蛛网膜下腔出血腰椎穿刺术后患者体位管理新模式的应用效果分析

目的 探讨体位管理新模式在蛛网膜下腔出血患者腰椎穿刺术后的应用效果。方法 选取2021年2—12月在首都医科大学附属北京天坛医院神经外科住院治疗，并在局部麻醉下行腰椎穿刺术的蛛网膜下腔出血患者（改良Fisher分级0～Ⅱ级）作为研究对象。采用随机数字表法将患者分为试验组和对照组。试验组采用穿刺后体位管理新模式进行护理，对照组接受穿刺后常规护理。对两组干预后即刻（4 h）和短期（24 h）头部、腰背部疼痛发生率，疼痛严重程度，以及术后24 h患者满意度等指标进行比较。  结果 试验组和对照组腰椎穿刺术后4 h（41.2% vs. 37.5%，P=0.627）和术后24 h（25.0% vs. 22.5%，P=0.710）头痛发生率的差异均不具有统计学意义，头痛严重程度分级的差异亦均无统计学意义（P=0.533，P=0.685）；对照组术后4 h（50.0% vs. 27.5%，P=0.003）和24 h（37.5% vs. 22.5%，P=0.038）腰背痛的发生率均显著高于试验组，且两组术后4 h和24 h腰背痛的疼痛程度分级差异亦均有统计学意义（P=0.005，P=0.033）。术后24 h对照组护理满意度总分为（78.19±3.17）分，试验组为（88.41±2.80）分，试验组显著高于对照组（P=0.003），试验组在尊重患者、护理技术、身体舒适、健康教育、沟通交流以及患者和家属参与护理等指标方面优于对照组，差异均有统计学意义。结论 体位管理新模式适用于有腰椎穿刺需求的蛛网膜下腔出血轻症患者，该模式通过缩短腰椎穿刺术后患者的卧床时间，在不增加术后头痛发生率的同时，显著降低患者术后短期内腰背部疼痛的发生率和严重程度，提升患者满意度，值得临床推广应用。     

腰穿后颅内CSF体积的变化与腰穿后头痛的关系

腰穿后头痛的病理生理至今仍不清楚.作者选20例具有神经系统症状的病人于腰穿前及腰穿后24小时行MRI检查,以了解颅内CSF体积与腰穿后头痛的关系,以及腰穿后枕大孔区诸解剖结构关系的变化情况.病人及方法:男8例,年龄25～71岁(平均41.5岁),女12例,年龄14～64岁(平均38.5岁).所有病人住院时均无头痛,未服止痛药,未行强化脊髓造影.用18号腰穿针行常规腰椎穿刺术,测初压后放出10mlCSF,然后测终压.术后卧床14小时.     

阴式宫切腰硬联合麻醉前输液对麻醉后血压的影响

目的观察腰硬联合麻醉前输液对麻醉后血压的影响。方法选择100例腰硬联合麻醉下行择期阴式子宫切除手术的患者，随机分成2组，实验组于麻醉前30min内静脉输入乳酸林格氏液500ml，麻醉后以3～4ml／（kg·h）继续输入乳酸林格氏液；对照组静脉以3～4ml／（kg·h）继续输入乳酸林格氏液并立即实施麻醉。观察2组病人麻醉后血压下降情况。结果实验组病人麻醉后血压下降的发生率为10％，对照组病人麻醉后血压下降发生率为40％。实验组血压下降发生率明显低于对照组，P〈0．005。结论腰硬联合麻醉前输入一定量的液体可有效预防麻醉后血压下降。     

腰大池置管外引流术在动脉瘤术后早期应用分析

目的探讨术后早期行腰大池置管外引流术对缓解动脉瘤性蛛网膜下腔出血患者头痛症状和缩短病人住院时间的影响。方法将我科2010年6月至2012年5月收治的72例动脉瘤性蛛网膜下腔出血患者分层随机分为两组：动脉瘤夹闭术后早期（24。48h）行腰大池置管外引流组（A组,39例）术后未行腰大池置管外引流分组（B组,33例）。结果A、B组患者的术后住院时间分别为（16．89±2．51）d和（21．42±2．54）d,两者相差显著（P〈0．05）。A、B组术后1周内头痛症状缓解率分别为74．36％（29／39）和15．15％（5／33）,两者相差显著（P〈0．05）。结论破裂动脉瘤夹闭术后早期（24～48h内）行腰大池置管外引流术,能够有效的减轻因蛛网膜下腔出血造成的头痛症状,缩短患者的住院时间。     

