诱导升压对动脉瘤性蛛网膜下腔出血患者脑血流量的影响

目的 本文旨在探讨对于动脉瘤性蛛网膜下腔出血患者，诱导升压对其脑血流量的影响。方法 选取2015年1月至2018年12月在我院就诊的诊断为动脉瘤性蛛网膜下腔出血的患者，随机分为诱导组和对照组。分别对两组患者实行诱导升压以及无诱导操作，在24~36小时后，评估两组患者的脑血流量（CBF），同时评估两组患者的动脉血压。结果 共有24名患者被纳入到本研究中，对照组和诱导组的临床资料无统计学的差异。在本研究中，在CTP1和CTP2两个时间点之间，诱导组患者的平均动脉血压为12 mmHg（95%置信区间，8.7~14.8 mm Hg），高于对照组。诱导组的所有患者在CTP2时间点时，仍然能够耐受诱导血压的升高。诱导组患者的总CBF变化为0.1（-31~43）ml/100g/min，而对照组为-8.3（-41~30）ml/100g/min，差异没有显著的统计学意义（P=0.24）。结论 诱导升压对于动脉瘤性蛛网膜下腔出血患者的脑血流量无显著的统计学影响。     

动脉瘤夹闭术对不同Fisher分级患者的蛛网膜下腔积血量及脑血管痉挛程度的影响

目的探讨动脉瘤夹闭术对不同Fisher分级患者的蛛网膜下腔积血量和脑血管痉挛程度的影响。方法选取我院2008-06—2014-11 90例动脉瘤性蛛网膜下腔出血患者为研究对象,依据不同Fisher分级分为FisherⅠ组、FisherⅡ组和FisherⅢ组,选取同期30例未破裂动脉瘤性蛛网膜下腔出血患者为对照组,观察患者术后血量和脑血管痉挛程度状况。结果FisherⅢ组第3天和第7天及第13天氧合血红蛋白含量、大脑中动脉血流速度明显的高于FisherⅠ组、FisherⅡ组,且FisherⅡ组和FisherⅢ组氧合血红蛋白含量、大脑中动脉血流速度均明显的高于对照组,差异有统计学意义(P0.05)。结论临床中FisherⅠ级和FisherⅡ级动脉瘤性蛛网膜下腔出血患者行动脉瘤夹闭术后积血量会增加,加重血管痉挛。而FisherⅢ分级动脉瘤性蛛网膜下腔出血患者行动脉瘤夹闭术后血量降低,减轻脑血管痉挛。     

多巴胺升压疗法对脑血管痉挛的评价

脑动脉瘤破裂出血患者由于血凝块及溶血物质的刺激,常可继发脑血管痉挛.尽管早期作动脉瘤根治手术,清除血肿,以及脑室清洗和引流,但发生脑血管痉挛仍难予避免,所以时常引起脑血流量(CBF)减少而发生脑缺血.又由于蛛网膜下腔出血后CBF之生理调节功能障碍,以及这些患者的脑血     

法舒地尔联用尼莫地平预防动脉瘤性蛛网膜下腔出血后迟发性脑血管痉挛的疗效观察

目的探讨法舒地尔联用尼莫地平对预防动脉瘤性蛛网膜下腔出血后脑血管痉挛的疗效及不良反应。方法在入院后即常规给予尼莫地平静脉持续泵入的同时,将50例动脉瘤性蛛网膜下腔出血患者在作动脉瘤栓塞治疗后,均给予腰大池引流及"3H"疗法,并随机分成2组,治疗组加用盐酸法舒地尔30mg静滴,3次/d,连用14d,观察2组血管痉挛的发生情况及不良反应。结果治疗组症状性脑血管痉挛1例,无症状性脑血管痉挛3例,对照组症状性脑血管痉挛3例,无症状性脑血管痉挛10例,2组间差异有统计学意义(P<0.05)。不良反应方面2组比较差异无统计学意义。结论法舒地尔联用尼莫地平在预防动脉瘤性蛛网膜下腔出血所致血管痉挛的疗效优于单用尼莫地平,安全性亦较高。     

