DOI: 10.1148/rg.226015180
(Radiographics. 2002;22:1395-1409.)
© RSNA, 2002
Bronchial and Nonbronchial Systemic Artery Embolization for Life-threatening Hemoptysis: A Comprehensive Review1
Woong Yoon, MD,
Jae Kyu Kim, MD,
Yun Hyun Kim, MD,
Tae Woong Chung, MD and
Heoung Keun Kang, MD
1 From the Department of Diagnostic Radiology, Chonnam National University Hospital, Chonnam National University Medical School, 8 Hak-1-dong, Dong-gu, Gwangju 501-757, South Korea. Recipient of a Certificate of Merit award for an education exhibit at the 2001 RSNA scientific assembly. Received December 19, 2001; revision requested April 23, 2002; final revision received July 26; accepted August 1. Address correspondence to W.Y. (e-mail: radyoon@cnuh.com).
 |
Abstract
|
|---|
Massive hemoptysis is one of the most dreaded of all respiratory emergencies and can have a variety of underlying causes. In 90% of cases, the source of massive hemoptysis is the bronchial circulation. Diagnostic studies for massive hemoptysis include radiography, bronchoscopy, and computed tomography (CT) of the chest. Bronchoscopy and chest radiography have been considered the primary methods for the diagnosis and localization of hemoptysis. Many researchers currently suggest that CT should be performed prior to bronchoscopy in all cases of massive hemoptysis. Bronchial artery embolization (BAE) is a safe and effective nonsurgical treatment for patients with massive hemoptysis. However, nonbronchial systemic arteries can be a significant source of massive hemoptysis and a cause of recurrence after successful BAE. Knowledge of the bronchial artery anatomy, together with an understanding of the pathophysiologic features of massive hemoptysis, are essential for planning and performing BAE in affected patients. In addition, interventional radiologists should be familiar with the techniques, results, and possible complications of BAE and with the characteristics of the various embolic agents used in the procedure.
© RSNA, 2002
Index Terms: Arteries, bronchial, 943.1264, 943.92 • Arteries, therapeutic embolization, 943.1264 • Bronchi, anatomy, 671.92 • Bronchi, interventional procedures • Lung, CT, 60.1211, • Lung, hemorrhage • Pulmonary angiography, 60.124
|
LEARNING OBJECTIVES
|
|---|
After reading this article and taking the test, the reader will be able to:
- List the most common causes of massive hemoptysis.
- Discuss the roles of CT and bronchoscopy in the diagnosis of massive hemoptysis.
- Describe the techniques, embolic materials, results, and complications associated with BAE for massive hemoptysis.
|
Introduction
|
|---|
Life-threatening hemoptysis is one of the most challenging conditions encountered in critical care and requires a thorough and timely investigation. Despite advances in medical and intensive care unit management, massive hemoptysis remains a serious threat. According to recently published data, 28% of chest clinicians had experienced a patient’s death from massive hemoptysis during a previous 1-year period (1). Conservative management of massive hemoptysis carries a mortality rate of 50%–100% (2). The cause of death is usually asphyxiation, not exsanguination (3). The reported mortality rates for surgery performed for massive hemoptysis range from 7.1% to 18.2% (4). However, the mortality rate increases significantly, up to about 40%, when the surgery is undertaken as an emergency procedure (4).
Bronchial artery embolization (BAE) has become an established procedure in the management of massive and recurrent hemoptysis; its use was first reported in 1973 by Remy et al (5). The efficacy, safety, and utility of BAE in controlling massive hemoptysis have been well documented in many subsequent reports (6–14). Because of poor pulmonary reserve and other medical comorbid conditions, most patients with massive hemoptysis are not surgical candidates (2,3). However, surgery remains the procedure of choice in the treatment of massive hemoptysis caused by specific conditions, such as hydatid cyst, thoracic vascular injury, bronchial adenoma, and aspergilloma that is resistant to other therapies (15). Even in surgical candidates, BAE is effective in preparing the patient for elective rather than high-risk emergency surgery (4).
In this article, we describe the definition and causes, pathophysiologic features, and diagnosis of massive hemoptysis and review the angiographic and computed tomographic (CT) anatomy of the bronchial circulation. We also discuss the technique, embolic materials, results, and complications associated with BAE. In addition, we describe the role of nonbronchial systemic artery embolization and present CT findings that are useful in predicting the existence of nonbronchial systemic arterial supply in patients with massive hemoptysis.
|
Massive Hemoptysis
|
|---|
Definition and Causes
Massive hemoptysis has been described as the expectoration of an amount of blood ranging from 100 mL to more than 1,000 mL over a period of 24 hours, and the most widely used criterion is the production of 300–600 mL per day (2–4,15). However, depending on the ability of the patient to maintain a patent airway, a life-threatening condition may be caused by a rather small amount of hemorrhage. Thus, a more functional definition of "massive" as an amount sufficient to cause a life-threatening condition should be used in deciding whether to undertake interventional management (15,16).
