RAPID OVERCORRECTION OF HYPONATREMIA FOLLOWING UNEXPECTED AQUARESIS DURING HYPERTONIC SALINE THERAPY IN AN OXCARBAZEPINE-TREATED PATIENT: A CASE REPORT

Dr. Jyoti Goyal*, Dr. Bhawesh Kumar Thakur, Dr. Anil Jain, Dr. Nickle Sasidharan, Dr. Jitendra Soni

Background: Oxcarbazepine is a well-recognized cause of drug-induced hyponatremia and may precipitate breakthrough seizures despite adequate compliance with antiepileptic therapy. While rapid sodium overcorrection is commonly described with vasopressin antagonists such as tolvaptan, sudden overcorrection during conventional 3% hypertonic saline therapy due to unexpected aquaresis is less frequently highlighted in literature. Case Presentation: We report a case of severe symptomatic hyponatremia in a patient with seizure disorder receiving multiple antiepileptic drugs including oxcarbazepine. The patient presented with breakthrough seizures and serum sodium of 118 mEq/L. Hypertonic 3% saline was initiated for symptomatic hyponatremia. Within a few hours, urine output increased abruptly from 100–150 mL/hour to 300–400 mL/hour, suggestive of sudden free water diuresis (aquaresis). Despite early discontinuation of hypertonic saline, serum sodium increased rapidly by nearly 20 mEq/L within less than 16 hours. Rescue therapy with 5% dextrose and desmopressin was initiated to prevent further overcorrection and reduce the risk of osmotic demyelination syndrome. Discussion: This case highlights an important but under-recognized phenomenon of rapid sodium auto-correction associated with sudden aquaresis during hypertonic saline therapy. Although this phenomenon is well described with tolvaptan and reversal of SIADH physiology, it is less commonly reported during routine 3% saline administration. The case emphasizes that abrupt increase in urine output may serve as an early bedside warning sign of impending overcorrection. Conclusion: Close monitoring of urine output is essential during correction of severe hyponatremia with hypertonic saline. Sudden polyuria should prompt urgent reassessment of sodium correction trajectory and consideration of early intervention with desmopressin-based strategies to prevent osmotic demyelination.