局麻药中毒处理 Microsoft Office Word 文档

第一篇：局麻药中毒处理 Microsoft Office Word 文档

ASRA recommendations on systemic toxicity of local anesthetics The American Society of Regional Anesthesia(ASRA)has developed a series of recommendations addressing the systemic toxicity of local anesthetics.The AAOS Council on Research, Quality Assessment and Technology reviewed the recommendations, and the AAOS Board of Directors, at its meeting on June 12, 2008, agreed to publish them inAAOS Now.Prevention of systemic local anesthetic toxicity

Be vigilant.Monitoring electrocardiogram, blood pressure, and arterial oxygen saturation is recommended.Communicate frequently with the patient to query for symptoms of toxicity.Limit local anesthetic(LA)dose based on site of injection, hypercapnia, advanced age, poor cardiac function, ischemic heart disease, cardiac conduction abnormalities(see notes), metabolic(especially mitochondrial)disease, or abnormally low plasma protein concentration.Aspirate syringe prior to each injection observing for blood or cerebrospinal fluid.Inject small volumes(5 mL), incrementally(45–60 sec intervals)observing for signs and symptoms of toxicity between each injection.Use a pharmacologic marker(e.g., epinephrine 5 mcg/mL of LA).Know the expected response, onset, duration, and limitations of “test dose” in identifying intravascular injection.Monitor the patient after completion of injection as peak blood concentrations may not occur for up to 30 minutes.Detection of systemic LA toxicity Be aware.The signs, symptoms, and timing of local anesthetic systemic toxicity are unpredictable.Because there is a potential antidote to this life-threatening event, the most important step in treating local anesthetic toxicity is to consider the diagnosis in any patient with altered mental status or cardio vascular instability following a regional anesthetic.Central nervous system(CNS)symptoms are often subtle or absent;cardiovascular signs, particularly hypotension or bradycardia, are often the only manifestation of severe local anesthetic toxicity;and the toxic syndrome can occur an hour or more after injection.CNS excitation(agitation, confusion, twitching, seizure), depression(drowsiness, obtundation, coma, or apnea), or nonspecific neurologic symptoms(metallic taste, circumoral paresthesias, diplopia, tinnitus, dizziness)are each typical of LA toxicity.Progressive hypotension and bradycardia, leading to asystole are typical of severe cardiovascular toxicity.Ventricular ectopy, multiform ventricular tachycardia, and ventricular fibrillation are also frequently seen.Treatment of systemic LA toxicity

Be prepared: The ASRA strongly advises anesthesiology departments to establish a plan for managing systemic local anesthetic toxicity at their facility.This should include stocking 20 percent lipid emulsion and the means for its rapid delivery close to every site where local anesthetics are used.Having a Local Anesthetic Toxicity Kit is encouraged.Get help and call for lipid or an LA Toxicity Kit, then focus attention on the following:

1.Airway management

2.Seizure suppression and, if needed，3.Cardiopulmonary resuscitation 4.Alert the nearest facility having cardiopulmonary bypass capability.Administer 20 percent lipid emulsion(values in parenthesis are for 70kg):

1.Bolus 1.5 mL/kg intravenously over 1 minute(~100mL)2.Continuous infusion 0.25 mL/kg/min(~500 mL over 30 minutes)3.Repeat bolus Q 5 minutes for persistent cardiovascular collapse.4.Double infusion rate if blood pressure returns but remains low.5.Continue infusion for a minimum of 30 minutes.Notes on prevention

Sedative hypnotic drugs reduce seizure risk but even light sedation may abolish the patient’s ability to recognize rising LA concentrations.Patients with severe cardiac dysfunction, particularly very low ejection fraction, severe conduction abnormality, or ongoing ischemia, may not be good candidates for plexus or peripheral nerve block or epidural anesthesia(blocks requiring larger doses of LA).Despite the prejudice that regional anesthesia is safer and that such patients might be ‘too sick’ for general anesthesia, they could be more susceptible to irreversible cardiovascular collapse with local anesthetic exposure(even with nonlipophilic LA)than with inhalational exposure.Consider alternatives such as spinal or small dose field block(subcutaneous injection).Notes on treatment

