Hydrostatic brain edema: basic mechanisms and clinical aspect

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Abstract
The term hydrostatic brain edema results from unfavorable hydrtostatic pressure gradiernts between blood vessels and brain tissue. Arterial hypertension combined with decompressive craniectomy produces extensive brain edema in the arterial boundary zone of the decompressive area. The increased hydrostatic pressure gradient enhances tissue damage and causes the biphasic opening of the blood-brain barrier (BBB). The hydrostatic pressure alone is capable of causing the initial BBB opening and this induced edema results in derangement of cerebral microcirculation and metabolism. With morphological opening and metabolic damage of the vascular wall, the second BBB opening is elicited by the amplified hydrostatic pressure gradient, which is similar to that in vasogenic edema. In the clinical aspect, the beneficial effect of decompressive craniectomy in the treatment of uncontrollable ICP and brain edema remains controversial. External decompression may have adverse effects on severe brain edema and swelling. In this regards, control of driving force for the formation of brain edema could be the treatment of choice as an initial step. In addition, recent reports provided by MR imaging indicated new information on the pathophysiological features of the patients with acute hypertension. In the patients with hypertension due to reversible posterior leucoencephalopathy (RPL) syndrome, MR images show reversible signal abnormalities in the bilateral occipital lobes, suggesting hydrostatic brain edema.