Symptomatic hydrocephalus following aneurysmal subarachnoid hemorrhage

The results of a series of 500 consecutive patients who underwent aneurysmal surgery between 1969 and 1980 are reported. The incidence of significant symptomatic hydrocephalus secondary to spontaneous rupture of an intracranial aneurysm was 16.4%. Hydrocephalus was most frequent after rupture of aneurysms of the anterior communicating artery. Only one-third of the patients had more than one episode of subarachnoid hemorrhage before surgery. In 64% of the patients with preoperative hydrocephalus, there was angiographic evidence of spasm. In certain cases, the hydrocephalus must be treated before the offending aneurysm can be managed.     

Reversible arterial hypotension after acute aneurysmal subarachnoid hemorrhage

The authors report five patients who developed transient arterial hypotension immediately after the rupture of cerebral aneurysms. They manifested deep coma (three cases), abnormal electrocardiogram (four cases), and remarkable pulmonary edema (two cases). The level of consciousness in all three patients who were in deep coma improved with the normalization of blood pressure. Although two patients died of recurrent hemorrhage, the other three patients were discharged in satisfactory condition. Serious clinical conditions that are not terminal and are caused by arterial hypotension immediately after the rupture of cerebral aneurysms are sometimes reversible with adequate treatment.     

动脉瘤性蛛网膜下腔出血后症状性脑血管痉挛的相关因素分析研究

目的探讨动脉瘤性蛛网膜下腔出血后患者症状性脑血管痉挛的相关因素。方法本研究选取71例确诊为动脉瘤性蛛网膜下腔出血的患者为研究对象,在72小时之内行TCD,获得颅内大脑中动脉流速（MCAV）、颈内动脉血流速度、Lindegaard比值、颅内血管痉挛指数（VI）;并同时收集所有患者临床特征：年龄,性别,Hunt-Hess分级,CT Fisher分级,WBC计数（WBC）,治疗方法（弹簧圈栓塞,外科夹闭或保守治疗）,吸烟史,高血压病史;同时观察患者有无症状性脑血管痉挛发生。用SPSS统计学软件进行统计学分析。结果 21例（29.6%）发生症状性脑血管痉挛,单因素分析结果表明：MCAV、Lindegarrd率、VI、WBC计数（WBC）、Hunt-Hess分级、Fisher分级6个因素与是否发生症状性脑血管痉挛明显相关;纳入多因素Logistic回归分析,仅有CT Fisher分级,MCA流速,痉挛指数进入方程。可见对于诊断症状性血管痉挛,最好的多变量模型是选用CT Fisher分级,MCA流速,痉挛指数为变量。结论 MCAV、Lindegarrd率、VI、WBC计数、Hunt-Hess分级、Fisher分级6个因素是发生症状性脑血管痉挛的最重要影响因素。     

动脉瘤性蛛网膜下腔出血后脑血管痉挛和围术期容量治疗

背景 动脉瘤破裂蛛网膜下腔出血后脑血管痉挛(cerebral vasospasm,CVS)是一个常见而严重的并发症.CVS造成的继发性脑组织缺血或迟发性脑损伤严重影响患者的预后,是动脉瘤性蛛网膜下腔出血(aneurysm subarachnoid hemorrhage,aSAH)患者伤残和死亡的主要因素. 目的 探究围术期液体治疗和循环容量管理在aSAH后CVS预防和治疗中的有效性,为减少脑动脉瘤手术后CVS发生、改善预后提供参考. 内容 探究动脉瘤破裂蛛网膜下腔出血后CVS病因、病理生理以及如何选择合适的液体进行容量治疗和三高疗法来防治CVS的发生. 趋向 深入研究脑动脉瘤破裂出血后CVS的发病机制和探讨围术期液体治疗以及循环容量管理,为临床防治CVS提供新的思路和方法.     

Review of the literature regarding the relationship of rebleeding and external ventricular drainage in patients with subarachnoid hemorrhage of aneurysmal origin

