老年急性脑卒中患者并发低钠血症的机制探讨

目的：探讨老年急性脑卒中患者并发低钠血症的发生率。临床特点及发生机制。方法：回顾分析41例老年急性脑卒中并发低钠血症患者的临床,血清钠及CT资料。结果：老年急性脑卒中并发低钠血症的发生率占同期住院老年脑卒中患者的16．02％,以出血性脑卒中为多见。并发低钠血症者发生昏迷和病死率均高于对照组（均P＜0．05）,低钠血症的发生与CT所见的病灶分布密切相关,病灶位于基底节区（含丘脑）及脑室内积血更易发生低钠血症。结论：下丘脑－垂体功能紊乱是引起老年急性脑座中并低钠血症的主要原因之一。     

急性脑卒中并发低钠血症的机制及其临床意义

我院自1995年1月～1996年12月共收治急性脑卒中患者212例,其中并发低钠血症者35例,报告如下。资料与方法一、一般资料212例患者,男153例,女59例;年龄36～8岁,平均57.5岁。均经头部CT检查证实为急性脑卒中。其中脑梗死者132例,脑出血者62例,蛛网膜下腔出血者18例,均符合第四届全国脑血管病学术会议修订的各类脑血管病诊断标准;均排除肾功能不全和影响血钠水平的各种疾患如甲状旁腺功能减退等。二、检测方法患者于入院24h内抽取外周静脉血5ml,取血清1.5ml,应用瑞士罗天公司生产的CoBasMirPlus全自动生化仪及该公司生产的试剂药盒进行血清钠…     

急性脑卒中并低钠血症52例临床分析

目的探讨急性脑卒中后低钠血症的发生率、临床特点及临床意义。方法回顾性分析336例急性脑卒中患者的临床资料,按是否并低钠血症分为低钠组和正常组,并对2组相关临床资料进行比较。结果 336例患者并发低钠血症52例,发生率15.5%。低钠血症的发生与卒中性质、病灶分布及脱水剂使用相关;低钠血症可使脑卒中症状加重、病情恶化。结论 出血性脑卒中、病灶位于脑室及基底节区、大剂量脱水剂使用患者更易发生低钠血症;低钠血症可作为病情判断及评估预后的指标。     

脑卒中并发上消化道出血的临床研究

目的掌握急性脑卒中患者并发上消化道出血的临床特点。方法对763例急性脑卒中患者并发上消化道出血的情况进行调查研究。结果在763例患者中,急性脑出血并发上消化道出血的发生率明显高于急性脑梗死组,病变累及脑干时尤为突出。伴意识障碍的患者并发上消化道出血的发生率较高。脑卒中并发上消化道出血发生时间多在发病后24h内出现,亦可发生于病程10d左右。并发上消化道出血的脑卒中患者死亡率明显高于未并发上消化道出血者。结论脑卒中并发上消化道出血预后不良,早期应采取措施,积极预防。     

老年病毒性脑炎患者并发低钠血症的机制探讨

目的 探讨老年病毒性脑炎患者并发低钠血症的发生率、临床特点及发生机制。方法 回顾分析41例老年病毒性脑炎中并发低钠血症患者的临床、血清钠及CT资料。结果 老年病毒性脑炎并发低钠血症的发生率占同期老年病毒性脑炎住院 患者的16％,并发低钠血症患者昏迷和病死率均高于对照组(P<0.05),低钠血症的发生与CT所见的病灶分布密切相关,病灶位于基底节区(含丘脑)更易发生低钠血症 结论 下丘脑-垂体功能紊乱是引起老年病毒性脑炎患者并发低钠血症的主要原因之一。     

急性缺血性脑卒中后早期可出现脑微出血灶

研究对象是237例急性缺血性脑卒中发病24h内及1周内患者。研究方法进行MRI扫描，利用眩加权梯度回波成像（GRE他）检测脑微出血（MB）灶。研究结果：75例，占31．6％和30例，占12．7％患者在基线时有MB和新发MB；基线时MB中分别有53％、32％和15％位于脑深部、叶区以及幕下区，     