Massive hemoptysis may result from various causes, and the frequency with which these causes occur differs greatly between the Western and the non-Western world. In the non-Western world, pulmonary tuberculosis, including tuberculosis bronchiectasis, is the most common underlying cause of massive hemoptysis. Bronchogenic carcinoma and chronic inflammatory lung diseases due to bronchiectasis, cystic fibrosis, or aspergillosis are the more prevalent causes of hemoptysis in Western countries (2,3,15). Other causes include lung abscess, pneumonia, chronic bronchitis, pulmonary interstitial fibrosis, pneumoconiosis, pulmonary artery aneurysm (Rasmussen aneurysm), congenital cardiac or pulmonary vascular anomalies, aortobronchial fistula, ruptured aortic aneurysm, and ruptured bronchial artery aneurysm.
Bronchial artery aneurysm or pseudoaneurysm is a rare entity, and the term aneurysm is used interchangeably with pseudoaneurysm in the literature (17–22). The cause of bronchial artery aneurysm is unknown, although bronchiectasis or recurrent bronchopulmonary inflammation, a mycotic origin, trauma, and Rendu-Osler-Weber syndrome are often associated with an aneurysm (21). Bronchial artery aneurysms can be characterized as either mediastinal (juxtaaortic) or intrapulmonary. The treatment options for bronchial artery aneurysm include transcatheter embolization, placement of a covered stent, and surgery (21,22).
Pathophysiologic Features
The source of massive hemoptysis is usually the bronchial circulation (90% of cases) rather than the pulmonary circulation (5%) (23). In a minority of cases (5%), massive hemoptysis may originate with the aorta (eg, aortobronchial fistula, ruptured aortic aneurysm) or the systemic arterial supply to the lungs (24–26). In many acute and chronic lung diseases, pulmonary circulation is reduced or occluded at the level of the pulmonary arterioles because of hypoxic vasoconstriction, intravascular thrombosis, and vasculitis (27). As a result, bronchial arteries proliferate and enlarge to replace the pulmonary circulation. The enlarged bronchial vessels, which exist in an area of active or chronic inflammation, may be ruptured due to erosion by a bacterial agent or due to elevated regional blood pressure. The arterial blood under systemic arterial pressure subsequently extravasates into the respiratory tree, resulting in massive hemoptysis (27,28).
Diagnosis
Diagnostic studies for massive hemoptysis include radiography, bronchoscopy, and CT of the chest (15,16,29,30). In patients with massive hemoptysis, the diagnostic work-up is usually performed both to find the cause of the bleeding and to localize the pulmonary lobes in which bleeding is suspected. Localization of the bleeding site prior to BAE is very important if the procedure is to be performed in a focused and efficient manner.
Conventional radiography is a basic study and is readily available even under emergency conditions. It may be helpful in diagnosing and localizing pneumonia, acute or chronic pulmonary tuberculosis, bronchogenic cancer, or lung abscess (29). However, radiographic findings are normal or nonlocalizing in 17%–81% of patients with hemoptysis (16,29–33). In a retrospective evaluation of 208 patients with hemoptysis, Hirshberg et al (31) found that radiography was considered to be diagnostic in only 50% of cases.
Bronchoscopy has long been considered by chest clinicians to be the primary method for diagnosis and localization of hemoptysis (34,35). Fiberoptic bronchoscopy (FOB) has proved efficacious in evaluating central bronchial lesions. A vasoactive drug can be infused locally during bronchoscopy to control bleeding (15).
It has been reported that FOB can help localize bleeding to one side or the other in 49%–92.9% of patients with hemoptysis (16,31,33). The role of FOB in the evaluation of patients who present with hemoptysis is still controversial, especially in cases in which chest radiographic findings are normal or nonlocalizing (29). The diagnostic accuracy of FOB in patients with hemoptysis and normal chest radiographs is low, ranging from 0% to 31% (29,31,32,36,37). The overall diagnostic accuracy of FOB in evaluating patients with hemoptysis is reported to be 10%–43% (29–33). In a recent article, Hsiao et al (16) documented that FOB prior to BAE is unnecessary in patients with hemoptysis of known cause if the site of bleeding can be determined on conventional radiographs. FOB has some disadvantages in the diagnosis and localization of massive, active hemoptysis. It is difficult to localize the bleeding site with FOB in patients with massive hemoptysis because of excessive blood in the bronchi. Moreover, endobronchial therapies are not effective in most cases of massive hemoptysis (15). The risks of FOB include possible airway compromise from sedation, delay in definitive treatment, hypoxemia, and high cost.