Acute hydrocephalus is a well-documented complication of subarachnoid hemorrhage. The insertion of external ventricular drainage (EVD) has been the standard of care in the management of this complication, aiming primarily at immediate improvement of the clinical condition of these patients, making them more suitable candidates for surgical or endovascular intervention. In our current communication, we review the pertinent literature regarding the relationship of rebleeding and EVD. Several studies have implicated a significantly increased risk of rebleeding in patients with EVD, compared with patients without it. Abrupt lowering of the intracranial pressure could lead to rebleeding due to decreased transmural pressure or removal of the clot sealing the previously ruptured aneurysm. However, a variety of parameters that could affect the rebleeding rate, such as the timing of surgery, the timing and duration of drainage, the size of the aneurysm, as well as the severity of the initial hemorrhage, do not seem to have been adequately explored in the majority of these studies. In addition, a number of clinical trials have failed to provide evidence for the negative role of EVD in the development of rebleeding. Conclusively, further long-term multi-center studies are required in order to establish the exact nature of the relationship between EVD and rebleeding after aneurysmal subarachnoid hemorrhage.A commentary on this paper is available at     

Removal of subarachnoid blood clots after subarachnoid hemorrhage

The difficulty in removing subarachnoid blood clots was evaluated in terms of the interval after subarachnoid hemorrhage. Subarachnoid blood clots were removed from a total of 30 cisterns with a Hounsfield unit of more than 70. In 20 cisterns, removal was performed within 24 hours, and in 10 between 24 and 72 hours after subarachnoid hemorrhage. In 16 of the 20 cisterns (80%) and in 4 of the 10 cisterns (40%), the density was reduced to a Hounsfield unit of less than 60 after removal of subarachnoid blood clots. Two typical cases are presented.     

Computed tomographic demonstrated infarcts after surgical and endovascular treatment of aneurysmal subarachnoid hemorrhage

Summary. Background. Cerebral infarction is a sequela of vasospasm. Other etiologies for infarction after subarachnoid hemorrhage (SAH), however, have not been well-studied. To determine the incidence and etiologies for infarction after SAH, we reviewed the head CT scans of all SAH patients at our center from 1993–2000.Methods. From 1993–2000, 679 consecutive patients were admitted with SAH, of which 619 patients underwent surgical or endovascular treatment. Two reviewers examined the head CT scans of all 619 patients for new infarct. Clinical outcome was collected from a prospective database.Findings. 505 patients were treated with surgical clipping; 114 with endovascular coiling. There were CT findings of new infarct in 189 patients (30%): 140 in the surgical group (28%) and 49 in the endovascular group (43%). The etiologies for infarct in the surgical group were vasospasm 79 (15%), perforator occlusion 40 (8%), large vessel occlusion 14 (3%), elevated intracranial pressure 4 (1%), thromboembolism 2 (0.4%), and systemic hypotension 1 (0.2%). Infarcts in the endovascular group were due to vasospasm 20 (18%), thromboembolism 12 (11%), large vessel occlusion/dissection 9 (8%), elevated intracranial pressure 4 (4%), perforator occlusion 3 (3%), and systemic hypotension 1 (1%). Hunt Hess Grade (P<0.001), Fisher Score (P<0.0001), and MGH Grade (P<0.001) were significantly associated with CT-demonstrated infarct. There was no significant difference in incidence of CT-infarcts when the period 1993–1996 was compared to 1997–2000.Conclusions. Despite advances in the treatment of SAH, there is still a significant incidence of associated radiographic infarcts. Hunt Hess Grade, Fisher Score, and MGH Grade were significantly associated with CT-demonstrated infarct.     

A randomized controlled study assessing outcome,cognition, autonomy and quality of life in over 70-year-old patients after aneurysmal subarachnoid hemorrhage

Background

Current aging of the population with good physiological status and the increasing incidence of subarachnoid hemorrhage (SAH) in elderly patients has enhanced the benefit of treatment in terms of independence and long-term quality of life (QoL).

动脉瘤性蛛网膜下腔出血后脑血管痉挛的低温治疗

脑血管痉挛(cerebral vasospasm,CVS)是导致动脉瘤性蛛网膜下腔出血(aneurysm subarachnoid hemorrhage,aSAH)患者死亡和残疾的主要原因之一.人们对SAH后CVS进行了广泛的研究,认为红细胞分解产物、血管内皮功能障碍以及分子机制在其发病起关键作用.目前对脑血管痉挛的治疗尚无确切治疗方法,近年来人们尝试应用低温治疗脑血管痉挛,现就SAH后CVS的病理生理机制和低温对于CVS的治疗进展作一综述.     

