化学物品中毒现场急救

化学物品中毒现场急救第1页/共164页ContentsBackgroundGeneralintroductionAcuteOrganophosphatepoisoningAcutecarbonmonoxidepoisoningAcutesedatives-hypnoticspoisoningAlcoholIntoxication/Withdrawal第2页/共164页BackgroundThereareabout9000000kindsofchemiclaPeoplehavemanyopportunitytotouchwithpoison第3页/共164页BackgroundThereare1751476poisoningpt’sinUSAin1993Poisoncontrolcenter(PCC)

isestablishedinChicago1953。Majorduty:componentof

poison;4.informationDangerous5.toxicologyfirstaid6.

generalknowledgeofpreservation第4页/共164页第5页/共164页第6页/共164页第7页/共164页BackgroundCountryside>city。Countryside----pesticideintoxication。City---food-poisoning,carbonmonoxidepoisoning,Hypnoticintoxication。EstablishPCCinBeijing,Shanghai,Shenyang第8页/共164页Whatispoison?Apoisonisanythingsomeoneeats(ingestion),breathes(inhalation),getsintheeyes(ocularexposure),orontheskin(dermalexposure),thatcancausesicknessordeathifitgetsintobodyoronthebody.Poisoncanbefoundinfourforms:solid,liquid,sprayandgas.第9页/共164页Generalintroductiontoxicsubstance:drug,chemical,badfoodandsoon.Acutepoisoning：shorttime，largedoseChronicpoisoning：longtime、smalldose第10页/共164页Etiopathogenisis

andpathogenesyCauseofapoisoningOccupationalpoisoningLifepoisoningAccidentalpoisoning,SuicidalAbuse，addication,homicdal第11页/共164页Pathogenesy--Absorption

Bymouth;inhalation（Powderdust、smoke、steam）,skinmucosa,muscleorintravenousinjectionRectum、urinarycanal、femalesheath

vagina、bladder、peritoneum、eyeInsectstingsorbite第12页/共164页Pathogenesis--metabolismspreadalloverbodybyblood

livermetabolismPoisonousnessPoisonousnessOxidation,deoxidize,hydrolyse,bonding第13页/共164页Pathogenesis---Eliminatebreatheoutbyrespiratorytract（gas，volatilematter）DischargebykidneyDischargebyalimentarytractSkinMilk第14页/共164页1.Localeffect强酸、强碱吸收组织水分与蛋白质脂肪结合组织细胞变性坏死第15页/共164页2.HypoxiaInhibitionrespiratoryfunction：ChangebloodconstituentInhibitioncellsrespiratory：cyanide，hydrogensulfideDestroyCardiovascularfunction第16页/共164页破坏酶蛋白质部分的金属或活性中心——氰化物抑制细胞色素氧化酶Fe++；一氧化碳抑制细胞色素氧化酶Fe+++从而破坏酶蛋白质分子中的金属，使细胞发生窒息毒物与基质竞争同一种酶而产生抑制作用,丙二酸结构与琥珀酸相似，抑制三羟酸循环中琥珀酸脱氢酶3.Inhibitoryenzymeactivity第17页/共164页与酶的活性剂作用：——氟化物与Mg++形成复合物，使Mg++失去激活磷酸葡萄糖变为酶的作用去除辅酶：——铅中毒时，造成烟酸的消耗增多，使辅酶I和辅酶II减少，抑制了脱氢酶的作用与基质直接作用：——氟乙酸直接与柠檬酸相结合形成氟柠檬酸，阻止三羧酸循环的继续进行第18页/共164页

Organophosphatepoisoning，可抑制体内的胆碱酯酶，使组织中乙酰胆碱过量积蓄，引起一系列以乙酰胆碱为传导介质的神经处于过度兴奋状态，最后则转为抑制Carbontetrachloridepoisoning，首先作用于CNS，使之产生交感神经冲动，体内产生大量单胺类物质，使内脏血管收缩引起供血不足，中毒数小时后可出现肝、肾损害4.Dromotropism

medium第19页/共164页

一氧化碳与氧竞争血红蛋白，而形成碳氧血红蛋白，破坏了正常的输氧功能异烟肼与维生素B及烟酸的结构相似，因此，异烟肼在体内可与维生素B竞争，而取代其作用，因而引起中毒