The role of CT in the evaluation of patients with hemoptysis has been validated (30,32,38). CT has proved to be of considerable value in diagnosing bronchiectasis, bronchogenic carcinoma, and aspergilloma in patients with massive hemoptysis (31,39). CT may demonstrate lesions that may not be visible on conventional radiographs, and contrast material–enhanced CT may help detect vascular lesions that cause massive hemoptysis. CT findings can suggest a specific diagnosis in 50% of patients in whom FOB findings are nondiagnostic and in 39%–88% of patients in whom chest radiographs are nondiagnostic (29,30,32,39). CT can also help localize the site of bleeding in 63%–100% of patients with hemoptysis, a rate that is higher than that for FOB (16,33). It has been stated that CT and FOB are not competitive but complementary tools for assessing patients with hemoptysis, and indeed, the combined use of FOB and CT does yield the best results in evaluating hemoptysis (33). However, many researchers are currently suggesting that CT should be performed prior to bronchoscopy in all patients with hemoptysis (15,30,32,38). State-of-the-art CT allows rapid scanning, making timely examination feasible in critically ill patients. In addition, bronchial and nonbronchial systemic feeder vessels can be detected at contrast-enhanced CT. In a prospective study of 40 patients with massive hemoptysis, 27 patients (67.5%) had a nonbronchial systemic arterial supply, and CT had an overall accuracy of 84% in identifying this finding (unpublished data).
|
Anatomy of the Bronchial Artery
|
|---|
Interventional radiologists who perform BAE should have a thorough knowledge of bronchial artery anatomy. The bronchial arteries have variable anatomy in terms of origin, branching pattern, and course (40). The bronchial arteries originate directly from the descending thoracic aorta, most commonly between the levels of the T5 and T6 vertebrae (3). Cauldwell et al (41) reported four classic bronchial artery branching patterns: two on the left and one on the right that presents as an intercostobronchial trunk (ICBT) (40% of cases); one on the left and one ICBT on the right (21%); two on the left and two on the right (one ICBT and one bronchial artery) (20%); and one on the left and two on the right (one ICBT and one bronchial artery) (9.7%) (Fig 1). The right ICBT is the most consistently seen vessel at angiography (80% of individuals) (Fig 2). The right ICBT usually arises from the right posterolateral aspect of the thoracic aorta and the normal right and left bronchial arteries from the anterolateral aspect of the aorta. Right and left bronchial arteries that arise from the aorta as a common trunk are not uncommon at angiography (Fig 3). The true prevalence of a common bronchial artery trunk is unknown.
View larger version (18K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 1. Diagrams illustrate the types of bronchial arterial supply: Type I, two bronchial arteries on the left and one on the right that manifests as an ICBT (40.6% of cases); Type II, one on the left and one ICBT on the right (21.3%); Type III, two on the left and two on the right (one ICBT and one bronchial artery) (20.6%); and Type IV, one on the left and two on the right (one ICBT and one bronchial artery) (9.7%).
|
|
View larger version (193K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 2. Right intercostobronchial artery. On a selective right ICBT angiogram, an intercostal branch (solid arrows) and the right bronchial artery (open arrows) are seen to arise from a common trunk.
|
|
View larger version (201K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 3. Common bronchial trunk. On a selective bronchial angiogram, the right intercostobronchial artery (black arrow) and a pathologic left bronchial artery (white arrow) are seen to arise from a common trunk and supply hypervascular lesions in the left lower lobe.
|
|
The bronchial arteries supply the trachea, extra- and intrapulmonary airways, bronchovascular bundles, nerves, supporting structures, regional lymph nodes, visceral pleura, and esophagus as well as the vasa vasorum of the aorta, pulmonary artery, and pulmonary vein (27).
Bronchial arteries that originate outside the area between the T5 and T6 vertebrae at the level of the major bronchi are considered to be anomalous (41,42). The reported prevalence of bronchial arteries with an anomalous origin ranges from 8.3% to 35% (42,43). These aberrant bronchial arteries may originate from the aortic arch, internal mammary artery (Fig 4), thyrocervical trunk (Fig 5), subclavian artery, costocervical trunk, brachiocephalic artery, pericardiacophrenic artery, inferior phrenic artery, or abdominal aorta. Aberrant bronchial arteries can be distinguished anatomically and angiographically from nonbronchial systemic collateral vessels in that they extend along the course of the major bronchi. In contrast, nonbronchial systemic collateral vessels enter the pulmonary parenchymathrough the adherent pleura or via the pulmonary ligament, and their course is not parallel to that of the bronchi (42). The majority of aberrant bronchial arteries originate from the aortic arch (41,42). The prevalence of bronchial arteries with origins outside the aorta is unknown. Interventional radiologists should be aware of the possible presence of aberrant bronchial arteries, especially when a significant bronchial arterial supply to areas of abnormal pulmonary parenchyma is not demonstrated during a catheter search or at descending thoracic aortography (44). In addition, bronchial arteries of anomalous origin should be suspected and investigated angiographically in patients who present with recurrent hemoptysis despite successful embolization and in those in whom the source of bleeding has not been detected (42).
