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27 Ιουν 2022 · This review aims to provide a brief overview of DKA from its pathophysiology to clinical presentation with in depth focus on up-to-date therapeutic management.
Symptomatic cerebral edema (CE) in pediatric patients with DKA is uncommon and is defined by diagnostic criteria, including abnormal motor or verbal responses to pain, decorticate posture, and abnormal neurogenic respiratory patterns.
Cerebral edema is described as occurring in DKA in 0.4 to nearly 5% of cases, due to referral bias and variable diagnostic criteria. Mortality in the context of cerebral edema is 21% with morbidity rates reported of 10-26%.
Cerebral edema is a condition where an excess of cerebral water accumulates due to primary neurological or non-neurological causes. Cerebral edema complicates many brain pathologies causing additional injury often in excess of the original neurological insult.
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
Diabetic ketoacidosis (DKA) is associated with a high mortality rate, especially if cerebral edema develops during the disease course. It is rarer and more severe in adults than in children. We present cases of two patients with cerebral edema‐related DKA.
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 ...