5.Competitionreceptor第20页/共164页6.Interferecellororganellaphysiologicfunctioncarbontetrachloride（CCl4）－－CHCl3（trichlormethane)－－肝细胞膜中的unsaturatedfattyacid－－lipidperoxidation－－mitochondria(线粒体)、endoplasmicreticulum(内质网)变性－－hepatocyte(肝细胞)deathPhenols(酚类)－－线粒体内oxidativephosphorylation(氧化磷酸化)uncoupling(解偶联)－－inhibitingadenosinetriphosphate(三磷酸腺苷)synthesis(合成)、store(贮存)。第21页/共164页ThefactorofinfluencetoxicactionPhysico-chemicalpropertyofpoisonfineparticle,solubility,evaporabilitySusceptibilityofindividualsex,age,nutrition,healthstatus,livinghabit

第22页/共164页DiagnosispoisoningHistorySignandsymptomconsciousstatebreathingheartratebloodpressurepupil,skin,mucosa第23页/共164页Laboratory

examinationDetectionofpoison:blood,gastricjuiceandurineBlood,urineexamination第24页/共164页TherapeuticprincipleCPRGetridoftheenvironmentDecreaseAbsorptionSpecificantidotesCleaningpoisoningastrointestinaltractHeteropathyPreventComplication第25页/共164页EmergentmanagementBreathingsupportCirculationsupportTreatmentcomaTreatmentconvulsion第26页/共164页SPECIFICANTIDOTESOrgnaophosphorus-----PralidoximeIodide，AtropineBenzodiazepines－－FlumazenilPain-killer－－NaloxoneIsoniazid－－vitaminB6第27页/共164页EliminatepoisonEmeticGastriclavageActivatedcarbonadsorptionCatharsisWhole-bowelirrigation第28页/共164页Emetic压舌板、刺激咽后壁饮温水200-300ml吐根糖浆+200ml水休克、意识不清—禁用摄入腐蚀性毒物----禁用第29页/共164页PurposeofGastriclavageEliminatepoisoningastric,preventabsorbPreparationforoperationorsomeexamination第30页/共164页IndicationandcontraindicationIndication

Non-corrosivepoisonContraindication

Corrosivepoison—strongacid,baseesophagealvarix,aneurysmofaortaSevereheartdisease，uppergastrointestinalbleeding，gastricperforation第31页/共164页Principleofgastriclavage一般毒物的洗胃原则

一次性彻底洗胃（10000-20000ml）、停止洗胃标准为无色无味。有机磷中毒的洗胃原则

首次足量20000-30000ml持续胃肠减压留置胃管接胃肠减压器

反复少量洗胃

2000-5000ml/1-2h第32页/共164页洗胃的操作步骤洗胃步骤：1.先将胃内容物尽量抽尽2.灌入300-500ml洗胃液3.再排出灌入液体4.反复灌洗直到洗胃液纯清无味注意事项:1.洗胃液每次进入不宜过多，进出要平衡。2.洗胃液性质尽可能视毒物而定，液温37℃3.掌握适应症与禁忌症第33页/共164页洗胃要注意和观察的几个问题洗胃与胃出血的关系少量可给保护胃粘膜药，大量停止洗胃、持续胃肠减压观察出血情况洗胃时要密切观察生命体征、腹部情况、洗出液的性质第34页/共164页CatharsisandWhole-bowelirrigation

硫酸钠--15-20+水200口服硫酸镁--15-20+水200口服（引起高血镁）20%甘露醇250胃管内灌入--1小时腹泻、3小时排空。1%盐水、肥皂水5000--高位连续灌肠清洗活性炭加入灌肠液，促进毒物吸附排出第35页/共164页

EliminatepoisonForceddiuresis强化利尿Bloodpurification（血液净化）

hemodialysisHD（血液透析）

hemoperfusion,HP（血液灌流）

plasmaexchangePE（血浆置换）Highpressureoxygen高压氧第36页/共164页HemodialysisHD

血液透析机理：血液经体外循环进入透析器，通过透析膜和透析液之间形成的溶液浓度梯度，促使血液内溶质弥散至透析液内。可透析毒物的性质：water-solubility水溶性、heavymetals,生物性毒物。种类：蛇毒、鱼胆、利眠宁、diamorphine海洛因、扑热息痛、Isoniazid异烟肼、aminoglycosides氨基糖甙类、arsenic砷、mercury汞等。第37页/共164页HemoperfusionHP

