Department of Clinical Pharmacy and Outcomes Sciences, South Carolina College of Pharmacy, University of South Carolina , Columbia, SC , USA.
Clin Toxicol (Phila). 2014 Jun;52(5):525-30. doi: 10.3109/15563650.2014.913175. Epub 2014 May 5.
Although clinical use of dexmedetomidine (DEX), an alpha2-adrenergic receptor agonist, has increased, its role in patients admitted to intensive care units secondary to toxicological sequelae has not been well established.
The primary objective of this study was to describe clinical and adverse effects observed in poisoned patients receiving DEX for sedation.
This was an observational case series with retrospective chart review of poisoned patients who received DEX for sedation at an academic medical center. The primary endpoint was incidence of adverse effects of DEX therapy including bradycardia, hypotension, seizures, and arrhythmias. For comparison, vital signs were collected hourly for the 5 h preceding the DEX therapy and every hour during DEX therapy until the therapy ended. Additional endpoints included therapy duration; time within target Richmond Agitation Sedation Score (RASS); and concomitant sedation, analgesia, and vasopressor requirements.
Twenty-two patients were included. Median initial and median DEX infusion rates were similar to the commonly used rates for sedation. Median heart rate was lower during the therapy (82 vs. 93 beats/minute, p < 0.05). Median systolic blood pressure before and during therapy was similar (111 vs. 109 mmHg, p = 0.745). Five patients experienced an adverse effect per study definitions during therapy. No additional adverse effects were noted. Median time within target RASS and duration of therapy was 6.5 and 44.5 h, respectively. Seventeen patients (77%) had concomitant use of other sedation and/or analgesia with four (23%) of these patients requiring additional agents after DEX initiation. Seven patients (32%) had concomitant vasopressor support with four (57%) of these patients requiring vasopressor support after DEX initiation.
Common adverse effects of DEX were noted in this study. The requirement for vasopressor support during therapy warrants further investigation into the safety of DEX in poisoned patients. Larger, comparative studies need to be performed before the use of DEX can be routinely recommended in poisoned patients.
尽管临床应用右美托咪定（DEX）作为一种α2-肾上腺素能受体激动剂有所增加，但它在因中毒后遗症而入住重症监护病房的患者中的作用尚未得到充分确立。
本研究的主要目的是描述接受 DEX 镇静治疗的中毒患者的临床和不良事件。
这是一项观察性病例系列研究，回顾性分析了在学术医疗中心接受 DEX 镇静治疗的中毒患者的病历。主要终点是 DEX 治疗的不良事件发生率，包括心动过缓、低血压、癫痫发作和心律失常。为了比较，在开始 DEX 治疗前的 5 小时内和 DEX 治疗期间每小时收集生命体征，直到治疗结束。其他终点包括治疗持续时间；目标 Richmond 镇静躁动评分（RASS）范围内的时间；以及同时需要镇静、镇痛和血管加压药。
共纳入 22 例患者。初始和 DEX 输注中位数率与常用镇静治疗率相似。治疗期间的中位数心率较低（82 比 93 次/分钟，p < 0.05）。治疗前后的中位数收缩压相似（111 比 109 mmHg，p = 0.745）。根据研究定义，5 例患者在治疗期间出现不良事件。没有发现其他不良事件。中位数目标 RASS 内时间和治疗持续时间分别为 6.5 和 44.5 小时。17 例（77%）患者同时使用其他镇静和/或镇痛药物，其中 4 例（23%）在开始 DEX 后需要额外的药物。7 例（32%）患者同时需要血管加压药支持，其中 4 例（57%）在开始 DEX 后需要血管加压药支持。
本研究中观察到 DEX 的常见不良事件。治疗期间需要血管加压药支持，这需要进一步研究 DEX 在中毒患者中的安全性。在 DEX 可常规推荐用于中毒患者之前，需要进行更大规模的、对照研究。