血浆PTX3对动脉瘤性蛛网膜下腔出血后脑血管痉挛的预测价值

目的 分析血浆正五聚蛋白3(Pentraxin 3,PTX3)对动脉瘤性蛛网膜下腔出血后脑血管痉挛的预测价值。方法 收集本院2016年2月-2019年2月186例动脉瘤性蛛网膜下腔出血患者作为研究对象,经颅多普勒检测仪检测大脑中动脉(Middle cerebral artery,MCA)流速,MCA平均流速(Mean velocity of MCA,MCA Vm)>120 cm/s,且同侧Lindegaard≥3为血管痉挛组(92例),其余为无血管痉挛组(94例); 收集2组一般资料; 酶联免疫吸附(Enzyme linked immunosorbent assay,ELISA)法检测血浆中PTX3水平; 绘制受试者工作特性曲线(Receiver operator characteristic curve,ROC)分析血浆中PTX3对动脉瘤性蛛网膜者发生脑血管痉挛的诊断价值; 以血浆PTX3水平<4.73 ng/mL和≥4.73 ng/mL分为PTX3低表达组和PTX3高表达组,分析血浆PTX3水平与一般资料的关系; Logistic分析影响动脉瘤性蛛网膜下腔出血患者发生脑血管痉挛的因素。结果 无血管痉挛组与血管痉挛组年龄、治疗方法、高血压病史、Fisher分级、Hunt-Hess分级存在明显差异(P<0.05); 与无血管痉挛组比较,血管痉挛组血浆PTX3水平升高(P<0.05); ROC曲线显示,血浆PTX3水平预测动脉瘤性蛛网膜下腔出血患者发生脑血管痉挛的ROC曲线下面积为0.777,截断值为4.73 ng/mL,其敏感性为68.50%、特异性为74.50%; 血浆PTX3水平与年龄、治疗方法、Fisher分级、Hunt-Hess分级关系密切(P<0.05); Logistic分析显示,PTX3、年龄、Fisher分级、Hunt-Hess分级是影响动脉瘤性蛛网膜下腔出血患者发生脑血管痉挛的独立危险因素。结论 动脉瘤性蛛网膜下腔出血脑血管痉挛患者血浆PTX3水平升高,PTX3对动脉瘤性蛛网膜下腔出血患者发生脑血管痉挛具有一定诊断价值。     

颅内动脉瘤性蛛网膜下腔出血患者手术前病情加重的多因素分析

目的探讨和分析颅内动脉瘤性蛛网膜下腔出血患者手术前病情加重的相关危险因素。方法选择2002年5月-2006年3月诊断明确的189例动脉瘤性蛛网膜下腔出血患者,均于首次发病后2周内接受手术治疗。根据手术前Hunt-Hess分级分为颅内动脉瘤手术前病情加重组(27例)和手术前病情未加重组(162例)。通过Logistic回归方程对11项与蛛网膜下腔出血相关的危险因素进行分析,从中归纳总结出与手术前病情加重最为相关的危险因素。结果颅内动脉瘤性蛛网膜下腔出血首诊Hunt-Hess分级(OR=2.739,95%CI:1.721～4.359;P=0.000)、意识障碍(OR=4.863,95%CI:1.687～14.020;P=0.003)和运动功能障碍(OR=3.579,95%CI:1.064～12.042;P=0.039)等3项因素与动脉瘤性蛛网膜下腔出血患者手术前病情加重相关;而与性别、年龄、失语、脑积水、脑内或脑室出血及高血压病史等因素无关,两组相比差异无统计学意义(P>0.05)。结论首诊Hunt-Hess分级≥3级、意识障碍和运动功能障碍等项指标可以作为预测动脉瘤性蛛网膜下腔出血患者手术前病情加重的独立危险因素,对预测患者病情的变化具有重要临床意义。     

