Lagerkranser M, Pehrsson K, Sylvén C
Acta Med Scand. 1982;212(4):267-71.
Five cases of neurogenic pulmonary oedema (NPE) are described. The causes were mechanical trauma to the skull, subarachnoid haemorrhage and epileptic seizure. In every case a frank pulmonary oedema was diagnosed that resolved within a few days. Treatment of the underlying disease resulted in a favourable outcome. The literature has been reviewed. The basic mechanism seems to be an increased intracranial pressure (ICP) precipitating an increased central sympathetic nerve activity mediated via peripheral alpha- or beta-adrenergic discharge. NPE results from a predominant alpha-receptor stimulation with massive increase in pre- and afterload. The major therapeutic efforts should be directed towards the underlying cause and, in addition, mechanical ventilation with passive hyperventilation is vital. High positive end-expiratory pressure should not be used without strict monitoring of ICP.
本文描述了5例神经源性肺水肿（NPE）病例。病因包括颅骨机械性创伤、蛛网膜下腔出血和癫痫发作。每例均诊断为明显的肺水肿，且在数天内消退。对基础疾病的治疗取得了良好效果。本文对相关文献进行了综述。其基本机制似乎是颅内压（ICP）升高，通过外周α或β肾上腺素能释放介导，促使中枢交感神经活动增强。NPE是由主要的α受体刺激导致前负荷和后负荷大量增加所致。主要治疗措施应针对基础病因，此外，机械通气及被动过度通气至关重要。在未严格监测ICP的情况下，不应使用高呼气末正压。
