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[重症监护患者的继发性神经肌肉缺陷]

[Secondary neuromuscular deficiencies in critical care patients].

作者信息

Souron V, Chollet S, Ordronneau J R, Chailleux E

机构信息

Département d'Anesthésie-Réanimation chirurgicale, Hôpital de Bicêtre, Le Kremlin-Bicêtre.

出版信息

Ann Fr Anesth Reanim. 1995;14(2):213-7.

PMID:7486279
Abstract

The authors report three cases of neuromuscular deficits occurring after a variable time of mechanical ventilation in ICU patients suffering from acute respiratory failure requiring sedation and neuromuscular blockade by pancuronium bromide. The clinical features of these deficits were similar : flaccid quadriparesia slowly reversible without sensory loss and difficult weaning from ventilation for two patients. The paraclinical investigations (measurements of creatine kinase, electrophysiological examination) permitted to distinguish two diseases: critical illness polyneuropathy (in patient with ARDS) and acute myopathy (in other patients with severe asthma) caused by corticosteroids and potentiated by neuromuscular blocking agents. This myopathy differs from the chronic myopathy caused by long term corticotherapy. After a status asthmaticus treated with corticosteroids and mechanical ventilation under muscle relaxants, creatine kinases should be measured in plasma and a neurological examination be performed. The value of neuromuscular blockade monitoring for the prevention of this myopathy should be assessed.

摘要

作者报告了3例在重症监护病房(ICU)因急性呼吸衰竭需要镇静及使用潘库溴铵进行神经肌肉阻滞的患者,在机械通气不同时间后出现神经肌肉功能缺损的病例。这些缺损的临床特征相似:弛缓性四肢瘫,可缓慢恢复,无感觉丧失,两名患者脱机困难。辅助检查(肌酸激酶测定、电生理检查)有助于区分两种疾病:由皮质类固醇引起并因神经肌肉阻滞剂而加重的危重病性多发性神经病(ARDS患者)和急性肌病(其他重症哮喘患者)。这种肌病不同于长期皮质激素治疗引起的慢性肌病。在使用皮质类固醇和肌肉松弛剂进行机械通气治疗哮喘持续状态后,应检测血浆肌酸激酶并进行神经学检查。应评估神经肌肉阻滞监测对预防这种肌病的价值。

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