# 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.

## Key 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.