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危重病性多发性神经病和肌病:导致肌肉无力和瘫痪的主要原因。

Critical illness polyneuropathy and myopathy: a major cause of muscle weakness and paralysis.

机构信息

Department of Anaesthesia, Intensive Care, and Perioperative Medicine, Division of Neuroanaesthesia and Neurocritical Care, University of Brescia, Spedali Civili, Brescia, Italy.

出版信息

Lancet Neurol. 2011 Oct;10(10):931-41. doi: 10.1016/S1474-4422(11)70178-8.

DOI:10.1016/S1474-4422(11)70178-8
PMID:21939902
Abstract

Critical illness polyneuropathy (CIP) and myopathy (CIM) are complications of critical illness that present with muscle weakness and failure to wean from the ventilator. In addition to prolonging mechanical ventilation and hospitalisation, CIP and CIM increase hospital mortality in patients who are critically ill and cause chronic disability in survivors of critical illness. Structural changes associated with CIP and CIM include axonal nerve degeneration, muscle myosin loss, and muscle necrosis. Functional changes can cause electrical inexcitability of nerves and muscles with reversible muscle weakness. Microvascular changes and cytopathic hypoxia might disrupt energy supply and use. An acquired sodium channelopathy causing reduced muscle membrane and nerve excitability is a possible unifying mechanism underlying CIP and CIM. The diagnosis of CIP, CIM, or combined CIP and CIM relies on clinical, electrophysiological, and muscle biopsy investigations. Control of hyperglycaemia might reduce the severity of these complications of critical illness, and early rehabilitation in the intensive care unit might improve the functional recovery and independence of patients.

摘要

危重病性多发性神经病(CIP)和肌病(CIM)是危重病的并发症,表现为肌肉无力和无法脱离呼吸机。除了延长机械通气和住院时间外,CIP 和 CIM 还会增加危重病患者的住院死亡率,并导致危重病幸存者出现慢性残疾。与 CIP 和 CIM 相关的结构变化包括轴突神经变性、肌肉肌球蛋白丧失和肌肉坏死。功能变化可导致神经和肌肉的电兴奋性丧失,出现可逆转的肌肉无力。微血管变化和细胞缺氧可能会破坏能量供应和利用。获得性钠通道病导致肌肉膜和神经兴奋性降低,可能是 CIP 和 CIM 的一种潜在统一机制。CIP、CIM 或两者合并的诊断依赖于临床、电生理和肌肉活检检查。控制高血糖可能会降低这些危重病并发症的严重程度,而重症监护病房的早期康复可能会改善患者的功能恢复和独立性。

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