脑出血患者不同剂量甘露醇治疗前后的尿酶变化

甘露醇作为治疗脑水肿、降低颅内压的首选药物，广泛应用于脑血管疾病的治疗。但近10余年来，关于甘露醇致肾功能损害的报道较多见诸献，引起临床医师的重视。笔对40例脑出血患使用不同剂量甘露醇治疗前后的血清尿素氮(BUN)、肌酐(Cr)、尿γ-谷氨酰转肽酶(γ-GT)和尿N-乙酰-β-氨基葡萄糖苷酶(NAG)的变化进行临床观察，以了解甘露醇的肾毒性作用以及尿酶对肾功能损害的早期监测价值。     

连续血液滤过联合甘露醇治疗颅内高压合并肾功能衰竭的临床研究

目的 探讨连续血液滤过联合甘露醇在颅内高压合并肾功能衰竭治疗中的应用价值。 方法 对珠江医院重症医学科收治的9例颅内高压合并肾功能衰竭患者行2～3次连续血液滤过联合甘露醇治疗,监测治疗前后患者颅内压数值、血肌酐及胱抑素浓度。 结果 在应用连续血液滤过联合甘露醇治疗后,患者颅内压数值较治疗前明显降低,血肌酐及胱抑素浓度较治疗前明显下降,差异有统计学意义(P＜0.05)。1例脑干出血患者于治疗第2天死于多器官功能衰竭,其余8例患者均未出现脑疝,平稳渡过脑水肿高峰期。 结论 连续血液滤过联合甘露醇是一种快速有效的治疗颅内高压合并肾功能衰竭的方法。     

甘露醇治疗脑出血致肾损害16例疗效观察

甘露醇是治疗脑水肿、降低颅内压的常用首选药物，但在应用过程中会出现一些不良反应，应引起大家的重视。我们在治疗65例脑出血中发现16例(24．6％)引起肾损害，现报道如下。     

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。     

老年慢性肾衰血透患者常见神经精神症状及相关影响因素

目的分析老年慢性肾衰血透患者常见神经精神症状及相关影响因素。方法对64例出现精神神经症状的老年慢性肾衰患者(治疗组)与无神经精神症状的慢性肾衰患者(对照组)的透析年龄、肾功能及血压水平等的关系进行比较。结果 2组患者血透失衡综合征、脑血管意外及尿毒症脑病患者的透析龄差异均有统计学意义(P0.05);治疗组尿毒症脑病患者的肾功能血肌酐水平、脑血管意外患者的血压水平均明显高于对照组(P0.05)。结论老年慢性肾衰患者出现精神神经症状与透析年龄、肾功能及血压水平等有一定关系。     

20%吡拉西坦注射液降低颅脑损伤患者颅内压的临床研究

目的探讨20%吡拉西坦注射液降低颅脑损伤患者颅内压(ICP)的效果。方法将颅脑损伤患者60例分为治疗组和对照组,治疗组快速静脉滴注20%吡拉西坦注射液,对照组快速静脉滴注20%甘露醇,所有患者均采用无创ICP监测仪监测ICP,同时观察药物的安全性、有效性及可能出现的各种副作用。结果治疗组和对照组给药后均能迅速降低ICP,两组临床疗效差异无显著性(P<0.05);治疗组无局部及全身不良反应的发生,对照组出现尿素氮及肌酐增高2例。结论 20%吡拉西坦注射液治疗颅脑损伤ICP增高疗效安全可靠,比甘露醇更适合有肝肾功能损害的患者。     

甘露醇治疗脑出血致急性肾功能衰竭21例分析

甘露醇治疗脑出血致急性肾功能衰竭２１例分析胡波陈洪英张兆武临床中常应用甘露醇、脱水、利尿等作用治疗脑水肿，降低颅内压。但在应用中出现的副作用并未引起重视。我们在治疗８９例脑出血中发现有２１例（２３．６％）引起急性肾功能衰竭（ＡＲＦ），现报道如下：一般...     

