Amiodarone pulmonary toxicityBMJ 1997; 314 doi: http://dx.doi.org/10.1136/bmj.314.7097.1831b (Published 21 June 1997) Cite this as: BMJ 1997;314:1831
Authors did not emphasise typical radiological and histological features sufficiently
- Andrew Leonard, Senior registrar in respiratory medicinea,
- Paul Corris, Consultant respiratory physiciana,
- Dinah Parums, Consultant cardiothoracic pathologista
- a Regional Cardiothoracic Centre, Freeman Hospital, Newcastle upon Tyne NE7 7DN
- b Department of Anaesthetics, Ninewells Hospital, Dundee DD2 1UB
- c Western General Hospital, Edinburgh EH4 2XU
- d University Hospital Groningen, 9700 RB Groningen, Netherlands
Editor—In their editorial on amiodarone pulmonary toxicity Gillian A J Jessurun and Harry J G M Crijns made several misleading statements about the diagnosis of this dangerous condition.1 Although they are correct in stating that pulmonary toxicity has rarely been reported after low doses of amiodarone or after short periods of treatment, they make statements relating to the clinical and pathological features that are not supported by the literature or our own experience. They suggest that hyperinflation is a common radiological manifestation of amiodarone toxicity, that the spirometric pattern usually suggests obstruction, and that the presence of lamellar inclusion bodies on electron microscopy is specific for amiodarone toxicity. These statements are incorrect and misleading.
The radiological findings in amiodarone lung vary, but the commonest pattern is of asymmetric bilateral alveolar opacification, which may mimic tuberculosis if seen in the upper zones and pulmonary oedema if seen in the midzones and lower zones; other patterns include solitary or multiple masses and lobar or segmental consolidation. Pleural effusions may be seen together with other findings but rarely alone. The radiological differential diagnosis therefore includes infection, heart failure, and malignancy. Computed tomography …
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