Ischaemic brain oedema.

摘要: Abstract Ischaemic brain oedema appears to involve two distinct processes, the relative contribution and time course of which depend on duration severity ischaemia, presence reperfusion. The first process involves an increase in tissue Na+ water content accompanying increased pinocytosis Na+, K+ ATPase activity across endothelium. This is apparent during early phase infarction before any structural damage evident. phenomenon augmented by A second results from a more indiscriminate delayed BBB breakdown that associated with both parenchyma vasculature itself. Although, level still seems be major osmotic force for formation at this stage, extravasation serum proteases additional potentially deleterious factor. importance protease action not yet clear, however, degradation extracellular matrix conceivably leads further disruption softening tissue, setting stage most pronounced forms swelling. number factors mediate or modulate ischaemic formation, current information comes experimental models, clinical data microcosmic lacking. Clinically significant develops fashion after large hemispheric strokes cause substantial mortality. Neurological signs appear least as good direct ICP measurement neuroimaging detecting gauging secondary produced stroke oedema. characteristics stroke, specifically involvement greater than half MCA territory, are, highly predictive development severe over subsequent hours days. None available medical therapies provide relief raised ICP, best, they are temporizing cases. Hemicraniectomy promising method avoiding death compression, but optimum timing manner patient selection currently being investigated. All approaches massive swelling clouded potential survival poor functional outcome. It possible manage blood pressure, osmolarity way selective fluid administration, other systemic exaggerate Broad guidelines treatment can therefore given time.