短期应用高渗盐水对重症蛛网膜下腔出血患者颅内压、脑血流量的影响

Objective To investigate the effect of 23.4% hypertonic saline(HTS)on intracranial pressure(ICP), cerebral peffusion pressure(CPP), cerebral blood flow(CBF)in poor-grade patients with subarachnoid hemorrhage(SAH).Methods Sixteen patients(Glasgow coma score ≤ 8)with poor-grade SAH received 23.4% hypertonic saline intravenously for elevated ICP.ICP, mean arterial pressure(MAP), CPP and the middle cerebral artery flow velocity(FV)were observed and recorded before and at 30, 60, 90,120, 150, 180 min after the injection respectively.Results Thirty minutes postinfusion, a significant increase in MAP, CPP, FV was seen together with a decrease in ICP(P<0.05).ICP remained reduced for 180 minutes, CPP and FV remained elevated for 90 minutes(P < 0.05).Conclusions HTS can significantly decrease ICP and improve CBF in patients with poor-grade subarachnoid hemorrhage and may be used for reversal of pathophysiologic changes caused by cerebral ischemia.     

高渗盐水对颅内压的影响

高渗盐水（ＨＳ）与甘露醇都可降低增高的颅内压（ＩＣＰ）；二者都降低脑组织水含量而使ＩＣＰ降低。ＨＳ在使脑水含量降低方面是通过使正常脑组织的去水作用，从而增加了颅内顺应性（ＣＣ）实现的；同时，ＨＳ通过使脑血管内皮和红细胞的去水作用而使脑血流（ＣＢＦ）增加，脑供氧增加。从而减少了头部创伤后的继发性脑损伤。     

高渗盐水对颅内压的影响

高渗盐水(HS)与甘露醇都可降低增高的颅内压(ICP);二者都降低脑组织水含量而使ICP降低。HS在使脑水含量降低方面是通过使正常脑组织的去水作用,从而增加了颅内顺应性(CC)实现的;同时,HS通过使脑血管内皮和红细胞的去水作用而使脑血流(CBF)增加,脑供氧增加。从而减少了头部创伤后的继发性脑损伤。     

蛛网膜下腔出血合并脑叶血肿

本文报告经尸检证实的蛛网膜下腔出血合并脑叶血肿４例，临床表现均突然起病，头痛伴呕吐，１例肢体瘫痪，２例有玻璃体下出血。２例发病后很快昏迷至死亡，２例蛛网膜下腔出血再发死亡。病理上脑叶血肿特征为位置浅表，形状不规则，血肿与蛛网膜下腔的积血相连。     

一氧化氮与蛛网膜下腔出血后的脑血管痉挛

近年来,一些研究表明一氧化氮的改变可能涉及到蛛网膜下腔出血(SAH)后脑血管痉挛的病理过程。本文就最新有关SAH后脑血管痉挛的发病机制及治疗措施作一综述。     

高渗盐水与甘露醇对颅脑手术患者脑氧代谢的影响

目的 比较3％高渗盐水（HTS）与20％甘露醇对颅脑手术患者脑氧代谢的影响。方法 择期大脑半球胶质瘤切除术患者40例，ASAⅠ级或Ⅱ级，随机分为2组（n=20）：3％HTS组（HTS组）和20％甘露醇组（M组）。采用静吸复合麻醉，呼气末异氟醚浓度为1 MAC、血液动力学稳定15．min后，分别于15 min内静脉输注3％HTS 5．35 ml／kg或20％，甘露醇1 g／kg。L3，4珠网膜下腔置管测脑脊液压力（CSFP），行右颈静脉球穿刺置管、采血，测定颈静脉球氧饱和度。分别于输注前（T0）、输注完即刻（T1）、输注完15min（T2）、30min（T3）、60min（T4）、120min（T5）监测CSFP;于T0、T3-T5时监测平均动脉压，采集颈静脉球部和桡动脉血，进行血气分析，计算动脉-静脉氧含量差（Da-jvO2）、脑氧摄取率（CERO2）。结果 与T0比较，2组CSFP在T2-T5时降低，Da-jvO2和CERO2在T4，5时降低（P〈0．05）;与M组比较，HTS组CSFP在T2时降低（P〈0．05）。结论 3％HTS与20%甘露醇均可有效地降低颅内压，改善颅脑手术患者的脑氧代谢。     