CT定向穿刺术治疗高血压基底节区出血时机的选择及其对患者预后的影响

目的探讨CT定向穿刺技术治疗高血压基底节区出血时机的选择及其对患者预后的影响。方法2007年5月至2010年10月收治经CT证实为高血压基底节区出血且出血量为30～60ml的患者109例,均采取CT定向脑内血肿穿刺术治疗,按手术时机分为三组：A组从发病到手术时间≤6h,B组6～24h,C组24～72h。比较三组患者术后3d内再出血率、术后3个月死亡率及日常生活能力（ADL）分级。结果A组患者术后再出血率（20．00％,8／40）明显高于B组（4．55％,2／44）和c组（0．00％）（P〈0．05）,而B组和C组之间无明显差异fP〉0．05）;术后3月c组死亡率（36．00％,9／25）明显高于B组（4．55％,2／44）和A组（12．50％,5／40）（P〈0．05）,而A组和B组之间无明显差异（P〉0．05）;术后3月c组ADL1-3级患者比例（37．50％,6／16）明显低于A组（71．43％,25／35）和B组（69．05％,29／42）（P〈0．05）,而A组和B组之间无明显差异（P〉0．05）。结论生命体征平稳的高血压基底节区出血患者,出血后6—24h手术可有效地降低患者再次出血率和死亡率,改善其预后。     

腰椎穿刺后头痛的研究进展

腰椎穿刺（简称腰穿）后头痛是临床常见的并发症，各家报道不一，发病率为2%—11%。自1898年德国医生Bier K首次用腰穿进行脊髓麻醉以来，腰穿已广泛用于临床诊断和治疗。尽管近年来对腰穿的方法学进行许多改进，减少了头痛的发生，但对腰穿后头痛的发生机制不明，有关腰穿后头痛的预防和治疗存在争议。本文就腰穿后头痛的发病机制、预防和治疗进展作一综述，与同道共享。     

7号注射针在小婴儿腰椎穿刺术中应用

腰椎穿刺术（简称腰穿）是儿科常见的临床诊疗操作方法之一，在小儿中枢神经系统疾病的诊断及治疗中起着重要作用。本科自2003年1月至今，用7号注射针头代替传统腰穿针对小婴儿进行腰椎穿刺术350例，取得良好效果，现总结如下。     

手足口病患儿腰穿检查60例临床分析

目的研究改良腰椎穿刺术联合术前镇静进行手足口病患儿腰穿的临床应用,提高穿刺成功率,减轻患儿腰穿痛苦。方法120例需做腰穿的手足口病患儿,根据小儿解剖、生理特点,改良方法组60例采用一次性静脉穿刺头皮针或5ml注射器针头进行腰穿,术前给予10%水合氯醛保留灌肠镇静,传统方法组60例采用常规方法操作。结果改良方法组一次性成功率达98.3%,传统方法组一次性成功率为85.0%,其差异有统计学意义（P〈0.05）。结论改良方法组应用改良腰椎穿刺术联合术前镇静进行手足口病患儿腰穿检查,明显提高了穿刺成功率,减轻了患儿腰穿痛苦,操作易行,值得临床推广。     

高血压脑出血颅内血肿微创清除术治疗时机选择初探

目的 研究高血压脑出血微创血肿清除术不同治疗时间的疗效，找出较佳手术时机。方法 按发病-治疗时间分为7～24h组和〉24h组，主要疗效评定指标病死率和死亡／残障率，次要疗效评定指标是神经功能缺损评分变化。结果 两组病例入选时可比性好（P〉0．05）。随访期为7～24h组和〉24h组的病死率分别是11．6％和11．4％，差异无显著意义（P〉0．05）；随访期为7～24h组和〉24h组的死亡／病残率分别是37．2％和61．4％，差异有显著意义（P〈0．05）；神经功能缺损评分差异有显著意义（P〈0．01），失访率5．7％。结论 发病后7～24h是微创术较佳手术时机。     