View larger version (216K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 4. Aberrant bronchial artery in a 46-year-old man who presented with massive hemoptysis. Thoracic aortography and a catheter search demonstrated only hypertrophic intercostal arteries with no identification of the right bronchial artery. Despite the embolization of multiple pathologic intercostal arteries, massive hemoptysis recurred after 1 day, and the patient underwent repeat angiography. Selective right internal mammary angiogram shows an aberrant right bronchial artery (arrows) that originates from the proximal portion of the right internal mammary artery. This aberrant bronchial artery was embolized, and the massive hemoptysis did not recur during a follow-up period of 1 year.
|
|
View larger version (187K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 5a. Aberrant bronchial artery. (a) Thoracic aortogram shows a hypertrophic right bronchial artery (arrow) and intercostal arteries that supply hypervascular lesions in both upper lobes. There is no evidence of hypervascularity in the right middle lobe or the lower lobes despite the visualization of significant parenchymal lesions at chest radiography. (b) Image obtained after selective injection of an aberrant bronchial artery that arises from the left thyrocervical trunk shows hypertrophic arteries that supply hypervascular lesions in the right lower and left upper lobes. Unlike systemic collateral vessels, the aberrant bronchial arteries extend along the course of the primary bronchi.
|
|
View larger version (161K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 5b. Aberrant bronchial artery. (a) Thoracic aortogram shows a hypertrophic right bronchial artery (arrow) and intercostal arteries that supply hypervascular lesions in both upper lobes. There is no evidence of hypervascularity in the right middle lobe or the lower lobes despite the visualization of significant parenchymal lesions at chest radiography. (b) Image obtained after selective injection of an aberrant bronchial artery that arises from the left thyrocervical trunk shows hypertrophic arteries that supply hypervascular lesions in the right lower and left upper lobes. Unlike systemic collateral vessels, the aberrant bronchial arteries extend along the course of the primary bronchi.
|
|
Two kinds of spinal arteries may be seen at bronchial and intercostal angiography during BAE. Dorsal and ventral radicular arteries (Fig 6) are small vessels that arise from segmental spinal arteries and supply the dorsal and ventral roots. An average of eight anterior medullary arteries reinforce the anterior spinal artery, which is the major independent source of spinal cord perfusion. The artery of Adamkiewicz, or greater anterior medullary artery, reinforces the circulation of lumbar enlargement of the spinal cord. This unilateral vessel has been observed to arise between T9 and T12 in 75% of cases (45). Anterior medullary arteries have a characteristic "hairpin" configuration at angiography (Fig 7). Radicular arteries are often visualized during BAE. In our experience, unintentional embolization of radicular arteries does not cause clinical problems like spinal cord ischemia. It has been stated that the presence of radicular arteries is not considered to be a contraindication for BAE (8,9,43). Anterior medullary arteries are rarely observed, but embolization and repeat angiography should be avoided because spinal cord ischemia may occur with embolization. It has been suggested that spinal arteries will arise from the intercostal branch of the right ICBT in 5%–10% of cases, but it is generally believed that the true prevalence is considerably lower (3).
In adults, normal bronchial arteries measure less than 1.5 mm in diameter at their origin and 0.5 mm at their point of entry into a bronchopulmonary segment (27). A bronchial artery larger than 2 mm at CT is most likely abnormal (46). Hypertrophic bronchial arteries are easily visualized as enhancing nodular or tubular structures within the mediastinum and around the central airway on contrast-enhanced CT scans (47) (Figs 8, 9). The primary locations of enlarged bronchial arteries at CT are the retroesophageal area, retrotracheal area, retrobronchial area, posterior wall of the main bronchus, and aortopulmonary window. Mediastinal lymph nodes, the azygos vein, and an enhancing esophageal wall can mimic the bronchial arteries at CT (48).
