Vol.2, No.9, 521-524 (2013) Case Reports in Clinical Medicine
Amiodarone-induced bronchiolitis obliterans
organizing pneumonia in patient following
percutaneous transluminal coronary angioplasty
Massimo Bolognesi1*, Diletta Bolognesi2
1General Practice Medicine-Primary Care , C esena, Ita ly; *Corresponding Author: massbolo1@tin.it
2Territorial Medicine-Primary Care, Cesena, Italy
Received 23 September 2013; revised 20 October 2013; accepted 18 November 2013
Copyright © 2013 Massimo Bolognesi, Diletta Bolognesi. This is an open access article distributed under the Creative Commons
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Background: Many patients are affected by idio-
pathicbronchiolitis obliterans organizing pneu-
monia (BOOP). There are several know n causes
of BOOP, and several systemic disorders have
BOOP as an associated primary pulmonary le-
sion. Numerous agents including cytotoxic and
noncytotoxic drugs have the potential to cause
pulmonary toxicity. Descriptions of amiodarone-
related BOOP continue to be reported through-
out the world. Case Report: We reported a pa-
tient with original clinical presentation who de-
veloped recurrent sustained ventricular tachy-
cardia (SVT) despite the presence of implant able
cardioverter-defibrillator (ICD), hypoxaemia and
interstitial pneumonitis in both lung bases. After
percutaneous transluminal coro nary angioplasty,
he developed bronchiolitis obliterans organizing
pneumonia (BOOP). Conclusions: To our know-
ledge, such complications after percutaneous
coronary procedure in patients with amiodarone
therapy for arrhythmia prophylaxis, are not very
frequent in literature.
Keywords: Percutaneous Tr ansluminal Coronary
Angioplasty; Amiodarone; BOOP
Bronchiolitis obliterans organizing pneumonia (BOOP)
is a distinct entity with various clinical, rad iographic and
histologic features [1]. The term Bronchiolitis obliterans
organizing pneumonia was first described in the early
1980s as a clinical pathologic syndrome characterized
symptomatically by subacute and chronic respiratory
illness, histopathologically by granulation tissue in the
bronchiolar lumen, alveolar ducts with some alveoli as-
sociated with a variable degree of interstitial and air
space infiltration by mononuclear cells with foamy
macrophages [2]. In most cases, the aetiology remains
unknown, although it has been associated with specific
diseases and causes including bacterial or viral infections,
diseases of the connective tissue, radiation therapy, mye-
lodysplastic syndrome, cocaine abuse, human immuno-
deficiency virus (HIV) infection, gastrointestinal disor-
ders, coronary artery bypassing grafting, and more vari-
ous pharmaceutical drugs [3]. Amiodarone is one of the
principal drugs involved in pulmonary toxicity, espe-
cially in patients undergoing cardiac surgery [4]. The
manifestations of pulmonary toxicity from amiodarone,
described in the literature include bronchiolitis obliter-
ans with or without sign s of organizing pneumonia, with
or without chronic interstitial fibrosis, pulmonary solitary
or multiple masses or respiratory distress syndrome [5-
11]. A tissue biopsy specimen is needed for a precise
diagnosis, but clinicoradiologic characteristics deter-
mined through biopsy-based studies may provide suffi-
cient diagnostic information. In fact, the ch est radiograph
showed the typical bilateral patchy (alveolar) infiltrate
and even more, the chest computed tomographic scan
showed the same findings, with bilateral areas of con-
solidation and ground glass opacities, usually with a pe-
ripheral location [6]. High-resolution chest computed
tomographic scans showed two types of linear opacities
that usually occurred in the lower lobes, frequently asso-
ciated with multifocal areas of consolidation, and usually
completely resolved with treatment [7]. We report here a
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M. Bolognesi, D. Bolognesi / Case Reports in Clinical Medicine 2 (2013) 521-524
case of a patient with classic clinical and radiological
description of amiodarone-induced BOOP seen immedi-
ately after percutaneous coronary intervention (PCI).