动脉瘤性蛛网膜下腔出血导致症状性脑血管痉挛的危险因素分析

目的 探讨导致动脉瘤性蛛网膜下腔出血后患者症状性脑血管痉挛的主要危险因素。方法 选取华中科技大学同济医学院附属同济医院2011～2013年收治的421例经头颅CT检查和/或腰穿确诊的自发性蛛网膜下腔出血患者,观察并记录患者每天的病情变化、年龄、性别、出血次数、血压、动脉瘤部位、动脉瘤大小、Hunt-Hess分级和Fisher分级及患者症状性血管痉挛的发生情况。对所有患者症状性血管痉挛的发生情况按年龄、性别、出血次数、血压、动脉瘤部位、动脉瘤大小,Hunt-Hess分级和Fisher分级等进行Logistic多因素逐步回归分析。结果 单因素分析表明FisherⅢ级者与Ⅰ～Ⅱ级者相比症状性血管痉挛发生率明显较高(P<0.05)、入院时临床状态不良组症状性血管痉挛发生率与良好组相比明显较高(P<0.05),反复SAH发作组症状性血管痉挛发生率与单次SAH发作者相比明显较高(P<0.05); 不同性别、不同年龄组患者、不同动脉瘤治疗方式组(手术夹闭或栓塞)患者症状性血管痉挛发生率的差异均不明显(P均>0.05)。结论 可根据蛛网膜下腔积血量、入院时临床状态和SAH发生次数预测症状性血管痉挛的发生。     

动脉内灌注法舒地尔治疗症状性脑血管痉挛

目的评价盐酸法舒地尔动脉内灌注治疗症状性脑血管痉挛的疗效。方法收集40例动脉瘤性蛛网膜下腔出血在介入手术治疗后出现症状性脑血管痉挛的病人,随机分为治疗组(n=20)和对照组(n=20),对照组给予尼莫地平治疗,治疗组给予尼莫地平+动脉内法舒地尔灌注治疗,观察治疗前后影像学及症状变化,并随访3个月GOS评分,评价远期疗效。结果两组病人年龄、性别、动脉瘤位置及Hunt-Hess分级无统计学差异(P0.05)。治疗组共行23次法舒地尔动脉内灌注,造影图像均有改善,完全缓解19次,不完全缓解4次。治疗组NIHSS评分在治疗前后有显著差异(P=0.03)。法舒地尔灌注治疗中无一例病人出现严重并发症。随访3个月,对照组恢复良好35%,治疗组85%。治疗组预后与对照组相比差异具有统计学意义(P0.05)。结论法舒地尔动脉内灌注治疗对蛛网膜下腔出血后症状性脑血管痉挛病人有较好的临床疗效及远期预后,控制法舒地尔的剂量和给药速率,安全可靠。     

非动脉瘤性自发性蛛网膜下腔出血分析

目的总结非动脉瘤性自发性蛛网膜下腔出血的临床特点。方法自发性SAH患者首次CTA和DSA均未发现动脉瘤和其他血管病变者,3～4周复查CTA或DSA,结果仍为阴性者诊断为非动脉瘤性SAH。分为中脑周围非动脉瘤性蛛网膜下腔出血(PMN)组和非中脑周围非动脉瘤性蛛网膜下腔出血(nPMN)组。结果 51例患者首次CTA和DSA未发现动脉瘤和其他血管病变,其中4例复查CTA或DSA发现动脉瘤,另有6例患者未复查即死亡。诊断为非动脉瘤性蛛网膜下腔出血共41例,其中PMN组29例,nPMN组12例。平均随访2.3年,两组均无死亡,全部的PMN病例和83.3%的nPMN病例预后良好。结论非中脑周围非动脉瘤性蛛网膜下腔出血(nPMN)临床过程和预后介于动脉瘤性SAH和PMNSAH之间,需要通过重复造影检查排除动脉瘤的可能。     

动脉瘤性蛛网膜下腔出血后脑血管痉挛危险因素的分析

目的 探讨动脉瘤性蛛网膜下腔出血后脑血管痉挛的危险因素.方法 回顾性分析93例动脉瘤性蛛网膜下腔出血患者的临床资料,研究脑血管痉挛的危险因素.结果 93例动脉瘤性蛛网膜下腔出血患者中共有28例患者(30.1％)发生脑血管痉挛.Hunt-Hess分级≥Ⅲ级血管痉挛发生率明显高于Hunt-Hess分级Ⅰ-Ⅱ级,差异有统计学意义(P＜0.01);Fisher分级≥Ⅲ级血管痉挛发生率明显高于Fisher分级Ⅰ-Ⅱ级,差异有统计学意义(P＜0.01);白细胞计数＞ 15×109的患者脑血管痉挛发生率(41.9％,18/43)明显升高(P＜0.05).结论 Hunt-Hess分级≥Ⅲ级、Fisher分级≥Ⅲ级、白细胞计数增高是蛛网膜下腔出血后脑血管痉挛的危险因素.     