View larger version (92K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 8. Bronchial artery. Contrast-enhanced CT scan shows a pathologic right bronchial artery (arrow) that originates from the anteromedial aspect of the thoracic aorta and a hypertrophic left bronchial artery in the aortopulmonary window (arrowheads).
|
|
|
Bronchial Artery Embolization
|
|---|
Technique
Prior to BAE, the number and origin sites of bronchial arteries from the aorta should be carefully evaluated to determine the optimal angiographic approach. This can be accomplished with a preliminary descending thoracic aortogram. Abnormal bronchial arteries are visualized on an initial thoracic aortogram in the majority of affected patients (Fig 10). A descending thoracic aortogram is also useful in the detection of nonbronchial systemic arteries that supply parenchymallesions (Fig 11) (49). Although cobra-type curved catheters are most commonly used for catheterization of the bronchial artery, several different types of catheters (eg, Simmons-1, headhunter, Yashiro-type) should be prepared for optimal selection of bronchial arteries. The usefulness of a microcatheter for selective BAE has been emphasized in many recent articles (2,3,50,51). This superselective catheterization permits stabilization of the catheter position within the bronchial artery and safe positioning in the bronchial circulation beyond the origin of spinal cord branches, which prevents severe complications (Fig 12). After catheterization of the bronchial artery, bronchial angiography is performed with manual injection of contrast medium.
View larger version (191K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 10a. Value of preliminary thoracic aortography. (a) Descending thoracic aortogram demonstrates two hypertrophic bronchial arteries (solid arrows) and one intervening intercostal artery (open arrow) that supply a hypervascular lesion in the right upper lobe. (b) On a selective upper bronchial angiogram, the bronchial artery that supplies the large hypervascular lesion is seen to have an anomalous origin from the inferior aspect of the aortic arch. Marked bronchopulmonary shunting is also noted. (c) Selective lower bronchial angiogram shows a hypertrophic artery that supplies the hypervascular lesion, along with marked bronchopulmonary shunting. (d) Selective intercostal angiogram shows a hypertrophic artery that supplies the hypervascular lesion, along with bronchopulmonary shunting. The two bronchial arteries and the intervening intercostal artery were selectively embolized with polyvinyl alcohol particles. Postembolization angiograms (not shown) demonstrated occlusion of each vessel, with no opacification of the hypervascular lesion and no pulmonary arterial shunting.
|
|
View larger version (198K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 10b. Value of preliminary thoracic aortography. (a) Descending thoracic aortogram demonstrates two hypertrophic bronchial arteries (solid arrows) and one intervening intercostal artery (open arrow) that supply a hypervascular lesion in the right upper lobe. (b) On a selective upper bronchial angiogram, the bronchial artery that supplies the large hypervascular lesion is seen to have an anomalous origin from the inferior aspect of the aortic arch. Marked bronchopulmonary shunting is also noted. (c) Selective lower bronchial angiogram shows a hypertrophic artery that supplies the hypervascular lesion, along with marked bronchopulmonary shunting. (d) Selective intercostal angiogram shows a hypertrophic artery that supplies the hypervascular lesion, along with bronchopulmonary shunting. The two bronchial arteries and the intervening intercostal artery were selectively embolized with polyvinyl alcohol particles. Postembolization angiograms (not shown) demonstrated occlusion of each vessel, with no opacification of the hypervascular lesion and no pulmonary arterial shunting.
|
|
View larger version (186K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 10c. Value of preliminary thoracic aortography. (a) Descending thoracic aortogram demonstrates two hypertrophic bronchial arteries (solid arrows) and one intervening intercostal artery (open arrow) that supply a hypervascular lesion in the right upper lobe. (b) On a selective upper bronchial angiogram, the bronchial artery that supplies the large hypervascular lesion is seen to have an anomalous origin from the inferior aspect of the aortic arch. Marked bronchopulmonary shunting is also noted. (c) Selective lower bronchial angiogram shows a hypertrophic artery that supplies the hypervascular lesion, along with marked bronchopulmonary shunting. (d) Selective intercostal angiogram shows a hypertrophic artery that supplies the hypervascular lesion, along with bronchopulmonary shunting. The two bronchial arteries and the intervening intercostal artery were selectively embolized with polyvinyl alcohol particles. Postembolization angiograms (not shown) demonstrated occlusion of each vessel, with no opacification of the hypervascular lesion and no pulmonary arterial shunting.
|
|
View larger version (158K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 10d. Value of preliminary thoracic aortography. (a) Descending thoracic aortogram demonstrates two hypertrophic bronchial arteries (solid arrows) and one intervening intercostal artery (open arrow) that supply a hypervascular lesion in the right upper lobe. (b) On a selective upper bronchial angiogram, the bronchial artery that supplies the large hypervascular lesion is seen to have an anomalous origin from the inferior aspect of the aortic arch. Marked bronchopulmonary shunting is also noted. (c) Selective lower bronchial angiogram shows a hypertrophic artery that supplies the hypervascular lesion, along with marked bronchopulmonary shunting. (d) Selective intercostal angiogram shows a hypertrophic artery that supplies the hypervascular lesion, along with bronchopulmonary shunting. The two bronchial arteries and the intervening intercostal artery were selectively embolized with polyvinyl alcohol particles. Postembolization angiograms (not shown) demonstrated occlusion of each vessel, with no opacification of the hypervascular lesion and no pulmonary arterial shunting.
