第一篇：局麻藥中毒處理 Microsoft Office Word 文檔

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(醫(yī)學(xué)高級)局部麻醉神經(jīng)阻滯與局麻藥中毒章節(jié)練習(xí)(2014-08-21)

簡便易行的變態(tài)反應(yīng)試驗(yàn)有()A．皮內(nèi)注射試驗(yàn)

B．神經(jīng)反射試驗(yàn)

C．嗜堿性細(xì)胞脫粒試驗(yàn)

D．結(jié)膜試驗(yàn)

E．阿托品試驗(yàn)

表面麻醉藥有哪幾種劑型()A．乳劑

B．溶液

C．軟膏

D．栓劑

E．凝膠

預(yù)防局麻藥中毒的措施包括()A．加入微量腎上腺素

B．最低有效局麻藥濃度

C．麻醉前應(yīng)用鎮(zhèn)靜藥

D．減小局麻藥用量

E．加快注藥速度

4.判斷題靜脈注射局麻藥后最易發(fā)生的即刻并發(fā)癥是組織壞死。()參考答案對5.判斷題利多卡因是酯類局麻藥。()參考答案錯6.判斷題可卡因只能用于表面麻醉。()參考答案錯 7 靜脈注射局麻藥后最易發(fā)生的即刻并發(fā)癥是()A．神經(jīng)炎

B．失語

C．血栓性靜脈炎

D．心肌抑制

E．通氣過度

利多卡因在靜脈局部麻醉總劑量不應(yīng)超過()A．0.5mg/kg B．3mg/kg C．1.5mg/kg D．2mg/kg E．2.5mg/kg 9 在第2骶后孔阻滯骶神經(jīng)最常見的并發(fā)癥是()A．損傷脊髓

B．血腫形成

C．穿刺針刺入盆腔

D．注藥入血管

E．脊麻

第三篇：Office處理技術(shù)心得體會

《Office處理技術(shù)》心得體會

姓名：邢王秀學(xué)號：200924101215班級：計(jì)本<2>班

本次的講座陳院長主要給我們講三大辦公工具，在日常的學(xué)習(xí)，工作中都能看到它的身影，在我們實(shí)習(xí)備課中，它們更是會發(fā)揮至關(guān)重要的作用。因此，作為培訓(xùn)的最后一課，由我院副院長陳煥東老師為了我們就office的基本處理做了專題講座。

陳院長通過word, PowrPoint,excel三大辦公工具展開的，這三大基礎(chǔ)軟件，在我們備課中占有十分重要，所以實(shí)習(xí)學(xué)校對我們這三方面的掌握要求很高，而我們自己更應(yīng)該認(rèn)真對待，因?yàn)檫@不光代表我們院，最主要的還是自己。作為一名信息老師這是基本的技能，必須掌握的。在講座過程中，老師邊講邊做一些演示，有時還讓同學(xué)們上去操作。從word到ppt，老師說了些重要內(nèi)容，一些概念性內(nèi)容。比如在講word的時候，提問到什么是文字的編輯和排版。請同學(xué)起來回答，答案都不是很準(zhǔn)確，老師做了解答，文字的編輯是對文字內(nèi)容的改變，文字的排版是對文字格式上的改變。介紹了表格的制作的步驟，同學(xué)上去演示。Excel中講到是統(tǒng)計(jì)函數(shù)，給出一個表，按內(nèi)容完成任務(wù)，輸入正確公式得到結(jié)果，最后是四個同學(xué)共同完成，這說明這方面的知識還沒有完全掌握。接下來是ppt制作，問了ppt的組成，ppt是由幻燈片組成的，而幻燈片是由信息對象組成。在講座的最后，老師要求我們每一位學(xué)生做關(guān)于今天內(nèi)容的測試，目的是鞏固知識。

通過了這次講座我學(xué)到了一些我以前沒有學(xué)到過的知識，Micosoft office看似很簡單，但是做起來是很有難度的。所以我們要認(rèn)真的對待。

第四篇：office 宏病毒處理方法

Office文檔是目前使用最多也是最常見的辦公文檔(它包含Word文檔，Excel文檔，PPT文檔等)，以至于Office軟件成了大家必備的軟件，由于Office軟件默認(rèn)的安全級別為中，所以O(shè)ffice文檔成了病毒攻擊的目標(biāo)，目前有許多Office文檔病毒，以最近教科局出現(xiàn)的宏病毒為例，成了大家頭疼的一件事，現(xiàn)就個人處理方法介紹如下，供大家參考與分享。

1、宏病毒的分析

Office文檔中的宏是Office中最高級別的部分，平時大家很少用到，它能把繁重的工作簡單化，默認(rèn)的安全級別為中，宏病毒正是利用這一點(diǎn)通過網(wǎng)絡(luò)、U盤等進(jìn)行傳播，中毒的電腦明顯反應(yīng)變慢，Office文檔大小在不斷變化，有的成倍增加，一個小小的電子表格就有2M之多，使用十分困難。

2、中毒后文件的特征

中毒后的Office文檔，除大小變大外，每次打開都要求啟用宏，不啟用便不能打開Office文檔，或者打開了，全是空白，如果使用殺毒軟件，則會把文檔刪除，給用戶帶來許多麻煩。Office軟件運(yùn)行緩慢，電腦經(jīng)常死機(jī)等。

3、處理方法：

在網(wǎng)上下載“Office病毒專殺”工具（下載地址：http:///5254.html），解壓后安裝，界面如下:

