10%高渗盐水治疗急性脑血管病的临床研究

目的观察10%高渗盐水治疗急性脑血管病的疗效及副作用。方法将30例清醒急性脑血管病患者分为两组:高渗盐水治疗组(HS组)和甘露醇治疗组(M组)。HS组静注10%盐水40 ml/12 h连续5 d;M组静滴20%甘露醇250 ml 30 min内滴完,1次/12 h连续5 d。用药前及用药后1、3、7 d测患者血清电解质、渗透压、肾功能。治疗前及治疗14 d后对患者进行神经功能缺损评分。结果高渗盐水组患者治疗后第1、3、7天血清Na~ 、Cl~-及渗透压虽有所升高但均无统计学意义,且患者无肾功能损害;甘露醇组患者治疗后第1、3、7天血清Na~ 、Cl~-及渗透压无明显升高,但出现肾功能损害。治疗14 d后高渗盐水组及甘露醇组患者神经功能缺损状况均有明显改善。结论10%高渗盐水可有效治疗急性脑血管病引起的颅内高压,与甘露醇相比效力相当且对肾功能无损害。10%高渗盐水作为降低急性脑血管病性颅内高压的药物是安全、有效的。     

胱抑素C与急性脑梗死患者病情严重程度及肾功能变化的关系

目的探讨胱抑素C(CysC)与急性脑梗死患者病情严重程度及肾功能变化的关系。方法选择急性脑梗死患者84例(研究组)和体检健康者84例(对照组),检测血清CysC水平,分析其与患者梗死灶面积及神经功能缺损程度的关系。采用500mL/d(A组)和375mL/d(B组)20%甘露醇进行治疗,观察治疗前、治疗后第5、14天血清CysC及肾功能的变化。结果研究组大、中、小梗死灶患者血清CysC水平高于对照组(P0.05);重、中、轻度神经功能缺损患者血清CysC水平高于对照组(P0.05)。治疗后,A组和B组患者血清肌酐(Cr)、尿素氮(BUN)、CysC水平均升高,其中血清CysC水平与治疗前比较差异有统计学意义(P0.05)。A组和B组患者治疗后第5、14天血清Cys、Cr、BUN水平比较差异无统计学意义(P0.05)。结论 CysC与急性脑梗死患者病情严重程度密切相关;在监测脑梗死患者甘露醇治疗对肾功能影响方面,CysC优于Cr、BUN,值得临床应用。     

糖化血红蛋白对急性脑梗死患者预后的影响

目的:探讨糖化血红蛋白(HbA1c)对急性脑梗死患者病情严重程度及预后的影响。方法:将140例合并糖尿病的急性脑梗死患者根据其入院48h内HbA1c水平分为3组,A组:HbA1c≥9.0%,B组:6.5%≤HbA1c<9.0%,C组:HbA1c在正常范围内,4.5%相似文献   

银杏叶提取物联合高压氧治疗急性脑梗死的临床观察与评价

目的评价银杏叶提取物舒血宁联合高压氧对急性脑梗死患者的临床疗效。方法将急性脑梗死患者230例随机分为A组舒血宁联合高压氧治疗100例,B组舒血宁与基础治疗80例,C组高压氧与基础治疗50例,疗程均为15 d×2。观察3组治疗前后的神经功能缺损评分,血液流变学变化及临床疗效,比较评价。结果 A组、B组、C组临床有效率分别为89.0%(89/100)、80.0%(64/80)和72.0%(36/50);3组治疗后神经功能缺损评分和血液流变学指标均有不同程度降低,A组最好,B组次之,C组降低较少,舒血宁与高压氧联用有协同作用。结论银杏叶提取物舒血宁联合高压氧治疗急性脑梗死的疗效显著,值得推广。     

依达拉奉联合尤瑞克林治疗进展性脑梗死44例

目的:探讨依达拉奉联合尤瑞克林治疗进展性脑梗死的临床疗效.方法:将收治的132例进展性脑梗死患者分成A、B、C组,每组44例,3组均予改善循环、抗血小板聚集等常规治疗.C组予胞二磷胆碱+血栓通静滴,波立维口服;B组在C组基础上加用依达拉奉静滴;A组在B组基础上加用尤瑞克林静滴,均14 d为1个疗程.于治疗前后进行临床神经功能缺损程度评分与日常生活活动能力量表评分,观察两组临床疗效,并监测不良反应.结果:A组对神经功能缺损的治疗效果及控制脑梗死进展性优于B、C组,且无明显不良反应.结论:依达拉奉联合尤瑞克林对进展性脑梗死具有很好的治疗效果.     