|
|
View larger version (191K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 11a. Value of preliminary thoracic aortography. (a) Descending thoracic aortogram shows a tortuous branch of the right inferior phrenic artery (arrows) that supplies a hypervascular lesion in the right lower lobe. (b) Selective right inferior phrenic angiogram shows a nonbronchial systemic artery that supplies the hypervascular lesion (arrows) in the right lower lobe. Filling of the pulmonary artery is also seen.
|
|
View larger version (179K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 11b. Value of preliminary thoracic aortography. (a) Descending thoracic aortogram shows a tortuous branch of the right inferior phrenic artery (arrows) that supplies a hypervascular lesion in the right lower lobe. (b) Selective right inferior phrenic angiogram shows a nonbronchial systemic artery that supplies the hypervascular lesion (arrows) in the right lower lobe. Filling of the pulmonary artery is also seen.
|
|
View larger version (168K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 12a. Superselective embolization with a microcatheter. (a) Selective intercostal angiogram shows hypervascular areas and a small amount of pulmonary arterial shunting (open arrow) at the periphery of the left lower lung field. Note the small radicular artery (solid arrow) that arises from the proximal portion of the intercostal artery. (b) Postembolization angiogram shows a microcatheter (arrows) that has been advanced into the intercostal artery beyond the origin of the radicular artery.
|
|
View larger version (172K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 12b. Superselective embolization with a microcatheter. (a) Selective intercostal angiogram shows hypervascular areas and a small amount of pulmonary arterial shunting (open arrow) at the periphery of the left lower lung field. Note the small radicular artery (solid arrow) that arises from the proximal portion of the intercostal artery. (b) Postembolization angiogram shows a microcatheter (arrows) that has been advanced into the intercostal artery beyond the origin of the radicular artery.
|
|
Angiographic findings in massive hemoptysis include hypertrophic and tortuous bronchial arteries, neovascularity, hypervascularity (Figs 3, 5, 10), shunting into the pulmonary artery or vein (Figs 13, 14), extravasation of contrast medium (Fig 15), and bronchial artery aneurysm (Fig 16). Although extravasation of contrast medium is considered a specific sign of bronchial bleeding, this finding is rarely seen, and its reported prevalence ranges from 3.6% to 10.7% (12,16). Thus, the determination of which arteries are to be embolized should be based on a combination of CT, bronchoscopic, and angiographic findings with clinical correlation. All angiograms, including intercostal arteriograms, must be carefully scrutinized for opacification of spinal arteries to avoid inadvertent embolization.
View larger version (209K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 13. Systemic artery-pulmonary artery shunt. Right bronchial angiogram demonstrates an enlarged bronchial artery that supplies a hypervascular lesion in the right upper lobe. There is massive bronchopulmonary shunting with visualization of the branches of the right upper lobar pulmonary arteries (arrows).
|
|
View larger version (149K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 14. Systemic artery-pulmonary vein shunt. Right ICBT angiogram shows a hypervascular staining lesion in the right lower lung as well as shunting with branches of the right inferior pulmonary vein (arrows).
|
|
View larger version (166K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 15. Contrast material extravasation. Right bronchial angiogram shows multifocal hypervascular lesions in the right lung and extravasation of contrast material into the right lower lobe bronchus (arrow).
|
|
View larger version (172K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 16a. Bronchial artery aneurysm. (a) Selective left bronchial angiogram demonstrates a large, hypervascular lesion in the left upper lobe with an aneurysm (arrow). (b) On an angiogram obtained after embolization with polyvinyl alcohol particles, neither the hypervascular lesion nor the aneurysm is visualized.
|
|
View larger version (163K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 16b. Bronchial artery aneurysm. (a) Selective left bronchial angiogram demonstrates a large, hypervascular lesion in the left upper lobe with an aneurysm (arrow). (b) On an angiogram obtained after embolization with polyvinyl alcohol particles, neither the hypervascular lesion nor the aneurysm is visualized.
|
|
Embolic Materials
A variety of embolic materials are used for BAE. Absorbable gelatin sponge is widely used because it is inexpensive, easy to handle, and has a controllable embolic size. However, disadvantages of absorbable gelatin sponge are its resolvability and lack of radiopacity. Its use may lead to recanalization of the embolized artery and may sometimes be responsible for recurrent bleeding (50). Polyvinyl alcohol particles are nonabsorbable embolic materials, and particles 350–500 µm in diameter are the most frequently used worldwide (51). Their use may prevent the early recurrence of hemoptysis due to recanalization of the embolized artery, as might be anticipated with absorbable gelatin sponge.