Arguably the most important factor in treating LA toxicity is aggressive airway management to avoid hypoxia, hypoventilation, and tissue acidosis, which all exacerbate LA-induced cardiovascular depression.Timing of lipid infusion in the LA toxic syndrome is controversial.The most conservative approach would be to wait until American Heart Association/Advanced Cardiovascular Life Support has proven unsuccessful in returning adequate circulation.This seems unreasonable given the many reports of early reversal of toxicity, suggesting that progression to cardiovascular collapse can be stopped by early intervention.An aggressive strategy would be to infuse lipid at the earliest sign of systemic toxicity.This may result in the unnecessary treatment of many patients given that only a fraction are expected to progress to cardiovascular collapse.The most reasonable approach at this time, lacking rigorous data supporting one extreme over the other, is somewhere in between.The clinical context, severity, and rate of progression of clinical signs of toxicity should guide the use of lipid therapy.Propofol should not be used when the patient exhibits signs of cardiovascular instability.There is considerable confusion about this point given that propofol is typically formulated in lipid emulsion.However, the lipid content is too low to provide a benefit, while propofol is sufficiently cardio-depressant that its use is discouraged when there is a risk of progression to cardiovascular collapse.Seizure suppression is a key element of LA toxicity treatment since it is important to prevent the metabolic acidosis that accompanies tonic-clonic seizures.The best means for achieving this includes benzodiazepines or pentothal.Prolonged monitoring is recommended after any signs of systemic LA toxicity.Cardiovascular depression due to local anesthetics can persist or return after treatment

第二篇：麻醉(医学高级)局部麻醉神经阻滞与局麻药中毒章节练习(2014-08-21)

简便易行的变态反应试验有()A．皮内注射试验

B．神经反射试验

C．嗜碱性细胞脱粒试验

D．结膜试验

E．阿托品试验

表面麻醉药有哪几种剂型()A．乳剂

B．溶液

C．软膏

D．栓剂

E．凝胶

预防局麻药中毒的措施包括()A．加入微量肾上腺素

B．最低有效局麻药浓度

C．麻醉前应用镇静药

D．减小局麻药用量

E．加快注药速度

4.判断题静脉注射局麻药后最易发生的即刻并发症是组织坏死。()参考答案对5.判断题利多卡因是酯类局麻药。()参考答案错6.判断题可卡因只能用于表面麻醉。()参考答案错 7 静脉注射局麻药后最易发生的即刻并发症是()A．神经炎

B．失语

C．血栓性静脉炎

D．心肌抑制

E．通气过度

利多卡因在静脉局部麻醉总剂量不应超过()A．0.5mg/kg B．3mg/kg C．1.5mg/kg D．2mg/kg E．2.5mg/kg 9 在第2骶后孔阻滞骶神经最常见的并发症是()A．损伤脊髓

B．血肿形成

C．穿刺针刺入盆腔

D．注药入血管

E．脊麻

第三篇：Office处理技术心得体会

《Office处理技术》心得体会

姓名：邢王秀学号：200924101215班级：计本<2>班

本次的讲座陈院长主要给我们讲三大办公工具，在日常的学习，工作中都能看到它的身影，在我们实习备课中，它们更是会发挥至关重要的作用。因此，作为培训的最后一课，由我院副院长陈焕东老师为了我们就office的基本处理做了专题讲座。

陈院长通过word, PowrPoint,excel三大办公工具展开的，这三大基础软件，在我们备课中占有十分重要，所以实习学校对我们这三方面的掌握要求很高，而我们自己更应该认真对待，因为这不光代表我们院，最主要的还是自己。作为一名信息老师这是基本的技能，必须掌握的。在讲座过程中，老师边讲边做一些演示，有时还让同学们上去操作。从word到ppt，老师说了些重要内容，一些概念性内容。比如在讲word的时候，提问到什么是文字的编辑和排版。请同学起来回答，答案都不是很准确，老师做了解答，文字的编辑是对文字内容的改变，文字的排版是对文字格式上的改变。介绍了表格的制作的步骤，同学上去演示。Excel中讲到是统计函数，给出一个表，按内容完成任务，输入正确公式得到结果，最后是四个同学共同完成，这说明这方面的知识还没有完全掌握。接下来是ppt制作，问了ppt的组成，ppt是由幻灯片组成的，而幻灯片是由信息对象组成。在讲座的最后，老师要求我们每一位学生做关于今天内容的测试，目的是巩固知识。

通过了这次讲座我学到了一些我以前没有学到过的知识，Micosoft office看似很简单，但是做起来是很有难度的。所以我们要认真的对待。

第四篇：office 宏病毒处理方法

Office文档是目前使用最多也是最常见的办公文档(它包含Word文档，Excel文档，PPT文档等)，以至于Office软件成了大家必备的软件，由于Office软件默认的安全级别为中，所以Office文档成了病毒攻击的目标，目前有许多Office文档病毒，以最近教科局出现的宏病毒为例，成了大家头疼的一件事，现就个人处理方法介绍如下，供大家参考与分享。

1、宏病毒的分析

Office文档中的宏是Office中最高级别的部分，平时大家很少用到，它能把繁重的工作简单化，默认的安全级别为中，宏病毒正是利用这一点通过网络、U盘等进行传播，中毒的电脑明显反应变慢，Office文档大小在不断变化，有的成倍增加，一个小小的电子表格就有2M之多，使用十分困难。

2、中毒后文件的特征

中毒后的Office文档，除大小变大外，每次打开都要求启用宏，不启用便不能打开Office文档，或者打开了，全是空白，如果使用杀毒软件，则会把文档删除，给用户带来许多麻烦。Office软件运行缓慢，电脑经常死机等。

