不同剂量甘露醇单用或合用速尿治疗颅高压的疗效观察

目的观察不同剂量甘露醇单用或合用速尿治疗颅高压的疗效。方法对60例各种原因行脑外科手术后出现颅内压增高的患者、依据使用不同剂量甘露醇单用或加用速尿而分为半量甘露醇(0.5 g/kg)组(A组)、全量甘露醇(1.0 g/kg)组(B组)、半量甘露醇 速尿(20 mg)组(C组)及全量甘露醇 速尿(20 mg)组(D组),通过颅内压监测,观察各组降低颅内压的效率、血浆渗透压及肾功能改变。结果(1)在降低颅内压的有效率、颅内压反跳率、药效持续时间上,C、D组明显优于A、B组(均P<0.05);降压幅度4组间差异无显著性。(2)连续降颅压治疗第5 d及第7 d时,各组均出现血浆渗透压的升高,与C组相比,B、D组升高更明显(P<0.05~0.01)。(3)连续使用甘露醇第5 d、7 d,与C组相比,B、D组血尿素氮、肌酐明显升高(均P<0.05)。结论半量甘露醇 速尿治疗颅内压增高疗效佳、安全性高。     

持续颅内压监测指导重型颅脑损伤开颅术后甘露醇的应用

目的探讨持续动态颅内压(ICP)监测指导重型颅脑损伤(sTBI)患者行开颅脑血肿清除术和(或)去骨瓣减压术后甘露醇使用的临床价值。方法对20例sTBI开颅术后患者行持续ICP监测,根据ICP数值作个体化甘露醇脱水降颅压,并与同期未行ICP监测的21例开颅术后患者的甘露醇应用时间和计量、术后并发症、预后进行比较。结果监测组甘露醇使用时间及计量较对照组低,监测组术后总并发症(迟发性脑血肿、大面积脑梗塞、弥漫性脑肿胀、电解质紊乱、急性肾功能损害)发生率较对照组低;监测组GOS预后评分优于对照组。结论持续动态ICP监测能及时反应sTBI开颅术后ICP的变化,通过个体化精准降颅压治疗有效控制ICP,维持脑灌注压,减少甘露醇的使用,减少术后并发症的发生,改善sTBI患者预后和生存率。     

闪光视觉诱发电位监测甘露醇降颅压效果的临床研究

目的利用闪光视觉诱发电位监测颅内高压患者颅压水平,研究降颅压效果与甘露醇用量以及其他影响因素的关系。方法选择60例颅内高压患者,应用NIP-200型无创颅内压监测仪监测患者每日颅压,计算最高颅压与最低颅压间的差值(降颅压效果),采用多元逐步回归方法分析降颅压效果与性别,年龄,最高颅压时的心率、血压以及降至最低颅压时甘露醇总用量的关系。结果60例患者最低颅压平均值为(213·4±66·8)mmH2O(83·5~364·5mmH2O),患者的颅压水平从入院至最低值时甘露醇总用量的平均值为(1870·8±861·9)ml(375~4000ml)。降颅压效果与最高颅压时的血压(舒张压和收缩压)和心率无相关性(P>0·05),与性别、年龄显著相关(P<0·05),与甘露醇用量显著相关(P<0·01)。结论甘露醇有明显的降颅压作用,但是用到一定的剂量后,便不再有降颅压作用。女性患者比男性患者降颅压的效果好。患者年龄越小,降颅压效果越好。     

复方甘油治疗脑水肿降低颅内压的疗效观察

通过32例高颅压患者甘油和甘露醇交替给药的疗效比较，结果显示两药的总有效率及降ICP作用类似；但两药降ICP的显效时间、持续时间不同，尿量及尿比重也有显著差异。所以甘露醇适于急性颅压增高患者的急救，而甘油适于需长期脱水治疗的患者。     

