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[神经源性肺水肿:脑膜出血的并发症——4例报告]

[Neurogenic pulmonary edema, complication of meningeal hemorrhage: report of 4 cases].

作者信息

Jourdan C, Artru F, Convert J, Mottolese C, Poirot I, Lamy B, Deschamps J, Chiara Y

出版信息

Agressologie. 1990 Jun;31(6):395-403.

PMID:2285114
Abstract

Neurogenic pulmonary edema (NPE) observed in 4 patients admitted in Neurosurgical Intensive Care au SAH by ruptured a vascular malformation. This complication is unusual (1.9%) and has been observed in comatose patients. For 3 patients, NEP resorption was rapid, from 12 to 72 hours with a treatment by CCPV with a P.E.E.P. and with restoring the hemodynamical parameter. The drug must be discussed according to eventual deleterous side effects on cardiac output and systemic resistances. The early hemodynamical study argues for an essentially hemodynamical mechanism due to the brutal symphatic discharge created by cerebral lesions and increasing. ICP, more than a toxic lesionnal edema, as the Weidner's study shows it in ultrastructural analysis of sheep lungs.

摘要

在神经外科重症监护病房收治的4例因血管畸形破裂导致蛛网膜下腔出血(SAH)的患者中观察到神经源性肺水肿(NPE)。这种并发症并不常见(1.9%),且在昏迷患者中观察到。对于3例患者,通过持续气道正压通气(CCPV)加呼气末正压通气(P.E.E.P.)治疗并恢复血流动力学参数后,神经源性肺水肿在12至72小时内迅速吸收。必须根据对心输出量和全身阻力可能产生的有害副作用来讨论用药。早期血流动力学研究表明,由于脑损伤导致的交感神经突然放电以及颅内压升高,主要是血流动力学机制起作用,而不是像魏德纳在绵羊肺超微结构分析中所显示的毒性损伤性水肿。

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