化学物品中毒现场急救

,单击此处编辑母版标题样式,单击此处编辑母版文本样式,第二级,第三级,第四级,第五级,*,Acute toxicity,Capital university of medical science Xuan wu hospital,Emergency Department,Contents,Background,General introduction,Acute Organophosphate poisoning,Acute carbon monoxide poisoning,Acute sedatives-hypnotics poisoning,Alcohol Intoxication /Withdrawal,Background,There are about 9000000 kinds of chemicla,People have many,opportunity,to,touch with,poison,Background,There are,1751476,poisoning pts in USA in 1993,Poison control center(PCC),is established in Chicago,1953,。,Major duty:,component of,poison;,4.,information,Dangerous 5. toxicology,first aid 6.,general knowledge of preservation,Background,Countryside,city,。,Countryside-pesticide intoxication,。,City-food-poisoning, carbon monoxide poisoning ,Hypnotic intoxication,。,Establish,PCC,in Beijing,Shanghai ,Shenyang,What is poison?,A poison is anything someone eats ( ingestion), breathes (inhalation) , gets in the eyes (ocular exposure), or on the skin (dermal exposure) ,that can cause sickness or death if it gets into body or on the body.,Poison can be found in four forms: solid, liquid, spray and gas.,General introduction,toxic substance : drug ,chemical , bad food and so on.,Acute poisoning,：,short time， large dose,Chronic poisoning,：,long time,、,small dose,Etiopathogenisis,and pathogenesy,Cause of a poisoning,Occupational poisoning,Life poisoning,Accidental poisoning ,Suicidal,Abuse ，addication , homicdal,Pathogenesy-,Absorption,By mouth; inhalation Powder dust、smoke、steam, skin mucosa, muscle or intravenous injection,Rectum 、 urinary canal、female sheath vagina、bladder、peritoneum、eye,Insect stings or bite,Pathogenesis -,metabolism,spread all over body by blood,liver metabolism,Poisonousness,Poisonousness,Oxidation,deoxidize, hydrolyse, bonding,Pathogenesis - Eliminate,breathe out by respiratory tractgas，volatile matter,Discharge by kidney,Discharge by alimentary tract,Skin,Milk,1.Local effect,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,2.Hypoxia,Inhibition respiratory function：,Change blood constituent,Inhibition cells respiratory,：,cyanide,，,hydrogen sulfide,Destroy Cardiovascular function,破坏酶蛋白质局部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.Inhibitory enzyme activity,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,Organophosphate poisoning，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，最后那么转为抑制,Carbon tetrachloride poisoning，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缺乏，中毒数小时后可出现肝、肾损害,4.Dromotropism,medium,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.Competition receptor,6.Interfere cell or organella physiologic function,carbon tetrachlorideCCl4CHCl3trichlormethane)肝细胞膜中的unsaturated fatty acidlipid peroxidationmitochondria(线粒体)、,endoplasmic reticulum(内质网)变性hepatocyte(肝细胞)death,Phenols(酚类)线粒体内oxidative phosphorylation(氧化磷酸化) uncoupling(解偶联)inhibiting adenosine triphosphate(三磷酸腺苷) synthesis(合成)、store(贮存)。,The factor of influence toxic action,Physico-chemical property of poison,fine particle,solubility,evaporability,Susceptibility of individual,sex,age,nutrition,health status,living habit,Diagnosis poisoning,History,Sign and symptom,conscious state,breathing,heart rate,blood pressure,pupil, skin , mucosa,Laboratory,examination,Detection of poison:,blood, gastric juice and urine,Blood ,urine examination,Therapeutic principle,CPR,Get rid of the environment,Decrease Absorption,Specific antidotes,Cleaning poison in gastrointestinal tract,Heteropathy,Prevent Complication,Emergent management,Breathing support,Circulation support,Treatment,coma,Treatment,convulsion,SPECIFIC ANTIDOTES,Orgnaophosphorus -Pralidoxime Iodide，Atropine,Benzodiazepines,Flumazenil,Pain -killer,Naloxone,Isoniazid,vitamin B6,Eliminate poison,Emetic,Gastric lavage,Activated carbon adsorption,Catharsis,Whole-bowel irrigation,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,Purpose,of Gastric lavage,Eliminate poison in gastric, prevent absorb,Preparation for operation or some examination,Indication,and,contraindication,Indication,Non-corrosive poison,Contraindication,Corrosive poison,strong acid ,base,esophageal varix, aneurysm of aorta,Severe heart disease，upper gastrointestinal bleeding，gastric perforation,Principle of gastric lavage,一般毒物的洗胃原那么 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那么 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,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,本卷须知: 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,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,Catharsis and,Whole-bowel irrigation,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,活性炭参加灌肠液，促进毒物吸附排出,Eliminate poison,Forced diuresis 强化利尿,Blood purification血液净化,hemodialysis HD血液透析,hemoperfusion,HP血液灌流,plasma exchange PE血浆置换,High pressure oxygen 高压氧,Hemodialysis HD,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、,heavy metals,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。