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Cerebrovascular Effects Of Cocaine

机译:可卡因的脑血管效应

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Over five million Americans using cocaine regularly, and a survey in South London showed an increase in crack cocaine use from 16% to 59% amongst drug users. Common manifestations such as chest pain, hypertension, and psychiatric disturbances occur, but we must be alert for other serious unexpected presentations. Misdiagnoses are likely, especially as an accurate history may not be forthcoming, with cocaine toxicity masquerading as other common diseases. Subarachnoid haemorrhage, strokes of varying aetiologies, seizures, headache and sudden death are recognised associations of cocaine abuse. Seizures, for instance, have been reported to make up almost 10% of cocaine related admissions to emergency departments, and patients with prior seizure history, poor compliance with antiepileptic medication, alcohol abuse and poor diet or sleep habits are at greater risk. Simple management principles coupled to a high index of suspicion, are efficacious in the assessment and treatment of cocaine toxicity. Introduction Cocaine is one of the major drugs of abuse in the United States, with over five million Americans using the drug regularly 1 . This has recently become a problem in Great Britain, with a survey among injecting drug users in south London showing an increase in crack cocaine use from 16% in 1990 to 59% in 1993. In the North Thames region of London in 1995-6, 4% of young people used cocaine as their main drug of abuse, with a further 7% using crack cocaine 2 . When asked if it were either the main or secondary drug of abuse, these figures rose to 12% & 16% respectively. 1 in 50 young people in Great Britain have tried cocaine and 1 in 100 have tried crack. A Department of Health study revealed that the only drug in Great Britain to show a significant increase in proportion of misuse was cocaine, increasing from 1% of 16 – 24 year olds in 1994 to 3% in 1998 3 .Cocaine has commonly recognised manifestations such as chest pain, hypertension, and psychiatric disturbances such as psychosis, paranoia, agitation, anxiety and depression, but more unexpected presentations may occur, many neurological, which may commonly be ascribed to other causes 4 . Subarachnoid haemorrhage, strokes of varying aetiologies, seizures, headache and sudden death are all relatively common associations of cocaine abuse 5 . This review summarises the relevant literature in relation to cerebrovascular effects of cocaine, and makes recommendations on important areas of management. Methodology A medical literature search was carried out using Medline (1966 to 2003), in both Ovid and Pubmed versions, and Internet search engines, using the keywords below. Papers were identified and evaluated, and further references were drawn from hand-searches of their bibliographies. Key words used were: cocaine, crack cocaine, cocaine-related disorders, toxicity, drug toxicity, overdose, cerebrovascular accident, and cerebrovascular disorders. History, Types & Patterns Of Use Cocaine, or benzoylmethylecgonine, is an alkaloid derived from the leaves of the coca plant, Erythroxylon coca 6 . It acts as a local anaesthetic with sympathomimetic and vasoconstrictor properties and has been widely abused as a mental stimulant. The Indians of Peru, Bolivia and Colombia have traditionally chewed coca mixed with lime for 2000 years, to reduce fatigue and hunger and to enable sustained periods of heavy labour. Coca Cola, and tonic drinks such as Vin Mariani, contained cocaine until 1903. Thirty years after the isolation of alkaloidal cocaine by the German chemist Gaedke in 1855, Sigmund Freud praised the use of cocaine as a central nervous system stimulant 6 . The Harrison Narcotics Act of 1914 finally forbade its inclusion in proprietary medicines and restricted its use to prescription only. Cocaine was little used until the 1960s when its popularity underwent a resurgence, along with other illicit drugs. The common route of use at this time was sniffing or snorting the hydrochloride sal
机译:超过五百万美国人定期使用可卡因,伦敦南部的一项调查显示,吸毒者中可卡因的使用率从16%增加到59%。常见的症状有胸痛,高血压和精神病,但我们必须警惕其他严重的意外症状。误诊是可能的,尤其是由于可能没有准确的病史,可卡因毒性像其他常见疾病一样被伪装。蛛网膜下腔出血,各种病因中风,癫痫发作,头痛和猝死是可卡因滥用的公认协会。例如,据报告,癫痫发作占急诊科可卡因相关入院人数的近10%,具有癫痫病史,抗癫痫药物依从性差,酗酒以及饮食或睡眠习惯差的患者面临更大的风险。简单的管理原则加上高度的可疑指数,对可卡因毒性的评估和治疗有效。简介可卡因是美国主要的滥用药物之一,有超过五百万美国人定期使用该药物1。这在英国最近成为一个问题,一项对伦敦南部注射吸毒者的调查显示,可卡因的使用量从1990年的16%增加到1993年的59%。在1995-6年的伦敦北泰晤士地区, 4%的年轻人使用可卡因作为主要的滥用药物,另有7%的人使用可卡因2。当被问到它是滥用的主要还是次要药物时,这些数字分别上升到12%和16%。英国每50名年轻人中就有1人尝试了可卡因,而每100名年轻人中就有1人尝试了可卡因。卫生部的一项研究表明,英国唯一显示滥用率显着增加的药物是可卡因,可卡因从1994年的16-24岁人群的1%增加到1998年的3%3。如胸痛,高血压和精神病,如精神病,偏执狂,躁动,焦虑和抑郁,但可能会出现更多意想不到的表现,许多神经系统疾病通常可归因于其他原因4。蛛网膜下腔出血,各种病因中风,癫痫发作,头痛和猝死都是可卡因滥用的相对普遍的关联5。这篇综述总结了有关可卡因脑血管效应的相关文献,并对重要的治疗领域提出了建议。方法论使用Ovid和Pubmed版本的Medline(1966年至2003年)和Internet搜索引擎使用以下关键字进行了医学文献搜索。对论文进行了鉴定和评估,并从他们的书目手工搜索中获得了更多参考。使用的关键词是:可卡因,可卡因,可卡因相关疾病,毒性,药物毒性,药物过量,脑血管意外和脑血管疾病。使用的历史,类型和方式可卡因或苯甲酰基甲基芽子碱是一种生物碱,衍生自古柯植物古柯叶6的叶。它作为具有拟交感神经药和血管收缩药特性的局部麻醉药,已被广泛用作精神兴奋剂。秘鲁,玻利维亚和哥伦比亚的印度人传统上将古柯与石灰混合咀嚼了2000年,以减轻疲劳和饥饿感,并使持续的繁重劳动成为可能。可口可乐和诸如Vin Mariani之类的补品饮料一直含有可卡因,直到1903年。德国化学家Gaedke在1855年分离出生物碱可卡因后30年,Sigmund Freud称赞可卡因作为中枢神经系统兴奋剂的用途6。 1914年的《哈里森麻醉品法》最终禁止将其纳入专有药物,并将其使用范围仅限于处方药。直到1960年代,可卡因与其他非法药物一起流行之后,才得到广泛使用。这时的常用用法是嗅探或吸食盐酸盐盐

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