辛伐他汀对蛛网膜下腔出血后迟发性脑血管痉挛的影响及作用机制

目的本研究拟观察辛伐他汀对蛛网膜下腔出血后迟发性脑血管痉挛的影响，并探讨其机制。方法随机将新西兰白兔36只均分为假手术组、自发性蛛网膜下腔出血（SAH）组和SAH＋辛伐他汀组（n=12）。假注血组动物行枕大池假穿刺假注血，其他2组受试动物行枕大池穿刺2次注血的方法，制作迟发性脑血管痉挛模型。于0～6d。经口给予SAH＋辛伐他汀组家兔辛伐他汀5mg／kg体重，其他动物给予等量的淀粉。所有受试动物在第1次穿刺后的第7天被处死，比较不同组间基底动脉内径、内径与血管壁厚度之比（D／T）的变化；并应用免疫组织化学、逆转录．聚合酶链反应（RT-PCR）的方法对家兔基底动脉的肿瘤坏死因子（TNF）-α、白细胞介素（IL）-1β和IL-6表达进行评价。结果与SAH组比较。SAH＋辛伐他汀组动物血管痉挛明显缓解（P〈0．05）、其血管壁促炎细胞因子TNF-α、IL-1β和IL-6表达显著减少（P〈0．05）。结论经口给予一定量的辛伐他汀（5mg／kg体重）能明显缓解蛛网膜下腔出血后迟发性脑血管痉挛，其作用机制可能与辛伐他汀的抗炎作用有关。     

动脉瘤性蛛网膜下腔出血患者再出血的护理

对12例动脉瘤性蛛网膜下腔再出血患者严密观察病情变化，去除诱发因素，加强基础护理及出院指导。结果12例中9例经开颅动脉瘤夹闭或介入弹簧圈栓塞后康复出院，3例Hunt-HessⅣ～Ⅴ级患者因出血量大致脑疝而死亡。提出根据疾病发生的危险因素采取相应的护理措施是降低病死率，提高救治率的关键。     

蛛网膜下腔出血并发脑血管痉挛基因多态性研究进展

背景 脑血管痉挛(cerebral vasospasm,CVS)是蛛网膜下腔出血(subarachnoid haemorrhage,SAH)的主要并发症,也是造成患者死亡和致残的主要原因.目前国内外较少涉及SAH并发CVS基因多态性领域的研究. 目的 人类对CVS基因多态性的深入研究,将会给我们在对这种灾难疾病的认识、识别和管理带来很多的好处. 内容 综述国内外对SAH后并发CVS基因多态性研究及其应用. 趋向 基因多态性及表达产物既可作为CVS发生的危险因子,又可以提示CVS治疗的预后,同时也可以为SAH后CVS的治疗提供新的靶点.     

高渗盐水在神经外科中的应用研究进展

背景脑水肿和颅内压(intracranial pressure,ICP)增高的治疗一直是神经外科患者围手术期治疗的重要组成部分,也是决定患者预后的重要因素之一,甘露醇作为目前临床控制颅内高压的基本药物,其副作用及治疗局限性正被临床医生所重视.探讨更加有效的治疗方法已经成为目前国内外学者研究的热点.目的针对高渗盐水(hypertonic saline,HS)在各种神经外科疾病引起的脑水肿和ICP增高的治疗中的应用作一综述.内容主要阐述近年来HS防治脑水肿及ICP增高的相对明确的作用机制及其在各种神经外科疾病中的运用研究.趋向HS作为甘露醇的替代品,在脑水肿和ICP增高的治疗中正日益发挥着重要的作用.     

Efficacy and safety of hypertonic saline solutions in the treatment of severe head injury

BACKGROUND: The present study was undertaken to evaluate the efficacy and safety of hypertonic saline (HS) in the treatment of intracranial hypertension after severe head injury. METHODS: This prospective, observational study was performed in an 11-bed neurosurgery intensive care unit of a teaching hospital. From February 2002 to September 2004, 18 severely head-injured patients with elevated intracranial pressure (ICP) and Glasgow Coma Scale scores of 5 to 8 (mean, 5.9 +/- 1.2) were admitted to the unit and treated according to a standard protocol. One dose per day of 3% saline was administered by rapid infusion (300 mL/20 min) when ICP values exceeded 20 mm Hg. After infusion, cerebral blood flow, ICP, blood pressure, end-tidal carbon dioxide, and heart rate were monitored continuously for 60 minutes and recorded. Serum osmolarity, sodium, potassium, chloride, arterial carbon dioxide pressure, arterial oxygen pressure, hemoglobin, lactic acid, and pH were measured immediately before infusion (zero time) and 20 and 60 minutes after infusion. Mean arterial pressure, cerebral perfusion pressure (CPP), mean flow velocity (MFV), and pulsatility index (PI) were also recorded and analyzed. RESULTS: Intracranial pressure fell immediately after initiation of infusion with further significant decreases observed at 20 and 60 minutes (30.4 +/- 8.5, 24.3 +/- 7.4, and 23.8 +/- 8.3 mm Hg, respectively; P < .01). At these respective times CPP increased significantly (78.7 +/- 8.7, 83.2 +/- 7.8, and 87.2 +/- 12.8 mm Hg), PI dropped rapidly (1.51 +/- 0.42, 1.38 +/- 0.32, and 1.34 +/- 0.33) and MFV increased (66.26 +/- 25.91, 71.92 +/- 28.13, and 68.74 +/- 28.44). Serum sodium increased from 141.3 +/- 7.2 to 146.3 +/- 7.2 mmol/L after 20 minutes and returned to 144.3 +/- 7.36 mmol/L at 60 minutes. Potassium concentrations decreased significantly from 3.9 +/- 0.39 to 3.55 +/- 0.35 mmol/L after 20 minutes (P < .01). Lactic acid values at 0, 20, and 60 minutes were 1.6 +/- 0.5, 1.47 +/- 0.48, and 1.38 +/- 0.53 mmol/L, respectively (P < .01). CONCLUSION: Rapid infusion of single dose daily of HS is a safe alternative for the treatment of elevated ICP in severe head injury. Further evaluations of long-term consequences and complications and of maximal tolerance to this treatment are required.     

