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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Acute hyponatremia caused by water intoxication can lead to cerebral edema and neurological manifestations such as impaired consciousness and seizures. While this association is well known, few reports have documented the chronological improvement of cerebral edema using sequential neuroimaging. Here, we present a case of acute water intoxication in which serial head computed tomography (CT) images clearly demonstrated the development and resolution of cerebral edema in parallel with changes in serum sodium concentration.
A 61-year-old woman with schizophrenia developed acute water intoxication following excessive water intake. Baseline head CT taken six months earlier had shown no abnormalities. On presentation, her level of consciousness was reduced, and initial head CT revealed diffuse cerebral edema. Laboratory tests demonstrated severe hyponatremia (serum sodium 116 mEq/L). A conservative management approach was selected based on the presumed acute onset. Her serum sodium level and clinical status were monitored closely, and follow-up head CT was performed the next day.
Within one day, her serum sodium concentration increased from 116 mEq/L to 136 mEq/L, and her consciousness returned to normal. Repeat head CT revealed marked resolution of the previously observed cerebral edema, corresponding with the normalization of serum sodium. No evidence of osmotic demyelination syndrome was detected during the course. This temporal association supports the hypothesis that changes in cerebral edema closely parallel shifts in serum sodium concentration.
This case highlights the importance of considering acute hyponatremia when cerebral edema is observed on neuroimaging in patients with suspected water intoxication. It also illustrates that cerebral edema and serum sodium levels can change concurrently without a significant temporal lag, emphasizing the clinical value of serial imaging in the acute phase.
