Amiodarone and the Development of ARDS After Lung Surgery: Discussion

The incidence of ARDS after the right pneumonectomy was 7.4 percent in all patients compared with 1.6 percent in the other types of lung surgery (x2 11.2; p<0.001), and in our retrospective study, ARDS was almost exclusively seen after the administration of amiodarone except after right-sided pneumonectomy. The evaluation of prophylactic antiarrhythmic treatment with amiodarone was stopped because the development of ARDS seemed related to amiodarone administration other buy birth control pills online. Pulmonary toxicity is the most serious noncardiac side effect attributed to amiodarone therapy. The overall incidence of amiodarone pulmonary toxicity has been estimated at 5 to 10 percent of treated patients.
Amiodarone-induced pulmonary disease usually appears as a subacute or chronic disease, although in some cases there may be rapid progression toward respiratory failure.
The most common presentation is that of a relatively benign subacute illness, characterized by cough, dyspnea, and sometimes weight loss. The chest roentgenogram of these patients most often shows diffuse parenchymal infiltrates, typically in an interstitial pattern.
Other patients may have a more abrupt onsej of an acute illness. These patients characteristically have significant fever, and the chest roentgenogram often shows localized opaque areas in an acinar pattern. The clinical presentation may strongly mimic an infectious pneumonia or in extreme cases, ARDS.
The mechanisms of amiodarone pulmonary toxicity are not completely understood. Currently, at least two different pathways of toxicity may exist: (1) an indirect mechanism characterized by influx of inflammatory or immune effector cells to the lung, similar to the findings described with other “hypersensitivity” reactions associated with inhalation of organic antigen that are seen in farmer’s lung or pigeon breeder’s disease; and (2) a direct toxic mechanism that results in lung parenchymal cell injury and a subsequent fibrotic response. Several mechanisms of direct toxicity have been proposed. Regardless of the mechanism of initial toxicity to the cell, Martin et al suggest an amiodarone-mediated increase in cytosolic-free calcium may be the ultimate intercellular mediator of cell injury.

This entry was posted in ARDS and tagged amiodarone therapy, arrhythmia, lung surgery, pneumonectomy, pulmonary toxicity.