DOI:10.2214/AJR.05.0786
AJR 2007; 189:W135-W137
© American Roentgen Ray Society
Pulmonary Hemorrhage in a Patient with Acute Coronary Syndrome
Gabriel C. Fernández-Perez1,
María Vázquez2,
Carlos Delgado1,
María Velasco1,
Ana Vázquez-Lima3 and
José Rodríguez-Pérez3
1 Department of Radiology, Povisa Medical Center, Salamanca St. 5, Vigo 36211,
Pontevedra, Spain.
2 Department of Cardiology, Povisa Medical Center, Vigo, Pontevedra,
Spain.
3 Intensive Care Unit, Povisa Medical Center, Vigo, Pontevedra, Spain.
Received May 11, 2005;
accepted after revision August 9, 2005.
Address correspondence to G. C. Fernández-Perez.
WEB This is a Web exclusive article.
Keywords: cardiopulmonary imaging • chest • pulmonary hemorrhage • radiography
Introduction
Massive pulmonary hemorrhage after treatment with antiplatelet drugs
is a rare event that can occur in patients with acute coronary syndrome (ACS).
The use of medications such as tirofiban (Aggrastat, Merck) and abciximab
(ReoPro, Eli Lilly) has been associated with improvement in short-term outcome
among patients with ACS who undergo coronary angioplasty
[1]. Pulmonary hemorrhage
appears as bilateral alveolar infiltrates on chest radiographs and can be
easily mistaken for acute pulmonary edema in the context of ACS
[2]. When the infiltrates do
not resolve with administration of diuretics, the radiologist must be aware of
the possibility of pulmonary hemorrhage because early treatment can increase
the probability of survival. We report the clinical and radiologic features of
a patient with ACS complicated by massive pulmonary hemorrhage due to use of
tirofiban.
Case Report
A 67-year-old man with preexisting ischemic heart disease was evaluated in
the emergency department for acute chest pain. Because ECG showed negative T
waves in V3 and V4 and progressive elevation of cardiac
enzyme levels, the diagnosis was ACS (unstable angina). Chest radiographs
obtained at the time were normal (Fig.
1A). Sonography showed septal akinesia with an ejection fraction
of 58%. Treatment with ß-blockers, nitrates, heparin, and aspirin was
begun. The pain resolved, but progressive changes occurred in the ECG,
negative T waves from V2 through V6; DI and aVL ECG
leads were detected. A standard IV infusion of tirofiban at a dose of 10
µg/kg over 3 minutes followed by a maintenance infusion of 0.15
µg/kg/min was initiated before the patient underwent coronary angiography
with the possibility of percutaneous coronary angioplasty. Coronary
angiography showed three diseased vessels. Chronic occlusion was present in
the right coronary artery and severe stenosis in the left circumflex and left
anterior descending coronary arteries. Percutaneous coronary angioplasty of
the left anterior descending artery was attempted, and the results were poor.
The patient was offered coronary artery bypass graft surgery.
One day after percutaneous coronary angioplasty, the patient reported
shortness of breath and hemoptysis. A chest radiograph showed bilateral
alveolar infiltrates (Fig. 1B).
Arterial blood gas measurements showed a decrease in
PO2. Management for cardiac failure was started, but the
radiologic findings showed no changes (Figs.
1C and
1D). Laboratory results showed
a decrease in hemoglobin concentration from 13.7 to 12 mg/dL. Platelet count,
activated partial thromboplastin time, and prothrombin time were normal.
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Fig. 1B —67-year-old man with acute coronary syndrome. Chest radiograph 24
hours after percutaneous coronary angioplasty shows bilateral alveolar
infiltrates with central distribution and thickened minor fissure. Cardiac
silhouette is similar to that in A. Radiographic differentiation of
diffuse alveolar hemorrhage from hydrostatic pulmonary edema is difficult.
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Fig. 1C —67-year-old man with acute coronary syndrome. Chest radiograph 48
hours after percutaneous coronary angioplasty shows extensive bilateral
diffuse confluent acinar ground-glass areas of increased pulmonary
consolidation. Despite therapy for cardiac failure, radiologic findings are
not altered.
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Fig. 1D —67-year-old man with acute coronary syndrome. Chest radiograph 4
days after percutaneous coronary angioplasty shows persistent extensive
bilateral alveolar infiltrates with no change. Presence of hemoptysis and
sparing of peripheral pulmonary parenchyma are clues to diagnosis.