不同浓度高渗盐水和甘露醇降颅压效果及不良反应的比较

目的比较3%、7.5%高渗盐水(HS)和20%甘露醇降颅压有效性、安全性。方法 24例重型颅脑损伤患者接受不同浓度高渗盐水及20%甘露醇治疗,用药后6h内测定颅内压(ICP)、平均动脉压(MAP)、中心静脉压(CVP)、血Na+、K+、Cl-、血浆渗透压、脑灌注量(CPP)、血清S100B浓度。结果用药后,三者均可有效降低颅内压,3%高渗盐水组可较好保持中心静脉压处于正常水平,7.5%高渗盐水降压较为平稳,3%、7.5%高渗盐水较20%甘露醇组,作用持续时间更长,提升平均动脉压、脑灌注量更有效,差异有统计学意义(P0.05)。三者血清SIOOB浓度均升高,高渗盐水组上升幅度均较甘露醇组小。3%、7.5%高渗盐水组低钠血症发生率明显低于20%甘露醇组。结论高渗盐水降颅压作用持续时间长,有助于减轻伤后血脑屏障继发性损伤,并发症少,不良反应小,可作为降低颅内压的一线治疗药物。     

脑出血患者甘露醇治疗前后尿微量蛋白变化及意义

目的 探讨脑出血患者甘露醇治疗前后尿β2微球蛋白(Uβ2-MG)、尿白蛋白(UIAb)、尿IgG(UIgG)变化及其早期肾功能损害.方法 用放射免疫(RIA)法检测30例脑出血患者甘露醇治疗前后Uβ2-MG、UIAb、UIgG.结果 甘露醇治疗前尿微量蛋白变化与对照组比较无差异性(P>0.05);治疗后尿微量蛋白变化与对照组及治疗前比较均具有非常显著的差异性(P<0.001).结论 甘露醇治疗后早期肾功能损害以肾小管的重吸收功能降低为主,从而提示在临床工作中应严格掌握甘露醇的适应证、剂量以及血浆渗透压的监测;并在甘露醇使用的同时尽量避免使用肾毒性及肾代谢的药物.     

急性脑血管病患者使用甘露醇早期肾功能损害的检测

目的　探讨尿视黄醇结合蛋白 (RBP)对判断急性脑血管病患者使用甘露醇后肾功能损害的临床价值 ,及甘露醇的剂量、时间与肾功能损害的关系。方法　用酶联免疫吸附法测定了 32例急性脑血管病患者使用甘露醇前后尿中 RBP含量。结果　用甘露醇治疗后尿 RBP较治疗前增高 (P<0 .0 5 ) ,甘露醇总剂量≥ 5 0 0 g时尿 RBP增高有统计学意义 (P<0 .0 5 )。结论　 (1)大剂量的甘露醇能诱发肾功能损害 ;(2 )尿 RBP可作为判断早期肾功能损害的灵敏指标之一。     

白蛋白辅助治疗大面积脑梗死临床效果观察

目的观察人血白蛋白辅助治疗大面积脑梗死的疗效。方法将80例急性大面积脑梗死患者随机分为联合治疗组和甘露醇组,2组均给予甘露醇降颅压及基础治疗,联合治疗组加用白蛋白20g静滴,1次/d,共7d。于治疗前、治疗第14天分别进行神经功能缺损评分、颅脑CT或MRI测量脑中线移位数据,计算出每日脑中线移位产生率。结果治疗后2组神经功能缺损程度评分均较治疗前减少,而联合治疗组较甘露醇组减少的更为明显(P0.05);联合治疗组显效率明显高于甘露醇组(P0.05);联合治疗组每日脑中线移位产生率明显低于甘露醇组(P0.01)。结论白蛋白辅助治疗急性大面积脑梗死,不仅可有效减少脑水肿发生,且可减轻神经功能缺损程度,改善预后。     

吡拉西坦注射液静滴对脑挫裂伤患者颅内压的影响

目的观察吡拉西坦对脑挫裂伤患者的降颅压作用及吡拉西坦对其GCS评分改善的临床观察。方法 2009-06~2010-12对我科收治除外视神经损伤的中型颅脑损伤患者(GCS 6~12分)80例,随机分为治疗组40例和对照组40例,治疗组应用甘露醇和吡拉西坦,对照组单纯应用甘露醇,应用无创颅内压监测仪监测2组患者颅内压情况,同时每日对患者进行GCS测评。结果 2组患者在首次应用甘露醇前和首次应用甘露醇后1 h测得颅内压无明显差别(P>0.05),而在甘露醇应用后3 h颅内压治疗组较对照组明显降低(P<0.01)。GCS评分1~4 d差别无统计学意义,治疗后6~7 d差别有统计学意义,治疗组明显优于对照组。结论通过无创颅内压监测,吡拉西坦除具有神经营养作用外,还具有明显的降颅压作用,和传统的降颅压药物甘露醇合用,可降低甘露醇的用量,减少甘露醇对肾功能的损害,吡拉西坦和甘露醇联合应用可以起到良好的互补和协同作用,降低颅内压和促进脑挫裂伤患者神经功能恢复。     

