Hyponatremia – A Rare but Serious Complication of Amiodarone: A Case Report and Review of the Literature
An 84-year-old Caucasian man with a past medical history of hypertension and diabetes was admitted to the hospital with a non-ST elevation myocardial infarction. Urgent left heart catheterization showed multivessel disease, and the patient subsequently underwent coronary artery bypass graft. On postoperative day 2, the patient developed atrial fibrillation with rapid ventricular response. He was started on intravenous amiodarone with a loading dose of 150 mg, followed by a continuous infusion of 1 mg/min. After 24 h, intravenous amiodarone was discontinued and switched to 400 mg orally every 8 h. The oral dose of amiodarone was tapered over 7 days to 400 mg daily. The patient's atrial fibrillation converted to normal sinus rhythm after the loading dose of amiodarone. He was discharged on postoperative day 7 on amiodarone 400 mg daily. At the time of discharge, his serum sodium was 136 mmol/l.\nThe patient then presented to the emergency room 11 days later due to altered mental status, weakness and loss of appetite. He was drowsy but arousable. Physical examination revealed normal vital signs and euvolemic status. There was no orthostatic blood pressure change. A neurological examination showed no focal deficit. Laboratory data revealed a serum sodium level of 105 mmol/l. Renal and liver function tests were normal. Thyroid stimulating hormone and cortisol levels were 0.7 µIU/ml (normal range: 0.350–5.000 µIU/ml) and 16 µg/dl (normal range: 3.09–22.40 µg/dl), respectively. Serum osmolality was 228 mOsm/kg and urine osmolality was 251 mOsm/kg. It was noted that the patient was on furosemide 20 mg daily prior to his admission. Repeat testing after discontinuation of furosemide revealed a serum osmolality of 256 mOsm/kg and a urine osmolality of 506 mOsm/kg. The fractioned excretion of sodium was greater than 1% and the urine sodium was 124 mmol/l.\nThe diagnosis of SIADH was made based on euvolemic hypoosmotic hyponatremia, with a urine osmolality greater than the serum osmolality, urine sodium level greater than 40 mmol/l, normal thyroid and adrenal function and the absence of other medications known to cause SIADH. The patient was initially treated with hypertonic (3%) saline. His serum sodium increased gradually to 117 and 123 mmol/l after 36 and 48 h of treatment, respectively. Hypertonic saline was discontinued after 3 days, and demeclocycline was added, together with fluid restriction. The patient's mental status improved and his serum sodium normalized after 10 days of treatment (fig. ).