Amiodarone‐induced acute lung toxicity in an ICU setting

Skroubis, T.; Galiatsou, Eftychia; Metafratzi, Zafiria M.; Karahaliou, A.; Kitsakos, Athanassios; Nakos, George

doi:10.1111/j.1399-6576.2005.00606.x

Cited by 25 publications

(10 citation statements)

References 15 publications

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“…18 Intravenous amiodarone accumulates more rapidly in the lungs and can contribute to pulmonary toxicity after the first dose or few doses of administration even without predisposing risk factors. 21 Long-term use of amiodarone therapy can result in heart failure (HF), thyroid dysfunction, and hepatic toxicity. The most common adverse effect of amiodarone is nausea and vomiting.…”

Section: Adverse Effects Of Amiodaronementioning

confidence: 99%

Amiodarone Use to Prevent Postoperative Atrial Fibrillation After Cardiac Surgery

McAlister

Davis

Whitcomb

et al. 2012

Dimensions of Critical Care Nursing

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Section: Adverse Effects Of Amiodaronementioning

confidence: 99%

Amiodarone Use to Prevent Postoperative Atrial Fibrillation After Cardiac Surgery

McAlister

Davis

Whitcomb

et al. 2012

Dimensions of Critical Care Nursing

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“…Chronic use of amiodarone is associated with adverse events like thyroid dysfunction, pulmonary and hepatic toxicity. Much less attention has been given to the acute toxic effects, although acute pulmonary and hepatocellular toxicity has been described [3][4][5][6] .…”

mentioning

confidence: 99%

No Elevation of Glutathione S-transferase-A1-1 by Amiodarone Loading in Intensive Care Unit Patients with Atrial Fibrillation

Hilkens

Pickkers

Peters

et al. 2009

Anaesth Intensive Care

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Hepatocellular toxicity is a putative side-effect of amiodarone. The hepatic detoxification enzyme glutathione S-transferase-A1-1 (GSTA1-1) is a sensitive indicator of hepatocellular damage. We investigated the occurrence of subclinical liver injury, as measured by plasma GSTA1-1 in intensive care unit patients with atrial fibrillation receiving amiodarone.Sixteen haemodynamically stable intensive care unit patients with atrial fibrillation were treated with amiodarone intravenously. Patients were given a loading dose of 150 mg followed by another 150 mg followed by a continuous infusion of 1200 mg/hour if atrial fibrillation persisted. Blood samples for GSTA1-1 (measured by an enzyme-linked immunosorbent assay) were taken at zero, one, three, six, 12 and 24 hours, transaminases and bilirubin at zero, six, 12 and 24 hours. Blood pressure and heart rate were continuously monitored. Effects were analysed for timedependent changes (one-way analysis of variance for repeated measures).Blood pressure increased from 125±8/60±3 mmHg at t=0 to 144±9/66±4 mmHg at t=24 hours (P <0.05), heart rate decreased from atrial fibrillation 124±5 to sinus rhythm 86±6 beats per minute (P <0.05). There was no significant elevation of GSTA1-1, transaminases or bilirubin during the observation period of 24 hours.Amiodarone does not cause elevation of GSTA1-1 as a marker of subclinical liver injury in haemodynamically stable intensive care unit patients with atrial fibrillation.

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“…We read with interest the report by Skroubis et al about the occurrence of amiodarone‐induced pulmonary toxicity (APT) in a patient suffering from post‐operative atrial fibrillation (1). We would like to highlight certain other issues regarding APT.…”

mentioning

confidence: 99%