,Hemoperfusion HP,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阔外表积的吸附剂上。,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。,plasma exchange PE,血浆置换,机理：将血液引入血浆别离器中，使血细胞与血浆别离，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%,Acute Organophosphate poisoning,Acute Organophosphate poisoning,Feature,：,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,Acute Organophosphate poisoning,Etiopathogenisis,：,Accidental,suicide,Pathogenesis,：,Poison metabolism,mechanism,acute poisoning;,chronic poisoning,Organophosphate,Absorption:,readily,Distribution:,blood brain barrier,Metabolism: in the liver,Elimination: primarily in the urine,Half-life : 4 hours,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,CENTRAL NERVOUS SYSTEM,ACh,(nic,),Skeletal Muscle,Somatic,Efferent,system,ACh,(nic),ACh,(nic,),ACh,(nic),ACh,(nic),NA,ACh,(mus),ACh,(mus),Blood vessels etc,Sweat Glands,Adrenal medulla,Sympathetic,system,Salivary glands,etc,Para-,sympathetic,system,Choline receptor, Muscarinic receptorM-R毒蕈碱,heart : restrain,blood vessel：dilatation,smooth muscle：contract,sphincter pupillae muscle: contract,contractglandular organ:secrete, Nicotinic receptorN-R 烟碱N1-R：gangliocyte;ganglioneureexcited N2-R：skeletal musclecontract,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样病症和中枢神经系统的病症。,MECHANISM OF TOXICITY,The organophosphates are powerful inhibitors of carboxylic ester hydrolases, including acetylcholinesterase (found in nervous tissues and erythrocytes) and butyrylcholinesterase (plasma or pseudocholinesterase). As a result of this enzyme inhibition, the substrate,acetylcholine accumulates,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。,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。,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,30,min,发病。,消化道吸收：,吸收快、10,min2h,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、26,h,发病。,主要致死因素：呼吸衰竭,Symptoms and Signs,Muscarinic: SLUDGE, bronchorrhea, bradycardia and miosis.,Nicotinic: muscle weakness, fasciculation or paralysis tarchycardia, bronchodilation, mydriasis.,CNS: restless, drowsy, confusion, tremor, ataxia, delirium, seizure, coma.,Muscarinic effects 毒蕈碱M,Urination,Miosis,Bronchospasm,Emesis,Lacrimation,Salivation,Bradycardia,hypotension,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,nicotinic,manifestations,.,muscular twitching,fasciculation ,tachycardia,hypertension,central nervous system,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,S,eizure,癫痫,.,Restrain,center,of,breath,and,circulate,degree,Slight,：,ChE,50-70%。,Muscarinic,symptom and sign;,Midrange,：,ChE,30-50%,Muscarinic,symptom and sign,nicotinic effects,Heavy,：,ChE,30%,Muscarinic,nicotinic,，central nervous system symptom and sign,Delayed neuropathy,急性中毒病症消失后2-3周,motoriusthe lower limbs palsy麻痹, amyotrophy肌萎缩,Nerve fibrofatty degeneration, nerve cell demyelinate脱髓鞘,有机磷抑制神经病靶酯酶neuropathy target esterase ，NTE),Delayed neuropathy,stages,Progression ：sense neuropathy,Stable phase,：,sensory disability last,312,month,remissive stage,：618,month motor function partly or complete recovery,，,spasm, motor nerve functional disturbance,。,Intermediate syndrome,发生在急性中毒恢复后14天,瘫痪颈屈肌、脑神经支配的肌肉、肢体近侧肌、呼吸肌,418天缓解,严重者呼吸衰竭,神经肌肉接头处突触后功能障碍,Laboratory examination,serum cholinesterase,Organophosphate,metabolic product,others,Diagnosis,History,garlic-like odor蒜臭味,typical symptom： Pupil size small, 胃肠道 病症、coma。,Laboratory examination： serum cholinesterase, Organophosphate metabolic product。,Atropine test：1-2mg-atropinization,Differential diagnosis,Muscarinic,poison,globe fish poison,acute gastroenteritis;AGE,Heatstroke,Hypnotic intoxication,Pesticide intoxication,Therapeutic principle,Get rid of the environment,Cannot use the hot water,Eliminate the poison,queasy、,gastric lavage,Specific antidotes,Atropine、PAM,Heteropathy,Oxygen therapy、diuresis,Emergency Management,Airway,Breathing,Cardiopulmonary resuscitation;CPR,CNS,：,convulsion use,valium and phenobarbital,，,forbid use,Succinylcholine or Morphine,。