胺碘酮致急性呼吸窘迫综合征一例

Z. Muzaffarr
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引用次数: 0

摘要

简介:胺碘酮是美国最常用的抗心律失常药物之一。不良反应已显示影响多个器官系统,包括心脏,甲状腺,肝脏,眼和肺。肺毒性可表现为间质性肺炎、嗜酸性肺炎、组织性肺炎和急性呼吸窘迫综合征(ARDS)1。这是一例胺碘酮引起的急性呼吸窘迫综合征。病例介绍:这是一个81岁的男性病例,有房颤史(每天服用胺碘酮200毫克),机械主动脉瓣置换术和糖尿病,以干咳史4周和用力时呼吸困难1周就诊。入院前,他接受了类固醇、阿奇霉素、头孢曲松和左氧氟沙星的社区获得性肺炎治疗。到达时,他发烧,但缺氧,需要用鼻插管吸氧。体格检查中发现一位表现不佳,嗜睡的老年绅士,双肺广泛的裂纹,更集中在上肺叶。实验室SARS冠状病毒RNA PCR阴性,白细胞增多14.7。计算机断层扫描显示广泛的双侧实变,肺上叶空气支气管征加重。随着他的临床状况恶化,需要使用无创通气并转移到重症监护病房,很明显这不是一个传染性过程;到目前为止,工作一直是阴性的。停用胺碘酮,患者开始使用地尔硫卓和脉冲剂量类固醇。四天之内,他的呼吸和精神状况都有所改善。讨论:胺碘酮肺毒性与较高剂量400mg有关,但1.6%的病例报告剂量低于400mg,使本病例独特。病理表现与直接的细胞毒作用和间接的免疫反应有关。患者通常表现为非生产性咳嗽和呼吸短促。影像学是诊断的关键,表现为弥漫性斑片状浸润,优先于右肺和上肺叶。治疗的重点是停药,每天40-60毫克的强的松在几个月内逐渐减少。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
A Rare Case of ARDS Caused by Amiodarone
Introduction: Amiodarone is one of the most commonly prescribed antiarrhythmic medications in the United States. Adverse effects have been shown to affect multiple organ systems including cardiac, thyroid, hepatic, ocular and pulmonary. Pulmonary toxicity can vary in presentation from interstitial pneumonitis, eosinophilic pneumonia, organizing pneumonia and acute respiratory distress syndrome (ARDS)1. This is a case of ARDS caused by Amiodarone. Case Presentation: This is a case of an 81 yo male with a history of atrial fibrillation (on Amiodarone 200 mg daily), mechanical aortic valve replacement and diabetes who presented to the hospital with a four week history of dry cough and one week of dyspnea on exertion. He was treated for community acquired pneumonia prior to admission with steroids, Azithromycin, Ceftriaxone and Levofloxacin. On arrival he was afebrile, but hypoxic requiring oxygen support with nasal cannula. Physical exam was concerning for an ill appearing, lethargic elderly gentleman with extensive crackles throughout both lung fields more concentrated in the upper lobes. Laboratory was significant for negative SARS Coronavirus RNA PCR and Leukocytosis 14.7. Computed-tomography revealed extensive bilateral consolidations with air bronchograms worse in the upper lobes. As his clinical status worsened requiring use of non-invasive ventilation and transfer to the intensive care unit, it became clear that this was not an infectious process;work up thus far had been negative. Amiodarone was discontinued and the patient was started on Diltiazem and pulse dose steroids. Within four days, his respiratory and mental status improved. Discussion: Amiodarone pulmonary toxicity has been associated with higher doses of 400 mg, but 1.6% of cases are reported with less, making this case unique. The pathology appears to be related to direct cytotoxic effect and indirect immunological reaction. Patients will usually present with a nonproductive cough and shortness of breath. Imaging is key for diagnosis, demonstrating diffuse patchy infiltrates;with a preference to the right lung and upper lobes. Treatment centers on discontinuation of the drug and 40-60 mg of Prednisone per day tapered over the period of a few months2.
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