速尿和甘露醇引起的颅内压、血清渗透压和电解质的变化

神经外科病人注射甘露醇使脑体积缩小常伴有一些副作用,例如颅压反跳,脑和循环血量一过性增多,凝血和血粘稠度变化,血清渗透压增高和电解质减少等。磺胺类利尿药—速尿主要抑制远端肾小管的再吸收,可用以降低脑含水量,因副作用较少可以取代甘露醇。作者分别测定甘露醇和速尿对颅内压,血清渗透压和电解质的影响并加以比较。本组共20例患脑动脉瘤、动静脉畸形或脑瘤的病人择期施行开颅术。术前均无高颅压体征。一律选用氟烷—笑气—氧麻醉,控制呼吸使PaCO_2保持在25～30托。一组一次注入甘露醇1克/公斤;另一组一次静注速尿1毫克/公斤,并在手术前,麻醉诱导,利尿开始、药效最高与利尿结束以及术后分别测定颅内压,血细胞压     

Treatment of systemic hypertension and intracranial hypertension in cases of brain hemorrhage

We studied the effects of nifedipine, chlorpromazine, reserpine, furosemide, and thiopental on the mean arterial blood pressure, mean intracranial pressure, and cerebral perfusion pressure in 38 patients with increased intracranial pressure resulting from either hemorrhagic cerebrovascular disease or systemic hypertension. These agents are widely used in neurosurgical practice for the treatment of systemic hypertension. Patients were assigned to two groups on the basis of their mean intracranial pressure. Group I comprised 20 patients with a mean intracranial pressure of 20-40 mm Hg (moderately increased ICP group), and Group II consisted of 18 patients with a mean intracranial pressure of greater than 40 mm Hg (severely increased ICP group). Nifedipine, chlorpromazine, and reserpine reduced mean arterial blood pressure by 18-20% in both groups (p less than 0.05 in each). In Group I these agents raised mean intracranial pressure by 10-35% and decreased cerebral perfusion pressure by 20-32% (p less than 0.05 for both), but in Group II these changes were more marked: mean intracranial pressure increased 38-64% and cerebral perfusion pressure decreased 40-54% (p less than 0.01 for both). Furosemide did not significantly reduce mean arterial blood pressure but slightly reduced mean intracranial pressure in each group. Thiopental reduced both mean arterial blood pressure and intracranial pressure in both groups. The effect on intracranial pressure was pronounced in Group II, in which mean arterial blood pressure fell by 18% (p less than 0.05) and mean intracranial pressure decreased 50% (p less than 0.01), whereas in Group I mean arterial blood pressure was reduced by 16% and mean intracranial pressure dropped 23% (p less than 0.05 in each).(ABSTRACT TRUNCATED AT 250 WORDS)     

犬颅脑爆震伤模型的建立和甘露醇早期治疗研究

目的：建立颅脑爆震伤动物模型,早期应用甘露醇治疗,探讨脑损伤病理变化及治疗效果。方法：杂种犬20只,制作成点爆炸源颅脑爆震伤模型,随机分为：对照组（n=8）及实验组（n=12）,实验组静注甘露醇（5ml/kg,1/6h）,观察每一组血流变、颅内压、脑组织病理及死亡率。结果：犬爆震伤后,红细胞压积、血液粘度、颅内压指标均出现持续升高、血小板则持续下降（P〈0.05）;与对照组比较,实验组红细胞压积、血液粘度、血小板、颅内压指标明显改善（P〈0.01）,受伤部位的存活神经元也明显增多（P〈0.01）,实验组死亡率（2/12）明显低于对照组（6/8）（P〈0.05）。结论：早期应用甘露醇可改善血液流变特性,改善脑部微循环,降低颅内压,减轻犬爆震伤后神经元的缺血性损害,降低死亡率。     

