Патофизиологические механизмы отека головного мозга при диабетическом кетоацидозе в детской практике

Abstract

Diabetic ketoacidosis is a frequent complication of type 1 diabetes mellitus in children and adolescents. One of the leading causes of death in this pathology is cerebral edema. This complication is often asymptomatic, which makes it difficult to diagnose. The main risk factors for cerebral edema in children include the true factors (low partial pressure of carbon dioxide, high blood urea nitrogen, concomitant psychiatric pathology, etc.) and iatrogenic factors (large volume of infusion therapy, rapid decrease in blood glucose levels, administration of bicarbonate, etc.). The pathophysiology of this complication is not yet fully understood. The main pathophysiological elements of cerebral edema in children with DKA include the disruption of blood-brain barrier permeability, edema of brain cells, and dysfunction of cell membranes. Important roles are also played by hypercapnia and reduction of osmotic pressure. Based on the character of pathophysiologic changes, cerebral edema in children and adolescents with DKA is subdivided into vasogenic and cytotoxic. Gaining a better understanding of the pathophysiological mechanisms of this complication will increase the quality of care provided in pediatric practice.