a Department of Medicine , VUMC , Nashville , TN , USA.
b Tennessee Poison Center , Nashville , TN , USA.
Clin Toxicol (Phila). 2018 Oct;56(10):873-879. doi: 10.1080/15563650.2018.1450986. Epub 2018 Mar 16.
Following clonidine ingestion, naloxone is seldom administered as it is considered ineffective in reversing somnolence, bradycardia, or hypotension. However, this conclusion has been based on administration of small doses (2 mg or less) of naloxone. The somnolence is frequently treated with endotracheal intubation (ETI), a procedure with significant morbidity.
We aimed to determine if naloxone administration reversed the effects of clonidine or caused any adverse effects.
We performed a retrospective descriptive cohort (IRB approved) of hospital medical records for pediatric patients (6 months-16 years) with clonidine exposure. Demographics, history, co-ingestants, clinical data, treatments, and outcome were recorded in a de-identified database.
The most common clinical findings in the 52 patients were sedation (n = 51), bradycardia (n = 44), and hypotension (n = 11). Of 51 somnolent patients, naloxone administration awoke 40 patients, five of which had co-ingestants. Nine patients experienced recurrent sedation that resolved with a repeat bolus of naloxone. Twenty somnolent bradycardic patients (11 less than 3 years old) received 10 mg naloxone via intravenous bolus. Thirteen awoke; bradycardia persisted in six of the awake patients. Of the remaining 31 patients, 22 awoke following 6 mg or less of naloxone. Naloxone reversed hypotension in 7 of 11 hypotensive patients. Only one hypotensive patient (with a coingestion) received vasopressors for hypotension. Three awake normotensive patients received vasopressors for bradycardia. Seven patients awoke and had normal vital signs following naloxone administration, but were chemically sedated and intubated for transport. There were no adverse events following the administration of any dose of naloxone.
Administration of naloxone to somnolent pediatric patients with clonidine toxicity awoke the majority (40/51) and resolved bradycardia and hypotension in some. Persistent bradycardia was benign. Hypotension was rare and clinically insignificant. No adverse effects occurred in any patient including the 21 patients who received 10 mg naloxone. Morbidity in this overdose may be due to ETI, a procedure that could be prevented if high-dose naloxone (10 mg) were administered. Administration of high-dose naloxone should be considered in all children with clonidine toxicity.
氯氮平摄入后，很少给予纳洛酮，因为它被认为不能有效逆转嗜睡、心动过缓和低血压。然而，这一结论是基于小剂量（2 毫克或更少）纳洛酮的给药。嗜睡通常通过气管插管（ETI）治疗，这一过程有显著的发病率。
我们旨在确定纳洛酮的给药是否能逆转氯氮平的作用或引起任何不良反应。
我们对接受氯氮平暴露的儿科患者（6 个月至 16 岁）进行了一项回顾性描述性队列研究（IRB 批准）。记录了人口统计学、病史、共服者、临床数据、治疗和结果，并在一个去识别数据库中。
52 名患者中最常见的临床发现是镇静（n=51）、心动过缓（n=44）和低血压（n=11）。在 51 名嗜睡的患者中，纳洛酮给药唤醒了 40 名患者，其中 5 名有共服者。9 名患者出现复发性镇静，重复给予纳洛酮可缓解。20 名嗜睡性心动过缓的患者（11 名小于 3 岁）接受了 10mg 纳洛酮静脉推注。13 名患者苏醒；6 名清醒患者的心动过缓持续存在。在其余 31 名患者中，22 名患者在给予 6mg 或更少的纳洛酮后苏醒。纳洛酮逆转了 11 名低血压患者中的 7 名患者的低血压。只有一名低血压患者（共服者）因低血压接受了升压治疗。3 名清醒的正常血压患者因心动过缓接受了升压治疗。7 名患者在给予纳洛酮后苏醒，生命体征正常，但因转运需要进行化学镇静和插管。给予任何剂量的纳洛酮后均未发生不良反应。
给予氯氮平毒性嗜睡的儿科患者纳洛酮可使大多数（40/51）患者苏醒，并在某些患者中缓解心动过缓和低血压。持续的心动过缓是良性的。低血压很少见，且无临床意义。没有任何不良反应发生在任何患者中，包括 21 名接受 10mg 纳洛酮的患者。这种药物过量的发病率可能是由于 ETI 引起的，如果给予高剂量纳洛酮（10mg），则可预防该并发症。在所有氯氮平中毒的儿童中，都应考虑给予高剂量纳洛酮。
