迟发性脑病,死亡)。结果研究组总有效率高于对照组(P<0.05);研究组催醒时间、住院时间均短于对照组(P<0.05),治疗后两组MMSE评分均升高(P<0.05),且研究组MMSE评分高于对照组(P<0.05);治疗后两组CK、LDH、ALT、AST水平均降低(P<0.05),且研究组CK、LDH、ALT、AST水平低于对照组(P<0.05);两组不良反应比较无明显差异(P>0.05);两组均随访6个月,结果显示研究组死亡1例(2.22%)、并发迟发性脑病2例(4.44%),对照组死亡3例(6.67%),并发迟发性脑病7例(15.56%),两组比较有统计学差异(P<0.05)。结论在急性一氧化碳中毒患者中应用大剂量纳洛酮联合高压氧治疗疗效显著,能促进病情好转,且预后及安全性均较好。