{'fraction_non_alphanumeric': 0.02900591382709096, 'fraction_numerical': 0.015488594762038862, 'mean_word_length': 5.3428571428571425, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Acute Diaphragm Paralysis Caused by Intravenous Administration of Amiodarone

We present a patient who developed diaphragm paralysis shortly after initiation of intravenous amiodarone therapy. It is a serious adverse effect and very important to know for clinicians. A 12-year-old, previously healthy boy presented with a first episode of ventricular tachycardia. After successful defibrillation, intravenous amiodarone was started, in view of recurrent tachyarryhthmia. But it was stopped at 72 hours in view of bradycardia, hypotension, and prolonged QT interval. Metoprolol was started, on which his cardiac rhythm was normal. He was conscious and oriented, and echocardiography, troponin T, blood glucose, and serum potassium, were in the normal range, so we planned for weaning from the ventilator. However, he had respiratory distress with paradoxical diaphragm movements and could not be weaned off the ventilator. Chest radiography was normal. His negative inspiratory pressure was just −5 cm Hg. We suspected diaphragm paralysis and rechecked that our patient was not on any neuromuscular blockers. Sonography confirmed diaphragm paralysis. His magnesium, calcium, potassium, phosphate, urine metanephrine, and thyroid hormone levels were normal. On the 18th day, again, a trial of weaning from the ventilator failed. He also had limb muscle weakness, and creatine phosphokinase (CPK) levels were 431 U/L. On the 50th day, some reduction in paradoxical movements was observed, and this time, we could take him off the ventilator. His distress was more in the supine position. Fluoroscopy confirmed restricted diaphragm movements (Figure 1). Our patient improved completely (conscious, oriented, able to speak, and walk) and was discharged on the 64th day in good general condition. Amiodarone is approved for the treatment of tachyarrhythmia. Being lipophilic, it is taken up by many tissues, which may explain its toxicity in various organs, including the lung, liver, heart, nerves, central nervous system, thyroid, and cornea. Reports of muscle toxicity/myopathy are few, and the mechanism is unclear. Histopathological abnormalities are mild vacuolation, with accumulation of lipid-like inclusion bodies, and muscle inflammation and necrosis. CPK levels may not correlate with the degree of myopathy. The first unusual characteristic about the present case is that diaphragm paralysis caused by amiodarone has not been reported previously. This case scored 7 points on application of the Naranjo Probability Scale for adverse drug reactions. This means that this adverse event is probably caused by amiodarone. The patient also received ceftriaxone, intravenous fluids, pantoprazole, dopamine, and midazolam, but these are used routinely in the intensive care unit, and chances of their causing this event are remote. It was not ethical to readminister the drug in view of the seriousness and prolonged duration of the adverse effect. The second unusual point is that the toxicity occurred very fast—in 3 days; however, it could have occurred earlier than that. Severe muscle cramps within 12 hours and diffuse alveolar hemorrhage within 2 days have been reported. Fortunately, our patient had spontaneous resolution (limb muscles improved in 1 month, earlier than the diaphragm) over a 2-month period; in a previous report, skeletal muscle weakness resolved within 1 month of stopping the drug. A literature search shows that amiodarone-induced myopathy 599176 AOPXXX10.1177/1060028015599176Annals of Pharmacotherapy research-article2015