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Ann Thorac Surg 2001;72:1760-1761
© 2001 The Society of Thoracic Surgeons
a Department of Cardiothoracic Surgery, The Boston Medical Center and Boston University School of Medicine, Boston, Massachussetts, USA
b Department of Radiology, The Boston Medical Center and Boston University School of Medicine, Boston, Massachussetts, USA
Accepted for publication January 5, 2001.
* Address reprint requests to Dr Lazar, Department of Cardiothoracic Surgery, The Boston Medical Center, 88 E Newton St, B-404, Boston, MA 02118, USA
e-mail: harold.lazar{at}bmc.org
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A 72-year-old, 87-kg white man presented with post-myocardial infarction angina and dyspnea on exertion. His medical history was significant for non-insulin-dependent diabetes mellitus, hypothyroidism, hypertension, and a 90 pack-year smoking history. His preoperative chest roentgenogram was unremarkable, and his forced expiratory volume in 1 second was 1.47 L (70% of predicted). A cardiac catheterization showed a 70% left main lesion and a 90% obtuse marginal lesion, with an ejection fraction of 50%. He had coronary artery bypass grafting using the left internal mammary artery to bypass the left anterior descending artery, and a saphenous vein graft to an obtuse marginal branch, with cross-clamp and cardiopulmonary bypass times of 44 and 67 minutes, respectively. He was extubated without any difficulty 6 hours postoperatively.
On the evening of the second postoperative day, atrial fibrillation with a rapid ventricular response developed. In addition to a ß-blocker, he was started on oral amiodarone with a loading dose of 3,600 mg for more than 3 days. Because of persistent atrial fibrillation and flutter, he was cardioverted, but he continued to alternate between sinus rhythm and atrial fibrillation and flutter. After an amiodarone loading dose, he was maintained on 400 mg twice a day for 4 days, followed by 400 mg daily. On the seventh postoperative day, after a total of 6,800 mg of amiodarone, low-grade fever and dyspnea developed, requiring supplemental oxygen to keep his saturation at 90% or greater. His white blood cell count increased to 15,000, and bilateral lower lobe infiltrates developed. A sputum culture grew no organisms, and a transthoracic echocardiogram showed no new wall motion abnormalities, preserved ejection fraction, and no pericardial collections. His weight was only 3 pounds above his preoperative weight. A high resolution computed tomographic scan of the chest showed bilateral lower lobe interstitial infiltrates and no pulmonary emboli (Fig 1A). The infiltrates were characterized by high attenuation (> 80 Hounsfield units) compatible with iodine uptake (Fig 1B). Amiodarone toxicity was suspected and the drug was stopped after a total dose of 7,200 mg over more than 8 days. During the next 7 days, his oxygen saturation continued to decline, and he was started on prednisone 40 mg orally three times daily. Results of sputum cultures for anaerobes, fungi, and viral strains were negative. Smears for tuberculosis organisms were also negative. He was intubated on the 25th postoperative day for adult respiratory distress syndrome and required 100% fraction of inspired oxygen, 15 cm positive end-expiratory pressure, and total paralysis for 10 days, just to keep his oxygen saturation more than 90%. During this time, he was maintained on intravenous diltiazem to treat intermittent atrial fibrillation. Gradually, his respiratory status stabilized, his fraction of inspired oxygen and positive end-expiratory pressure requirements decreased, and so prednisone dosage was tapered. A percutaneous tracheostomy was done on the 55th postoperative day. Sixty days after stopping the amiodarone, the infiltrates cleared and he was weaned from the respirator. Eighteen months after his coronary artery bypass grafting he is living a normal lifestyle, without angina or dyspnea, and remains in normal sinus rhythm.
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The diagnosis of APT is one of exclusion because the signs and symptoms are similar to those of congestive heart failure, pneumonia, and volume overload, which are more common after cardiac operations. When APT is suspected, amiodarone should be discontinued. If the drug is necessary for life-threatening ventricular arrhythmias, the dose should be reduced significantly. Because the half-life of amiodarone is estimated to be 45 days, APT might progress and resolution might not occur for months. The value of steroids is not known. In general, steroids are recommended when there is severe impairment of gas exchange such that supplemental oxygen is required to keep oxygen saturation above 90%. They must be tapered slowly because rapid withdrawal has resulted in APT recurrences in some patients [3, 4]. The mortality rate is especially high in patients with underlying lung disease and compromised pulmonary function and in those with low ejection fractions. This partially explains the higher incidence of mortality in cardiac surgical patients.
Patients with preoperative amiodarone doses of 350 to 750 mg/d for prolonged periods and those with decreased diffusing lung capacity (DLCO) and older age are more likely to develop APT [5]. Preoperative chest roentgenogram appearance and spirometry and lung volume changes have not been predictors for the development of postoperative APT [5]. In our patient, APT occurred after only 8 days of therapy, with a cumulative dose of only 7,200 mg. As the usage of amiodarone increases, surgeons must be aware of the possibility of APT when respiratory insufficiency occurs early in the postoperative period, even after a short course of amiodarone therapy.
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This article has been cited by other articles:
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  M. Argyriou, P. Hountis, N. Antonopoulos, and M. Mathioudaki Acute Fatal Post-CABG Low Dose Amiodarone Lung Toxicity Asian Cardiovascular and Thoracic Annals, December 1, 2007; 15(6): e66 - e68. [Abstract] [Full Text] [PDF]
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 S. M. Bagshaw, P. D. Galbraith, L. B. Mitchell, R. Sauve, D. V. Exner, and W. A. Ghali Prophylactic Amiodarone for Prevention of Atrial Fibrillation After Cardiac Surgery: A Meta-Analysis Ann. Thorac. Surg., November 1, 2006; 82(5): 1927 - 1937. [Abstract] [Full Text] [PDF]
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 A. A. Patel, C. M. White, E. L. Gillespie, J. Kluger, and C. I. Coleman Safety of amiodarone in the prevention of postoperative atrial fibrillation: A meta-analysis Am. J. Health Syst. Pharm., May 1, 2006; 63(9): 829 - 837. [Abstract] [Full Text] [PDF]
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 R. Kailasam, C. A. Palin, and C. W. Hogue Jr Atrial Fibrillation After Cardiac Surgery: An Evidence-Based Approach to Prevention Seminars in Cardiothoracic and Vascular Anesthesia, March 1, 2005; 9(1): 77 - 85. [Abstract] [PDF]
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D. Lardinois, A. Handschin, and W. Weder Acute amiodarone-induced pulmonary toxicity after lung operation Ann. Thorac. Surg., June 1, 2002; 73(6): 2033 - 2034. [Full Text] [PDF]
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