Fluid Intake Related to Brain Edema in Acute Middle Cerebral Artery Infarction

Abstract

Evidence of the appropriate amount of fluid intake during the first few days after acute stroke was scarce. Concerns were raised in patients with acute malignant middle cerebral infarction, who tended to have malignant brain edema later. The purpose of the study was to evaluate the effect of fluid intake on the occurrence of malignant brain edema in patients with acute middle cerebral artery infarction. Patients with acute middle cerebral artery infarction who had National Institute of Health Stroke Scale (NIHSS) score of at least 15 were included. Baseline characteristics and amount of fluid intake during the first few days were compared in patients with and without malignant brain edema. One hundred ninety-three patients were studied. Mean NIHSS score was 20. Malignant brain edema occurred in 69 patients (36%). Higher amount of fluid intake (>1650 ml or >28 ml/kg/day or >93% of daily maintenance fluid) showed a significant association with malignant brain edema (OR = 13.86, 95% CI 5.11-37.60, p value <0.001). Decompressive surgery was performed in 35 patients (18%). With mean follow-up of 12 months, 49 patients (49/184, 27%) had favorable outcomes (modified Rankin scale (mRS) 0-2) at final follow-up. Seventy-nine patients (79/184, 43%) died. In the subgroup of patients with malignant brain edema, 39 patients (39/65, 60%) died and only 11% (7/65 patients) had favorable outcome. High amount of fluid intake in the first few days of acute middle cerebral infarction was related to the occurrence of malignant brain edema.

Mitochondrial dysfunction in neurological disorders: Exploring mitochondrial transplantation

“…The reduction of ATP triggers ischemic cascades such as membrane ion pump failure, plasma membrane depolarization and efflux of cellular potassium, influx of sodium, calcium, chloride, and water 48 . All of these factors lead to opening of mPTP, liberation of cytochrome c, activation of caspase 3 and consequently, execution of apoptotic death 49 .…”

Blood-brain barrier dysfunction and recovery after ischemic stroke

“…Ischemic insults can rapidly induce cerebral edema, referring to the excess accumulation of fluid in the intracellular (cytotoxic edema) or extracellular (vasogenic edema) spaces in the brain. Stepwise development of cerebral edema occurs after ischemia, with cytotoxic edema occurring minutes after ischemia onset followed by a relatively late onset of vasogenic edema, the latter in particular related to BBB breakdown (Dharmasaroja, 2016; Stokum et al, 2016). BBB disruption can permit a large inflow of hematogenous fluid into the extravascular space, leading to progressive elevation of brain water content and tissue swelling (Dharmasaroja, 2016; Rosenberg, 1999; Stokum et al, 2016).…”

“…Stepwise development of cerebral edema occurs after ischemia, with cytotoxic edema occurring minutes after ischemia onset followed by a relatively late onset of vasogenic edema, the latter in particular related to BBB breakdown (Dharmasaroja, 2016; Stokum et al, 2016). BBB disruption can permit a large inflow of hematogenous fluid into the extravascular space, leading to progressive elevation of brain water content and tissue swelling (Dharmasaroja, 2016; Rosenberg, 1999; Stokum et al, 2016). In patients with acute ischemic stroke, BBB disruption identified by magnetic resonance imaging (MRI) during the first 3 hours after symptom onset is associated with the development of vasogenic edema (Giraud et al, 2015).…”

Mitochondria in Ischemic Stroke: New Insight and Implications

“…Compared to other brain cells, neurons have higher energy demand, but their energy reserves are limited. Depletion of ATP is one of the major initiator, which triggers the ischemic cascades such as, membrane ion pump failure, efflux of cellular potassium, influx of sodium, chloride and water, and membrane depolarization [ 12 - 14 ]. Multiple mechanisms, including excitotoxicity, mitochondrial response, free radical release, acidotoxity, protein misfolding, and inflammation have been extensively studied as the events leading to the cellular death and neuronal loss after stroke [ 15 - 17 ], which are depicted in Fig.…”