Hyponatraemic seizure in a healthy adult due to stress-associated non-osmotic vasopressin–mediated antidiuresis on a low-solute background: a case report

TL;DR

A healthy man had a seizure due to low sodium from stress-induced water retention and low-solute intake, showing how stress can cause electrolyte imbalance.

Contribution

This case report identifies a dual-hit mechanism involving stress-induced vasopressin secretion and low-solute intake leading to hyponatraemia and seizures.

Findings

Stress-induced non-osmotic vasopressin secretion combined with low-solute intake caused acute hyponatraemia and a seizure.

Autocorrection led to rapid normalization of sodium levels without complications like osmotic demyelination syndrome.

Strict monitoring during sodium correction is essential to prevent neurological complications.

Abstract

Hyponatraemia 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.

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.

This 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.