Changes of the plasma ketone body level and arterial ketone body ratio at the onset of mild aneurysmal subarachnoid hemorrhage

Abstract

Objective: The purpose of this study was to investigate the physiologic changes of ketone bodies in patients with aneurysmal subarachnoid hemorrhage. We tested the hypothesis that the plasma ketone bodies are associated with the vasoconstrictor and lipolysis effect of circulating catecholamine.

Methods: Twenty-four patients with mild aneurysmal subarachnoid hemorrhage and 18 healthy volunteers were enrolled in this study. We collected arterial blood samples immediately after admission and 30 days later to measure the levels of 3-hydroxybutyrate, acetoacetate, epinephrine and norepinephrine.

Result: At the onset of aneurysmal subarachnoid hemorrhage, the plasma ketone body (3-hydroxybutyrate + acetoacetate) level and the epinephrine and norepinephrine concentrations were significantly elevated, but the arterial ketone body ratio (acetoacetate/3-hydroxybutyrate) was significantly decreased compared with that of the control group. There was a negative correlation between the plasma ketone body level and the arterial ketone body ratio. There was a positive correlation between the plasma ketone body level and epinephrine level. Thirty days after admission, the ketone body, epinephrine and norepinephrine levels, as well as the arterial ketone body ratio, showed no significant differences between the patients and controls.

Conclusion: At the onset of mild aneurysmal subarachnoid hemorrhage, the plasma ketone body level was significantly increased, while the arterial ketone body ratio was significantly decreased.     

脑灌注压对动脉瘤性蛛网膜下腔出血后迟发性脑缺血的预测价值

目的探讨脑灌注压(CPP)对动脉瘤性蛛网膜下腔出血(aSAH)后迟发性脑缺血(DCI)发生的预测价值。方法纳入2016年1月至12月在我院就诊并进行CPP检测的50例aSAH患者,其中19例发生DCI。统计所有患者低于各CPP阈值的时间总比例,通过ROC曲线及二元logisctic回归分析比较CPP与DCI的相关性。结果 CPP低于50 mmHg、55 mmHg、60 mmHg、65 mmHg的时间比例对DCI的预测阈值分别为0.28%(AUC=0.778)、3.0%(AUC=0.756)、10.8%(AUC=0.749)、16.1%(AUC=0.718),经二元logistic回归分析显示均与DCI的发生相关(P0.05)。而CPP低于70 mmHg、75 mmHg、80 mmHg的时间比例对DCI的预测阈值分别为24.8%(AUC=0.697)、49.6%(AUC=0.686)、55.9%(AUC=0.672),经二元logistic回归分析显示均与DCI无相关性(P0.05)。结论 aSAH患者发生DCI的风险与CPP降低有关,而维持CPP在70 mmHg以上可能有助于预防DCI发生。     

CT血管成像和CT灌注点征的联合应用在选择中等量脑出血超早期手术方式中的价值

目的探讨联合应用CT血管成像(CTA)、CT灌注(CTP)点征在基底节中等量脑出血超早期抽吸术或开颅手术的手术方式选择中的应用价值。方法选择中等量基底节脑出血(出血量30～60ml)且家属同意超早期手术治疗221例,根据入院后患者是否同意行颅脑CTA及CTP检查,分为研究组(同意检查者)105例,对照组(不同意检查者)116例,研究组CTA或CTP点征阳性者,入开颅手术亚组32例,CTA和CTP点征阴性者入抽吸亚组73例。对照组根据患者家属知情同意后选择的手术方式,分为开颅亚组39例,抽吸亚组77例。对比研究组与对照组患者治疗效果的差异,评估联合应用CTA、CTP点征在基底节中等量脑出血超早期手术方式选择中的应用价值。结果研究组有效率、术后血肿增大率、病死率、颅内感染率分别为77.1%、3.8%、3.8%、2.9%,对照组分别为52.6%、18.1%、15.6%、12.1%,2组比较差异有统计学意义。(P0.05)。结论联合应用CTA、CTP点征选择基底节中等量脑出血手术方式,可明显改善患者预后。     

Reduction of pulmonary edema after SAH with a pulmonary artery catheter-guided hemodynamic management protocol

