Osmotic Demyelination Syndrome Following Gastric Bleeding

Figure

Magnetic resonance imaging of the brain on the day of admission, 10 days after hyponatremia of 102 mmol/L. Transverse section at the level of the brainstem, FLAIR sequence. Extensive pathological signal hyperintensities in the entire pons (Figure, arrows). Contrast-enhanced sequences show no evidence of blood–brain barrier disruption. The changes on magnetic resonance imaging do not reliably correlate with the clinical course. Photo: Radiologie Center Niederhein

A male patient in his 30s developed a speech impairment and paralysis of all limbs within 3 days. Clinical examination revealed dysarthria, bilateral abducens and facial nerve palsies, pseudobulbar palsy, and high-grade tetraparesis (strength grade I/V). Electrolytes were within the normal range on admission. The patient had been treated 10 days prior for bleeding from an ulcer at the gastroesophageal junction. His initial sodium level rose from 102 mmol/L to 122 mmol/L the following day (reference range, 136–145 mmol/L). Magnetic resonance imaging of the brain showed pathological signal hyperintensities in the entire pons (Figure, arrows). Thus, the diagnosis of osmotic demyelination syndrome (ODS) with central pontine myelinolysis (CPM) was made. After 5 weeks of treatment, the patient was discharged able to walk independently. The triggering factor—hyponatremia alongside rapid sodium correction—typically precedes symptoms and demyelination with a latency of 1–14 days. Thus, this case underscores the importance of ODS prevention.

Dr. Peter Albrecht, EVK Wesel, Neurologie, [e-mail]

Conflict of interest statement: The author states that no conflict of interest exists.

Translated from the original German by Christine Rye.

Cite this as: Albrecht P: Osmotic demyelination syndrome following gastric bleeding. Dtsch Arztebl Int 2026; 123: 156. DOI: 10.3238/arztebl.m2025.0222