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Original Report |
Department of Imaging, Hammersmith Hospital, Du Cane Rd., London W12 0HS, England.
Received March 23, 2004;
accepted after revision July 6, 2004.
Address correspondence to J. E. Jackson.
Abstract
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CONCLUSION. Peripheral pulmonary artery pseudoaneurysms occur in up to 11% of patients undergoing bronchial angiography for hemoptysis. These are often most easily appreciated on bronchial and/or nonbronchial systemic arterial angiograms because of complete reversal of flow in pulmonary artery branches in the diseased lung. Embolization of bronchial and nonbronchial systemic arteries alone may not be sufficient therapy to control hemoptysis, and occlusion of the pseudoaneurysm itself via a pulmonary artery approach is recommended.
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We identified eight patients (male-female ratio, 6:2) with a mean age of 63 years (age range, 34-74 years) in whom peripheral pulmonary artery pseudoaneurysms were found, ranging from 5 to 9 mm (Table 1). One (patient 4) had two pseudoaneurysms and the other seven had one each. Three (patients 2, 3, and 4) had fibrocavitary pulmonary disease consistent with postprimary tuberculosis. One of these individuals had undergone a previous thoracoplasty, and another had silicosis and progressive massive fibrosis. Two of the patients with fibrocavitary disease (patients 3 and 4) had aspergillomas (radiographic changes consistent with complicating mycetoma formation and positive Aspergillus precipitins). Two additional patients (patients 5 and 7) had active tuberculosis (one with a multidrug-resistant organism) at the time of presentation with hemoptysis. The remaining three patients did not have a history of previous tuberculosis; two (patients 1 and 6) had lower zone bronchiectasis, one of whom had undergone a previous lower lobectomy with residual bronchiectasis involving a portion of the remaining middle lobe. The final patient (patient 8) had an aspergilloma in a preexisting upper lobe cavity of unknown cause. At the time of admission, three patients (in addition to those two with active tuberculosis) had proven bacterial pulmonary infection, two with Pseudomonas species and one with a mixed growth.
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All patients underwent aortography performed with a pigtail catheter positioned just beyond the left subclavian artery to show the bronchial and nonbronchial artery supply to both lungs arising from the descending thoracic aorta. Selective catheterization of these vessels was performed. In the presence of apical lung disease, subclavian arteriography was also undertaken followed by selective catheterization of any branch contributing a supply to the lungs.
In six of the eight patients, a peripheral pulmonary aneurysm was shown on bronchial or nonbronchial systemic artery angiograms because of the presence of systemic arterial-to-pulmonary artery shunting (Figs. 1A, 1B, 2A, 2B, 3A, 3B, 3C, 3D, 3E, 4A, 4B, 4C, 4D, 5A, 5B, 5C, and 5D). In five of these patients, pulmonary artery catheterization was performed with the systemic arterial catheter in place to aid selective catheterization of the diseased peripheral pulmonary artery branch. In these five patients, embolization of the aneurysmal pulmonary artery branch was performed with coils (n = 4) (Figs. 3A, 3B, 3C, 3D, 3E, 4A, 4B, 4C, and 4D) or N-butyl-2-cyanoacrylate (n = 1) (Figs. 5A, 5B, 5C, and 5D) before the systemic arterial supply to the lung was occluded with polyvinyl alcohol (PVA). One of these individuals (patient 2) was transferred from the ICU of a nearby hospital, having required intubation for respiratory failure due to massive hemoptysis. Initial bronchial angiography at that time revealed the presence of a peripheral pulmonary artery pseudoaneurysm, but its importance was not appreciated and bronchial and nonbronchial systemic artery embolization alone was performed. He was transferred back to the referring hospital, but during subsequent attempted extubation, hemoptysis recurred. At a second embolization session, the pseudoaneurysm was embolized (Figs. 5A, 5B, 5C, and 5D), and he was subsequently extubated without problem.