血液灌流机理：血液流经灌流器，血液中的毒物被吸附到具有广大表面积的吸附剂上。吸附剂：活性炭、合成树脂毒物性质：脂溶性、大分子化合物、易与血浆蛋白结合的药物、毒物。种类：安定类、苯巴比妥类、抗抑郁类、有机磷类、伴有肝衰竭、肾衰竭者。第38页/共164页plasmaexchangePE

血浆置换机理：将血液引入血浆分离器中，使血细胞与血浆分离，弃去全部血浆，注入新鲜血浆和平衡液。毒物性质：与血浆蛋白结合率高（大于60%）第39页/共164页AcuteOrganophosphatepoisoning第40页/共164页AcuteOrganophosphatepoisoningFeature：毒性大、起病快;发病迅速；中毒途径多；诊断要快、准确；抢救及时。Classify分类：剧毒、高毒、中毒、低毒

第41页/共164页AcuteOrganophosphatepoisoningEtiopathogenisis：Accidental

suicidePathogenesis：

Poisonmetabolism

mechanism

acutepoisoning;chronicpoisoning第42页/共164页Organophosphate

Absorption:readilyDistribution:bloodbrainbarrier

Metabolism:intheliverElimination:primarilyintheurineHalf-life:4hours第43页/共164页Mechanism体内胆碱能神经的化学介质--乙酰胆碱交感、副交感神经节前纤维副交感神经节后纤维横纹肌的运动神经--肌肉接头交感神经节后纤维（支配泪腺、血管平滑肌）中枢神经系统胆碱能神经末梢----胆碱酯酶第44页/共164页CENTRALNERVOUSSYSTEMACh(nic)SkeletalMuscleSomaticEfferentsystemACh(nic)ACh(nic)ACh(nic)ACh(nic)NA

ACh(mus)

ACh(mus)BloodvesselsetcSweatGlandsAdrenalmedullaSympatheticsystemSalivaryglandsetcPara-sympatheticsystem第45页/共164页Cholinereceptor①Muscarinicreceptor（M-R）毒蕈碱

heart:restrainbloodvessel：dilatation

smoothmuscle：contractsphincterpupillaemuscle:contractcontractglandularorgan:secrete②Nicotinicreceptor（N-R）烟碱

N1-R：gangliocyte;ganglioneure—excitedN2-R：skeletalmuscle——contract第46页/共164页第47页/共164页第48页/共164页急性有机磷中毒--机理

有机磷毒物与胆碱酯酶acetylcholinesterase(AchE)结合，形成磷酰化胆碱酯酶，失去水解活性，造成乙酰胆碱acetylcholine蓄积产生毒蕈碱（M）样、烟碱（N）样症状和中枢神经系统的症状。第49页/共164页MECHANISMOFTOXICITY

Theorganophosphatesarepowerfulinhibitorsofcarboxylicesterhydrolases,includingacetylcholinesterase(foundinnervoustissuesanderythrocytes)andbutyrylcholinesterase(plasmaorpseudocholinesterase).Asaresultofthisenzymeinhibition,thesubstrateacetylcholineaccumulates

第50页/共164页急性有机磷中毒--机理中枢神经系统：脑内Ach含量增高---大脑多部位先兴奋后抑制。惊厥、呼吸中枢抑制。神经--肌肉接头：神经--肌肉接头的传递阻断，导致肌无力和肌麻痹。呼吸系统：呼吸肌麻痹、气道分泌物阻塞。第51页/共164页急性有机磷中毒--机理循环系统：

*对心脏直接毒性：心动过缓、心肌收缩力降低、各种心律失常

*抑制交感心血管中枢：外周血管扩张、血压下降。

*兴奋心血管迷走中枢：心动过缓、心肌收缩力降低、血压下降。神经节、腺体、平滑肌：腺体分泌增加、肠蠕动增加。第52页/共164页中毒途径及特点呼吸道吸收：有机磷沸点低、易挥发，易从呼吸道吸收,30min发病。消化道吸收：吸收快、10min－2h发病。皮肤黏膜吸收：有机磷是脂溶性，能透过皮肤黏膜入血，潜伏期长、2－6h发病。主要致死因素：呼吸衰竭第53页/共164页SymptomsandSignsMuscarinic:SLUDGE,bronchorrhea,bradycardiaandmiosis.Nicotinic:muscleweakness,fasciculationorparalysistarchycardia,bronchodilation,mydriasis.CNS:restless,drowsy,confusion,tremor,ataxia,delirium,seizure,coma.第54页/共164页Muscariniceffects