高渗盐水联合吡拉西坦对重症脑出血患者颅内压及NIHSS评分的影响

目的:探讨高渗盐水联合吡拉西坦对重症脑出血患者颅内压及美国国立卫生院神经功能缺损量表(NIHSS)评分的影响.方法:回顾性分析2018年6月至2019年12月商丘市第一人民医院收治的130例重症脑出血患者临床资料,根据治疗方案的不同分为对照组(65例,给予吡拉西坦联合甘露醇治疗)和观察组(65例,给予高渗盐水联合吡拉西...     

奥扎格雷钠联合阿司匹林治疗急性脑梗死的临床疗效

目的:观察奥扎格雷钠联合阿司匹林对急性缺血性脑梗死患者的临床疗效及安全性。方法:84例急性缺血性脑梗死患者随机分为A组29例、B组28例、C组27例,分别给予阿司匹林、奥扎格雷钠、奥扎格雷钠联合阿司匹林治疗,观察用药14 d后3组的神经功能改善情况,并观察不良反应。结果:C组与A组和B组相比神经功能缺损评分及凝血指标降低显著,差异有统计学意义(P<0.05),临床疗效差异无统计学意义。用药前后肝肾功能无明显变化,不良反应发生率无明显差异。结论:奥扎格雷钠联合阿司匹林对于抗血小板聚集明显优于单用阿司匹林或奥扎格雷钠,具有良好的安全性。     

去大骨瓣减压颞肌贴敷术治疗大面积脑梗死患者几种护理模式的临床应用效果

目的:对比研究不同护理模式在去大骨瓣减压颞肌贴敷术治疗大面积脑梗死患者临床护理中的应用价值。方法:将襄阳市中心医院收治的120例大面积脑梗死患者随机分为A组、B组、C组,各组40例。A组进行常规护理,B组进行临床护理路径表护理,C组进行循证护理。于3组患者护理干预前后,根据美国国立卫生研究院卒中量表(National Institutes of Health Stroke Scale,NIHSS)评分标准评价患者神经功能缺损程度,并根据格拉斯哥预后分级(Glasgow outcome scale,GOS)评价3组患者预后情况。结果:护理3个月、6个月后,C组患者NIHSS评分低于A组、B组(P<0.05),A组、 B组比较,差异无统计学意义(P> 0.0 5)。在预后良好率,A组、 B组、 C组依次为5 0%、6 2.5%、 8 2.5%, C组高于A组、 B组(P <0.0 5), A组、 B组比较,差异无统计学意义(P> 0.0 5)。结论:于大面积脑梗死患者行去大骨瓣减压颞肌贴敷术治疗中行循证护理能有效提高护理效果,改善患者神经功能缺损程度及预后。     

左旋氨氯地平对脑梗死后血压调控及临床预后的观察

目的:研究左旋氨氯地平治疗急性脑梗死对血压调控及临床预后的影响。方法:急性脑梗死患者60例,随机分为A、B、C3组各20例,均根据脑梗死病情给予常规静脉药物治疗;同时A组给予口服苯磺酸左旋氨氯地平片2.5mg(8Am);B组口服硝苯地平缓释片10mg(8pm);C组必要时服用利尿剂控制血压。于入院时及治疗各时段进行血压、空腹血糖及血乳酸浓度监测;神经功能缺损程度评定;检测颈内动脉内膜厚度,计算中风体积等。结果:治疗7d时,A组患者血压,血糖及血乳酸浓度均明显低于B、C组(P0.05)。治疗1个月时临床疗效比较,A组无变化率明显低于B、C组(P0.05)。治疗3个月后颈内动脉内膜厚度及梗死病灶比较,A组显著小于B、C组(P0.05,0.01)。结论:左旋氨氯地平对脑梗死患者急性期和恢复期预后均具有显著的临床优势,可作为脑梗死患者血压调控治疗用药的首选。     