,Cerebral edema,：,mannitol,、,glucocorticosteroid,pneumonedema,：,Atropine,，,aminophylline and morphine cant be use,Specific antidotes,Cholinesterase resurrecter胆碱酯酶复活剂N样病症效果好,碘解磷定(pyraloxime methoiodide),氯磷定pyraldoxime methylchloride,Atropine, block muscarinic receptors, causing inhibition of all muscarinic functions.,Early , enough, association, repetitions,阿托品类生物碱,-,莨 菪 碱,颠茄,曼佗罗,The effect of,Atropine,atropine poisoning,BLURRED VISION,CONFUSION,restlessness,coma;,CONSTIPATION,URINARY,RETENTION,atropinization,mydriasis,Tachycardia,Blushing,Skin and,mucousdry,dry,crackles,disappear,Symptomatic treatment,keeping Water-Electrolyte and acid-base balance,Prevention and cure pulmonary infection,make use of sedative,Plasmapheresis,Prevention and cure intermediate syndrome,Acute carbon monoxide poisoning,Acute carbon monoxide poisoning,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30,mg/m3,吸入过量可发生急性中毒,Acute carbon monoxide poisoning,浓度，暴露时间，min 病症,0.0005 100 无明显病症,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,Acute carbon monoxide poisoning,Etiology,living,poisoning,burn coal,water-heater,occupational,poisoning,misoperation,No protection,Accidental,poisonin,coal mine,accident,Suicidal,homicdal,Mechanism,CO+Hb COHb,CO+Fe,+,restraint,cell respiration,Cant carrying,oxygen,hypoxia,CO+Hb,O2+Hb,=,260,CO-Hb,O2-Hb,=,3600,1,Clinical manifestation,Slight,：,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,：,HbCO50%，,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。,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。,Laboratory examination,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,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,Emergency treatment,Get rid of the environment,Oxygen therapy,：,Hyperbaric oxygen treatment,only after severe carbon monoxide poisoning in otherwise stable patients,respiratory failure,：,mechanical ventilation,exchange blood, blood transfusion,Diuresis:,prevention and cure brain edema,promote,recovery of function,：,sugar,、,vitamin,ATP、,coenzyme,A、,cytochrome,C。,acute sedatives-hypnotics poisoning,Background,Sedative-hypnotics are a group of drugs that cause CNS depression.,Benzodiazepines (BZD),barbiturates,nonbarbiturate nonbenzodiazepine sedative-hypnotics (NBNB),the most commonly used agents,Background,acute sedative-hypnotics poisoning,withdrawal syndrome,Etiology,Benzodiazepines (BZD),Long acting (half life 30h):,chlordiazepoxide (利眠宁),diazepam地西泮、安定,flurazepam 氟安定,Short acting (half life 6-30h):,alprazolam(阿普唑仑),Ultrashort acting :,triazolam(三唑仑),Etiology,Barbiturates,Ultrashort acting,Methohexital (Brevital,甲己炔巴比妥,),thiopental (Pentothal,硫喷妥那,),Short acting,pentobarbital (Nembutal,戊巴比妥,),secobarbital (Seconal,司可巴比妥,),Intermediate acting,Amobarbital (Amytal,异戊巴比妥,),butalbital (Fioricet, Fiorinal,异丁巴比妥,),Long acting,Phenobarbital (Luminal,鲁米那,),Nonbarbiturate, nonbenzodiazepine sedative-hypnotics (NBNB),Chloral hydrate (,水合氯醛,),Ethchlorvynol (,乙氯维诺,),Glutethimide (,导眠能,),Methyprylon (,甲乙哌酮,),Meprobamate (,眠尔通,),Etiology,一、,Pharmacokinetics,：,Pharmacokinetics of the BZD,Most BZD are extensively metabolized by the liver.,Some are metabolized to products which are active,and may have a much longer half life than the parent,drug.,The major route of metabolism is N-,demethylation,.,in the elderly,Cimetidine,Pathogenesis,Pathogenesis,2、Pharmacokinetics of Barbiturates,Barbiturates with low lipid solubility are excreted in the unchanged form by the kidneys. ie phenobarbital苯巴比妥.,Barbiturates with high lipid solubility are metabolized to more polar compounds in the liver before being excreted via the kidneys. ie thiopental 硫喷妥.,3,、,Pharmacokinetics of NBNB,Most NBNB are extensively metabolized by the liver,Pathogenesis,BZD,In the CNS, benzodiazepines exert their clinical effect by enhancing the activity of the inhibitory neurotransmitter GABA.,(The clinical effects of GABA release and,GABA-gated chloride channels,include sleep induction and excitement inhibition),Barbiturates,in,prolongation of the duration,of opening of,GABA-gated chloride channels, leading to,hyperpolarization,of the membrane and suppression of neurotransmission.,。