颅内破裂动脉瘤栓塞术后腰大池引流术治疗体会

目的 探讨颅内破裂动脉瘤栓塞术后持续腰大池引流治疗价值。方法 回顾性分析2015年1月至2016年12月收治的63例颅内破裂动脉瘤的临床资料;均行血管内栓塞治疗,术后行腰大池引流术30例（观察组）,行腰椎穿刺术33例（对照组）。结果 术后1 d,两组脑脊液红细胞计数无统计学差异（P>0.05）;术后4、7、10 d,两组脑脊液红细胞计数较术后1 d均明显降低（P<0.05）,而且,观察组均明显低于对照组（P<0.05）。观察组术后脑血管痉挛发生率和脑积水发生率均明显低于对照组（P<0.05）,而两组术后癫痫发生率、颅内感染发生率均无统计学差异（P>0.05）。术后6个月,观察组改良Rankin量表评分与对照组无统计学差异（P>0.05）。结论 颅内破裂动脉瘤栓塞术后持续腰大池引流可显著减少脑血管痉挛和降低脑积水的发生率。     

Syndrome of cerebrospinal fluid hypovolemia following lumbar puncture cerebrospinal fluid leak in a patient with idiopathic intracranial hypertension

An 11-year-old girl presented with headache of 3 months' duration. There was bilateral disc edema. The cerebrospinal fluid pressure was 50 cm of water with normal cerebrospinal fluid cytology and biochemistry. She developed severe headache (different and disabling), dizziness, vomiting, and backache on sitting up 6 hours after lumbar puncture, and lying supine relieved all of her symptoms. Intravenous fluids, analgesics, and complete bed rest did not relieve her symptoms over the next 72 hours. She was completely relieved of her symptoms on receiving two tablets of Caffergot containing 200 mg of caffeine and 2 mg of ergotamine 72 hours after lumbar puncture. The symptoms recurred 48 hours later, and a repeat dose of Caffergot was required. Magnetic resonance imaging (MRI) done 96 hours after lumbar puncture revealed the entire dura overlying the brain, including the posterior fossa, showing intense enhancement on contrast injection with leak at the lumbar puncture site. Oral caffeine (coffee, three times a day) was advised over 1 week. The patient remained asymptomatic, and a repeat MRI scan after 10 days showed complete clearing of the cerebrospinal fluid leak with no dural enhancement. The syndrome of cerebrospinal fluid hypovolemia following lumbar puncture is reported in a girl with idiopathic intracranial hypertension.     

Safety and efficacy of intravenous tissue plasminogen activator and heparin in acute middle cerebral artery stroke.

BACKGROUND AND PURPOSE: There is little reported of the safety and efficacy of high-dose intravenous recombinant tissue plasminogen activator (alteplase) in combination with heparin anticoagulation in patients presenting with acute ischemic stroke. METHODS: Thirty-two patients with severe hemispheric stroke syndrome caused by angiographically proven middle cerebral artery and/or intracranial internal carotid artery occlusion were treated with 100 mg alteplase by intravenous infusion over 90 minutes within a mean +/- SD of 226 +/- 68 minutes after symptom onset. Recanalization was assessed by digital subtraction angiography in all patients immediately after treatment and by transcranial Doppler monitoring (n = 30) and/or a third angiogram (n = 5) 12-24 hours later. RESULTS: Complete or partial reperfusion was observed in 11 patients (34%) 90 minutes after the initiation of alteplase infusion and in 17 patients (53%) within 12-24 hours. Hemorrhagic infarction without clinical deterioration was detected by follow-up computed tomography in nine patients (28%). Fatal parenchymal hemorrhage occurred in three patients (9%) with huge middle cerebral artery infarcts. Serious hemorrhage from the puncture site occurred in two patients (6%). Good clinical outcome correlated with reperfusion (p less than 0.05) and the presence of grade 2 collateral blood flow (p less than 0.01). CONCLUSIONS: When 100 mg of recombinant tissue plasminogen activator was given within the first 6 hours of acute stroke together with heparin the incidence of deleterious hemorrhage was less than 10%. Reperfusion and effective collateral blood flow seem to be two important factors associated with a small infarct volume and good clinical outcome.     