血浆NT-proBNP水平在高渗盐水和甘露醇治疗脑出血患者中的应用价值

目的:比较高渗盐水和甘露醇治疗脑出血患者的预后及NT-proBNP水平的变化,以判断NTproBNP对脑出血患者病情及治疗的指导意义。方法:将2016年1月-2019年12月广东省佛山市中医院就诊的符合研究要求的自发性脑出血138例患者随机分为高渗盐水组和甘露醇组,比较两组患者住院费用、住院天数、入选时GCS评分及出院时GCS评分、治疗第1天(用药前)及治疗第2-4天(用药后第1-3天)清晨6时患者NT-proBNP水平。结果:两组的性别、年龄、质量指数、高血压、高血脂、糖尿病、冠心病、脑梗死及烟酒嗜好等基础资料无明显差异(P均0.05);两组患者入院时的GCS评分无明显差异(P0.05),但两组的医疗总费用、住院天数、出院GCS评分、死亡率均有明显差异(P均0.05)。两组用药前NT-proBNP无明显差异(P0.05),用药后第1-3天两组各时间点NT-proBNP均逐渐明显下降,且高渗盐水组下降幅度明显优于甘露醇组(P均0.05)。结论:高渗盐水组治疗脑出血较甘露醇组预后好,NT-proBNP可以作为脑出血患者病情及其神经功能预后的评价指标之一。     

23.4%高渗盐水对不同程度颅内高压的影响

目的:以甘露醇作对照,探讨23.4％高渗盐水治疗不同程度颅内高压的效果。方法:对15名昏迷的、有侧脑室引流指征的脑出血患者进行共52例次降颅内压治疗。每次治疗随机决定静脉推注23.4％高渗盐水30 mL(HS组),或静滴20％甘露醇250 mL(Mannitol组)。持续监测用药前至用药后6h内的颅内压(ICP)。记录用药前的ICP、最大降幅和最大降幅百分比。结果:HS组:最大降幅与用药前的ICP之间有直线相关关系(P<0.01),最大降幅百分比与用药前的ICP之间无直线相关关系;Mannitol组:最大降幅、最大降幅百分比分别与用药前的ICP之间有直线相关关系(P分别<0.01、<0.05)。结论:23.4％高渗盐水和甘露醇均能安全、有效地降低颅内高压;但23.4％高渗盐水的降颅内高压效力比甘露醇稳定,尤其是当ICP升幅较小时,高渗盐水的降颅内压效力略高于甘露醇。     

高渗盐溶液对神经外科手术患者血流动力学和呼吸功能的影响

目的：观察高渗盐溶液对神经外科手术患者血流动力学和呼吸功能的影响。方法60例拟行择期神经外科开颅手术的患者（18～65岁）,随机分为高渗盐组和甘露醇组,高渗盐组所有患者在麻醉诱导后30 min内给与3%氯化钠溶液500 mL,对照组诱导后30 min内给与20%甘露醇500 mL,后两组患者输入乳酸林格液5 mL？kg-1？h-1。监测平均动脉压（MAP）、心率（HR）、心排量（CO）、胸腔液体含量（TFC）和氧合指数（OI）,同时观察硬脑膜张力、出血量、尿量、手术时间和拔管时间。结果与基础值相比,两组患者MAP和CO在麻醉诱导后显著降低,后逐渐升高,且高渗盐组更持久。与基础值相比,两组患者TFC和OI无明显改变,甘露醇和高渗盐均能显著地增加TFC和降低OI,甘露醇组在术毕恢复。高渗盐组具有更好的降低硬脑膜张力的作用。高渗盐组尿量为355±42 mL,而甘露醇组为680±59 mL。高渗盐组拔管时间为38±4 min,而甘露醇组为26±3 min。结论甘露醇和高渗盐都具有很好的稳定血流动力学和降低颅内压的作用,但是高渗盐可显著增加心排量和胸腔液体含量。     