Intracisternal infusion of magnesium sulfate solution improved reduced cerebral blood flow induced by experimental subarachnoid hemorrhage in the rat

Magnesium has neuroprotective and antivasospastic properties in the presence of subarachnoid hemorrhage (SAH). The present study investigated the effect of intracisternal administration of magnesium on cerebral vasospasm in the experimental SAH rat model. The rat double-SAH model (0.2 mL autologous blood injected twice into the cisterna magna) was used. Normal saline (SAH group, N = 8) or 10 mmol/L magnesium sulfate in normal saline (SAH + MG group, N = 8) was infused into the cisterna magna at 1.5 μL/min for 30 min on day 5. Control rats without SAH also received intracisternal infusion of normal saline (control group, N = 6). Local cerebral blood flow (CBF) at 24 locations and the weighted average were quantitatively measured by the autoradiographic technique using [¹⁴C]iodoantipyrine during infusion. The weighted average CBF was significantly reduced (P < 0.01, Student’s t-test) in the SAH group (0.78 ± 0.16 mL g⁻¹ min⁻¹) compared to the control group (1.0 ± 0.15 mL g⁻¹ min⁻¹) and was significantly improved (P < 0.01, Student’s t-test) in the SAH + MG group (0.98 ± 0.18 mL g⁻¹ min⁻¹). Local CBF was significantly reduced (P < 0.05, unpaired t test) in 16 locations in the SAH group and significantly improved (P < 0.05, unpaired t test) in 12 locations in the SAH + MG group. Intracisternal infusion of magnesium sulfate significantly improved reduced CBF induced by experimental SAH in the rat.     

Enhancement of cerebral blood flow using systemic hypertonic saline therapy improves outcome in patients with poor-grade spontaneous subarachnoid hemorrhage

OBJECT: Systemic administration of 23.5% hypertonic saline enhances cerebral blood flow (CBF) in patients with poor-grade spontaneous subarachnoid hemorrhage (SAH). Whether the increment of change in CBF correlates with changes in autoregulation of CBF or outcome at discharge remains unknown. METHODS: Thirty-five patients with poor-grade spontaneous SAH received 2 ml/kg 23.5% hypertonic saline intravenously, and they underwent bedside transcranial Doppler (TCD) ultrasonography and intracranial pressure (ICP) monitoring. Seventeen of them underwent Xe-enhanced computed tomography (CT) scanning for measuring CBF. Outcome was assessed using the modified Rankin Scale (mRS) at discharge from the hospital. The data were analyzed using repeated-measurement analysis of variance and Dunnett correction. A comparison was made between patients with favorable and unfavorable outcomes using multivariate logistic regression. RESULTS: The authors observed a maximum increase in blood pressure by 10.3% (p < 0.05) and cerebral perfusion pressure (CPP) by 21.2% (p < 0.01) at 30 minutes, followed by a maximum decrease in ICP by 93.1% (p < 0.01) at 60 minutes. Changes in ICP and CPP persisted for longer than 180 and 90 minutes, respectively. The results of TCD ultrasonography showed that the baseline autoregulation was impaired on the ipsilateral side of ruptured aneurysm, and increments in flow velocities were higher and lasted longer on the contralateral side (48.75% compared with 31.96% [p = 0.045] and 180 minutes compared with 90 minutes [p < 0.05], respectively). The autoregulation was briefly impaired on the contralateral side during the infusion. A dose-dependent effect of CBF increments on favorable outcome was seen on Xe-CT scans (mRS Score 1-3, odds ratio 1.27 per 1 ml/100 g tissue x min, p = 0.045). CONCLUSIONS: Bolus systemic hypertonic saline therapy may be used for reversal of cerebral ischemia to normal perfusion in patients with poor-grade SAH.     