Preoperative hypoxemia in conscious patients after subarachnoid hemorrhage

We retrospectively examined partial arterial pressure of oxygen (Pao₂) afer subarachnoid hemorrhage (SAH), adjusted for patient-related risk factors for hypoxemia in 51 adult patients with no disturbance of consciousness undergoing surgery for clipping of intracranial aneurysms. A control group of 174 patients undergoing other operations were used for comparison. Arterial blood gas analysis was performed while patients were spontaneously breathing room air in the supine position before induction of anesthesia. The Pao₂ in the SAH patients was significantly lower (p<0.0001) than that in the control group after adjustment for age, obesity, and smoking status. In three patients in the SAH group, Pao₂ was less than 60 mmHg. Close monitoring of arterial oxygenation with pulse oximetry is desirable, and supplemental oxygen should be considered during transfer from the patients' room to the operating suite, even for conscious patients of SAH without cardiopulmonary disease.     

蛛网膜下腔出血后皮层微血管及神经元的超微结构改变

目的 观察蛛网膜下腔出血(SAH)后皮层微血管及神经元超微结构的动态变化.方法 将SD大鼠随机分为正常、假手术和手术组,采用改良血管内穿刺法制作大鼠蛛网膜下腔出血的动物模型,通过透射电子显微镜观察不同时间点各组脑组织皮层微血管及神经元的超微结构改变.结果 蛛网膜下腔出血后1 h即可观察到皮层神经元和血管内皮细胞出现轻度水肿,其后水肿逐渐加重,并出现线粒体的嵴膜融合、消失,粗面内质网脱颗粒,毛细血管内皮细胞核固缩,甚至部分微血管闭塞;出血后48 h损伤达到高峰,神经元坏死增多,部分呈裸核改变;随后水肿逐渐减退,于7 d时基本恢复正常.结论 蛛网膜下腔出血后皮层微血管及神经元存在明显的病理性损伤与修复过程,及早保护血管内皮结构与功能的完整,改善微循环功能,对蛛网膜下腔出血的治疗和预后具有重要意义.

Abstract：

Objective To investigate the dynamic ultrastructural changes of micrangiums and neurons in cortex after subarachnoid hemorrhage (SAH). Methods The SD rats were divided into three groups: normal control group, sham-operated control group and SAH group. A modified endovascular perforation model was used to induce SAH in rats. In each group, the brains were collected at different time points for observation on the ultrastructural changes of micrangiums and neurons in cortex under the transmission electron microscopy (TEM). Results The mild edema could be obviously seen in cortex micrangiums and neurons at 1 h after SAH. Thereafter, the edema became serious gradually, membrane and cristae fusion appeared or disappeared, rough endoplasmic reticulum degranulated, and there was pyrosis of capillary endothelial cell nuclei, even blockage of partial capillaries. At the 48th h week aftyer onset of SAH, pathologic changes reached the peak: neurons necrosis increased, and partial showed naked nucleus. Then, the edem was gradually alleviated and returned basically to the normal state at the 7th day.Conclusion There were obviously pathologic changes and repair procedures in cortex micrangiums and neurons after SAH. It was very important for the therapy and prognosis of SAH to protect structural and functional integrity as soon as possible and improve microcirculation.     

Postoperative central conduction time and cerebral blood flow in patients with aneurysmal subarachnoid hemorrhage: Relationship with prognosis and ischemic conditions

Cerebral blood flow (CBF) and somatosensory evoked potential (SEP) were monitored periodically on 32 patients who underwent aneurysm clipping within 3 days after subarachnoid hemorrhage (SAH). From the SEP data, central conduction time (CCT) was obtained, and CCT fluctuations were categorized into three types. Patients with CCT prolongation over 7.5 ms within 10 days after SAH tended to have poor recovery of CBF and unfavorable outcome. Therefore, periodical monitoring of CCT was considered as a useful indicator for predicting prognosis and post-SAH changes of cerebral blood flow.     

细胞凋亡在蛛网膜下腔出血后脑血管痉挛发病中的作用

背景 脑血管痉挛(cerebral vasospasm,CVS)是蛛网膜下腔出血(subarachnoid hemorrhage,SAH)和颅内动脉瘤术后致死或致残的主要并发症之一,如何有效地治疗脑血管痉挛成为防治SAH的主要目标,但其确切机制尚不清楚,新近许多研究表明细胞凋亡可能在SAH后CVS的发病中发挥重要作用....     

HLA-type of cerebral vasospasm patients after aneurysmal subarachnoid hemorrhage

We studied human lymphocyte antigen (HLA) types in a group of 45 patients who had aneurysmal subarachnoid hemorrhage (SAH). A significantly increased frequency of HLA antigen A31 and a significantly decreased frequency of HLA antigen B40 were found. In patients with delayed ischemic neurological deficit (DIND) following aneurysmal SAH and HLA typing, HLA-Bw60 antigen showed significant increases; in patients who did not develop HLA-Aw33 and-Cw4 antigens showed significant. Among the patients with Fisher's Group 3 on CT, in particular, these antigens significantly increased when compared with controls from the same geographic area. These results suggest that HLA-Bw60 antigen plays a role as a predisposing factor of DIND resulting from vasospasm following aneurysmal SAH, and that HLA-Aw33 and-Cw4 exert protective influence against DIND.     