低钾血症和低钠血症对急性缺血性脑卒中溶栓患者短期预后的影响

目的研究低钾血症和低钠血症对急性缺血性脑卒中溶栓患者短期预后的影响。方法选取2018年11月～2019年5月于抚顺市中心医院收治的住院并且接受静脉溶栓治疗的患者共108例,其中急性缺血性脑卒中患者(45例),急性缺血性脑卒中伴低钠血症患者(36例),急性缺血性脑卒中伴低钾血症(27例),比较三组患者溶栓前,溶栓后24 h、3d的美国国立卫生研究院卒中量表(NIHSS)评分,溶栓后14 d改良Rankin量表(mRs)评分及出血转化率是否有差异。再将低钾血症组分为A组(轻度低钾)、B组(中度低钾)、C组(重度低钾),低钠血症组分为a组(轻度低钠)、b组(中度低钠)、c组(重度低钠),分别比较各组间溶栓前,溶栓后24 h、3d的NIHSS评分,溶栓后14 d mRs评分是否有差异。结果三组患者溶栓前NIHSS评分不存在显著差异(P>0.05),三组患者溶栓后24 h、3d的NIHSS评分及14 d后mRs评分均有所下降,其中伴有低钠血症的溶栓患者下降幅度不如其他两组,差异有统计学意义(P<0.05),出血转化率三组不存在显著差异(P>0.05)。A、B、C三组在溶栓前,溶栓后24 h,3d的NIHSS评分,溶栓后14 d mRs评分上差异均无统计学意义(P>0.05)。a、b、c三组比较,溶栓后24 h、3d的NIHSS评分,溶栓后14 d mRs评分差异存在统计学意义(P<0.05)。结论低钠血症对急性缺血性脑卒中溶栓患者短期预后存在不良影响,且血钠浓度越低,影响越大。     

急性脑卒中合并上消化道出血的治疗体会

目的对急性脑卒中患者并发上消化道出血的原因进行分析,探讨胃管内注入云南白药及硫糖铝口服混悬液治疗急性脑卒中合并上消化道出血的疗效及安全性。方法选择急性脑卒中并发上消化道出血患者76例,将其按随机原则分为观察组与对照组,对照组奥美拉唑注射液40mg加生理盐水100mL中静滴,2次/d;观察组在常规治疗基础上,给予云南白药1粒,硫糖铝口服混悬液10mL胃管注射,3次/d。观察治疗后12、24、48h止血情况和空腹胃液pH,治疗1周后评价疗效,记录不良反应。结果 2组均经有效的止血及降颅压治疗,观察组总有效率(97.3%)明显优于对照组(71.0%)。治疗后12、24、48h观察组止血率分别为73.6%、81.3%、97.3%,均显著高于对照组。治疗后12、24、48h,观察组和对照组空腹胃液pH值显著高于治疗前水平,差异有统计学意义。2组均无严重不良反应。结论分析急性脑卒中患者并发上消化道出血的原因,给予胃管内注入云南白药及硫糖铝口服混悬液,可提高治疗效果,有助于患者快速康复,在临床上具有重要意义。     

迟发性外伤性颅内血肿122例临床分析

目的探讨迟发性外伤性颅内血肿(DTIH)的临床特点、诱发因素及防治措施。方法 对我科自2001—01~2003-06收治的122例DTIH病人的临床及影像学资料进行回顾性分析。结果 DTIH占颅脑损伤病人的8.97％,死亡率23.8％。占同期颅脑损伤术中急性脑膨出病因的35.7％。中老年患者占DTIH患者的45.9％。DTIH发生在24h内占82％,72h内占97.5％。结论 DTIH多发生在颅脑损伤后72h内,伤后24h内发生率较高。多见于中老年患者。DITH是颅脑损伤术中发生急性脑膨出的重要原因。早期诊断和早期治疗是预后良好的关键。     

新生儿缺氧缺血性脑病合并低钠血症的分析

目的：早期诊断低钠血症，及时治疗，降低HIE死亡率。方法：对1999－01～2001-12我院收治的新生儿缺氧缺血性脑病患者，于入院24h内抽取静脉血检查血清电解质。血钠＜130mmol/L诊断为低钠血症并给予治疗，共105例。以积极治疗原发病为基础，在吸氧、保护脑代谢等综合治疗的同时，对轻度低钠血症患者给予限水、利尿等治疗，对中、重度低钠血症患者补钠。按3％氯化钠12ml/kg提高10mmol/L血钠计算，经静滴注3％氯化钠或生理盐水，无胃肠功能障碍者分次口服生理盐水提高血钠。结果：轻度低钠血症42例，占40．0％；中度52例，占49．52％；重度11例，占10．48％。痊愈83人，治愈率79．05％，死亡14人，死亡率13．33％。因病情危重自动出院8人，占7．62％。结论：新生儿缺氧缺血性脑病合并低钠血症临床无特异表现，监测血电解质可早期发现低钠血症，并及时限水、补钠等治疗，以提高HIE治愈率。     

