ArticleInternational journal of emergency medicine2026
Hyponatraemic seizure in a healthy adult due to stress-associated non-osmotic vasopressin-mediated antidiuresis on a low-solute background: a case report.
Article in International journal of emergency medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundHyponatraemia is the most common electrolyte disorder and a recognised precipitant of acute symptomatic seizures. In addition to drug-induced, endocrine, and central nervous system causes, acute psychological stress can provoke non-osmotic AVP secretion with inappropriate antidiuresis (SIAD-like physiology) and, when combined with low-solute intake (“beer-potomania” spectrum), impair free-water clearance. A critical challenge is autocorrection—a rapid, spontaneous rise in serum sodium once stress abates and solute intake resumes. While this may prevent recurrence, it also carries a high risk of osmotic demyelination syndrome (ODS) if unrecognised. CASE PRESENTATION: A healthy 40-year-old Korean man experienced a generalised tonic–clonic seizure after approximately 10–12 h of police interrogation with fasting and marked stress; history suggested recent low-solute intake with episodic heavy alcohol use. On arrival he was euvolaemic with sodium 121.6 mmol/L, serum osmolality 262 mOsm/kg, urine osmolality 540 mOsm/kg, and urine sodium 48 mmol/L. Brain MRI and EEG were normal; an incidental zygomatic–temporal vascular malformation was non-causal. Hypertonic saline was considered but deferred given clinical improvement and anticipated autocorrection. He received isotonic saline (about 1 L over 24 h) with sodium monitored every 2–4 h. Levels rose to 133.3 mmol/L within 11 h and 135.4 mmol/L by 36 h, then stabilised. He required no antiseizure therapy and was discharged on day 2. At 1 month, sodium was 139.8 mmol/L with no ODS.
conclusionThis case illustrates a dual-hit mechanism- stress-associated non-osmotic arginine vasopressin secretion with inappropriate antidiuresis (SIAD-like physiology) on a low-solute background-leading to acute symptomatic hyponatraemia. It highlights autocorrection as a distinct physiological phenomenon that mandates strict monitoring and readiness to re-lower sodium to ensure safe outcomes.
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