高渗盐水复苏对急性脑损伤伴失血性休克患者颅内压脑氧代谢的影响

目的　研究高渗盐水 (HTS)复苏对急性脑损伤伴失血性休克患者颅内压、脑氧代谢的影响。方法　 4 6例急性脑损伤伴失血性休克患者随机分为 3组 :HTS治疗组、甘露醇 (MT)治疗组和平衡液对照组。在平衡液复苏基础上 ,分别在 15min内快速静脉输入 7 5 %HTS 4mL/kg和 2 0 %MT 0 5g/kg。于治疗后 15、30、6 0、12 0min通过侧脑室置管监测颅内压 (ICP) ,计算脑灌注压 (CPP) ;同时分别抽取动脉、颈内静脉球部血行血气分析 ,监测颈静脉血氧饱和度 (SjvO2 )及脑动静脉氧含量差 (Da -jvO2 )。结果　与对照组比较 ,HTS能明显降低ICP ,增加CPP ,改善脑氧供需平衡 (P <0 0 1) ;与MT组比较 ,HTS组降低ICP幅度与其相似(P >0 0 5 ) ,而降ICP作用维持时间较长 ,于治疗后 12 0minICP、CPP值与MT组比较差异有显著意义 (P <0 0 1)。结论　HTS降低ICP效果确切 ,且维持时间较长 ,同时可改善脑氧代谢 ,适于急性脑损伤伴失血性休克患者的急救治疗     

Treatment of acute hyponatremia: ensuring the excretion of a predictable amount of electrolyte-free water

BACKGROUND: Hypertonic saline is the recommended therapy to shrink swollen brain cells in patients with acute hyponatremia accompanied by seizures. OBJECTIVES: In the absence of hypertonic saline, hypertonic mannitol will shrink the cell volume. Because mannitol is excreted rapidly, our aim was to ensure that it would be excreted with electrolyte-free water (EFW) and to evaluate the renal mechanisms responsible for EFW excretion. DESIGN: A randomized, prospective, placebo-controlled study in rats was carried out in a research laboratory. SUBJECTS: Adult male Wistar rats. INTERVENTIONS: The control group of rats (n = 6) was administered hypotonic saline, a loop diuretic, vasopressin, and glucose by the intraperitoneal route; in the experimental group (n = 6), glucose was replaced with mannitol. Plasma electrolytes were measured at 0 and 210 mins, and balances for water, sodium, and potassium were obtained from 0 to 90 mins and from 90 to 210 mins. MEASUREMENTS AND MAIN RESULTS: Virtually 100% of the administered mannitol was excreted within 210 mins, and half was excreted in the first 90 mins. The urine contained EFW only in the mannitol group because of a larger volume in the first 90 mins (EFW, 3.7 mL) and to a lower excretion of NaCl in the next 120 mins (EFW, 3.5 mL). CONCLUSIONS: The combined use of mannitol and a loop diuretic caused the excretion of a predictable volume of EFW because the urine was iso-osmotic to plasma and contained all the administered mannitol. The calculated decrease in intracellular fluid volume was equivalent when mannitol was retained or excreted.     

甘露醇致不同年龄蛛网膜下腔出血患者急性肾损害的对比分析

目的对比分析不同年龄首次发生蛛网膜下腔出血（SAH）患者应用甘露醇致急性肾损害的临床特点。方法选择1989年2月2005年12月收治的SAH患者1361例，有94例合并甘露醇肾病，其中中年组（〈60岁）35例，老年组（〉60岁）59例。观察应用甘露醇后急性肾损害出现的时间、肾损害的预后、应用肾毒性药物情况以及甘露醇应用剂量和时间。结果老年组患者尿常规出现异常时间为应用甘露醇后4d（中位数），肾功能异常出现时间为5d（中位数），急性肾功能衰竭（ARF）出现时间为5d（中位数），ARF发生率为20．3％；中年组分别为7d、11d、9d和2．8％（P〈0．05或P〈0．01），说明老年患者对甘露醇的耐受性差，甘露醇肾病出现早、肾损害重、预后差。老年组有43例使用了速尿（占72．9％），总剂量为400mg（中位数）；中年组35例使用了速尿（占100．0％），总剂量为800mg（中位数），两组比较差异有统计学意义（P〈0．01）；大剂量甘露醇联合应用速尿的患者甘露醇肾病发生率低。老年组病死率为3．4％（2／59例），中年组无死亡病例。结论老年SAH患者应用甘露醇易于诱发急性肾损害，联合使用速尿对防止急性肾功能衰竭具有重要意义。     

