右美托咪定诱导的多尿是肾发生机制的基础。病例报告。

L. Vaz Rodrigues , D. Roriz , F. Salgado-Seixas , S. Marinho , P.R. Ferreira
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引用次数: 0

摘要

右美托咪定的α-肾上腺素受体激动剂作为一种镇静、催眠和镇痛剂在麻醉室越来越受欢迎,随着围手术期的广泛使用,人们越来越担心副作用。心动过缓和低血压是常见的不良反应,但也有一些报告称尿量过多,可能是由于血管加压素分泌和收集管的通透性。多尿症通常会随着停药而消退,并且尚未报告显著的发病率。为了最大限度地减少并发症(主要是钠血症和神经系统症状),必须尽早识别、清除药物并进行治疗。本病例报告描述了一例右美托咪定相关的多尿综合征,该综合征是在无阿片类药物全身麻醉下进行头颈部大手术时发生的。提出了临床效果的肾发生机制,并通过获得的分析数据得到了加强。术中多尿的方法也被描绘出来。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
A nephrogenic mechanism underlies dexmedetomidine-induced polyuria. A case report

Dexmedetomidine’s α-adrenoreceptor agonism has been gaining popularity in the anesthetic room as a sedative-hypnotic and analgesic agent, and with extensive perioperative use rising concern about side effects is necessary.

Bradycardia and hypotension are common adverse effects, but there are also several reports of excessive urine output, possibly due to vasopressin secretion and permeability of collecting ducts.

Polyuria usually resolves with discontinuation of the drug, and significant morbidity has not been reported. Early identification, removal of the agent, and treatment are imperative to minimize complications - mainly natremia and neurological symptoms.

This case report describes a dexmedetomidine-related polyuric syndrome during opioid-free general anesthesia for major head and neck surgery. A nephrogenic mechanism for the clinical effect is proposed and reinforced by analytical data obtained. An intra-operative polyuria approach is also delineated.

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