P 587. Osmotic Myelinolysis—A Rare but Severe Complication of Diabetic Ketoacidosis

Background: Diabetes mellitus type I in childhood often manifests in the form of ketoacidosis. Most often, no severe consequences arise.

Goal: We report on a 9-year-old boy, who, at the time of the initial diagnosis, presented with severe ketoacidosis (pH 6.87, BE-33). After admission, his clinical condition worsened rapidly, he developed anisocoria. A magnetic resonance imaging confirmed cerebral edema with loss of reserve spaces. Bithalamic diffusion restriction was present, indicating osmotic myelinolysis. After metabolic recompensation, the patient remained altered for quite a long time, and he also had severely compromised motor function. Despite comprehensive early neurorehabilitation, severe residual deficits persist after 3 months, particularly dysarthria, and a severe movement disorder, making a wheelchair indispensable.

Results: The pathophysiologic mechanisms that promote the occurrence of cerebral edema in ketoacidosis are not sufficiently understood. Excessive rehydration, early bicarbonate administration, a rapid decrease in plasma osmolality, and cerebral hypoxia are considered as potential contributing factors. Osmotic myelinolysis is a rare but disastrous complication that probably reflects the duration and severity of metabolic decompensation. In the presented case, the first clinical changes probably occurred several hours to days before therapy were started, which speaks for a protracted course.

Conclusion: Early recognition and therapy of ketoacidosis are essential elements for a favorable outcome.