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In one patient, a pulmonary artery aneurysm was identified during bronchial arteriography, but only the systemic arterial supply to the lung was embolized, again with PVA.
In the two remaining patients, pulmonary artery aneurysmal disease was not shown during bronchial arteriography, despite marked systemic arterial-to-pulmonary artery shunting in both. These two patients underwent bronchial arteriography and embolization of all of the abnormal bronchial artery and systemic arterial branches identified but presented with recurrent hemoptysis. Pulmonary arteriography was therefore performed and depicted a single aneurysm in one patient, which was embolized with coils. In the second individual, selective peripheral pulmonary artery angiograms showed two pulmonary artery pseudoaneurysms, and these were catheterized and embolized with platinum microcoils.
All eight individuals were successfully treated and discharged after embolization without further hemoptysis during their inpatient stay. Hemoptysis recurred during follow-up in four of the eight patients, however, at 1 month (patient 7), 2 months (patient 8), 6 months (patient 6), and 3 years (patient 3) after embolization. All four underwent further bronchial angiography at which the previously embolized pulmonary artery aneurysms were not visualized and were presumed thrombosed; bronchial embolization was repeated in these individuals. The patient presenting again at 1 month (patient 7) remains alive and well without further hemoptysis at 3-year follow-up. The patient presenting again at 2 months (patient 8) continued to have hemoptysis and underwent subsequent embolization of several peripheral pulmonary artery vessels, although there was no evidence of further pulmonary artery aneurysmal disease. Despite this treatment, small-volume hemoptysis continued, and the patient underwent surgical resection of a mycetoma 2 months later. She remains well at 18-month follow-up.
The patient presenting again at 6 months (patient 6) died of cardiac arrest 8 months after this second embolization, without further hemoptysis, while being investigated as an inpatient for weight loss. Patient 3 remained well for 1 year further (4 years after his initial bronchial and pulmonary artery embolization) but then died after a massive hemoptysis without preceding warning bleeding.
Two further patients have died, one of severe pneumonia (patient 2) 6 weeks after successful embolization without recurrent hemoptysis. The other (patient 1) had no further hemoptysis for 3 years although he had recurrent chest infections. He subsequently died without hemoptysis; his records at the time of his death were unobtainable, and his cause of death is therefore not known. The patient with multidrug-resistant tuberculosis (patient 5) underwent a pneumonectomy because of severe unremitting infection 2 months after embolization and remains well at 3-year follow-up. The last patient (patient 4) has remained well without further hemoptysis at 4 years.
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Incidence
Auerbach [3] described
finding such aneurysms in 45 (4%) of 1,114 consecutive autopsies of patients
with chronic pulmonary tuberculosis. In 38 of these aneurysms, rupture was the
immediate cause of death.
Remy et al. [4] prospectively studied 72 patients presenting with hemoptysis with both bronchial and pulmonary angiography to detect a pulmonary source of hemorrhage and showed pulmonary artery pseudoaneurysms in six individuals (8.3%). Five of these patients had cavitary tuberculosis, one complicated by an aspergilloma. The two other patients were both alcoholics who developed pseudoaneurysms related to pyogenic lung abscesses. Of the three patients with pseudoaneurysms due to cavitary tuberculosis, one was treated surgically with cessation of bleeding for 18 months. This patient then died, however, of massive hemoptysis. The other two individuals were treated by embolization without rebleeding in one at 4 years. Follow-up of the second patient was for only 9 months, and it is unclear whether hemoptysis persisted. Of the two patients with mycotic pseudoaneurysms, one died of septic shock 2 days after embolization and the other survived without rebleeding to a follow-up of 7 months.
Sanyika et al. [5] reported three pseudoaneurysms in a total of 59 patients (5%) treated for massive hemoptysis by embolization with Gianturco coils. Two of these patients were discharged from the hospital on antituberculous chemotherapy and presumably, therefore, had active tuberculosis. The third patient in this series was described as having had "suppurative lung disease" and undergoing pneumonectomy. No short- or long-term follow-up was given.
