Ayata Cenk, Ropper Allan H
Neurology Service, St. Elizabeth's Medical Center, Tufts University School of Medicine, Boston, MA 02135, USA.
J Clin Neurosci. 2002 Mar;9(2):113-24. doi: 10.1054/jocn.2001.1031.
Ischaemic brain oedema appears to involve two distinct processes, the relative contribution and time course of which depend on the duration and severity of ischaemia, and the presence of reperfusion. The first process involves an increase in tissue Na+ and water content accompanying increased pinocytosis and Na+, K+ ATPase activity across the endothelium. This is apparent during the early phase of infarction and before any structural damage is evident. This phenomenon is augmented by reperfusion. A second process results from a more indiscriminate and delayed BBB breakdown that is associated with infarction of both the parenchyma and the vasculature itself. Although, tissue Na+ level still seems to be the major osmotic force for oedema formation at this second stage, the extravasation of serum proteases is an additional potentially deleterious factor. The relative importance of protease action is not yet clear, however, degradation of the extracellular matrix conceivably leads to further BBB disruption and softening of the tissue, setting the stage for the most pronounced forms of brain swelling. A number of factors mediate or modulate ischaemic oedema formation, however, most current information comes from experimental models, and clinical data on this microcosmic level is lacking. Clinically significant brain oedema develops in a delayed fashion after large hemispheric strokes and is a cause of substantial mortality. Neurological signs appear to be at least as good as direct ICP measurement and neuroimaging in detecting and gauging the secondary damage produced by stroke oedema. The neuroimaging characteristics of the stroke, specifically the early involvement of greater than half of the MCA territory, are, however, highly predictive of the development of severe oedema over the subsequent hours and days. None of the available medical therapies provide substantial relief from the oedema and raised ICP, or at best, they are temporizing in most cases. Hemicraniectomy appears most promising as a method of avoiding death from brain compression, but the optimum timing and manner of patient selection are currently being investigated. All approaches to massive ischaemic brain swelling are clouded by the potential for survival with poor functional outcome. It is possible to manage blood pressure, serum osmolarity by way of selective fluid administration, and a number of other systemic factors that exaggerate brain oedema. Broad guidelines for treatment of stroke oedema can therefore be given at this time.
缺血性脑水肿似乎涉及两个不同的过程，其相对贡献和时间进程取决于缺血的持续时间和严重程度以及再灌注的情况。第一个过程涉及伴随跨内皮细胞胞饮作用增加和钠钾ATP酶活性增强而出现的组织钠和水含量增加。这在梗死早期且在任何结构损伤明显之前就很明显。再灌注会加剧这种现象。第二个过程是由于血脑屏障更广泛且延迟的破坏所致，这与实质和血管系统本身的梗死有关。尽管在第二阶段组织钠水平似乎仍是水肿形成的主要渗透驱动力，但血清蛋白酶的外渗是另一个潜在的有害因素。然而，蛋白酶作用的相对重要性尚不清楚，细胞外基质的降解可能导致血脑屏障进一步破坏和组织软化，为最明显的脑肿胀形式奠定基础。许多因素介导或调节缺血性水肿的形成，然而，目前的大多数信息来自实验模型，缺乏这一微观层面的临床数据。临床上显著的脑水肿在大面积半球性卒中后延迟出现，是导致大量死亡的原因。在检测和评估卒中水肿产生的继发性损伤方面，神经体征似乎至少与直接颅内压测量和神经影像学一样有效。然而，卒中的神经影像学特征，特别是大脑中动脉区域超过一半在早期受累，对随后数小时和数天内严重水肿的发展具有高度预测性。现有的任何药物治疗都不能显著减轻水肿和升高的颅内压，或者在大多数情况下充其量只是暂时缓解。颅骨切除术作为一种避免因脑受压而死亡的方法似乎最有前景，但目前正在研究最佳的手术时机和患者选择方式。所有针对大面积缺血性脑肿胀的治疗方法都因可能出现功能预后不良的存活情况而变得复杂。通过选择性补液来控制血压、血清渗透压以及许多其他会加重脑水肿的全身因素是可行的。因此，目前可以给出治疗卒中水肿的广泛指导原则。