甘露醇治疗脑血管意外致肾损害32例分析

甘露醇作为一种渗透性利尿药，是治疗脑水肿、降低颅内压的首选药物，但在；陆床应用中其出现的副作用已引起重视。我们近年来在95年-98年间治疗脑血管病人中发现32例出现肾脏损害，现报道如下：1资料与方法1．1一般资料32例男对例，女11例，年龄54一用岁，平均67岁。诊断依据，儿例均经脑CT证实，其中脑出血对例，大面积脑梗死9例。本文32例中有高血压病史22例，糖尿病史IO例，其中冠心病史5例，均无肾脏病史，治疗前查血尿素氮、肌耷及尿液分析均在正常范围。1．2治疗方法32例发病后即给予20％甘露醇液25（）al每4－6h一次。快速计叽为…     

经颈总动脉推注rhbFGF治疗重症颅脑损伤的初步观察

目的：探讨经颈总动脉灌注甘露醇开放血脑屏障后,再经颈总动脉推注重组人碱性成纤维生长因子（rhbFGF)对重型颅脑损伤患的作用。方法：重型颅脑损伤（GCS≤8分）患12例,在经伤侧大脑半球颈总动脉穿刺,用20％甘露醇50ml灌注后推注rhbFGF80万单位,每天一次,共10－18d,术前对伤作GCS评分,肢体肌力语言功能,CT,ECT,TCD检查,用药后5d,10d,1个月,3个月复行上述检查。结果：用药2－5d出现肢体功能好转,脑血供改善,脑水肿吸收,10d后肢体功能明显恢复,脑血供和颅内血流流速接近正常,脑水肿消退,而失语恢复和脑干损伤患的肢体,意识恢复时间较长（1－3个月）。结论：经颈总动脉灌注甘露醇开放血脑屏障后,患推注rhbFGF可以有效增加局部脑血流,促进脑外伤病人的康复。     

甘露醇治疗急性脑梗死致急性肾功能衰竭12例观察

我院自 2 0 0 1～ 2 0 0 3年 6月 ,应用甘露醇治疗急性脑梗死致急性肾功能衰竭 12例 ,报告如下。1　一般资料12例均系大面积脑梗死患者 ,既往有糖尿病史 ,年龄 68～75岁 ,其中大面积额、颞、顶叶、基底节区脑梗死 5例 ,大面积枕叶、顶叶脑梗死 3例 ,大面积颞叶脑梗死 2例 ,大面积小脑梗死 2例。2　结果12例入院后急查肾功能均正常 ,给予 2 0 %甘露醇 12 5ml快速静滴 ,1次 /6h。 10例于应用甘露醇第 3d出现肌酐及尿素氮明显升高 ,2例于应用甘露醇第 6d出现肌酐和尿素氮明显升高 ,发现肾功能异常后立即停用甘露醇 ,改用甘油氯化钠、白蛋白等 ,…     

Mannitol therapy in perinatal hypoxic-ischemic brain damage in rats

To study the efficacy of mannitol in reducing cerebral edema and improving the ultimate neuropathologic outcome in perinatal cerebral hypoxia-ischemia, 67 7-day postnatal rats were subjected to unilateral common carotid artery ligation followed by exposure to 8% oxygen at 37 degrees C for 3 hours. Twenty-seven rat pups received a subcutaneous injection of 0.1 ml mannitol in a dosage of 4 mg/kg body wt immediately following cerebral hypoxia-ischemia and every 12 hours thereafter for a total of four doses. Control animals received either no therapy (n = 16) or an equivalent volume of normal saline (n = 24). Mannitol injections in six rat pups not subjected to hypoxia-ischemia produced no mortality but significantly increased serum osmolality from 287 to 361 mos/l (p less than 0.01). Preliminary studies indicated that substantial mortality occurred when greater doses of mannitol were administered to rats. After 48 hours of recovery from hypoxia-ischemia, the animals were killed and their brains were examined for either tissue water content (33 rat pups) or the presence of neuropathologic alterations (34 rat pups). Mannitol significantly reduced (p less than 0.001) brain water content, as a reflection of cerebral edema, in both the ipsilateral (88.5% compared with 90.6% in controls) and the contralateral (85.0% compared with 87.2% in controls) cerebral hemispheres. Mannitol therapy did not ameliorate the incidence, distribution, or severity of tissue injury in the cerebral cortex, subcortical white matter, hippocampus, striatum, or thalamus of the ipsilateral cerebral hemisphere compared with the controls. Thus, while mannitol substantially reduces the extent of cerebral edema following hypoxia-ischemia, no beneficial affect on ultimate brain damage occurs.(ABSTRACT TRUNCATED AT 250 WORDS)     