The First 10 Thrombolysis for Acute Ischemic Stroke in Lao People's Democratic Republic under Teleconsultation from Thailand

Background: Acute ischemic stroke patients in Lao People's Democratic Republic (Lao PDR) are unable to access the intravenous thrombolytic therapy using recombinant tissue plasminogen activator (rtPA) due to various reasons. Aims: This study aimed to evaluate the feasibility and safety of thrombolytic therapy administration at Mittaphab Hospital, Lao PDR under the international telestroke consultation system from King Chulalongkorn Memorial Hospital, Thailand. Methods: Acute ischemic stroke patients who presented at Mittaphab Hospital within 4.5 hours after the onset and received thrombolytic therapy between December 2016 and June 2017 were studied. An immediate real time teleconsultation with 24 hours availability between neurologists at Mittaphab hospital and the Chulalongkorn stroke team was performed in all cases for patient evaluation and decision for thrombolytic treatment. Results: There were 205 patients with acute stroke, 28 patients (14%) arrived at the hospital within 4.5 hours after the onset. Ten patients (5%) were eligible for intravenous rtPA. The mean duration from onset to hospital arrival was 122.50 minutes and the mean door to needle time was 108 minutes. The mean National Institute of Health stroke scale (NIHSS) before thrombolysis was 10. At 90 days, the mean NIHSS was 3 and the mean mRS was 2. Seventy percent of patients had good outcome (mRS ≤2). Only one patient developed massive cerebral infarction. None of the patient developed symptomatic intracerebral hemorrhage or major bleedings. Conclusions: Telestroke consultation from Thailand can facilitate the thrombolytic therapy for acute ischemic stroke patients in Lao PDR.     

急性脑出血并发全身炎症反应综合征致多器官功能障碍综合征患者血清一氧化氮、一氧化氮合酶的变化

目的　探讨急性脑出血并发全身炎症反应综合征(SIRS)致多器官功能障碍综合征(MODS)的可能机制及一氧化氮(NO)、一氧化氮合酶(NOS)在急性脑出血致MODS发生发展中的作用。方法　观察急性脑出血并发SIRS及导致MODS的发生率。应用硝酸还原酶法及比色法动态监测73例急性脑出血患者血清NO及NOS的水平,并以20名健康人为对照。结果　脑出血并发SIRS的发生率为47. 95% (35 /73),其中74. 29% (26 /35)导致MODS。73例患者血清NO及NOS水平均明显高于正常对照组,且随病情的加重呈上升的趋势(均P<0. 01);重型MODS组较轻型组、死亡MODS组较存活组差异有极显著性(均P<0 01)。结论脑出血并发SIRS是导致MODS的主要机制,NO、NOS参与了脑出血并发SIRS及导致MODS的病理生理过程,并可作为一客观指标判断脑出血的病情及预后。     

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。     

急性幕上性脑出血患者脑水肿体积与高迁移率族蛋白B1的关系

目的 探讨脑出血后高迁移率族蛋白B1(high mobility group protein B1,HMGB1)水平的变化及其与脑出血后继发性脑水肿的关系。方法 收集152例幕上性脑出血患者的入院各基线资料及发病24 h时的HMGB1水平和发病后3或4 d复查头颅CT显示的相对水肿体积。结果 初入院的HMGBl水平要显著高于对照组(P<0.05),且24 h患者HMGBl水平与第3或4 d CT复查显示的相对水肿体积呈正相关(r=0.87,P=0.001)。结论 脑出血后HMGBl水平显著升高,且与脑水肿体积进展程度呈正相关。     

急性卒中合并应激性溃疡的危险因素

应激性溃疡是卒中最严重的并发症之一,发病机制不清。多表现为呕血、便血或二者兼有,严重者可出现失血性休克。急性出血性卒中并发应激性溃疡的发生率明显高于急性缺血性卒中,病变累及脑干时尤为突出。伴意识障碍的患者并发应激性溃疡的发生率较高。其发生可加重脑损害和出现多器官功能衰竭,对卒中预后影响较大。并发应激性溃疡的卒中患者病死率明显高于未并发者。卒中并发应激性溃疡预后不良,应早期识别其发生的危险因素,从而积极预防及治疗。     

Cerebral salt wasting syndrome in patients with aneurysmal subarachnoid hemorrhage

