Abstract: FR-PO0877
But Why the Status Epilepticus? Central Pontine Myelinolysis After Moderate Hyponatremia with Appropriate Correction: A Case Highlighting Thiazide-Associated Risk in Older Adults
Session Information
- Fluid, Electrolyte, and Acid-Base Disorders: Case Reports - 1
October 23, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Rodil, Alexandra Isabel, Hospital Damas, Ponce, Puerto Rico
- Veguilla Rivera, Nahomie Ivette, Hospital Damas, Ponce, Puerto Rico
Introduction
Osmotic demyelination syndrome (ODS) is classically associated with rapid correction of severe hyponatremia (serum sodium <120 mmol/L) characterized by encephalopathy, followed by weakness (quadriparesis), speech difficulties, and potential locked-in syndrome. Current recommendations limit correction to 8–10 mmol/L per 24 hours. Occurrence of ODS outside these conditions is rare.
Case Description
We present a 77-year-old male with a history of hypertension on chronic use of HCTZ, poor oral solute intake, and high free water consumption secondary to strenuous exercise, who presents with progressive confusion. Initial serum sodium 127 mmol/L. The patient received a 1L bolus of isotonic saline, resulting in an increase in serum sodium to 131 mmol/L (+4 mmol/L) within 6 hours. Over the first 24 hours, the net correction was approximately 5 mmol/L, remaining within guideline-recommended limits. Despite this, the patient developed acute neurologic deterioration with persistent seizures, requiring hypertonic saline administration and ICU admission. Between 48 and 72 hours, serum sodium increased gradually to 137–139 mmol/L, corresponding to a total correction of approximately 12 mmol/L (averaging ~4 mmol/L per day). Persistent encephalopathy disproportionate to correction led to high suspicion for ODS, later confirmed by Brain MRI.
Discussion
This case demonstrates that ODS can occur despite moderate hyponatremia and strict adherence to recommended correction limits, challenging the assumption that guideline-concordant therapy is universally protective. Predisposing factors included advanced age, thiazide diuretic use, and low solute intake, impairing free water excretion and increasing vulnerability to osmotic shifts. These factors may lower the threshold for demyelination despite guideline-concordant management. Correction thresholds alone may not be universally protective. High-risk patients may require more conservative correction strategies and close neurologic monitoring.