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.     

Effect of remifentanil on intracranial pressure and cerebral blood flow velocity in patients with head trauma

BACKGROUND: Remifentanil, an ultra-short-acting opioid, is used as an on-top analgesic in head trauma patients during transient painful procedures, e.g. endotracheal suctioning, physiotherapy, on the intensive care unit. However, previous studies have shown that opioids may increase intracranial pressure and decrease cerebral blood flow. METHODS: The present study investigates the effect of remifentanil on mean arterial blood pressure, intracranial pressure measured with intraparenchymal or epidural probes, and on cerebral blood flow velocity assessed by transcranial Doppler flowmetry in 20 head trauma patients sedated with propofol and sufentanil. Ventilation was adjusted for a target PaCO2 of 4.7-5.1 kPa. After baseline measurements a bolus of remifentanil (0.5 microg x kg(-1) i.v.) was administrated followed by a continuous infusion of remifentanil (0.25 microg x kg(-1) x min(-1) i.v.) for 20 min. RESULTS: There was no change in mean arterial blood pressure, intracranial pressure, and cerebral blood flow velocity in response to remifentanil infusion over time. Statistical analysis was performed using the Wilcoxon Signed Rank test. CONCLUSIONS: These data suggest that remifentanil can be used for on-top analgesia in head trauma patients without adverse effects on cerebrovascular haemodynamics, cerebral perfusion pressure or intracranial pressure.     

Cerebral blood flow and intracranial pressure during experimental subarachnoid haemorrhage

Summary The relationships of intracranial pressure (ICP), systemic blood pressure (SBP) and cerebral blood flow (CBF) during experimental subarachnoid haemorrhage were investigated in cats. Continuous monitoring of regional cerebral blood flow (rCBF) was done by a thermal diffusion method using a Peltier stack. During haemorrhage ICP rose within 5.4±0.97 minutes from 10.5±4.9 to 176.1±27.8 mmHg. This strong increase of ICP resulted in a temporary arrest of cerebral circulation. The Cushing response during the haemorrhage could not improve the cerebral circulation, but in contrast caused a further increase of ICP. After the haemorrhage the cerebral blood flow normalised within minutes. It is concluded, that the Cushing response during a subarachnoid haemorrhage should be regarded as a deleterious rather than a beneficial mechanism.     

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.     

Effect of controlled blood pressure increase on cerebral blood flow velocity and oxygenation in patients with subarachnoid haemorrhage

Background

Patients with aneurysmal subarachnoid haemorrhage (SAH) might have impaired cerebral autoregulation, that is, CBF – and thereby oxygen delivery – passively increase with an increase in CPP. This physiological study aimed to investigate the cerebral haemodynamic effects of controlled blood pressure increase in the early phase after SAH before any signs of delayed cerebral ischaemia (DCI) occurred.

Methods

The study was carried out within 5 days after ictus. Data were recorded at baseline and after 20 min of noradrenaline infusion to increase mean arterial blood pressure (MAP) by a maximum of 30 mmHg and to an absolute level of no more than 130 mmHg. The primary outcome was the difference in middle cerebral artery blood flow velocity (MCAv) measured by transcranial Doppler (TCD), while differences in intracranial pressure (ICP), brain tissue oxygen tension (PbtO₂), and microdialysis markers of cerebral oxidative metabolism and cell injury were assessed as exploratory outcomes. Data were analysed using Wilcoxon signed-rank test with correction for multiplicity for the exploratory outcomes using the Benjamini-Hochberg correction.

Results

Thirty-six participants underwent the intervention 4 (median, IQR: 3–4.75) days after ictus. MAP was increased from 82 (IQR: 76–85) to 95 (IQR: 88–98) mmHg (p-value: <.001). MCAv remained stable (baseline, median 57, IQR: 46–70 cm/s; controlled blood pressure increase, median: 55, IQR: 48–71 cm/s; p-value: .054), whereas PbtO₂ increased significantly (baseline, median: 24, 95%CI: 19–31 mmHg; controlled blood pressure increase, median: 27, 95%CI: 24–33 mmHg; p-value <.001). The remaining exploratory outcomes were unchanged.

Conclusion

In this study of patients with SAH, MCAv was not significantly affected by a brief course of controlled blood pressure increase; despite this, PbtO₂ increased. This suggests that autoregulation might not be impaired in these patients or other mechanisms could mediate the increase in brain oxygenation. Alternatively, a CBF increase did occur that, in turn, increased cerebral oxygenation, but was not detected by TCD. Trial registration: clinicaltrials.gov (NCT03987139; 14 June 2019).