OBJECTIVE: Hydroelectrolytic disturbances are part of the complications of subarachnoid hemorrhage. Cerebral salt wasting syndrome (CSWS) must be considered when hyponatremia is associated with a decrease in circulating volume. We performed this study to determine the clinical characteristics and management paradigm of patients with serum sodium concentration abnormalities and aneurysmatic subarachnoid hemorrhage. METHODS: We analyzed retrospectively clinical and laboratory data from eight patients with subarachnoid hemorrhage due to rupture of an intracranial saccular aneurysm and cerebral salt wasting syndrome. Their course, as well as their clinical findings and treatment, are described. RESULTS: In eight patients, hyponatremia that lasted for more than 24 hours was detected (serum sodium under 135 mEq/l). The sodium disturbance occurred between day 3 and day 10 in all cases, in six of them in day 7 or day 8. The specific treatment for CSWS was to increase volume delivery according to the characteristics of the patient. Except for one case, none of the remaining patients required more than 72 hours of treatment to correct hyponatremia. No treatment-related complications were found CONCLUSION: Cerebral salt wasting syndrome, occurring in some patients with subarachnoid hemorrhage, is more commonly related to certain specific anatomic locations of the ruptured aneurysm, responds to sodium replacement therapy and fluids and can be diagnosed and treated based on the clinical, hydroelectrolytic and hemodynamic course of the patient. Further studies are needed to define the underlying mechanism of this condition.     

Anticoagulant-related hemorrhage in acute cerebral embolism

Five patients with nonseptic cerebral embolism of cardiac origin are reported in whom early anticoagulant therapy resulted in clinical deterioration or death from frank hemorrhage into the acute infarct. In each patient an initial CT scan excluded the presence of intracerebral hemorrhage and a second CT scan, after clinical deterioration had occurred, documented frank hemorrhage into the infarcted zone. All five patients had large infarctions in the right middle cerebral artery territory and three patients were mildly hypertensive. Four patients received heparin within 36 hours of their stroke and one was on warfarin at time of the embolism. Clinical deterioration occurred after intervals of several hours (2 cases), 5-6 days (2 cases) and 30 days (1 case). In only 2 patients was anticoagulant activity excessive at time of clinical deterioration. This report illustrates the danger of early anticoagulant therapy of acute nonseptic cerebral embolism, particularly in the setting of large infarction.     

Recent advances in pathophysiology and treatment of acute ischemic stroke]

The pathophysiology of ischemic neuronal cell damage has been studied extensively. Intracellular calcium ions, excitatory amino acids, nitric oxide, oxygen free radicals, proteolysis, apoptosis, and so on play important roles. There are also gene expressions following cerebral ischemia, such as the immediately early gene, heat shock protein, cytokines, adhesion molecule, and growth factor, etc. In vessels of the ischemic brain, activation of platelets, leukocytes, the coagulation cascade, and fibrin generation occur and aggravate the cerebral microcirculatory disturbance. Treatment of acute ischemic stroke must be based on the clinical type (atherothrombotic, lacunar or cardioembolic) and the time after onset. Fibrinolysis by tissue plasminogen activator (intravenous administration) is approved in the USA for patients with cerebral infarction within 3 hours after onset. Efficacy of anticoagulant therapy using heparin was not verified by the International Stroke Trial (IST). In Japan selective anti-thrombin agent (argatroban) is used in patients with atherothrombotic cerebral infarction within 48 hours after onset. Results of IST and Chinese Acute Stroke Trial (CAST) showed aspirin within 48 hours after onset of cerebral infarction reduced recurrence of ischemic stroke during the acute stage and death within 6 months.     

不同类型急性脑卒中血压变化的动态观察

目的　探讨不同类型急性脑卒中患者血压的变化规律。方法　 96例急性脑卒中患者 ,42例脑出血 ,5 4例脑梗死。以同期 65例Ⅰ期高血压作对照 ,全部患者均作 1～ 3d的 2 4h动态血压测定。并于第 2d始每隔 12h记录 1次 ,连续记录 7d ,至第14d再记录 1次。结果　脑出血组与脑梗死组 2 4h及夜间平均收缩压和舒张压均较对照组升高 ,有显著性差异 (P <0 0 5 )。但脑出血组较脑梗死组更明显 ,两组有显著性差异 (P <0 0 5 )。而高血压患者发生脑梗死、脑出血的危险性分别是非高血压患者的 3～ 4倍。急性脑卒中后 84%患者血压迅速升高 ,于 12h达到高峰 ,4d内逐渐下降至低水平。结论　血压的昼夜波动变化特点与发生脑卒中的类型有密切关系。急性脑卒中后血压的变化呈先升后降的自然规律。高血压患者急性卒中的发生率明显高于非高血压患者。