Cerebral edema is the most feared complication of DKA in children. Clinically apparent cerebral edema occurs in 1% of childhood DKA. One third to one half of children who develop cerebral edema as a consequence of DKA die and another one-third suffer severe permanent neurologic disability. It is unclear if asymptomatic or subclinical cerebral edema occurs commonly in pediatric DKA or if it is present prior to the initiation of treatment. Cerebral edema is more commonly seen in children presenting with severe DKA, a new onset type 1 diabetic, younger age, and a child with longer duration of symptoms prior to treatment.

A number of possible mechanisms may contribute to cerebral edema in DKA. There is uncertainty about whether the pathophysiology is a result of vasogenic edema or cytotoxic edema. Some studies have suggested that cerebral hypoperfusion and subsequent reperfusion may play a role in the pathogenesis of cerebral edema. It is thought the reperfusion, in addition to the breakdown of the blood–brain barrier endothelium, causes vasodilatation and vasogenic edema. Other studies have proposed the edema formation is due to cytotoxic edema from increased brain osmolality where, in a chronic hyperosmolar state due to hyperglycemia, cerebral cells compete with the osmotic force of serum by storing intracellular osmoles.