Acute Amiodarone-induced Pulmonary Toxicity: An Association of Risk Factors in a Child Operated by Arterial Switch Operation Fabien Labombarda, MD,* Phalla Ou, MD, † Bertrand Stos, MD, † Jacques de Blic, MD, † Elisabeth Villain, MD, † and Daniel Sidi, MD, PhD † *Department of Cardiology, University Hospital of Caen, Caen, France; † University Rene Descartes Paris V, UFR Necker–Enfants Malades, Department of Pediatric Radiology, Paris, France ABSTRACT Amiodarone is an antiarrhythmic benzoflurane drug with an imposing adverse effect profile. Amiodarone pulmonary toxicity is the major complication. It is well described in adults, whereas it is extremely rare in pediatric patients. This is a case of a child with supraventricular tachycardia post repair of transposition of the great vessels who developed amiodarone toxicity. Key Words. Amiodarone; Transposition of the Great Arteries; Toxicity; Pediatric Introduction A miodarone-induced pulmonary toxicity is well described in adults, whereas it is extremely rare in children. We report a case of a 3-month-old child presented with an association of risk factors for amiodarone pulmonary toxicity. Observation L.A. is a newborn who had been operated at the 11th day of life by an arterial switch operation for a simple transposition of the great arteries. Postoperative period was eventless until the ninth postoperative day, when an atrial tachycardia access occurred. Arrhythmia was successfully treated by oral amiodarone with a loading dosage of 500 mg/m 2 of body surface area (30 mg/kg/ day) for 5 days, and then a daily dosage of 250 mg/m 2 of body surface area (15 mg/kg/day) for 3 months, according to the protocol of our department. He was hospitalized 3 months later for dyspnea, which increased since 2 weeks. Clinical exam showed a moderate respiratory dis- tress with a respiratory rate of 45/min. Pulmo- nary auscultation revealed crepitations at the top of right lung. Electrocardiogram was in sinus rhythm, with a right axis deviation and a right ventricular hypertrophy. Chest X-ray showed a cardiomegaly by dilatation of the right ventricle, and diffuse flocculent opacities in bilateral whole lungs (Figure 1A). There was no biological marker of inflammation. Echocardiography con- firmed the good anatomical result of the surgery but a dilated right ventricle. Pulmonary arterial pressure was high, with a mean pressure esti- mated at 55 mm Hg. Chest computed tomography scan showed diffuse ground-glass opacities in bilateral whole lobes (Figure 1B). Bronchial fiberscopy revealed a diffuse inflammation of the bronchus, and bron- choalveolar lavage fluid showed a prevalence of large foamy macrophages with characteristic lamellated inclusions (Figure 1C). Pulmonary function test showed a severe bronchial obstruc- tion, with reduction of carbon monoxide (CO) diffusion. No infectious agent was found on secre- tions, blood culture, or serology. Dyspnea was thought to be secondary to amio- darone toxicity. Amiodarone was stopped and prednisolone corticotherapy at 2 mg/kg dose was begun. After 2 months, the child remained moder- ately polypneic. Chest radiography was normal and chest tomography scan showed a regression of initial lesions. The mean pulmonary arterial pressure was measured at 25 mm Hg on echo- cardiography. Pulmonary function test showed a significant diminution of the plethysmo- graphic resistances. After this evolution, we retained the diagnosis of amiodarone pulmonary toxicity. 365 © 2008 Copyright the Authors Journal Compilation © 2008 Wiley Periodicals, Inc. Congenit Heart Dis. 2008;3:365–367