In our series, almost 11% of patients undergoing bronchial angiography for hemoptysis had visible pulmonary artery pseudoaneurysms, and in the subset of patients with chronic pulmonary tuberculosis, the incidence was 14%. These figures are higher than those previously reported; these findings might simply reflect a more diligent search for aneurysmal disease and the routine use of digital subtraction angiography (which was not used in prospective series of Remy et al. [4]).
Etiology
Thirty-five percent (27/76) of all individuals undergoing bronchial
angiography for hemoptysis during this study period had either chronic
(n = 22) or active (n = 5) pulmonary tuberculosis. A
pulmonary artery pseudoaneurysm was seen in 18.5% (5/27) of these overall and
in 13.6% (3/22) of those with chronic disease. Two of five patients with
active tuberculosis had pulmonary aneurysmal disease, but it is not possible
to draw any conclusions from this finding because of the small numbers
involved. Of perhaps greater significance, however, is the high incidence
(37.5%, 3/8) of pulmonary artery pseudoaneurysms in patients with mycetomas
complicating either chronic tuberculosis or sarcoidosis, although once again,
the numbers are small.
Pathogenesis
The development of pulmonary artery pseudoaneurysms in patients with
chronic pulmonary tuberculosis has been well described. Auerbach
[3] concluded on the basis of
histopathologic changes observed in three of his autopsies that "the
aneurysm develops as a result of the progressive destruction and replacement
of the elastic fibers of the pulmonary artery from without inward by
granulation tissue" from the outer wall of a tuberculous cavity. As the
cavity undergoes progressive healing, the granulation tissue within its wall
continuously increases, and it is this granulation tissue that destroys the
elastic fibers of the artery in a circumscribed area, resulting in aneurysmal
formation.
That aneurysmal development occurred secondary to "healing" of the cavity was supported, Auerbach [3] suggested, by two observations: 62% of his 45 cases had chronic pulmonary tuberculosis for periods ranging from 2 to 19 years, and there was a considerably smaller incidence of aneurysmal disease in the much larger group of autopsies he performed on individuals with tuberculosis of less than 2 years' duration.
Bronchial Supply
Enlargement of normal bronchopulmonary anastomoses is common in patients
with chronic inflammatory lung disease resulting in the frequently observed
angiographic finding of systemic arterial-to-pulmonary artery shunting.
Because this occurs in areas of lung involved by more severe disease, which is
where pulmonary artery pseudoaneurysms are more likely to develop, these
pseudoaneurysms are seen on the systemic arterial angiograms. In fact, because
of the complete reversal of flow within pulmonary artery branches that may
occur secondary to the systemic arterial-to-pulmonary artery shunting,
paradoxically, pulmonary aneurysmal disease may be better seen on systemic
rather than on pulmonary arteriography. Of the eight patients in our series,
the pseudoaneurysm was initially visible on the bronchial or nonbronchial
systemic artery arteriograms in six. This is an important point, which, to our
knowledge, has received little attention in the literature to date.
Remy et al. [4] described Rasmussen's pseudoaneurysms as having both bronchial and pulmonary artery perfusion, which was unusual in our series; in almost all our patients, the degree of systemic arterial-to-pulmonary artery shunting was such that there was complete reversal of blood flow within pulmonary artery branches with no antegrade flow on subsequent pulmonary artery angiograms to whole segments or lobes of the affected lung. Any pseudoaneurysm within such an area is, therefore, only perfused by systemic blood via bronchopulmonary anastomoses.
In two of the patients presented here, pulmonary artery pseudoaneurysms were seen only on subsequent pulmonary angiography. Both these individuals continued to have hemoptysis after embolization of abnormal bronchial and nonbronchial systemic arteries. The policy in our unit is to proceed to pulmonary angiography in any patient who either continues to bleed or who has early recurrent bleeding within the first few weeks after what is believed to have been an adequate bronchial artery embolization. These two individuals, therefore, underwent pulmonary angiography, which revealed their pulmonary artery aneurysmal disease.