It is essential to avoid the use of embolic materials that can pass through the bronchopulmonary anastomosis. Experimental study has demonstrated a bronchopulmonary anastomosis of 325 µm in the human lung (52). Pulmonary infarction via bronchial artery–pulmonary artery shunts or systemic artery embolization via bronchial artery–pulmonary vein shunts may occur when embolic agents less than 325 µm in diameter are used. In addition, it is important to avoid using embolic agents that produce distal occlusion to such an extent that normal peripheral branches that supply the bronchi, esophagus, or vasa vasorum of the pulmonary artery or aorta become occluded, possibly leading to disastrous complications (eg, bronchial, esophageal, pulmonary arterial, or aortic wall necrosis) (3). To avoid the complications indicated earlier, we recommend the use of polyvinyl alcohol particles with a diameter of 350–500 µm for BAE.
Bronchopulmonary fistula is a common finding at bronchial angiography in patients with massive hemoptysis. Regardless of whether a bronchopulmonary fistula is demonstrated at bronchial angiography, we perform BAE with the same technique and the same size of embolic materials (polyvinyl alcohol particles over 350 µm in diameter or absorbable gelatin sponge), and we have not encountered any clinical problems related to pulmonary infarction or systemic embolization. Thus, we recommend the use of the same strategy even when a bronchopulmonary fistula is visualized at bronchial angiography.
Liquid embolic agents (eg, isobutyl-2 cyanoacrylate, absolute ethanol) are not currently used because of the high risk of severe complications such as tissue necrosis. Stainless steel platinum coils are generally not used for BAE because they tend to occlude more proximal vessels and may preclude repeat embolization if hemoptysis recurs. However, they may be used to occlude a pulmonary artery aneurysm and may occasionally be used in the internal mammary artery to prevent embolization of a normal vascular territory and development of collateral vessels (Fig 17) (3,53).
View larger version (195K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 17a. Coil embolization. (a) Selective right internal mammary angiogram shows small branches that supply a hypervascular staining lesion in the right upper lobe, as well as a pseudoaneurysm (arrow). (b) On a postembolization angiogram obtained after deposition of two coils (arrows) at both the proximal and distal portions of the origin site of the small branches and use of additional polyvinyl alcohol particles, neither the hypervascular lesion nor the pseudoaneurysm is visualized.
|
|
View larger version (181K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 17b. Coil embolization. (a) Selective right internal mammary angiogram shows small branches that supply a hypervascular staining lesion in the right upper lobe, as well as a pseudoaneurysm (arrow). (b) On a postembolization angiogram obtained after deposition of two coils (arrows) at both the proximal and distal portions of the origin site of the small branches and use of additional polyvinyl alcohol particles, neither the hypervascular lesion nor the pseudoaneurysm is visualized.
|
|
Results
Previous studies have shown that BAE is very effective in controlling acute massive hemoptysis. The initial nonrecurrence rates for BAE have been reported to be 73%–98%, with a mean follow-up period ranging from 1 day to 1 month (7–14,54). Immediate success rates have increased recently because of the introduction of superselective embolization and the refinement of embolic agents and techniques. However, the long-term success rate of BAE in hemoptysis is unfavorable. Long-term recurrence rates have been reported to be 10%–52%, with a mean follow-up period ranging from 1 to 46 months (2,3,55). However, the long-term success rate can be improved with repeat BAE. Hemoptysis may recur after successful BAE if the disease process is not controlled with drug therapy or surgery because embolization does not address the underlying disease but rather treats the symptom. In this sense, BAE is a palliative procedure that prepares the patient for elective surgery for localized disease or continued antimicrobial therapy (51).
Recurrent bleeding may be caused by recanalization of embolized vessels, incomplete embolization, revascularization by the collateral circulation, inadequate treatment of the underlying disease, progression of basic lung disease, or nonbronchial systemic arterial supply (2,3,51,55). Recurrence rate may also be influenced by the cause of the hemoptysis. Recurrent bleeding is more common in patients with chronic tuberculosis, aspergilloma, or neoplasm. In one study of 103 patients who underwent BAE, 16 patients (15.5%) required repeat embolization; all 16 had hemoptysis due to chronic tuberculosis (56). It is believed that this was due mainly to hypertrophy of the collateral nonbronchial systemic arteries. In a series by Katoh et al (55), 75% of patients with aspergilloma experienced recurrence of hemoptysis after undergoing initial embolization. Hayakawa et al (11) reported that BAE failed within 1 month in 42% of patients with neoplasm. A neoplasm receives its blood supply from multiple feeder vessels other than the bronchial artery and invades the vascular structure aggressively.