Introduction: The frequency of pulmonary edema, which occurs with high frequency following subarachnoid hemorrhage (SAH), can be worsened by hypervolemic, hypertensive, hemodilution therapy for vasospasm. This study compares the complication rates for patients with SAH before and after institution of a pulmonary artery catheter-guided hemodynamic management protocol. Methods: Complication and outcome data were prospectively collected on 453 patients with spontaneous SAH. The patients were divided into groups treated from July 1998 through January 2000 (n=174) and from February 2002 through June 2002 (n=279). In group I, treatment consisted of hypervolemia (central venous pressures: >8 mmHg) and hypertension (mean arterial pressure: 110–130 mmHg). In group II, normovolemia was the goal, defined using a pulmonary artery catheter (wedge pressure: 10–14 mmHg). Cardiac output was enhanced (index: >4.5 L/minute/m2), and blood pressure elevations were moderated (mean pressure: >100 mmHg). Results: The average age, comorbidity, hemorrhage severity, and incidence of vasospasm were almost identical between the two groups. Statistically significant reductions were noted in patients in group II for two types of complications as well as for mortality. The rate of pulmonary edema (from 14 to 6%) and the rate of sepsis (from 14 to 6%) were both decreased (p≤0.03). Mortality decreased from 34 to 29% (p=0.04). Other complications, such as myocardial infarction, were not affected. Conclusions: These data show that a significant reduction in the frequency of pulmonary edema after SAH can be attained using a pulmonary artery catheter-guided hemodynamic management protocol.     

Subarachnoid blood infusion versus raised intracranial pressure: Effects on the amino acid pattern in the extracellular fluid of the rabbit hippocampus

Abstract

In order to evaluate the role of a hemorrhage versus that of a transient increase in intracranial pressure in subarachnoid hemorrhage, the two components were induced separately in rabbits. Extracellular glutamate, sampled from the hippocampus with microdialysis, was used to evaluate the degree of CNS tissue damage. In four rabbits, autologous arterial blood was infused in the cisterna magna in a volume that would not affect the intracranial pressure. The other group of animals was infused with saline to elevate the intracranial pressure from 10 to > 100 mmHg. The increase of intracranial pressure per se did not induce significant changes in extracellular glutamate. However, 20-60 min after infusion of blood, a significant glutamate increase was recorded. Furthermore, aspartate, alanine, glycine and serine were also raised. The results indicate that blood in the subarachnoid space damages the brain primarily by inducing ischemia. Furthermore, the parameters employed gave no indication that an increase in intracranial pressure had a deleterious effect on CNS tissue. [Neurol Res 1999; 21: 404-408]     

Relationship of hypotension and cerebral vasospasm in patients with aneurysmal subarachnoid hemorrhage

OBJECTIVES: Changes in systemic arterial blood pressure and the degree of cerebral vasospasm were investigated in 125 patients with aneurysmal subarachnoid hemorrhage.METHODS: Systemic arterial blood pressure was measured every 2 hours in each patient for a period of more than 2 weeks, and a fall in systemic blood pressure (FBP) was defined as a decrease of >40 mmHg of systolic blood pressure between two consecutive measurements.RESULTS: A total of 91 FBPs occurred in 52 (41.6%) of 125 patients despite specific post-operative management to prevent hypovolemia. Five (5.5%) of the 91 FBPs occurred just before the onset of symptomatic vasospasm. Symptomatic vasospasm was observed in 36 (69.2%) of 52 patients with FBP and in 32 (43.8%) of 73 patients without FBP (p<0.01, chi-squared test). A hypodense area on computed tomographic scans in association with cerebral vasospasm was observed in 25 (48.1%) of 52 patients with FBP and in 21 (28.8%) of 73 patients without FBP (p<0.05).DISCUSSION: We conclude that FBP might result from delayed cerebral vasospasm and/or brain dysfunction owing to subarachnoid hemorrhage itself.     

Whole brain CT perfusion combined with CT angiography in patients with subarachnoid hemorrhage and cerebral vasospasm

Objective

To assess cerebral vasospasm (CVS) and monitor cerebral microcirculatory changes in patients with acute subarachnoid hemorrhage (SAH) via CT angiography (CTA) combined with whole-brain CT perfusion (CTP) techniques.