高渗盐水可降低重型颅脑创伤患者颅内压

目的:评价高渗盐水和甘露醇降低重型颅脑创伤患者颅内压(ICP)的效果。方法:我院治疗的重型颅脑损伤患者132例,随机分为高渗盐水组65例和甘露醇组67例,在常规治疗基础上,分别给予3%高渗盐水5.4 mL/kg和20%甘露醇5.0 mL/kg静脉滴注。评价2组治疗期间的药物起效时间、最大ICP下降幅度、累积颅内压负荷(CICPB)、平均ICP负荷时间、压力累及时间(PTD)、ICU停留时间和格拉斯哥预后评分(GOS)。结果:2组起效时间、最大ICP下降幅度组间比较差异无统计学意义(P0.05);高渗盐水组PTD、CICPB和ICP负荷时间均小于甘露醇组(P0.05);2组ICU停留时间、GOS评分和临床预后差异无统计学意义(P0.05)。以GOS评分为因变量的多元线性回归分析结果显示,PTD、CICPB、ICP负荷时间与GOS呈负相关(P0.05),起效时间、最大ICP下降幅度与GOS不相关(P0.05)。结论:高渗盐水稳定重型颅脑损伤患者ICP的效果优于甘露醇,但不能改善临床预后。     

Global brain water increases after experimental focal cerebral ischemia: effect of hypertonic saline

OBJECTIVE: Isolated experiments suggest that global cerebral edema is a sequela of large hemispheric ischemic lesions, presumably as an extension of the initial ischemic insult into areas of vital, noninjured tissue. Diuretics and osmotic agents are controversial and poorly defined therapeutic modalities after large infarction. By using a rat model of middle cerebral artery occlusion (MCAO), we tested the hypothesis that significant edema occurs in the contralateral uninjured hemisphere and that this postischemic complication can be manipulated by hypertonic saline therapy. DESIGN: Prospective laboratory animal study. SETTING: Research laboratory in a teaching hospital. SUBJECTS: Halothane-anesthetized, male Wistar rats. INTERVENTIONS: Under controlled conditions of normoxia, normocarbia, and normothermia, rats were subjected to 2 hrs of MCAO. MEASUREMENTS AND MAIN RESULTS: Adequacy of MCAO and reperfusion was assessed by laser Doppler flowmetry. All animals except naive rats received continuous infusion of 0.9% saline at 0.5 mL/hr throughout the experiment. Brains were harvested, and tissue water content was estimated by comparing the wet-to-dry weight ratios of ipsilateral and contralateral cerebral hemispheres at 12 hrs, 24 hrs, or 2, 3, or 7 days postischemia. Naive and sham-operated rats served as control cohorts. In a second series of randomized experiments, wet-to-dry weight ratios were determined in rats treated with continuous intravenous infusion of 7.5% hypertonic saline (0.5 mL/hr; acetate/chloride, 50:50) and were compared with well-studied antiedema therapy: 20% mannitol (2.5 g/kg bolus every 6 hrs) or furosemide (2.5 mg/kg bolus every 6 hrs). Treatments were started at 24 hrs of reperfusion, and brain water was assessed at 2 days of reperfusion. In a third series of experiments, wet-to-dry ratios were determined in brains harvested at 2 days of reperfusion from rats that were subjected to 2 hrs of MCAO and did not receive any intravenous fluids. All values are mean +/- SEM. There were no differences between sham-operated and naive control cohorts. At 24 hrs of reperfusion, water content was higher in both ipsilateral ischemic (82.80 +/- 0.86%) and contralateral hemispheres (80.53 +/- 0.29%), compared with naive animals (ipsilateral, 79.62 +/- 0.12%; contralateral, 79.53 +/- 0.13%). Maximal cerebral edema was measured at 2 days in both hemispheres (ipsilateral, 83.94 +/- 0.47%; contralateral, 80.63 +/- 0.13%). Edema was present for up to 3 days in contralateral tissue (80.27 +/- 0.26%) and persisted to 7 days in the injured hemisphere (81.07 +/- 0.34%). Maximal edema (as assessed at 2 days postocclusion) was robustly attenuated with hypertonic saline therapy (ipsilateral, 81.59 +/- 0.52%; contralateral, 78.44 +/- 0.22%). The efficacy of hypertonic saline was equivalent to furosemide (ipsilateral, 82.09 +/- 0.50%; contralateral, 79.13 +/- 0.17%) but less robust than mannitol (ipsilateral, 79.89 +/- 0.36%; contralateral, 78.73 +/- 0.17%). CONCLUSIONS: These data demonstrate that cerebral edema persists in both injured and contralateral hemispheres for days after MCAO. The global, maximal increase in brain water is responsive to continuous 7.5% hypertonic saline treatment begun at 24 hrs postischemia and to standard diuretic/osmotic agents. These results may have implications for diuretic and osmotic therapy in clinical ischemic stroke.     