BALB/c小鼠肾缺血再灌注损伤模型的建立与评价

背景：对于一些药物研究，小鼠是理想的造模工具，但由于小鼠耐受性相对较差，肾脏及肾蒂小且难于寻找，容易增加实验误差，导致造模失败。 目的：探讨BALB/c小鼠肾缺血再灌注损伤模型的建立方法，评价肾脏缺血时间对肾缺血再灌注损伤的影响。 方法：采用微型动脉夹夹闭小鼠双侧肾蒂的方法建立雄性BALB/c小鼠肾缺血再灌注损伤模型，根据肾缺血时间不同分为 0 min组(对照组)、30 min组、35 min组、45 min组，肾再灌注后24 h观察肾功能和肾脏病理组织学的变化，比较不同的肾脏缺血时间对上述指标的影响；观察45 min组小鼠肾缺血再灌注损伤后的生存率。 结果与结论：模型成功率95.9%，与对照组相比，肾缺血30 min组、35 min组和45 min组再灌注后24 h血清肌酐、尿素氮和肾脏病理组织学评分均升高，肾缺血45 min组生存率明显下降，差异均有显著性意义(P < 0.05)。结果提示，应用微型动脉夹夹闭小鼠双侧肾蒂的方法可制备稳定肾缺血再灌注损伤模型，雄性小鼠肾缺血35~45 min是造模较为理想的肾缺血时间，所得模型效果满意。     

The influence of repeated doses, route and time of administration on the neuroprotective effects of BIII 277 CL in a rat model of focal cerebral ischemia.

Objective. We investigated the influence of dose, route and time of administration on the neuroprotective effects of the noncompetitive N-methyl-D-aspartic acid antagonist BIII 277 CL ([2R-[2alpha, 3(R*), 6alpha]]-1,2,3,4,5,6-hexahydro-3-(2-methoxy-propyl)-6,11,11-trimethyl-2,6-methao-3-benzazocin-9-ol hydrochloride). Methods. Focal cerebral ischemia was induced in isoflurane-anaesthetized Fischer rats by permanent occlusion of the left middle cerebral artery. Rats were treated with BIII 277 CL three times at doses of 1 and 3 mg/kg intraperitoneally (IP) (5 to 10 minutes and 4 and 24 hours after occlusion) or twice with 0.1, 0.3, and 1.0 mg/kg subcutaneously (SC) (5 to 10 minutes and 3 hours after occlusion) or twice with 1 mg/kg SC (30 minutes and 3 hours 30 minutes; 1 and 4 hours; 2 and 5 hours; or 4 and 7 hours after occlusion). Other rats received (+)MK-801 (dizocilpine) three times at doses of 0.3, 1.0, and 3.0 mg/kg IP (5 to 10 minutes and 4 and 24 hours after occlusion). Control rats received an equal volume of saline. Infarct volume was determined 48 hours after occlusion by standard histological techniques. Results. IP administration of BIII 277 CL caused a dose-dependent reduction of infarct volume (1 mg/kg, 13%; 3 mg/kg, 25%). (+)MK-801 had similar effects (0.3 mg/kg, 13%; 1.0 mg/kg, 21%; 3 mg/kg, 27%). BIII 277 CL also dose-dependently reduced the infarct volume after SC administration (0.1 mg/kg, 14%; 0.3 mg/kg, 30%; 1.0 mg/kg, 28%). Furthermore, significant neuroprotective effects of BIII 277 CL were observed even when initial treatment was delayed up to 1 hour after occlusion (30 minutes, 28%; 1 hour, 23%; 2 hours, 5%; 4 hours, 4%). Conclusions. These results indicate that BIII 277 CL shows significant neuroprotective effects at doses as low as 0.1 mg/kg SC. The effects after IP administration are comparable with those of (+)MK-801, and significant effects were observed even when the BIII 277 CL was first administered up to 1 hour after the beginning of ischemia.     

Normobaric hyperoxia reduces MRI diffusion abnormalities and infarct size in experimental stroke

BACKGROUND: Hyperbaric oxygen therapy is considered an important stroke treatment strategy. BACKGROUND: To determine whether normobaric oxygen is neuroprotective, and, if so, what the therapeutic time window is. METHODS: Experiment 1-Serial diffusion- and perfusion-weighted MRI (DWI and PWI) was performed after middle cerebral artery filament occlusion (MCAO) in rats randomized to FiO(2) 30% (normoxia) or FiO(2) 100% (hyperoxia). Experiment 2-48-hour lesion volumes were analyzed in rats subjected to 2-hour MCAO and randomized to normoxia or hyperoxia starting 15, 30, or 45 minutes after MCAO and ending 15 minutes after reperfusion. RESULTS: Experiment 1-Lesion apparent diffusion coefficient (ADC) values were persistently low in normoxic animals. In hyperoxia-treated rats, ADC values in cortical border zones showed progressive recovery from 66 +/- 3% of contralateral before hyperoxia, to 104 +/- 20% at approximately 2 hours. Striatal ADC values showed early but ill-sustained improvement. ADC lesion volumes increased progressively in the normoxia group. In the hyperoxia group, ADC lesion volumes tended to decrease after starting hyperoxia; however, lesions later increased in size, and 2-hour lesion volumes were not significantly different from baseline. PWI showed stable right MCA hypoperfusion in all animals. Experiment 2-Hyperoxia within 30 minutes significantly reduced total and cortical lesion volumes at 48 hours after stroke. Striatal lesion volumes were significantly reduced in the hyperoxia-15 group. CONCLUSION: In rats subjected to transient stroke, 100% oxygen administered within 30 minutes salvages ischemic brain tissue, especially in the cerebral cortex. Reducing the time to treatment enhances the degree of neuroprotection.     