Embolization Technique
The technique used to occlude pulmonary artery pseudoaneurysms is usually
that of coil embolization of the pulmonary artery branch supplying the
aneurysmal sac [4,
6,
7], but filling of the sac
itself with coils has also been described
[4,
8]. Both techniques were
reported as being successful. In three patients presented here, the aneurysmal
sac itself was filled with embolic material, whereas in four patients, the
pulmonary artery immediately proximal to the neck of the pseudoaneurysm was
occluded. The latter circumstance may still allow perfusion of the aneurysmal
sac via bronchopulmonary anastomoses distal to the emboli, but occlusion of
the feeding bronchial or nonbronchial systemic arteries, which was achieved in
all individuals, should encourage pseudoaneurysm thrombosis. These
embolization techniques appear to have been successful in terms of aneurysm
obliteration because none of them showed recanalization in the four patients
who required repeat angiography.
Prognosis
Four patients had recurrent hemoptysis between 1 month and 3 years after
initial embolization, and one of these individuals was the only patient to die
as a result of bleeding 4 years after his initial presentation. Four patients
remain well without hemoptysis at follow-up periods of 18 months, 3 years (two
patients), and 4 years, but two of these patients also required surgery. These
results are similar to those expected in patients who have hemoptysis due to
chronic lung disease without a pulmonary artery aneurysm who are treated by
bronchial artery embolization
[9,
10] and simply reflect the
palliative nature of embolization in such patients.
That pulmonary artery pseudoaneurysms are a potent cause of bleeding and require treatment is supported by the fact that in three patients in whom bronchial artery embolization alone was initially performed (patients 2, 3, and 4), hemoptysis continued until the pseudoaneurysms were occluded via a pulmonary artery approach. It is therefore our policy to embolize all pulmonary artery pseudoaneurysms via this approach when first identified. The one patient in whom this procedure was not performed in this series (patient 1) was treated before the importance of embolization of pulmonary artery pseudoaneurysms was recognized and fortunately did not have further hemoptysis.
In the patients who underwent repeat bronchial angiography for recurrent hemoptysis, the previously embolized pseudoaneurysms were not opacified and it was assumed that these were thrombosed. In retrospect, in one of these individuals, the pseudoaneurysm was not seen at the time of the original bronchial angiogram; for this reason, pulmonary angiography should perhaps have been repeated to confirm aneurysm thrombosis. This individual underwent repeat bronchial artery embolization alone and survived 1 year longer before dying of massive hemoptysis; he was the only patient in this series to have died as a result of bleeding. It is likely, in view of this information, that the pseudoaneurysm had recurred.
In the three other patients who had recurrent hemoptysis, pseudoaneurysm thrombosis was more certain because in all of them, the pulmonary arteries involved by the aneurysmal disease were directly visualized because of filling via bronchial and nonbronchial collateral vessels; in one patient, pulmonary angiography was also performed and confirmed pseudoaneurysm occlusion. Recurrent bleeding in these three patients presumably occurred, therefore, from friable vessels within adjacent abnormal lung exposed to increased pressure from hypertrophied bronchial and nonbronchial systemic arteries.
Conclusion
Pulmonary artery pseudoaneurysms occur in up to 11% of patients undergoing
bronchial angiography for hemoptysis and in approximately 14% of those with
chronic pulmonary tuberculosis. In most individuals, these pseudoaneurysms are
well seen and may indeed be more easily appreciated on bronchial or
nonbronchial systemic arterial angiograms because of complete reversal of flow
in pulmonary artery branches in the diseased lung. Embolization of bronchial
and nonbronchial systemic arteries alone may not be sufficient therapy to
control hemoptysis, and occlusion of the pseudoaneurysm itself via a pulmonary
artery approach is recommended. Hemoptysis may recur even in the presence of
confirmed pseudoaneurysm occlusion but generally responds well to repeat
embolization of bronchial and nonbronchial systemic arteries.
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