Methods

Sixty patients with SAH (SAH group) and 10 patients without SAH (control group) were selected for a prospective study. CTP combined with CTA and digital subtraction angiography (DSA) studies were performed on patients with initial onset of SAH less than three days. CTA and DSA as well as the CTP parameters such as cerebral blood volume (CBV), cerebral blood flow (CBF), mean transit time (MTT), and time-to-peak (TTP) were acquired and analyzed. The relationship of CTA and CTP measurements was assessed in these acute SAH patients.

Results

CTP techniques were used to achieve the perfusion maps of the whole brain in patients with acute SAH. Compared to the control group, mean CBF value was significantly lower while both MTT and TTP values were significantly higher in SAH group (all p < 0.05). Further analysis revealed that mean CBF in patients with CVS, sCVS, Fisher III–IV and Hunt–Hess III–V significantly decreased when compared to patients with nCVS, asCVS, Fisher I–II and Hunt–Hess I–II (p < 0.05). Furthermore both MTT and TTP values were also significantly reduced in patient with CVS, sCVS, Fisher III–IV and Hunt–Hess III–V (p < 0.05).

Conclusion

The study demonstrated that changes of microcirculation in patients with SAH could be assessed by whole-brain CTP. CTP combined with CTA could detect both macroscopic evident vasospasm on CTA and alterations of microcirculation on CTP. Mean CBF was significantly lower in patients with SAH.     

Post-operative changes of cerebral circulation and metabolism in the acute stage of low-grade aneurysmal subarachnoid hemorrhage

Abstract

Objective: Pre- and post-operative cerebral circulation and metabolism were evaluated in patients with low-grade acute aneurysmal subarachnoid hemorrhage (SAH) who underwent early surgery to investigate the effects on brain dysfunction.

Methods: Positron emission tomography (PET) was performed to measure the regional cerebral blood flow (CBF), cerebral metabolic rate of oxygen (CMRO₂), oxygen extraction fraction (OEF) and cerebral blood volume in four patients (one male and three females, mean age: 60.3 years) with low-grade SAH within 30 hours of onset. Post-operative PET was performed on the seventh post-operative day. No patient suffered clinical deterioration during the study. Pre-operative PET scans demonstrated significant global reduction of CBF and CMRO₂, compared to 16 normal control subjects, and no significant change in OEF. CBF and CMRO₂ reduction post-operatively improved to the normal control values. Post-operative OEF was significantly increased compared to the normal control value.

Conclusions: Patients with low-grade SAH have impairment of cerebral circulation and metabolism in the acute period, which improves after surgery. Early surgery for low-grade SAH, necessary to avoid rerupture of the aneurysm, did not worsen the impairment of cerebral circulation and metabolism. However, measures to protect the brain from perioperative damage are necessary to achieve the optimum outcome.     

Significance of a reduced cerebral blood flow during the first 12 hours after traumatic brain injury

Background: It is controversial whether a low cerebral blood flow (CBF) simply reflects the severity of injury or whether ischemia contributes to the brain’s injury. It is also not clear whether posttraumatic cerebral hypoperfusion results from intracranial hypertension or from pathologic changes of the cerebral vasculature. The answers to these questions have important implications for whether and how to treat a low CBF. Methods: We performed a retrospective analysis of 77 patients with severe traumatic brain injury who had measurement of CBF within 12 hours of injury. CBF was measured using xenon-enhanced computed tomography (XeCT). Global CBF, physiological parameters at the time of XeCT, and outcome measures were analyzed. Results: Average global CBF for the 77 patients was 36±16 mL/100g/minutes. Nine patients had an average global CBF <18 (average 12±5). The remaining 68 patients had a global CBF of 39±15. The initial ICP was >20 mmHg in 90% and >30 mmHg in 80% of patients in the group with CBF<18, compared to 33% and 16%, respectively, in the patients with CBF≥18. Mortality was 90% at 6 months postinjury in patients with CBF<18. Mortality in the patients with CBF>18 was 19% at 6 months after injury. Conclusion: In patients with CBF<18 mL/100 g/minutes, intracranial hypertension plays a major causative role in the reduction in CBF. Treatment would most likely be directed at controlling intracranial pressure, but the early, severe intracranial hypertension also probably indicates a severe brain injury. For levels of CBF between 18 and 40 mL/100 g/minutes, the presence of regional hypoperfusion was a more important factor in reducing the average CBF.