Sensitivity and specificity of in vivo diffusion-weighted MRI in acute spinal cord injury

The aim of this study was to test the sensitivity and specificity of diffusion-weighted MRI for the detection of acute spinal cord injury. Forty female New Zealand white rabbits were randomly divided into four groups: the mild, moderate and severe injury groups, and the control (sham operation) group. Contusion of the spinal cord was induced using a weight-drop impactor. All animals were imaged using T1-weighted, T2-weighted, and diffusion-weighted imaging (DWI) sequences at 30 minutes, 6 hours, and 24 hours after injury. One animal from each group was killed at each time point for histologic examination of the spinal cord. DWI had a sensitivity of 100% at all time points, whereas T2-weighted MRI had a sensitivity of 43.33% at 30 minutes after injury, 81.48% at 6 hours after injury, and 95.83% at 24 hours after injury. Conversely, the specificity of DWI was lower than that of T2-weighted MRI at all time points. One animal in the control group had a non-specific high signal on DWI. Significant systematic differences were seen between DWI and T2-weighted MRI at both 30 minutes and 6 hours after injury. The apparent diffusion coefficient values of the lesion were lower than those of adjacent unaffected regions in the mild and moderate injury groups, but higher than adjacent unaffected regions in the severe injury group. The histological findings were reliably correlated with the magnetic resonance findings. We found that DWI has a higher sensitivity, but a lower specificity, than conventional MRI for the detection of early pathological changes after contusive injury.     

巴曲酶对NJS小鼠短暂性脑缺血发作后神经细胞的保护和改善认知功能的作用

目的 观察巴曲酶对小鼠短暂性脑缺血发作（TIA）后神经细胞的保护和改善认知功能的作用。方法 选择自发性高胆固醇血症小鼠56只，分为对照组（缺血发作但未用药），缺血前2小时用药组，缺血后2小时用药组，缺血后24小时用药组。缺血后72小时测定各组小鼠的认知行为学指标和海马CA1区神经元凋亡数。结果 缺血前2小时用药组和缺血后2小时用药组神经元凋亡数较对照组少，认知功能恢复好于对照组，缺血后24小时用药组各指标与对照组相比无统计学差异。结论 巴曲酶对小鼠TIA后神经元有保护作用和促进认知功能恢复，但应早期用药。     

Streptokinase treatment versus calcium overload blockade in experimental thromboembolic stroke

Thromboembolic brain ischemia was produced in dogs using an autologous blood clot model. The effect of postembolic treatment with flunarizine and streptokinase on hemispheric cerebral metabolic rate for oxygen (CMRO2), oxygen extraction ratio (OER), and cerebral blood flow (CBF) was studied by positron emission tomography (oxygen-15 technique) 24 hours after the insult. We studied five groups of experimental dogs and compared them with a control group of nonembolized dogs. Group I received no treatment, Group II was treated locally with 500,000 IU streptokinase starting 30 minutes after the insult, Group III received streptokinase locally 30 minutes after the insult and 0.1 mg/kg i.v. flunarizine immediately after the insult and 2 hours later, Group IV received flunarizine as Group III, and Group V was orally pretreated with 0.5 mg/kg/day flunarizine during 2 weeks preceding embolization. Compared with the contralateral hemisphere, in the embolized hemisphere a significant reduction of CMRO2 (-25% to -40%) and CBF in normocapnia (-35%) and hypercapnia (-50%) was observed in Groups I, II, and V. In Groups III and IV, CMRO2, OER, and CBF of the embolized hemisphere were within the normal range during normocapnia and hypercapnia; the extent of the ischemic lesions was markedly less than in the other groups of experimental dogs. We conclude that flunarizine treatment after experimental thromboembolic stroke had a favorable influence on brain tissue. Chronic preventive flunarizine treatment failed to have a beneficial effect.