Department of Neurosurgery, University of Maryland School of Medicine, 22 S. Greene St., Suite S12D, Baltimore, MD, 21201-1595, USA.
Division of Neurocritical Care and Emergency Neurology, Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
Neurocrit Care. 2018 Jun;28(3):276-287. doi: 10.1007/s12028-017-0474-8.
We sought to review the role that cerebral edema plays in neurologic outcome following cardiac arrest, to understand whether cerebral edema might be an appropriate therapeutic target for neuroprotection in patients who survive cardiopulmonary resuscitation. Articles indexed in PubMed and written in English. Following cardiac arrest, cerebral edema is a cardinal feature of brain injury and is a powerful prognosticator of neurologic outcome. Like other conditions characterized by cerebral ischemia/reperfusion, neuroprotection after cardiac arrest has proven to be difficult to achieve. Neuroprotection after cardiac arrest generally has focused on protecting neurons, not the microvascular endothelium or blood-brain barrier. Limited preclinical data suggest that strategies to reduce cerebral edema may improve neurologic outcome. Ongoing research will be necessary to determine whether targeting cerebral edema will improve patient outcomes after cardiac arrest.
我们试图回顾脑水肿在心脏骤停后神经功能结果中的作用,以了解脑水肿是否可能成为心肺复苏后存活患者神经保护的合适治疗靶点。在 PubMed 中索引并以英文撰写的文章。心脏骤停后,脑水肿是脑损伤的主要特征,也是神经功能结果的有力预后指标。与其他以脑缺血/再灌注为特征的疾病一样,心脏骤停后的神经保护已被证明难以实现。心脏骤停后的神经保护通常侧重于保护神经元,而不是微血管内皮细胞或血脑屏障。有限的临床前数据表明,减少脑水肿的策略可能改善神经功能结果。需要进行正在进行的研究,以确定靶向脑水肿是否会改善心脏骤停后的患者预后。