Abstract
We read with interest the study by Volbers et al.,1 who found that perihemorrhagic edema (PHE) independently predicted functional outcome after acute intracerebral hemorrhage (ICH) and was associated with inflammatory markers and hematoma expansion. Cerebral edema formation has a multifactorial etiology with time-dependent contributing factors like increased hydrostatic pressure, transcapillary efflux of electrolytes and fluids, clot retraction, thrombin production, inflammatory activation, erythrocyte lysis, iron deposition, and hemoglobin-induced neurotoxicity. Sudden blood pressure (BP) increases may promote arterial bleeding and hematoma growth; BP rises and falls may contribute to disruption of the blood–brain barrier and enhance vasogenic edema. Excessive BP fluctuations may lead to further cell injury and amplify the secondary brain damage by affecting blood flow and brain perfusion in the area of impaired cerebral autoregulation surrounding the hematoma.
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