Department of Internal Medicine, Texas TechUniversity Health Sciences Center, Lubbock, TX 79430-9410, USA.
Pharmacotherapy. 2010 Feb;30(2):218. doi: 10.1592/phco.30.2.218.
Pleural effusion is an uncommon manifestation of amiodarone toxicity and is usually associated with amiodarone-induced interstitial pneumonitis. We describe a 70-year-old woman who came to the emergency department with bilateral pleuritic chest pain and malaise 4 weeks after her amiodarone dose was increased from 200 mg/day to 600 mg/day. She had bilateral exudative pleural effusions without associated pneumonitis. She was diagnosed with amiodarone-induced pleural effusions after a thorough workup during her hospitalization excluded other causes for the effusions. Due to intractable arrhythmias, the patient's amiodarone was not discontinued, and she was discharged home. Four days later at a follow-up visit at the pulmonary clinic, the patient complained of worsening chest pain as well as dyspnea and cough. A computed tomography scan showed left-sided pleural effusion with multiple loculations. She underwent a pulmonary vein isolation procedure, and amiodarone was discontinued. She was treated with prednisone 40 mg/day, tapered over the next 2 weeks. Three weeks after the amiodarone was stopped, the patient was asymptomatic, and a chest radiograph showed complete resolution of the effusions. Review of the patient's medical records revealed that she had experienced similar symptoms and exudative pleural effusions 2 years earlier after a similar dose escalation of amiodarone; the symptoms and pleural effusions resolved after the amiodarone dosage was reduced. Use of the Naranjo adverse drug reaction probability scale indicated that the association between the pleural effusions and amiodarone was highly probable (score of 9). This case report emphasizes that amiodarone should be considered in the differential diagnosis of patients with exudative effusions after a thorough workup has excluded other causes. Amiodarone should be replaced with alternative antiarrhythmic therapy if clinically feasible, and corticosteroids may be beneficial.
胸腔积液是胺碘酮中毒的一种罕见表现,通常与胺碘酮引起的间质性肺炎有关。我们描述了一位 70 岁的女性,她在胺碘酮剂量从 200mg/天增加到 600mg/天后 4 周时因双侧胸痛和不适来到急诊室。她有双侧渗出性胸腔积液,没有伴发肺炎。在住院期间经过全面检查排除了胸腔积液的其他原因后,她被诊断为胺碘酮引起的胸腔积液。由于心律失常难以控制,该患者的胺碘酮未被停用,并出院回家。在随后的 4 天,在肺病诊所的随访就诊中,患者抱怨胸痛加重,伴有呼吸困难和咳嗽。计算机断层扫描显示左侧胸腔积液伴多个分隔。她接受了肺静脉隔离手术,并停用了胺碘酮。她接受了泼尼松 40mg/天的治疗,在接下来的 2 周内逐渐减量。胺碘酮停用 3 周后,患者无症状,胸部 X 光片显示胸腔积液完全吸收。回顾患者的病历,发现她在 2 年前胺碘酮剂量类似增加后也经历了类似的症状和渗出性胸腔积液;胺碘酮剂量减少后症状和胸腔积液缓解。使用 Naranjo 药物不良反应概率量表表明,胸腔积液与胺碘酮之间的关联高度可能(评分 9)。本病例报告强调,在排除其他原因后,对于渗出性胸腔积液的患者,应考虑胺碘酮在鉴别诊断中的作用。如果临床可行,应将胺碘酮替换为替代抗心律失常治疗,并且皮质类固醇可能有益。