Background:
Amiodarone is a potent class III antiarrhythmic widely used in atrial fibrillation (AF) management, including short-term therapy after catheter ablation. While thyroid, pulmonary, and hepatic toxicities are well recognized, hyponatraemia due to syndrome of inappropriate antidiuretic hormone secretion (SIADH) is extremely rare and potentially lifethreatening.
Case presentation:
A 65year old man with persistent AF underwent successful cryoballoon pulmonary vein isolation (PVI). He received amiodarone loading (200 mg TID for 10 days, then 200 mg OD). Within 7–10 days, he developed dizziness, nausea, epigastric discomfort, and mild confusion. Laboratory studies revealed severe hyponatraemia (Na 105 mmol/L) with low plasma osmolality and inappropriately high urine sodium, consistent with SIADH. Amiodarone was discontinued immediately, fluid restriction was initiated, and sodium normalized within 7 days.
Outcome:
The patient recovered completely, remained in sinus rhythm without further antiarrhythmic therapy, and had no recurrence of hyponatraemia at 3-month follow-up.
Conclusion:
Amiodarone-induced SIADH is rare but potentially lifethreatening. Our case demonstrates that even short-term periprocedural use can precipitate severe hyponatraemia. Clinicians should monitor sodium closely, recognize early symptoms, and discontinue amiodarone promptly.
Learning points:
- Amiodarone can induce severe SIADH, even after short-term therapy post AF ablation.
- Early monitoring of serum sodium during amiodarone loading is essential.
- Prompt discontinuation and supportive care lead to full recovery in most cases.
