Marcelino Gretchen P, Collantes Cyril Manuel C, Oommen Jomi K, Wang Shan, Baldassari Heather, Muralidharan Rajanandini, Hanna Adel
P T. 2019 Jul;44(7):416-423.
Amiodarone (Cordarone, Pfizer Inc) is an antiarrhythmic medication with a well-known toxicity profile, including rare cases of hyponatremia as a result of syndrome of inappropriate antidiuretic hormone (SIADH). We report on such a case in which a patient was found to be hyponatremic after evaluation. An 88-year-old male who presented to the emergency department was found to be hyponatremic secondary to amiodarone-induced SIADH following a fall, with possible seizure and traumatic brain injury. He had a history of hypertension, paroxysmal atrial fibrillation, emphysema, myocardial infarction, benign prostatic hyperplasia, chronic kidney disease, Meniere's disease, anemia, and gastroesophageal reflux. Upon admission, his urine sodium level was elevated, and his serum sodium, urine osmolality, and anion gap were below normal. In the setting of hyponatremia, the patient's amiodarone was held: he had been taking amiodarone 200 mg once daily for nine months prior to admission. He was treated with intravenous (IV) normal saline over four days. He was fluid-restricted and his sodium levels were closely monitored every two hours. Within 19 hours, his serum sodium levels had improved. Amiodarone was restarted approximately three days later. Upon follow-up after discharge, the patient remained on amiodarone for the next two months. His serum sodium level ranged from 126 mEq/L to 131 mEq/L over a two-week period. He was supplemented with sodium chloride tablets and has been otherwise stable. Amiodarone may cause acute or chronic SIADH, with a wide range of symptoms. Seizures have not been reported in the literature but our patient had a witnessed seizure, although his electroencephalogram (EEG) was negative. Syndrome of inappropriate antidiuretic hormone can occur with any formulation of amiodarone in a dose-dependent fashion. Our patient's sodium levels stabilized within two weeks after amiodarone was resumed. The mechanism of amiodarone-induced SIADH remains unclear.
胺碘酮(可达龙,辉瑞公司)是一种抗心律失常药物,具有众所周知的毒性特征,包括因抗利尿激素分泌不当综合征(SIADH)导致的罕见低钠血症病例。我们报告了这样一例经评估发现患者存在低钠血症的病例。一名88岁男性因跌倒后出现胺碘酮诱导的SIADH继发低钠血症,可能有癫痫发作和创伤性脑损伤,被送往急诊科。他有高血压、阵发性心房颤动、肺气肿、心肌梗死、良性前列腺增生、慢性肾脏病、梅尼埃病、贫血和胃食管反流病史。入院时,他的尿钠水平升高,血清钠、尿渗透压和阴离子间隙低于正常水平。在低钠血症的情况下,停用了患者的胺碘酮:入院前他已服用胺碘酮200毫克,每日一次,共九个月。他接受了四天的静脉生理盐水治疗。他被限制液体摄入,每两小时密切监测钠水平。19小时内,他的血清钠水平有所改善。大约三天后重新开始使用胺碘酮。出院后随访时,患者在接下来的两个月内继续使用胺碘酮。在两周时间内,他的血清钠水平在126毫当量/升至131毫当量/升之间。他补充了氯化钠片,其他方面情况稳定。胺碘酮可能导致急性或慢性SIADH,症状范围广泛。文献中未报道过癫痫发作,但我们的患者有一次癫痫发作被目击到,尽管他的脑电图(EEG)结果为阴性。抗利尿激素分泌不当综合征可因任何剂型的胺碘酮以剂量依赖方式发生。胺碘酮恢复使用后两周内,我们患者的钠水平稳定下来。胺碘酮诱导SIADH的机制仍不清楚。