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17 Αυγ 2022 · Subclinical cerebral edema, as detected by ventricular narrowing on imaging studies or alterations in brain water distribution on magnetic resonance imaging (MRI), has been reported in the majority of children with DKA, even in the absence of neurologic signs or symptoms (image 1) [6,15,16].
This review critically examines the literature on the pathophysiology of CE and attempts to categorize the findings by types of brain injury that contribute to its development: cytotoxic, vasogenic, and osmotic. Utilizing this scheme, we propose a multifactorial pathway for the development of CE in patients with DKA.
1 Φεβ 2000 · The case for a multifactorial cause of cerebral edema in DKA. Mild edema and other histopathology exists before treatment. Rare reports of symptomatic cerebral edema presenting before any possible influence of therapy on the brain. Inconsistent correlations of cerebral edema with serum. Osmolality. Sodium concentration. Acid base status.
The purpose of this study was to investigate the pathophysiology of DKA-related cerebral edema through the use of diffusion and perfusion MRI.
This review critically examines the literature on the pathophysiology of CE and attempts to categorize the findings by types of brain injury that contribute to its development: cytotoxic, vasogenic, and osmotic.
cerebral edema, as detected by subtle brain computed tomography (CT) or magnetic resonance imaging (MRI) changes, can occur in as much of 50% of DKA patients. Hence, early identification of clinically relevant cerebral edema in DKA relies on clinical criteria rather than solely on radiological tests [5]. Clinical identification of
Fourth, data suggest that the predominant pathophysiology early after initial cerebral injury (broadly defined) is cerebral ischemia, followed in the subacute stages by a more vasogenic process. Finally, impaired cerebral autoregulation is documented in both TBI and DKA, either reflecting the disease severity or playing a role in the ...