早期应用尼莫地平治疗脑出血的临床疗效报告

目的 :探讨用尼莫地平降低血压 ,提升颅内压 ,从而控制高血压脑内出血。方法 :将 6 5例脑出血病人随机分为两组 ,治疗组 35例 ,用尼莫地平 10mg静滴 ;对照组 30例 ,用 2 0 %甘露唇 2 5 0ml,每日 2次或 3次 ,两组治疗 7天 ,2周内复查头颅CT。结果 :治疗组的血压平均由 179/ 10 4降至 15 1/ 91mmHg ,对照组由 181/ 10 8降为 180 /10 3mmHg ,两组比较有统计学意义 (P <0 0 1) ,对照组血肿扩大 18例 (6 0 % ) ,治疗组为 3例 (8 5 7% ) ,两组比较有统计学意义 (P <0 0 1)。对照组死亡 7例 ,因脑疝 6例 ,并发症死亡 1例 ;治疗组因肺部感染和消化道出血死亡 1例。结论 :尼莫地平可扩张血管 ,降低血压和提高颅内压 ,使破损血管壁的跨壁压力梯度下降 ,有止血和防止再出血的功能 ,可作为首选抢救药物之一 ,发病早期患者无脑疝或因颅高压引起的昏迷 ,就不要用甘露醇类的降低颅内压的药物 ,以免血肿扩大     

Effect of steroids on intracranial pressure and pressure-volume index in patients with hydrocephalus

It is well-established that steroids (glucocorticoids) have a beneficial clinical effects on patients with increased intracranial pressure, but there is still a controversy on the mode of action of steroids. The purpose of this study is to investigate the effects of steroids on continuous intracranial pressure and on intracranial compliance using pressure-volume index (PVI). Thirteen hydrocephalic patients, ranging from 9 to 70 years old, without intracranial mass lesion nor brain edema were studied. The patients were divided into two groups. Group I: Five patients were monitored the continuous intracranial pressure for 24 hours again following the administration of steroids on continuous intracranial pressure. The method of the administration of steroids was that betamethasone 8 mg for initial dose was administered intravenously and followed by 4 mg intramuscularly every 6 hours. There was little change in the baseline pressure and the amplitude on continuous intracranial pressure monitoring before and after the administration of steroids. But the maximum pressure and the maximum amplitude significantly decreased after the administration of steroids. The % time B-wave and the maximum continuous time of B-wave also decreased significantly. Group II: Eight patients were studied in order to investigate the effects of steroids on the intracranial compliance. PVI was measured according to Marmarou's method before and after the intravenous administration of steroids (beta-methasone 0.5 mg/kg). PVI increased in 7 out of 8 cases after the administration of steroids, which was statistically significant. It can be concluded that steroids increase the intracranial compliance and inhibit the rise of intracranial pressure.(ABSTRACT TRUNCATED AT 250 WORDS)     

The mechanism of intracranial pressure-reducing effect of mannitol

The effect of mannitol to decrease the raised ICP is well documented and mannitol is now widely used in clinical practice. However, its mechanism of lowering ICP still remains controversial, especially under the condition of vasogenic edema. The objective of this study is to reexamine and delineate the mechanism of ICP reducing effect of mannitol, using quantitative vasogenic edema model, specific gravimetric technique to measure the brain water content, and the method to estimate the CSF dynamics without disturbing the physiological condition of intracranial compartments in cats. Quantitative increase of water content of the white matter was produced by the infusion of 0.5 ml of normal saline though stereotaxically inserted 25-G needle into the left frontal white matter. In control group, cats were sacrificed and water content of the gray and white matter of each coronary sliced brain was measured by specific gravimetric technique. In the mannitol group, 20% of mannitol (2 g/kg) was administrated via femoral vein within 3 minutes. The maximum reduction of ICP was achieved at the average of 30 minutes. At this time, the cats were sacrificed and the water content of brain was measured in the same way as in the control group. PVI, Ro, If (Marmarou) were calculated before and after mannitol administration. In parameter group, BP, ICP, CVP, serum osmotic pressure and osmolarity were measured without terminating the experiment. The changes of water content of the gray and white matter before and after mannitol administration in the area of infusion edema were 80.7% to 80.8% and 76.8% to 77.1% respectively.(ABSTRACT TRUNCATED AT 250 WORDS)     

Comparison of Hypertonic Saline and Mannitol on Whole Blood Coagulation In Vitro Assessed by Thromboelastometry

Background  

Hypertonic saline (HS) is an alternative to mannitol for decreasing intracranial pressure in traumatic brain injury and before craniotomy. Both HS and mannitol may interfere with blood coagulation but their influence on coagulation has not been compared in controlled situations. Therefore, we evaluated different strengths of HS and 15% mannitol on blood coagulation in vitro.     