This report concerns an 81-year-old man suffering from
ischemic dilated cardiomyopathy and permanent atrial
fibrillation. The patient had had previous myocardial
infarction and sustained ventricular tachycardia (SVT)
with impairment of theleft ventricular systolic function
that required multiple drugs, including amiodarone, and
implantable cardioverter-defibrillator (ICD). Significant
multivessel coronary artery disease with severe left ven-
tricular dysfunction, estimate by ejection fraction to 30%,
requireda percutaneous coronary intervention (PCI) by
dualangioplasty with drug-eluting stent. This procedure
was carried out under poor clinical conditions. This pa-
tient was in long term treatment with L-tiroxin a for jatro-
genic hypothyroidism. After discharge, at home, he de-
veloped symptoms of an upper respiratory infection,
worsened shortness of breath and cough and was again
admitted to hospital. Postero-anterior chest radiograph
recorded the first time in supine position (see Figure 1,
Panel B) and 2 days later in sitting positio n (see Figure 1,
Panel A), showed a worsening of infiltration of the bilat-
eral inferior lobe of the lungs with mild pleu ral effu sion.
Pneumonia was initially diagnosed and an antibiotic
therapy (Levofloxacina and Ceftriaxone) was started,
while a cardiac ablation was performed for recurrent
SVT (see Figure 2). After four days the patient remained
symptomatic despite antibiotics and symptomatic man-
agement. A subsequent chest high-resolution computed
tomography (HRCT) scan (see Figure 3) showed exten-
sive bilateral opacities which were more pronounced in
the lower lobes, particularly in the right lobe. In additio n
to the chest HRCT, which confirmed the bilateral pres-
ence of basal pulmonary infiltrates, the pulmonary func-
tion tests showed reduced. Then, amiodaronew as dis-
continued and the patient began an anti-inflammatory
treatment with steroids at high dose for presumed BO OP.
Other medications such ascarvedilol, furosemide, ACE
inhibitors, digoxin, ceftriaxone and nebulised broncho-
dilators were continued. There was a dramatic improve-
ment in the clinical as well as radiological status within
72 hours, and a chest x ray sh owed f airly good resolu tion
of infiltrates (see Figure 4). Thus, the presumptive di-
agnosis of acute amiodarone toxicity was confirmed.
Pulmonary drug toxicity is a common and possibly
underdiagnosed cause of acute and chronic lung disease
[8]. There are numerous drugs with potential toxic ef-
fects on the lungs: one of these is amiodarone. As Nacca
et al. describes in our case study [9], diagnosis of amio-
darone pulmonary toxicity is often one of exclusion as
there are no specific laboratory analyses to confirm this.
Therefore, the diagnosis is based on a combination of
clinical suspicion, history, radiographic and clinical evi-
dence, with the exclusion of alternative etiologies. Chest
X ray and subsequent chest HRCT show bilateral dif-
fuse or patchy infiltrates, more commonly in the right
lobe. Furthermore, pleural thickening and/or effusion has
been described. Pulmonary function tests typically reveal
either a restrictive or mixed obstructive/restrictive pat-
tern with a decreased diffusion lung capacity of 15% -
20% [10]. In fact, the earliest abnormality in amiodar-
one pulmonary toxicity is a decrease in the diffusion ca-
pacity for carbon monoxide. The aim of this report is to
emphasize the possibility of this dangerous disease in
patients undergoing cardiovascular surgery or other pro-
cedures such as percutaneous coronary angioplasty, es-
pecially when they are in long term therapy with amio-
darone, and when signs of iatrogenic effects such as hy-
pothyroidismare already present. The clinician must keep
Chest x ray findings
Sitting position Supine position
Figure 1. Chest x ray, in supine (Panel B) and sitting positions (Panel A), shows a progressive
worsening of bilateral patchy infiltrates in the lower lungs with mild pleural effusion.
Copyright © 2013 SciRes. OPEN ACCESS
M. Bolognesi, D. Bolognesi / Case Reports in Clinical Medicine 2 (2013) 521-524 523
Figure 2. ECG shows sustained ventricular tachycardia.
chest computed tomography (CT) scan
Figure 3. Chest HRCT scan shows findings similar to the chest radiograph, with bi-
lateral areas of consolidation and ground glass opacities with a peripheral location.
Figure 4. Chest x ray shows full resolution of infiltrates with
normal radiographic a pp ea ra nc es .
this in mind because medical decision depends on clini-
cal skills rather than any definitive diagnostic tests or
proven therapies. Pulmonary toxicity can be fatal. A high
index of suspicion is necessary in establishing the diag-
nosis of amiodarone-induced BOOP, since most cases are
reversible if detected early. In summary, the toxicity of
amiodarone should be considered in the differential di-
agnosis of all patients who are being treated with this
medication and presenting progressive or acute respira-
tory symptoms, especially those with a history of chronic
lung disease, supplemental oxygen therapy and after car-
diac surgery.
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