3、处理方法：

在网上下载“Office病毒专杀”工具（下载地址：http:///5254.html），解压后安装，界面如下:

点击全盘杀毒，即可对电脑中的Office

病毒进行全面查杀。

备注：该软件使用前要关闭其他杀毒软件！

第五篇：有机磷农药中毒的急诊处理

一、有机磷酸酯类杀虫剂中毒的急诊处理

（一）有机磷酸酯类理化性质及中毒机理有机磷酸酯多为有特殊气味的油状液体，挥发性很强，少数为黄白色固体，易溶于多种有机溶剂，不溶或微溶于水。遇强碱性物质可迅速被分解、破坏，毒性减低或消失。但敌百虫例外，其在碱性溶液中能变成毒性更强的敌敌畏。有机磷酸酯类进入人体后，其磷酸根与胆碱酯酶活性部分紧密结合，形成磷酰化胆碱酯酶，使其丧失水解乙酰胆碱的能力，导致胆碱能神经释放的乙酰胆碱过多积聚，引起胆碱能神经及部分中枢神经功能过度兴奋，继而转入抑制和衰竭，产生中毒症状。

（二）诊断要点病人接触过毒物或吞服过有机磷酸酯类杀虫剂是确定诊断的重要依据之一，如果从患者的胃内容物、呼吸道分泌物，以及皮肤、衣物等，嗅到有机磷酸酯的特殊蒜臭气味，对诊断有帮助。

根据其中毒的程度，临床表现可分为轻、中、重三种情况。

轻者有头痛、头晕、流涎、恶心、呕吐、腹痛、多汗、乏力、肢体麻木、视力模糊等症状。

中度者，除上述症状外，进而出现精神恍惚，言语不利，步态蹒跚，呼吸困难，肌束颤动，中度瞳孔缩小等。

重度者，病情进展迅速，瞳孔极小，对光反应迟钝，严重时血压下降，心率加快，口及呼吸道有大量分泌物，导致呼吸困难，口唇及指端明显紫绀，甚至于呼吸衰竭，病人呈现昏迷、大小便失禁状态。

为肯定临床诊断和协助判断病情轻重，可测定血胆碱酯酶活动。正常人血胆碱酯酶活力为80％～100％，如果血胆碱酯酶活力降为50％～70％，为轻度有机磷酸酯类中毒，血胆碱酯酶活力降为30％～50％为中度中毒，血胆碱酯酶活力降为30％以下，为重度中毒。

（三）急救措施1．防止毒物继续进入人体将病人移离有毒物的现场后，除敌百虫中毒外，均可用2～5％碳酸氢钠溶液清洗污染的皮肤，用清水或肥皂水也可。如果毒物污染眼睛，可用生理盐水或2％碳酸氢钠溶液冲洗眼部，然后滴1％阿托品1～2滴。经消化道中毒者应用2％碳酸氢钠溶液或清水完全、彻底、干净地及时洗胃，直洗到洗胃液无有机磷酸酯的蒜臭味为止。为清除已被吸收的毒物又从胃肠道粘膜排到胃内，必要时考虑再次洗胃。之后的处理见前述急救原则一节。

2．特效解毒剂的选用（1）阿托品：可对抗蓄积过多的乙酰胆碱，缓解临床症状。根据轻、中、重三种病情而选用不同的剂量。轻者给予阿托品1～2mg，皮下或肌内注射，每隔1～2h重复用药。中度中毒者予以阿托品2～5mg，静注，每15～20min重复一次。重度者给阿托品5～10mg，每10～15min重复一次，待达到阿托品化以后或症状明显缓解时，可酌情减少药量或延长用药间隔时间。达到阿托品化的临床依据如下为瞳孔散大，但对光反应存在。病人面色逐渐潮红，心率稍增快，但低于140次／min，口及皮肤趋于干燥，肺水肿减轻。病人对刺激有一定的反应。严防上述临床表现转向过分，否则容易阿托品过量或中毒。待治疗达到阿托品化后，经过减量，尚需予以维持治疗，以免出现中毒表现的反覆。

（2）胆碱酯酶复能剂：以解磷定、氯磷定或双复磷较为常用，其能恢复胆碱酯酶的活力，也可解除肌束颤动和抽搐。但中毒时间过长时磷酰化胆碱酯酶已老化，不能再与解磷定类药物形成磷酸化解磷定，也就难以恢复胆酯酶的活力了。因此，应用此类解毒药要早用，剂量也需根据轻、中、重三种不同病情调正，一般用量可予以解磷定0.5～1g，加入葡萄糖液500ml中静脉点滴，中度以上中毒者，首剂还可予以静脉注射0.5g。胆碱酯酶复能剂与阿托品联合应用抢救急性有机磷酸酯类中毒收效可有很大提高。