毒蕈碱（M）UrinationMiosisBronchospasmEmesisLacrimationSalivationBradycardiahypotension尿频、尿失禁缩瞳，视力模糊气管痉挛，分泌增加呕吐、腹泻、腹痛流泪、流汗、流口水肺水肿心跳减慢，血压下降第55页/共164页nicotinicmanifestations.musculartwitching,fasciculation,tachycardia,hypertension第56页/共164页centralnervoussystem

manifestations:Headache头痛,Drowsiness

昏睡,Confusion

意识混乱,Slurred

speech言语不清,Emotional

lability

情感不稳,Ataxia

共济失调,Tremor

震颤,Delirium

精神错乱,Seizure

癫痫.

Restrain

centerofbreathand

circulate第57页/共164页degree

Slight：ChE50-70%。Muscarinicsymptomandsign;Midrange：ChE30-50%,

Muscarinicsymptomandsign,nicotiniceffectsHeavy：ChE30%,

Muscarinic,nicotinic，centralnervoussystemsymptomandsign第58页/共164页Delayedneuropathy急性中毒症状消失后2-3周motorius—thelowerlimbspalsy麻痹,amyotrophy肌萎缩Nervefibrofattydegeneration,nervecelldemyelinate脱髓鞘有机磷抑制神经病靶酯酶（neuropathytargetesterase，NTE)第59页/共164页Delayedneuropathy－

stagesProgression：senseneuropathyStablephase：sensorydisabilitylast3－12monthremissivestage

：6－18monthmotorfunctionpartlyorcompleterecovery，spasm,motornervefunctionaldisturbance。第60页/共164页Intermediatesyndrome发生在急性中毒恢复后1－4天瘫痪（颈屈肌、脑神经支配的肌肉、肢体近侧肌、呼吸肌）4－18天缓解严重者呼吸衰竭神经肌肉接头处突触后功能障碍第61页/共164页LaboratoryexaminationserumcholinesteraseOrganophosphatemetabolicproduct

others第62页/共164页Diagnosis

Historygarlic-likeodor蒜臭味typicalsymptom：Pupilsizesmall,胃肠道症状、coma。Laboratoryexamination：serumcholinesterase,Organophosphatemetabolicproduct。Atropinetest：1-2mg---atropinization第63页/共164页DifferentialdiagnosisMuscarinicpoisonglobefishpoisonacutegastroenteritis;AGEHeatstrokeHypnoticintoxicationPesticideintoxication第64页/共164页TherapeuticprincipleGetridoftheenvironment

CannotusethehotwaterEliminatethepoisonqueasy、gastriclavageSpecificantidotesAtropine、PAMHeteropathyOxygentherapy、diuresis第65页/共164页EmergencyManagement

AirwayBreathingCardiopulmonaryresuscitation;CPRCNS：convulsionuse

valiumandphenobarbital，forbiduse

SuccinylcholineorMorphine。Cerebraledema：mannitol、glucocorticosteroidpneumonedema：Atropine，aminophyllineandmorphinecan’tbeuse第66页/共164页SpecificantidotesCholinesterase

resurrecter胆碱酯酶复活剂－N样症状效果好碘解磷定(pyraloximemethoiodide)氯磷定（pyraldoximemethylchloride）Atropine,blockmuscarinicreceptors,causinginhibitionofallmuscarinicfunctions.

Early,enough,association,repetitions第67页/共164页阿托品类生物碱--莨菪碱颠茄曼佗罗第68页/共164页TheeffectofAtropine

atropinepoisoningBLURREDVISIONCONFUSIONrestlessness

coma;CONSTIPATIONURINARYRETENTION

atropinizationmydriasisTachycardiaBlushingSkinandmucousdrydrycrackles

disappear第69页/共164页Symptomatictreatment

keepingWater-Electrolyteandacid-basebalancePreventionandcurepulmonaryinfection

makeuseofsedativePlasmapheresisPreventionandcureintermediatesyndrome第70页/共164页Acutecarbonmonoxidepoisoning第71页/共164页Acutecarbonmonoxidepoisoning无色、无臭、不溶于水的窒息性气体比重：0.967含碳物质不完全燃烧产生的气体空气中最高允许浓度0.05%或30mg/m3吸入过量可发生急性中毒第72页/共164页Acutecarbonmonoxidepoisoning浓度，％ 暴露时间，min 症状0.0005 100 无明显症状0.003 360 对中枢神经有害0.04-0.05 短时间 呼吸困难0.05-0.1 短时间 头痛、晕眩0.1-0.2 短时间 短时间内死亡1 短时间 立即死亡第73页/共164页Acutecarbonmonoxidepoisoning

