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

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.

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Journal
International Journal of Emergency Medicine
Published
2026-02-13
DOI
https://doi.org/10.1186/s12245-026-01137-w
Primary Topic
Electrolyte and hormonal disorders
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article
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article

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

Ninh Xuan Nguyen, Ngoc Tien Pham, Huong Thi Thanh Le, Thị Kim Thanh Võ et al.
International Journal of Emergency Medicine
Electrolyte and hormonal disorders
article

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

Ninh Xuan Nguyen, Ngoc Tien Pham, Huong Thi Thanh Le, Thị Kim Thanh Võ, Hang Ngoc Thuy Tran, Quoc Viet Tran
article en

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.

International Journal of Emergency MedicineVol. 19(1)
Vinmec Times City International Hospital (VN)
Good health and well-being
Openalex Percentile: Top 57%
Electrolyte and hormonal disorders
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