Abstract: FR-PO0872
Rapid-Onset Hyponatremia After Intravenous Amiodarone
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
Author
- Shetta, Raghda Ali, The University of Texas Health Science Center at Houston John P and Katherine G McGovern Medical School, Houston, Texas, United States
Introduction
Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is a common cause of euvolemic hyponatremia, often related to malignancy, pulmonary disease, or medications. Amiodarone-induced SIADH is rare, particularly with intravenous use, but clinically significant due to the potential for rapid sodium decline.
Case Description
A 29-year-old male with non-Hodgkin lymphoma (in remission) and severe non-ischemic cardiomyopathy (EF 10%) status post AICD placement presented after multiple ICD shocks. He was found to be in supraventricular tachycardia (HR ~180 bpm), refractory to Adenosine and IV Amiodarone bolus, requiring synchronized cardioversion. He was started on an IV Amiodarone infusion and admitted to the ICU.
Initial labs showed sodium 143 mmol/L, potassium 3.1 mmol/L, magnesium 1.6 mg/dL, and creatinine 0.84 mg/dL. Within 24 hours of Amiodarone infusion, sodium decreased to 127 mmol/L. Evaluation revealed serum osmolality 277 mOsm/kg, urine osmolality 508 mOsm/kg, and urine sodium 30 mmol/L. The patient was clinically euvolemic and asymptomatic. Home Furosemide and Spironolactone were held.
Amiodarone-induced SIADH was suspected based on temporal association and laboratory findings. The infusion was discontinued by hospital day 3. Serum sodium improved gradually to 137 mmol/L by day 7 without other interventions. His home diuretics were restarted safely upon discharge without significant changes in his serum Sodium level.
Discussion
Amiodarone-induced SIADH remains rare, with prior reviews describing roughly 10–15 published cases and additional sporadic reports since; proposed mechanisms include Amiodarone’s channel-modulating effects on renal or neural tissues, leading to inappropriate ADH release, enhanced renal sensitivity to ADH, or altered aquaretic/vasopressin-receptor signaling. In our case, rapid hypotonic hyponatremia with inappropriately concentrated urine soon after IV Amiodarone initiation, euvolemia, early withholding of diuretics, and prompt improvement after discontinuation strongly support Amiodarone-induced SIADH.