Etiology

livingpoisoning

burncoalwater-heateroccupationalpoisoningmisoperationNoprotectionAccidentalpoisonincoalmineaccidentSuicidalhomicdal第74页/共164页MechanismCO+HbCOHbCO+Fe++restraint

cellrespirationCan’tcarryingoxygenhypoxiaCO+HbO2+Hb=260CO-HbO2-Hb=36001第75页/共164页ClinicalmanifestationSlight：HbCO10-20%，头痛、眩晕、心悸、恶心、呕吐、短暂晕厥。吸空气可好转。Midrange：HbCO30-40%，昏迷、虚脱。皮肤樱桃红。吸空气或高压氧可很快清醒，数日恢复，不留后遗症。Heavy：HbCO>50%，深昏迷、各种反射消失、瞳孔散大、血压下降呼吸抑制。严重者昏迷数天出现脏器功能障碍。第76页/共164页临床表现--迟发脑病意识障碍恢复后经过2-60天的“假愈期”3%-10%病人出现脑病：

神经意识障碍：痴呆、谵妄、去皮层状态。

锥体外系神经障碍：震颤麻痹综合征。

锥体系神经损害：偏瘫、病理反射（+）

大脑皮层局灶性功能障碍：失语、失明、继发癫痫。第77页/共164页Laboratoryexamination血COHb测定：特异性、判断严重程度动脉血气分析脑电图：弥漫性低波幅慢波头部CT：具有鉴别诊断意义第78页/共164页诊断和鉴别诊断有吸入CO病史典型临床表现实验室检查：定性或定量阳性、心肌酶增高其他：心电图、头颅CT、脑电图除外：安眠药中毒，其他有毒气体中毒、脑血管意外、糖尿病酮症酸中毒第79页/共164页EmergencytreatmentGetridoftheenvironmentOxygentherapy：Hyperbaricoxygentreatmentonlyafterseverecarbonmonoxidepoisoninginotherwisestablepatientsrespiratoryfailure：mechanicalventilationexchangeblood,bloodtransfusionDiuresis:preventionandcurebrainedema

promoterecoveryoffunction：sugar、vitaminATP、coenzymeA、cytochromeC。第80页/共164页acutesedatives-hypnoticspoisoning第81页/共164页Background

Sedative-hypnoticsareagroupofdrugsthatcauseCNSdepression.Benzodiazepines(BZD)barbituratesnonbarbituratenonbenzodiazepinesedative-hypnotics(NBNB)themostcommonlyusedagents第82页/共164页Backgroundacutesedative-hypnoticspoisoningwithdrawalsyndrome第83页/共164页EtiologyBenzodiazepines(BZD)Longacting(halflife>30h): chlordiazepoxide(利眠宁) diazepam（地西泮、安定）

flurazepam（氟安定）

Shortacting(halflife6-30h): alprazolam(阿普唑仑)Ultrashortacting: triazolam(三唑仑)第84页/共164页EtiologyBarbiturates

UltrashortactingMethohexital(Brevital甲己炔巴比妥)thiopental(Pentothal硫喷妥那)Shortactingpentobarbital(Nembutal戊巴比妥)secobarbital(Seconal司可巴比妥)IntermediateactingAmobarbital(Amytal异戊巴比妥)butalbital(Fioricet,Fiorinal异丁巴比妥) LongactingPhenobarbital(Luminal鲁米那)第85页/共164页Nonbarbiturate,nonbenzodiazepinesedative-hypnotics(NBNB) Chloralhydrate(水合氯醛) Ethchlorvynol(乙氯维诺) Glutethimide(导眠能) Methyprylon(甲乙哌酮) Meprobamate(眠尔通)Etiology第86页/共164页一、Pharmacokinetics

