Masullo Lawrence N, Miller Michael A, Baker S David, Bose Sudip, Levsky Marc
Darnall Army Community Hospital, Ft Hood, TX 76544, USA.
Clin Toxicol (Phila). 2006;44(2):165-8. doi: 10.1080/15563650500514525.
Despite the frequency of use of citalopram, its clinical effects and pharmacokinetics in overdose in the pediatric patient are not well described. We describe the clinical course and drug levels following the ingestion of citalopram by a 10-month-old female.
A 10 month-old female ingested an unknown amount of citalopram. Approximately 40 min after ingestion, the child developed horizontal nystagmus, followed by a generalized, tonic-clonic seizure that lasted 2 to 3 min very shortly thereafter. The child received 1 mg of midazolam intramuscularly (IM), followed by 1 mg of midazolam intravenously (IV) for termination of this seizure, and was given a loading dose of 20 mg/kg of fosphenytoin IV. Elective orotracheal intubation was done to protect the airway. Despite the use of midazolam and fosphenytoin, the child had another seizure approximately 85 min following the ingestion. A third seizure was noted at approximately 100 min post-ingestion. In the course of treatment, activated charcoal was administered via nasogastric tube, and IV midazolam and phenobarbital were given. The child was transferred to a nearby facility with pediatric intensive care capabilities in stable condition. The child did not experience any hypotension or dysrhythmia, and the electrocardiographic QTc and QRS complex were normal throughout the clinical course. During the subsequent 48 h, the child awoke and regained normal function. This child's recovery was uneventful, and the child was discharged home without sequelae. Plasma levels of citalopram were 1400 ng/ml, 583 ng/ml, 416 ng/ml, and 296 ng/ml, at one, six, 13, and 23 h post-ingestion, respectively. The first level likely represents a predistributional level with subsequent levels giving an elimination t1/2 of 17.38 h.
We report a case of citalopram poisoning in a 10-month-old infant with refractory seizures, and an absence of cardiovascular events with subsequent excellent outcome. The elimination of the parent drug corresponds to an approximate t1/2 of 15-20 h in this single case.
尽管西酞普兰使用频繁，但其在儿科患者过量用药时的临床效果及药代动力学情况尚未得到充分描述。我们描述了一名10个月大女性摄入西酞普兰后的临床过程及药物水平。
一名10个月大的女性摄入了未知量的西酞普兰。摄入后约40分钟，患儿出现水平眼球震颤，随后很快发生了持续2至3分钟的全身性强直阵挛性惊厥。患儿肌肉注射（IM）1毫克咪达唑仑，随后静脉注射（IV）1毫克咪达唑仑以终止惊厥，并静脉给予20毫克/千克的磷苯妥英负荷剂量。进行了选择性气管插管以保护气道。尽管使用了咪达唑仑和磷苯妥英，患儿在摄入后约85分钟又发生了一次惊厥。在摄入后约100分钟观察到第三次惊厥。在治疗过程中，通过鼻胃管给予活性炭，并静脉注射咪达唑仑和苯巴比妥。患儿被转移到附近具备儿科重症监护能力的机构，情况稳定。患儿未出现任何低血压或心律失常，在整个临床过程中心电图QTc和QRS波群均正常。在随后的48小时内，患儿苏醒并恢复了正常功能。该患儿恢复顺利，出院时无后遗症。摄入西酞普兰后1小时、6小时、13小时和23小时的血浆水平分别为1400纳克/毫升、583纳克/毫升、416纳克/毫升和296纳克/毫升。第一个水平可能代表分布前水平，随后的水平给出的消除半衰期为17.38小时。
我们报告了一例10个月大婴儿西酞普兰中毒的病例，该患儿惊厥难治，但未发生心血管事件，随后预后良好。在这一单一病例中，母体药物的消除半衰期约为15 - 20小时。