,NBNB,similar to the action of Barbiturates,二、,The mechanism of action,Pathogenesis,Benzodiazepines-,Pathogenesis,BZD,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,1,2,3,抑制中枢神经系统,BZD,GABA,chloride channel,Cl,-,Cl,-,hyperpolarization,Clinical,Benzodiazepine,blurred vision, dizziness, confusion, drowsiness, anxiety, agitation, and unresponsiveness or coma.,BZD overdose in itself is remarkably safe. most patients with benzodiazepine overdose can be managed in the ED and released home after appropriate care.,When combined with other sedatives (most frequently alcohol), patients with benzodiazepine overdose can present with profoundly depressed levels of consciousness. .,Clinical,Barbiturates,Mild intoxication is characterized by ataxia, incoordination, nystagmus, slurred speech, and altered level of consciousness.,Moderate poisoning leads to respiratory depression and hyporeflexia.,Severe poisoning leads to flaccid areflexic coma, apnea, and hypotension.,Occasionally, hyperreflexia, rigidity, clonus, and Babinski signs are present.,Miosis is common, but mydriasis may be present with certain agents.,Generally, 10 times the hypnotic dose produces severe toxicity.,Chloral hydrate,Mild intoxication is characterized by ataxia, lethargy,Severe poisoning leads to,stupor, coma, pinpoint pupils, hypotension, slow or rapid and shallow respiration, hypothermia, areflexia, and muscle flaccidity.,Arrhythmias,Clinical,Clinical,Glutethimide (Doriden),Loss of brainstem reflexes,Flaccidity,Anticholinergic effects,Delayed gastric emptying,May cause hyperthermia or heatstroke,Methaqualone (Quaalude),Resembles barbiturate poisoning,Has more pronounced motor problems (eg, ataxia) and is known as wallbanger because of this phenomenon.,Can lead to severe muscular hypertonicity and seizures,Clinical,Lab Studies,Obtain a complete blood count (CBC), arterial blood gas (ABG), glucose, chemistry,Imaging Studies:,Obtain an abdominal x-ray. Chloral hydrate is radiopaque.,Other Tests:,Obtain an electrocardiogram (ECG); Co-ingested drugs may have direct cardiac effects (eg, tricyclic antidepressants).,Quantitative serum drug concentrations are recommended for patients with serious toxicity,Barbiturates: For short-acting drugs, the lethal dose is 3 g or a serum concentration higher than 3.5 mg/dL. For long-acting drugs, the lethal dose is 5-10 g or a concentration higher than 8 mg/dL.,Chloral hydrate: The lethal dose is 10 g and a concentration higher than 100 mg/mL is toxic,Lab Studies,Diagnosis,History,Symptom and sign,serum drug concentrations,Differentials,Toxicity, Alcohols,Hypoglycemia,Diabetic Ketoacidosis,Neoplasms, Brain,Treatment,Emergency Department Care,Establish ABCs, obtain IV access, provide oxygen,Ensure adequate airway and ventilation. Do endotracheal intubation if necessary.,Fluid resuscitation and anti-shock,Naloxone is recommended to the patients with comma.,Prevention of absorption,Gastric lavage may be performed if the patient presents obtunded within 2hour of ingestion,Activated charcoal is recommended for sedative-hypnotic overdoses. Multi-dose activated charcoal (20-50 g q4h) is recommended for overdoses with barbiturates, glutethimide, and meprobamate.,Treatment,Elimination enhancement,Alkaline diuresis enhances elimination of phenobarbital and other long-acting barbiturates. It is recommended for all symptomatic patients with long-acting barbiturate toxicity.,Consider hemodialysis or hemoperfusion in glutethimide, methyprylon, phenobarbital, meprobamate, and chloral hydrate poisoning.,Treatment,Detoxicant Flumazenil,Flumazenil competitively and reversibly binds benzodiazepine receptors (ie, GABA).,The use of flumazenil for suspected benzodiazepine overdoses is controversial. If used, it should be administered slowly (0.2 mg/min up to 3-5 mg) because large doses cause agitation and withdrawal.,This drug is contraindicated in patients with increased intracranial pressure (ICP) or closed head injury (CHI), those with a history of epilepsy, or those known to have ingested a tricyclic antidepressant (TCA) agent,Treatment,Treatment of complication,Pneumonia,Arrhythmias,Acute renal failure,Prognosis,prophylaxis,Acute alcoholic intoxication,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-acute alcoholic intoxication,西方国家成人70有饮酒史。,美国成人中14出现酒精依赖(,alcoholdependence),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4060,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