甘露醇在脑血管病患者中的应用

甘露醇一直作为治疗脑水肿和降低颅内压的常规药物，但目前临床疗效争议较大，而且缺乏循证医学证据。文章就甘露醇的药理学作用、脱水降颅压的作用机制及其在缺血性和出血性脑血管病患者中的临床应用做了综述。     

Potassium Sparing Diuretics as Adjunct to Mannitol Therapy in Neurocritical Care Patients with Cerebral Edema: Effects on Potassium Homeostasis and Cardiac Arrhythmias

Background  

Mannitol therapy to treat cerebral edema induces osmotic diuresis and electrolyte loss. In neurocritical care patients, potassium is the electrolyte that most often needs replacement. Objective of this study was to evaluate the effects of adding potassium sparing diuretic (canrenone) to mannitol therapy on potassium urinary excretion, potassium plasma levels, and incidence of new cardiac arrhythmias in patients receiving neurocritical care for cerebral edema.     

Is mannitol safe for patients with intracerebral hemorrhages? Renal considerations

OBJECTIVES: Mannitol, a drug widely used to decrease intracranial pressure, can cause renal failure. The goal of this study is to determine the renal safety of mannitol therapy in patients with intraparenchymal hemorrhages. MATERIAL AND METHODS: 51 patients with intracerebral hemorrhages were treated with mannitol according to guideline of American Heart Association. Serum urea and creatinine levels were measured before mannitol administration and on the 2nd, 5th and 14th day. RESULTS: Transient elevation of urea and creatinine concentration was noticed, however, none of patients developed anuria or oliguria. CONCLUSIONS: Our study points out safety of mannitol therapy under control of osmolality, although control of urea and creatinine concentrations in special group of patients (persons with history of renal failure or diabetes) should be considered.     

脑出血后迟发型、反常性水肿4例报道及其发生机制初探

目的:报道4例脑出血后迟发型反常性水肿患者的临床特征,同时利用影像学检测的方法,对其发生机制进行初步的探讨。对象和方法:本研究报道的4例脑出血后迟发型反常性水肿患者均为2005.6~2006.3月间我院住院患者。作者利用CT、MR等影像学检测方法,对甘露醇影像学特征和患者脑水肿影像学特征进行对比分析,提出脑出血后迟发型反常性水肿的发生机制的假说。结果:甘露醇CT扫描显示低密度的CT影像学特征,同时,随着甘露醇浓度的降低,其CT密度值也相应的减小。核磁共振扫描结果提示,与脑组织相比,甘露醇表现短T1、长T2信号的磁场特征。研究结果表明,脑出血后迟发型反常性水肿患者的水肿表现与甘露醇CT、MR影像特征十分相似。结论:脑出血后迟发型反常性水肿的临床转归、影像学特征与常规脑水肿不同,可能是一个独立的病理实体。该病理过程的发生可能与脑出血后甘露醇的大量、长时程应用有关。     