：PharmacokineticsoftheBZDMostBZDareextensivelymetabolizedbytheliver.Somearemetabolizedtoproductswhichareactiveandmayhaveamuchlongerhalflifethantheparentdrug.ThemajorrouteofmetabolismisN-demethylation. intheelderly Cimetidine

Pathogenesis第87页/共164页Pathogenesis2、PharmacokineticsofBarbituratesBarbiturateswithlowlipidsolubilityareexcretedintheunchangedformbythekidneys.iephenobarbital（苯巴比妥）.Barbiturateswithhighlipidsolubilityaremetabolizedtomorepolarcompoundsintheliverbeforebeingexcretedviathekidneys.iethiopental（硫喷妥）.第88页/共164页3、PharmacokineticsofNBNBMostNBNBareextensivelymetabolizedbytheliverPathogenesis第89页/共164页

BZD IntheCNS,benzodiazepinesexerttheirclinicaleffectbyenhancingtheactivityoftheinhibitoryneurotransmitterGABA. (TheclinicaleffectsofGABAreleaseandGABA-gatedchloridechannelsincludesleepinductionandexcitementinhibition)Barbiturates inprolongationofthedurationofopeningofGABA-gatedchloridechannels,leadingtohyperpolarizationofthemembraneandsuppressionofneurotransmission.。NBNB similartotheactionofBarbiturates二、ThemechanismofactionPathogenesis第90页/共164页Benzodiazepines--PathogenesisBZD受体+GABA受体+CI+通道感觉运动区，有镇静催眠作用蛋白复合物BZD边缘系统，抗焦虑和抗惊厥不清ω1ω2ω3抑制中枢神经系统第91页/共164页BZDGABAchloridechannelCl-Cl-＋＋＋＋＋－－－－－hyperpolarization第92页/共164页ClinicalBenzodiazepineblurredvision,dizziness,confusion,drowsiness,anxiety,agitation,andunresponsivenessorcoma.BZDoverdoseinitselfisremarkablysafe.mostpatientswithbenzodiazepineoverdosecanbemanagedintheEDandreleasedhomeafterappropriatecare.Whencombinedwithothersedatives(mostfrequentlyalcohol),patientswithbenzodiazepineoverdosecanpresentwithprofoundlydepressedlevelsofconsciousness..

第93页/共164页ClinicalBarbituratesMildintoxicationischaracterizedbyataxia,incoordination,nystagmus,slurredspeech,andalteredlevelofconsciousness.Moderatepoisoningleadstorespiratorydepressionandhyporeflexia.Severepoisoningleadstoflaccidareflexiccoma,apnea,andhypotension.Occasionally,hyperreflexia,rigidity,clonus,andBabinskisignsarepresent.Miosisiscommon,butmydriasismaybepresentwithcertainagents.Generally,10timesthehypnoticdoseproducesseveretoxicity.第94页/共164页ChloralhydrateMildintoxicationischaracterizedbyataxia,lethargySeverepoisoningleadsto

stupor,coma,pinpointpupils,hypotension,sloworrapidandshallowrespiration,hypothermia,areflexia,andmuscleflaccidity.ArrhythmiasClinical第95页/共164页ClinicalGlutethimide(Doriden)LossofbrainstemreflexesFlaccidityAnticholinergiceffectsDelayedgastricemptyingMaycausehyperthermiaorheatstroke第96页/共164页Methaqualone(Quaalude)ResemblesbarbituratepoisoningHasmorepronouncedmotorproblems(eg,ataxia)andisknownaswallbangerbecauseofthisphenomenon.CanleadtoseveremuscularhypertonicityandseizuresClinical第97页/共164页LabStudies

Obtainacompletebloodcount(CBC),arterialbloodgas(ABG),glucose,chemistry,ImagingStudies:

Obtainanabdominalx-ray.Chloralhydrateisradiopaque.OtherTests:Obtainanelectrocardiogram(ECG);Co-ingesteddrugsmayhavedirectcardiaceffects(eg,tricyclicantidepressants).

