锂中毒的临床特点及处理。

A Amdisen
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引用次数: 82

摘要

锂盐,特别是碳酸盐和柠檬酸盐,以前被广泛使用,形成碱性盐混合物的一部分,用于治疗属于尿酸素质的许多疾病。这些障碍包括躁狂、抑郁、急性躁狂、急性忧郁症和周期性抑郁症。直接声称对周期性抑郁有满意的预防效果。建议每日服用3至26毫摩尔的锂作为标准。在所述期间(1860年至1930年),只有极少数病例报告了轻微或中度中毒症状,当时这些治疗指数良好的含锂预防性药物的普及程度达到顶峰。1949年,凯德引入了他的锂中毒治疗方案,这种治疗方案偶然有效,但剂量很高,直到出现躁狂症恢复的迹象,锂中毒才成为一个严重的临床问题。对于维持剂量,凯德原则上推荐,但很少坚持,17mmol /天。慢性锂中毒开始时伴有肾脏的隐性疼痛,随后出现“前驱”症状,当达到中度严重程度时,肾脏恶性循环加速,肾功能下降迫在眉睫。在这一点之后,慢性中毒类似于急性中毒。在这一阶段或早期阶段进行积极的排毒,使患者有很好的康复机会。晚期出现少尿、半昏迷或昏迷,伴有潜伏性惊厥运动,恢复不确定。目前还没有针对锂中毒的特效解药。血液透析是治疗急性锂中毒最有效的方法。对于肾功能受损或潜在肾功能受损的患者,腹膜透析可能是另一种治疗方法,但效果较差。强制利尿要求肾功能不受损,比停止治疗并辅以纠正水和电解质平衡更有效。钠不建议过量摄入。接受锂预防治疗的患者在门诊接受治疗。中毒的预防取决于患者和临床医生之间的合作,并可能在大多数患者中使用较小的低风险剂量。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Clinical features and management of lithium poisoning.

Lithium salts, in particular the carbonate and citrate, were formerly in widespread use, forming part of alkaline salt mixtures which were used for treatment of the many disorders belonging to the uric acid diathesis. Among these disorders were mania, depression, acute mania, acute melancholia and periodic depression. Satisfactory prophylactic effects on periodic depression were directly claimed. Daily doses of 3 to 26 mmol of lithium were recommended as standards. Only slight or moderate symptoms of poisoning were reported in a very few cases during the period in question (1860 to 1930), when the popularity of these lithium-containing prophylactic drugs with a favourable therapeutic index was at its peak. Lithium intoxication was not a serious clinical problem until 1949 when Cade introduced his fortuitously effective, but nevertheless high, dosage regimen which was continued until signs of recovery from mania appeared. For the maintenance dose, Cade in principle recommended, but seldom adhered to, 17 mmol/day. Chronic lithium intoxication starts insidiously with silent affliction of the kidneys followed by 'prodromal' symptoms, and when moderate severity has been reached, an accelerating renal vicious circle with decreasing kidney function is imminent. After this point the chronic intoxication resembles acute intoxication. Active detoxification at this, or an earlier stage, leaves the patient with a good chance of recovery. At a later stage, with the occurrence of oliguria, semi-coma or coma, and latent convulsive movement, recovery is less certain. There is no specific antidote for the toxic effects of lithium. Haemodialysis is the most effective treatment for acute lithium poisoning. For patients with impaired, or potentially impaired renal function, peritoneal dialysis may be an alternative, but less effective, treatment. Forced diuresis demands unimpaired renal function, and is little more effective than withdrawal of treatment, supplemented with correction of water and electrolyte balance. Sodium overloading is not recommended. Patients on lithium prophylaxis are treated on an outpatient basis. Prevention of intoxication depends on cooperation between patient and clinician, and possibly on the use of smaller, low risk dosages in most patients.

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