Isovolume hypertonic solutes (sodium chloride or mannitol) in the treatment of refractory posttraumatic intracranial hypertension: 2 mL/kg 7.5% saline is more effective than 2 mL/kg 20% mannitol

OBJECTIVE: To evaluate the clinical benefit of increasing the osmotic load of the hypertonic solution administered for the treatment of refractory intracranial hypertension episodes in patients with severe head injury. DESIGN: Prospective, randomized study. SETTINGS: A trauma center in a university hospital. PATIENTS: Twenty consecutive patients with head trauma and persistent coma who required infusions of an osmotic agent to treat episodes of intracranial hypertension resistant to well-conducted standard modes of therapy were studied. Intracranial hypertension was considered refractory when it persisted despite deep sedation, optimal hemodynamic status, and, in some patients, drainage of cerebral spinal fluid. INTERVENTIONS: Patients were randomly assigned to receive isovolume infusions of either 7.5% hypertonic saline solution (2400 mOsm/kg/H(2)O) or 20% mannitol (1160 mOsm/kg/H(2)O). The patients were given 2 mL/kg (body weight) of either solution, i.e., 361 +/- 13 mOsm of saline or 175 +/- 12 mOsm of mannitol per injection. MEASUREMENTS AND MAIN RESULTS: The main variables studied were the number and the duration of episodes of intracranial hypertension per day during the study period, which was stopped after the last episode of intracranial hypertension was recorded from intracranial pressure monitoring or after the allocated treatment failure. Patients in the HHS group were monitored for 7 +/- 5 days and those in the mannitol group for 7 +/- 6 days (not significant). The rate of failure for each treatment was also evaluated. Failure was defined as the persistence of intracranial hypertension despite two successive infusions of the same osmotic agent. The mean number of osmotic solute infusions was 3.7 +/- 5.3 in the mannitol group and 3.3 +/- 4.1 in the hypertonic saline solution group (not significant). The mean number (6.9 +/- 5.6 vs. 13.3 +/- 14.6 episodes) of intracranial hypertension episodes per day and the daily duration (67 +/- 85 vs. 131 +/- 123 min) of intracranial hypertension episodes were significantly lower in the hypertonic saline solution group (p <.01). The rate of clinical failure was also significantly lower in the hypertonic saline solution group: 1 of 10 patients vs. 7 of 10 patients (p <.01). CONCLUSION: In this study, when a hypertonic solute was required for the treatment of refractory intracranial hypertension episodes in patients with severe head trauma, increasing the osmotic load by giving 2 mL/kg (body weight) of 7.5% saline (361 +/- 13 mOsm) was more effective than giving 2 mL/kg (body weight) of 20% mannitol (175 +/- 12 mOsm). Within the limitations of the present study, these data suggest that giving 2 mL/kg hypertonic saline solution (approximately 480 mOsm/70 kg body weight) is an effective and safe initial treatment for intracranial hypertension episodes in head-trauma patients when osmotherapy is indicated.