犬颅脑爆震伤早期救治的实验研究

目的观察早期运用大剂量青霉素钠、甘露醇对颅脑爆震伤实验犬的救治效果。方法杂种雄性犬30只,使用简单随机化的方法将犬分为:对照组(6只)、外伤组(12只)及治疗组(12只),外伤组和治疗组制作成颅脑爆震伤模型,治疗组运用大剂量青霉素钠、甘露醇进行治疗,然后观察每一组犬的血浆内皮素(ET)、肿瘤坏死因子(TNF)、谷丙转氨酶(ALT)、淀粉酶(AMY)、尿素氮(BUN)、肌酸激酶(CK)水平,以及颅内压(ICP)、头颅CT表现、细菌定性培养结果和犬生存时间。结果与对照组相比,外伤组伤后6h血浆ET、TNF及伤后12h血浆ALT、AMY、BUN、CK、ICP水平均显著升高(P0.01),伤后24 和48h,治疗组的ET、TNF、ALTAMY、BUN和CK水平均明显低于外伤组(P0.05)。头颅CT检查示治疗组脑水肿明显轻于外伤组;伤后48h,治疗组血液细菌培养阳性率8.33%(1/12),显著低于外伤组的83.33%(10/12)(P0.01);治疗组的生存时间为(138.6±8.0)h,明显长于外伤组的(96.53.0)h(P0.01)。结论颅脑爆震伤后早期运用大剂量青霉素钠、甘露醇治疗可减轻机体感染,降低颅内压,减轻脑组织水肿及机体继发损伤,延长动物的生存时间。     

连续应用7．5％高渗盐水治疗重型颅脑损伤的临床观察

目的 探讨7．5％高渗盐水治疗重型颅脑损伤的效果及副作用。方法 将50例颅脑损伤患者随机分为高渗盐水治疗组（HTS组，26例）和甘露醇治疗组（M组，24例）。HTS组静脉滴注7．5％高渗盐水2ml／kg，M组静脉滴注甘露醇250ml，均为q8h，连续7d。用药前及用药后第1、3、7天测患者血电解质、渗透压和肾功能，用药前及用药后2周对患者进行GCS评分。结果 与用药前相比，用药后6h两组患者的平均动脉压、心率、呼吸均无统计学差异（P〉0．05），而HTS组患者中心静脉压在用药后明显升高（P〈0．05）。用药后第1、3、7天HTS组患者血K^＋、Na^＋、Cl^-、尿素氮、肌酐及血浆渗透压均无显著改变；M组血K^＋、Na^＋、Cl^-、肌酐及血浆渗透压无显著改变（P〉0．05），但用药后第7天尿素氮值较同期HTS组明显升高（P〈0．05）。用药2周后，两组患者GCS评分均有明显改善（P〈0．05）。结论 7．5％高渗盐水降低颅脑损伤引起的高颅内压是安全、有效的，连续使用效果好、副作用少。     

Encephalopathy and Cerebral Edema in the Setting of Acute Liver Failure: Pathogenesis and Management

Cerebral edema is a potential life-threatening complication in patients with acute liver failure who progress to grade III/IV encephalopathy. The incidence is variably reported but appears to be most prevalent in those patients with hyperacute liver failure as opposed to subacute forms of liver failure. In those patients who are deemed at risk of cerebral edema and raised intracranial pressure, insertion of an intra-cranial pressure monitoring device may be considered to optimize treatment and interventions. The pathogenesis of cerebral edema in this setting remains controversial, although recent work suggests a pivotal role for arterial ammonia, whose effects appear to be potentiated by the presence of systemic inflammation. Recent work has also suggested the import of free radical formation occurring at a mitochondrial level as being the potential mediator of cellular dysfunction as opposed to ammonia per se. Treatment of such patients requires a multi-disciplinary approach incorporating both hepatology and critical care. In a significant proportion of such cases, consideration of liver transplantation may be required. Treatment should be focused at optimizing liver function and regenerative capacity and minimizing the inflammatory milieu. Controlled studies are lacking and much of the management has been extrapolated from neurocritical care. Sustained elevation of intracranial pressure may be responsive to mannitol or hypertonic saline bolus, and in those with hyperemia indomethacin has been reported as beneficial in case series. Recently, interest has developed into the use of cooling in the management of patients with acute liver failure and raised intracranial pressure. Animal studies support this treatment option as do case series, although randomized trials are still awaited.