Darrouj Jamil, Puri Nitin, Prince Erin, Lomonaco Anthony, Spevetz Antoinette, Gerber David R
Pulmonary and Critical Care Medicine Division, Cooper University Hospital, Camden, NJ, USA.
Ann Pharmacother. 2008 Nov;42(11):1703-5. doi: 10.1345/aph.1K678. Epub 2008 Sep 9.
To report a case of alcohol withdrawal and delirium tremens successfully treated with adjunctive dexmedetomidine.
A 30-year-old man with a history of alcohol abuse was admitted to the general medical unit because of altered mental status and agitation. He was initially treated for alcohol withdrawal with benzodiazepines; his condition then deteriorated and he was transferred to the intensive care unit. Because of the patient's poor response to benzodiazepines (oxazepam and lorazepam, with midazolam the last one used), intravenous dexmedetomidine was started at an initial dose of 0.2 microg/kg/h and titrated to 0.7 microg/kg/h to the patient's comfort. Midazolam was subsequently tapered to discontinuation due to excessive sedation. In the intensive care unit, the patient's symptoms remained controlled with use of dexmedetomidine alone. He remained in the intensive care unit for 40 hours; dexmedetomidine was then tapered to discontinuation and the patient was transferred back to the general medical unit on oral oxazepam and thiamine, which had been started in the emergency department. He was discharged after 5 days.
A review of the PubMed database (1989-2007) failed to identify any other instances of dexmedetomidine having been used as the principal agent to treat alcohol withdrawal. The use of sedative to treat delirium tremens is well documented, with benzodiazepines being the agents of choice. The clinical utility of benzodiazepines is limited by their stimulation of the gamma-aminobutyric acid receptors, an effect not shared by dexmedetomidine, a central alpha(2)-receptor agonist that induces a state of cooperative sedation and does not suppress respiratory drive.
In patients with delirium tremens, dexmedetomidine should be considered as an option for primary treatment. This case illustrates the need for further studies to investigate other potential uses for dexmedetomidine.
报告1例成功使用右美托咪定辅助治疗酒精戒断和震颤谵妄的病例。
一名有酒精滥用史的30岁男性因精神状态改变和烦躁不安入住普通内科病房。他最初接受苯二氮䓬类药物治疗酒精戒断；随后病情恶化，被转入重症监护病房。由于患者对苯二氮䓬类药物（奥沙西泮和劳拉西泮，最后使用的是咪达唑仑）反应不佳，开始静脉输注右美托咪定，初始剂量为0.2微克/千克/小时，并根据患者舒适度滴定至0.7微克/千克/小时。随后由于过度镇静，咪达唑仑逐渐减量至停用。在重症监护病房，仅使用右美托咪定就能控制患者症状。他在重症监护病房住了40小时；然后右美托咪定逐渐减量至停用，患者转回普通内科病房，口服在急诊科就已开始使用的奥沙西泮和硫胺素。5天后他出院。
检索PubMed数据库（1989 - 2007年）未发现右美托咪定被用作治疗酒精戒断主要药物的其他病例。使用镇静剂治疗震颤谵妄已有充分记录，苯二氮䓬类药物是首选药物。苯二氮䓬类药物的临床效用受其对γ-氨基丁酸受体的刺激作用限制，而右美托咪定不具有这种作用，右美托咪定是一种中枢α2受体激动剂，可诱导协同镇静状态且不抑制呼吸驱动。
对于震颤谵妄患者，应考虑将右美托咪定作为主要治疗选择。本病例说明需要进一步研究以探究右美托咪定的其他潜在用途。