點(diǎn)擊全盤殺毒，即可對電腦中的Office

病毒進(jìn)行全面查殺。

備注：該軟件使用前要關(guān)閉其他殺毒軟件！

第五篇：有機(jī)磷農(nóng)藥中毒的急診處理

一、有機(jī)磷酸酯類殺蟲劑中毒的急診處理

（一）有機(jī)磷酸酯類理化性質(zhì)及中毒機(jī)理有機(jī)磷酸酯多為有特殊氣味的油狀液體，揮發(fā)性很強(qiáng)，少數(shù)為黃白色固體，易溶于多種有機(jī)溶劑，不溶或微溶于水。遇強(qiáng)堿性物質(zhì)可迅速被分解、破壞，毒性減低或消失。但敵百蟲例外，其在堿性溶液中能變成毒性更強(qiáng)的敵敵畏。有機(jī)磷酸酯類進(jìn)入人體后，其磷酸根與膽堿酯酶活性部分緊密結(jié)合，形成磷酰化膽堿酯酶，使其喪失水解乙酰膽堿的能力，導(dǎo)致膽堿能神經(jīng)釋放的乙酰膽堿過多積聚，引起膽堿能神經(jīng)及部分中樞神經(jīng)功能過度興奮，繼而轉(zhuǎn)入抑制和衰竭，產(chǎn)生中毒癥狀。

（二）診斷要點(diǎn)病人接觸過毒物或吞服過有機(jī)磷酸酯類殺蟲劑是確定診斷的重要依據(jù)之一，如果從患者的胃內(nèi)容物、呼吸道分泌物，以及皮膚、衣物等，嗅到有機(jī)磷酸酯的特殊蒜臭氣味，對診斷有幫助。

根據(jù)其中毒的程度，臨床表現(xiàn)可分為輕、中、重三種情況。

輕者有頭痛、頭暈、流涎、惡心、嘔吐、腹痛、多汗、乏力、肢體麻木、視力模糊等癥狀。

中度者，除上述癥狀外，進(jìn)而出現(xiàn)精神恍惚，言語不利，步態(tài)蹣跚，呼吸困難，肌束顫動，中度瞳孔縮小等。

重度者，病情進(jìn)展迅速，瞳孔極小，對光反應(yīng)遲鈍，嚴(yán)重時血壓下降，心率加快，口及呼吸道有大量分泌物，導(dǎo)致呼吸困難，口唇及指端明顯紫紺，甚至于呼吸衰竭，病人呈現(xiàn)昏迷、大小便失禁狀態(tài)。

為肯定臨床診斷和協(xié)助判斷病情輕重，可測定血膽堿酯酶活動。正常人血膽堿酯酶活力為80％～100％，如果血膽堿酯酶活力降為50％～70％，為輕度有機(jī)磷酸酯類中毒，血膽堿酯酶活力降為30％～50％為中度中毒，血膽堿酯酶活力降為30％以下，為重度中毒。

（三）急救措施1．防止毒物繼續(xù)進(jìn)入人體將病人移離有毒物的現(xiàn)場后，除敵百蟲中毒外，均可用2～5％碳酸氫鈉溶液清洗污染的皮膚，用清水或肥皂水也可。如果毒物污染眼睛，可用生理鹽水或2％碳酸氫鈉溶液沖洗眼部，然后滴1％阿托品1～2滴。經(jīng)消化道中毒者應(yīng)用2％碳酸氫鈉溶液或清水完全、徹底、干凈地及時洗胃，直洗到洗胃液無有機(jī)磷酸酯的蒜臭味為止。為清除已被吸收的毒物又從胃腸道粘膜排到胃內(nèi)，必要時考慮再次洗胃。之后的處理見前述急救原則一節(jié)。

2．特效解毒劑的選用（1）阿托品：可對抗蓄積過多的乙酰膽堿，緩解臨床癥狀。根據(jù)輕、中、重三種病情而選用不同的劑量。輕者給予阿托品1～2mg，皮下或肌內(nèi)注射，每隔1～2h重復(fù)用藥。中度中毒者予以阿托品2～5mg，靜注，每15～20min重復(fù)一次。重度者給阿托品5～10mg，每10～15min重復(fù)一次，待達(dá)到阿托品化以后或癥狀明顯緩解時，可酌情減少藥量或延長用藥間隔時間。達(dá)到阿托品化的臨床依據(jù)如下為瞳孔散大，但對光反應(yīng)存在。病人面色逐漸潮紅，心率稍增快，但低于140次／min，口及皮膚趨于干燥，肺水腫減輕。病人對刺激有一定的反應(yīng)。嚴(yán)防上述臨床表現(xiàn)轉(zhuǎn)向過分，否則容易阿托品過量或中毒。待治療達(dá)到阿托品化后，經(jīng)過減量，尚需予以維持治療，以免出現(xiàn)中毒表現(xiàn)的反覆。

（2）膽堿酯酶復(fù)能劑：以解磷定、氯磷定或雙復(fù)磷較為常用，其能恢復(fù)膽堿酯酶的活力，也可解除肌束顫動和抽搐。但中毒時間過長時磷酰化膽堿酯酶已老化，不能再與解磷定類藥物形成磷酸化解磷定，也就難以恢復(fù)膽酯酶的活力了。因此，應(yīng)用此類解毒藥要早用，劑量也需根據(jù)輕、中、重三種不同病情調(diào)正，一般用量可予以解磷定0.5～1g，加入葡萄糖液500ml中靜脈點(diǎn)滴，中度以上中毒者，首劑還可予以靜脈注射0.5g。膽堿酯酶復(fù)能劑與阿托品聯(lián)合應(yīng)用搶救急性有機(jī)磷酸酯類中毒收效可有很大提高。