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Over several days, the PO2 severely decreased, and
the patient needed endotracheal intubation with mechanical ventilation. The
hemoglobin concentration decreased to 8.4 mg/dL, and alveolar infiltrates
persisted on chest radiographs. Bronchoscopic examination showed clots and
blood in the trachea and bronchial tree without active bleeding. CT
(Fig. 1E) showed bilateral
ground-glass patch lesions interpreted as areas of pulmonary hemorrhage
associated with reticular and parenchymal opacifications due to adult
respiratory distress syndrome. The patient's condition was complicated by
unstable hemodynamic events and nosocomial infections. He died 30 days after
arriving at the hospital.
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Fig. 1E —67-year-old man with acute coronary syndrome. CT scan several days
after D shows ground-glass patch lesions (arrows) due to
pulmonary hemorrhage and parenchymal opacifications interpreted as adult
respiratory distress syndrome.
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Discussion
Tirofiban is a nonpeptide inhibitor of the platelet glycoprotein IIb/IIIa
receptor (GP IIb/IIIa), the final common pathway for platelet aggregation. The
use of GP IIb/IIIa inhibitors is recommended in the care of patients with
unstable angina and non-ST segment elevation myocardial infarction
[1]. These agents are related
to medicines such as aspirin, nitrates, ß-blockers, and heparin because
they reduce not only the occurrence of ischemic events 48 hours after
myocardial infarction but also mortality due to refractory ischemia and new
myocardial infarction. GP IIb/IIIa inhibitors also are used in the care of
patients undergoing percutaneous cornonary angioplasty to substantially reduce
major adverse cardiac events. In this setting, tirofiban and similar drugs,
such as abciximab, a chimeric mouse-human monoclonal antibody directed against
the GP IIb/IIIa receptor, are widely used in coronary care units
[3].
The most frequent complications of the use of GP IIb/IIIa inhibitors are
reversible thrombocytopenia and hemorrhage
[4-6].
Bleeding problems, including arterial access and gastrointestinal and
genitourinary hemorrhage, are easily recognized. Intracranial hemorrhage is
another possible but infrequent complication. The incidence of bleeding
complications has been associated with the dose-weight relation; with renal
failure, in which the dose should be halved; and with concomitant use of other
anticoagulant drugs [2]. Choi
et al. [7] reported a relation
between bleeding complications and female sex, older age, complicated or
prolonged percutaneous cornonary angioplasty, the presence of underlying
pulmonary problems such as chronic obstructive pulmonary disease and pulmonary
hypertension, high pulmonary capillary wedge pressure, and use of
defibrillation before percutaneous cornonary angioplasty.
Massive pulmonary hemorrhage is a rare complication that occurs most often
when GP IIb/IIIa inhibitors are used in association with other platelet
antiaggregating agents, such as aspirin, ticlopidine, and clopidogrel. Kalra
et al. [2] found seven
documented cases in a study involving 2,553 patients treated with abciximab,
an incidence of 0.27%. However, the number of patients in whom intrapulmonary
bleeding might have been mild and unrecognized or incorrectly diagnosed is
unknown. In this regard, massive pulmonary hemorrhage has been infrequently
reported; we found no reference in the radiology literature.
Hypoxemia and hemoptysis with new alveolar infiltrates on chest radiography
can be easily mistaken for pulmonary edema, infection, and even aspiration. If
this error occurs, patients can be incorrectly treated for heart failure or
with antibiotics, and the outcome could be fatal in many cases. Our patient
reported dyspnea and hemoptysis, but both signs are common in pulmonary edema.
Thus in this case the first radiologic diagnosis was pulmonary edema.
The presence of bilateral infiltrates not altered with diuretics must
remind us to be cautious in reaching the correct diagnosis, particularly in a
patient with ACS treated with GP IIb/IIIa inhibitors. Another clue is a
decrease in hemoglobin concentration, but this finding usually is delayed.
Early suspicion of pulmonary hemorrhage should lead to prompt withdrawal of
infusion of GP IIa/IIIb inhibitors, heparin, and additional antiplatelet drugs
to try to stop the pulmonary bleeding. When pulmonary hemorrhage is suspected,
bronchoscopy should be performed because the findings may lead to the
diagnosis. The procedure also can have a therapeutic role: Balloon tamponade
can be performed in the bleeding area, or iced saline lavage can be used if
the bleeding point is not located
[8].
In conclusion, if a patient with ACS being treated with infusion of a GP
IIa/IIIb inhibitor reports dyspnea and hemoptysis and alveolar infiltrates are
found, the possibility of pulmonary hemorrhage must be considered,
particularly if the radiologic findings remain unchanged over several hours.
Early treatment is mandatory for avoiding fatal consequences.
References
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- Topol EJ, Moliterno DJ, Herrmann HC, et al. Comparison of two
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Introduction
Case Report