动脉瘤性蛛网膜下腔出血后再出血的急诊专科化护理经验

目的 探讨急诊专科化护理在预防和减少动脉瘤性蛛网膜下腔出血后再出血的影响。方法 回顾分析我院2012年1月～2015年12月之间96例急诊接受专科化护理干预措施的动脉瘤性蛛网膜下腔出血患者术前再出血的临床资料。结果 96例患者中有10签字后转院治疗,30例发病6h内接受手术治疗,其余56例则在72h内接受手术。共有14例患者出现病情加重,其中6例出现再出血,再出血率6.3%。结论 对于急诊就诊动脉瘤性蛛网膜下腔出血患者尽早开启专科化护理,有助于减少术前再出血的发生。     

Brainstem hypoperfusion in severe symptomatic vasospasm following aneurysmal subarachnoid hemorrhage: role of basilar artery vasospasm

Summary Background. The hemodynamic effects of vertebrobasilar vasospasm are ill defined. The purpose of this study was to determine the effects of basilar artery (BA) vasospasm on brainstem (BS) perfusion. Methods. Forty-five patients with delayed ischemic neurological deficits (DIND) following aneurysmal subarachnoid hemorrhage (SAH) underwent cerebral angiography prior to decision-making concerning endovascular treatment. BA diameter was compared with baseline angiogram. Regional brainstem (BS) cerebral blood flow (CBF) was qualitatively estimated by ^99mTc ethyl cysteinate dimer single photon emission computed tomography (ECD-SPECT). Findings. Delayed BS hypoperfusion was found in 22 (48.9%) of 45 patients and BA narrowing of more than 20% was found in 23 (51.1%). Seventeen of 23 (73.9%) patients with BA narrowing of more than 20% experienced BS hypoperfusion compared to 6 of 22 (27.3%) patients with minimal or no narrowing (p = 0.0072). Patients with severe and moderate BS hypoperfusion had higher degree of BA narrowing compared to patients with normal BS perfusion and mild BS hypoperfusion (p < 0.001). The three-month outcome of patients n-22) with BS hypoperfusion was significantly worse compared to patients (n-23) with unimpaired (p = 0.0377, odd ratio for poor outcome 4, 1.15–13.9 95% confidence interval). Interpretation. These findings suggest that the incidence of BA vasospasm in patients with severe symptomatic vasospasm is high and patients with significant BA vasospasm are at higher risk to experience BS ischemia. Further studies should be done to evaluate the effects of endovascular therapy on BS perfusion and the impact of BS ischemia on morbidity and mortality of patients with severe symptomatic vasospasm.     

Patients in poor neurological condition after subarachnoid hemorrhage: Early management and long-term outcome

Summary We report management and outcome data on 118 patients that presented to our emergency room over a 4 year interval (1990–1994) in poor neurological condition after subarachnoid hemorrhage. All patients were treated following a strict protocol. After initial evaluation, patients underwent a head computerized tomography (CT) scan to try to understand the mechanism of coma. If CT did not show destruction of vital brain areas, a ventriculostomy was inserted and ICP measured. If ICP was less than 20 mm Hg, or if standard treatment of increased ICP was able to lower the ICP to a value less than 20 mmHg, patients were evaluated with cerebral angiogram to determine the location of the raptured aneurysm. The lesion was then treated by craniotomy for aneurysm clipping or endovascular obliteration. Postoperative monitoring for vasospasm with clinical exam and transcranial doppler studies was performed routinely. If vasospasm developed, this was managed aggressively with hypertensive, hypervolemic and hemodilutional therapy and, at times, endovascular treatment with angioplasty or papaverine. Outcome was measured at 1 year or more after treatment. Among patients who met criteria for aneurysm treatment, 47% had excellent or good neurologic outcome. There was a 30% mortality rate in these patients. In patients with high ICP, poor brainstem function or destruction of vital brain areas on CT, comfort measures only were offered and almost all died. It is concluded that an approach of early aneurysm obliteration and aggressive medical and endovascular management of vasospasm is warranted in patients in poor neurological conditions after subarachnoid hemorrhage.