第98页/共164页QuantitativeserumdrugconcentrationsarerecommendedforpatientswithserioustoxicityBarbiturates:Forshort-actingdrugs,thelethaldoseis3goraserumconcentrationhigherthan3.5mg/dL.Forlong-actingdrugs,thelethaldoseis5-10goraconcentrationhigherthan8mg/dL.Chloralhydrate:Thelethaldoseis10gandaconcentrationhigherthan100mg/mListoxicLabStudies

第99页/共164页DiagnosisHistorySymptomandsignserumdrugconcentrations第100页/共164页DifferentialsToxicity,AlcoholsHypoglycemiaDiabeticKetoacidosisNeoplasms,Brain第101页/共164页TreatmentEmergencyDepartmentCareEstablishABCs,obtainIVaccess,provideoxygenEnsureadequateairwayandventilation.Doendotrachealintubationifnecessary.Fluidresuscitationandanti-shockNaloxoneisrecommendedtothepatientswithcomma.第102页/共164页PreventionofabsorptionGastriclavagemaybeperformedifthepatientpresentsobtundedwithin2hourofingestionActivatedcharcoalisrecommendedforsedative-hypnoticoverdoses.Multi-doseactivatedcharcoal(20-50gq4h)isrecommendedforoverdoseswithbarbiturates,glutethimide,andmeprobamate.Treatment第103页/共164页EliminationenhancementAlkalinediuresisenhanceseliminationofphenobarbitalandotherlong-actingbarbiturates.Itisrecommendedforallsymptomaticpatientswithlong-actingbarbituratetoxicity.Considerhemodialysisorhemoperfusioninglutethimide,methyprylon,phenobarbital,meprobamate,andchloralhydratepoisoning.Treatment第104页/共164页DetoxicantFlumazenilFlumazenilcompetitivelyandreversiblybindsbenzodiazepinereceptors(ie,GABA).Theuseofflumazenilforsuspectedbenzodiazepineoverdosesiscontroversial.Ifused,itshouldbeadministeredslowly(0.2mg/minupto3-5mg)becauselargedosescauseagitationandwithdrawal.Thisdrugiscontraindicatedinpatientswithincreasedintracranialpressure(ICP)orclosedheadinjury(CHI),thosewithahistoryofepilepsy,orthoseknowntohaveingestedatricyclicantidepressant(TCA)agentTreatment第105页/共164页TreatmentofcomplicationPneumoniaArrhythmiasAcuterenalfailure第106页/共164页Prognosisprophylaxis第107页/共164页Acutealcoholicintoxication烃类羟基衍生物，属于微毒品无色、易挥发、易燃液体，能与大多数有机溶剂混溶，更易溶于水，具有醇香气味。分子量46.07，沸点78.5℃Overdose--acutealcoholicintoxication西方国家成人70％有饮酒史。美国成人中14％出现酒精依赖(alcoholdependence)第108页/共164页发酵微生物对糖类发酵而成，主要成分乙醇。蒸馏酒：烈性酒(如白酒、烧酒、大曲酒、白兰地、威士忌)，含乙醇40％～60％发酵酒：果酒、啤酒和黄酒，乙醇20％以下配制酒：竹叶青酒、青梅酒、玫瑰酒等以蒸馏酒或发酵酒为酒基加用添加剂含乙醇含量低．酒精广泛应用于工业、医药、日常化学制品和酒类饮料。许多产品酒精含量达50％～99％日常酒精中毒常为烈性酒引起第109页/共164页WhatisaStandardDrink?第110页/共164页Mechanism（1）Metabolismofalcoholinthebody

Spirits,beer,wineAbsorbedintheupperGItract说明I：1、吸收部位（肠道）2、是否与食物混合3、酒饮料的种类90%changeintoacetaldehydeintheliver,thenethanoicacid,CO2andwater10%byurinaryorrespiratorysystem说明II：1、正常人每小时可代谢7-20ml酒精2、嗜酒者可代谢25ml3、酒精为“燃烧食品”，嗜酒者靠饮酒获得能量阻碍营养物质的摄入第111页/共164页Mechanism（2）Alcoholism:1、Lackofsomenutritionalelements2、IncreasethesecretionofACTH3、Damagestoliver4、Combineswithlecithinanddepositsinthenervoussystem.