重型颅脑损伤术后凝血功能障碍病人残留血肿或迟发性颅内出血的处理

目的 探讨重型颅脑损伤术后凝血功能障碍病人残留血肿或迟发性颅内出血的处理对策。方法 回顾性分析2016年1月至2018年9月收治的29例重型颅脑损伤开颅术后病人的临床资料。所有病人术中均行颅内压传感器植入监测颅内压,术后凝血功能障碍并有残留血肿或迟发性颅内血肿。17例采用软通道置管引流术治疗（引流组）,12例采用保守治疗（对照组）。结果 引流组术后ICP呈明显下降趋势（P<0.05）,而且明显低于对照组（P<0.05）。引流组NICU住院时间、甘露醇用量及使用时间较对照组均明显减少（P<0.05）,而且引流组再次开颅手术率、肾功能损害发生率和电解质紊乱发生率均明显低于对照组（P<0.05）。两组颅内感染发生率、肺部感染及术后6个月GOS评分均无统计学差异（P>0.05）。结论 软通道置管引流术简单易行,创伤小,手术时间短,适用于重型颅脑损伤术后凝血功能障碍并有残留血肿或迟发性颅内血肿的病人,可以有效的降低颅内压、减少并发症,但需严格掌握手术适应证。     

In vivo multiparametric monitoring of brain functions under intracranial hypertension following mannitol administration

OBJECTIVE: Over the last 20 years, mannitol has replaced other osmotic diuretics. Its beneficial effects on intracranial pressure (ICP), cerebral perfusion pressure (CPP), cerebral blood flow (CBF) and brain metabolism are widely accepted. In the present study, we tested the effect of mannitol injection on brain hemodynamic, metabolic, ionic and electrical state in rats exposed to intracranial hypertension. METHODS: The parameters monitored simultaneously included ICP, CBF using the laser Doppler flowmetry, mitochondrial NADH redox state by the fluorometric technique, extracellular K(+) and H(+) levels, DC potential, ECoG, blood pressure and calculated CPP. ICP was elevated to 30 mmHg for 30 minutes and mannitol was injected 15 minutes post-ICP elevation. RESULTS: Our results showed that mannitol decreased ICP, and improved the levels of MAP, CPP and CBF. Moreover, mannitol completely prevented mortality following intracranial hypertension in rats. CONCLUSION: It seems that the multiparametric monitoring approach, used in intracranial hypertension models, is an important tool for brain functional state evaluation.     

Analysis of epidural pressure pulse wave (EDP-PW) and common carotid blood velocity (CBFV) in acute intracranial hypertension

The changes in the two consistent components of epidural pressure pulse wave (EDP-PW), P₁ and P₂ waves, and mean velocity of common carotid blood flow (CBFV) were studied in 21 patients with acute intracranial hypertension to investigate the origin of the amplitude change in these components. The amplitudes of P₂ wave increased progressively with the rise of EDP, but those of P₁ wave remained nearly in variable at EDP of more than20–30 mmHg which is incompatible with the changes in CBFV. Jugular vein compression caused in rapid rise of EDP and a proportionate increase in the magnitudes of both waves. Hyperventilation and mannitol administration caused a disproportionate reduction in the amplitudes of P₂ wave with a fall of EDP. But mannitol at high EDP (more than 40 mmHg) causeda mild fall of EDP and some increase in the amplitudes of P₂ wave. These results indicate that the variations in the amplitudes of P₁ wave reflect the changes in vascular resistance of the large intracranial conductive arteries, while those of P₂ wave result from the changes in the volume of the cerebral bulk. The increase in the amplitudes of P₂ wave induced by mannitol at high EDP may suggest a defective autoregulation of the cerebral vessels.     

Intravenous glycerol and mannitol therapy in children with intracranial hypertension

Acute intracranial hypertension may respond to intravenous mannitol, but frequent administration can cause cerebral edema or renal problems. We evaluated the use of 20% glycerol administered intravenously as an alternative to mannitol. Intravenous glycerol and mannitol were equally effective in lowering acute elevations of intracranial pressure. The duration of effect was similar for both agents. Side effects of intravenous glycerol were related to concentration, rate, and frequency of administration. In severe encephalopathies, such as Reye syndrome, we recommend infusions of 20% glycerol or 20% mannitol at a dose of 0.5-1.0 gm per kilogram. Glycerol should be administered in 0.45% or 0.9% saline, no faster than 1.5 ml (3.3 mOsm) per minute.