第112页/共164页Mechanism（3）Possiblereasonsfordependence1、DecreasedactivityofMAOinCNS2、TetrahydroisowuinolinoccupancytotheopiatereceptorinCNS3、InfluencetotheGABAactivityandmetabolismintheCNS第113页/共164页Physicaleffectsofexcessiveuseofalcohol第114页/共164页Neuropsychiatriceffectsofexcessiveuseofalcohol第115页/共164页Clinicalfeatures（1）Acutealcoholism1、FirststageMildde-repressionofcortexElation,talkativeConcentrationofbloodalcohol:30-50mg/100ml第116页/共164页Clinicalfeatures（2）

2、SecondstageModeratede-repressionofcortexManiasyndrome,irritabilityConcentrationofbloodalcohol:60-100mg/100ml第117页/共164页Clinicalfeatures（3）

3、ThirdstageSevererde-repressionofcortexIn-congruentexcitementHallucinationanddelusionConfusionDeliriumConcentrationofbloodalcohol:100-150mg/100ml第118页/共164页Clinicalfeatures（4）

4、LaststageFullrepressionofCNSfunctionConsciousdisturbanceAbnormalsignsinNSEpilepsyInstabilityofvitalsignsConcentrationofbloodalcohol:150-200mg/100mlorhigher第119页/共164页Clinicalfeatures（5）AlcoholdependenceAlcoholdependencesyndromepsychologicaldependencephysicaldependenceWithdrawalsyndrome第120页/共164页Mechanism（1）Metabolismofalcoholinthebody

Spirits,beer,wineAbsorbedintheupperGItract说明I：1、吸收部位（肠道）2、是否与食物混合3、酒饮料的种类90%changeintoacetaldehydeintheliver,thenethanoicacid,CO2andwater10%byurinaryorrespiratorysystem说明II：1、正常人每小时可代谢7-20ml酒精2、嗜酒者可代谢25ml3、酒精为“燃烧食品”，嗜酒者靠饮酒获得能量阻碍营养物质的摄入第121页/共164页Mechanism（2）Alcoholism:1、Lackofsomenutritionalelements2、IncreasethesecretionofACTH3、Damagestoliver4、Combineswithlecithinanddepositsinthenervoussystem.

第122页/共164页Mechanism（3）Possiblereasonsfordependence1、DecreasedactivityofMAOinCNS2、TetrahydroisowuinolinoccupancytotheopiatereceptorinCNS3、InfluencetotheGABAactivityandmetabolismintheCNS第123页/共164页Physicaleffectsofexcessiveuseofalcohol第124页/共164页Neuropsychiatriceffectsofexcessiveuseofalcohol第125页/共164页Clinicalfeatures（1）Acutealcoholism1、FirststageMildde-repressionofcortexElation,talkativeConcentrationofbloodalcohol:30-50mg/100ml第126页/共164页Clinicalfeatures（2）

2、SecondstageModeratede-repressionofcortexManiasyndrome,irritabilityConcentrationofbloodalcohol:60-100mg/100ml第127页/共164页Clinicalfeatures（3）

3、ThirdstageSevererde-repressionofcortexIn-congruentexcitementHallucinationanddelusionConfusionDeliriumConcentrationofbloodalcohol:100-150mg/100ml第128页/共164页Clinicalfeatures（4）

4、LaststageFullrepressionofCNSfunctionConsciousdisturbanceAbnormalsignsinNSEpilepsyInstabilityofvitalsignsConcentrationofbloodalcohol:150-200mg/100mlorhigher第129页/共164页Clinicalfeatures（5）AlcoholdependenceAlcoholdependencesyndromepsychologicaldependencephysicaldependenceWithdrawalsyndrome第130页/共164页醇浓度与临床表现

血乙醇浓度临床表现

rng／L非嗜酒者嗜酒者200~500精细运动失调500~1000欣快感、群集性、共济失调无或轻度症状1000~2000情绪不定、言语不清清醒、欣快感共济失调、嗜睡、恶心共济失调2000~3000昏睡、恍惚、语无伦次情绪不稳运动障碍3000~4000昏迷嗜睡5000呼吸抑制、死亡昏睡或昏迷第131页/共164页临床表现无酒精耐受者酒醉清醒后，可有头痛、头晕、无力、恶心、震颤等症状；耐受者，症状较轻。重症中毒轻度酸碱平衡和电解质失常、低血糖和肺炎急性肌病，表现肌肉肿胀、疼痛或伴有肌球蛋白尿。第132页/共164页实验室检查血清乙醇浓度测定成人乙醇LD50为5～8g／kg，儿童为3g／kg血液生化检查急性中毒可出现低血糖、低钾血症、低镁血症和低钙血症动脉血气急性中毒者表现轻度代谢性酸中毒心电图可出现心律失常和心肌损害的心电变头颅CT严重酒精中毒病人