Complications
Several complications of BAE have been reported in the literature. Chest pain is the most common complication, with a reported prevalence of 24%–91% (12,43,57). Chest pain is likely related to an ischemic phenomenon caused by embolization and is usually transient. In addition, dysphagia due to embolization of esophageal branches may be encountered, with a reported prevalence of 0.7%–18.2% (12,57). Dysphagia also regresses spontaneously. Subintimal dissection of the aorta or the bronchial artery during BAE is the other minor complication, with a reported prevalence of 1%–6.3% (8,9,11,13,14). There are usually no symptoms or problems related to the subintimal dissection.
The most disastrous complication of BAE is spinal cord ischemia due to the inadvertent occlusion of spinal arteries. The prevalence of spinal cord ischemia after BAE is reported to be 1.4%–6.5% (12,13,50,58). As discussed earlier, the visualization of radicular branches on bronchial or intercostal angiograms is not an absolute contraindication for BAE. However, when the anterior medullary artery (artery of Adamkiewicz) is visualized at angiography, embolization should not be performed.
Other rare complications that have been reported in the literature include aortic and bronchial necrosis, bronchoesophageal fistula, non–target organ embolization (eg, ischemic colitis), pulmonary infarction, referred pain to the ipsilateral forehead and orbit, and transient cortical blindness (59–64). It is hypothesized that cortical blindness develops because of embolism to the occipital cortex, either via a bronchial artery–pulmonary vein shunt or via collateral vessels between the bronchial and vertebral arteries (64).
|
Nonbronchial Systemic Arterial Supply
|
|---|
Nonbronchial systemic arteries can be a significant source of massive hemoptysis, especially in patients with pleural involvement caused by an underlying disease. Missing the nonbronchial systemic arteries at initial angiography may result in early recurrent bleeding after successful embolization of the bronchial artery. Many investigators have documented that a concerted search for nonbronchial systemic arterial supply should be made (3,10,53,56,58). In the presence of pleural thickening, nonbronchial systemic feeder vessels that originate from various arteries (eg, intercostal artery [Figs 10, 12], branches of the subclavian and axillary arteries [Figs 18–20], internal mammary artery [Fig 21], inferior phrenic artery [Fig 11]) (3,10,47,53,55) may develop along the pleural surface and become enlarged as a result of the inflammatory process. Pleural thickening that is noted at chest radiography negatively influences the long-term success rate of BAE (65). CT may help predict the presence of nonbronchial systemic collateral vessels as a source of bleeding in patients with massive hemoptysis. In our experience, pleural thickening of more than 3 mm and tortuous enhancing vascular structures within hypertrophic extrapleural fat seen at contrast-enhanced CT are signs of nonbronchial systemic arterial supply in patients with massive hemoptysis (Figs 21, 22) (unpublished data). Use of CT to predict the presence of nonbronchial systemic vessels that supply a parenchymal lesion is important prior to BAE because it helps in localizing the site of bleeding and in selecting systemic vessels for the interventional approach.
View larger version (143K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 18. Nonbronchial systemic artery. Right subclavian angiogram shows an enlarged superior thoracic artery, lateral thoracic artery, and subscapular artery and numerous small branches from the subclavian and axillary arteries that supply a hypervascular lesion in the right upper lobe, along with systemic artery-pulmonary artery shunting (arrows).
|
|
View larger version (190K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 19. Nonbronchial systemic artery. Selective left thyrocervical angiogram shows tortuous branches that supply a hypervascular lesion in the left upper lung, with a pseudoaneurysm (solid arrow) and systemic artery-pulmonary artery shunting (open arrow).
|
|
View larger version (173K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 20. Nonbronchial systemic artery. Selective right lateral thoracic angiogram shows a hypervascular lesion with systemic artery-pulmonary artery shunting (arrows) in the periphery of the right upper lobe.
|
|
View larger version (169K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 21a. Prediction of nonbronchial systemic arterial supply. (a) Contrast-enhanced CT scan shows irregular pleural thickening at the left apical thorax with tortuous vascular structures within a hypertrophic extrapleural layer of fat (arrows). (b) On a left subclavian angiogram, a tortuous, enlarged internal mammary artery (solid arrows) and its branches are seen to supply a hypervascular lesion in left upper lobe. A hypertrophic lateral thoracic artery (open arrows) also supplies the hypervascular lesion.
|
|
View larger version (187K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 21b. Prediction of nonbronchial systemic arterial supply. (a) Contrast-enhanced CT scan shows irregular pleural thickening at the left apical thorax with tortuous vascular structures within a hypertrophic extrapleural layer of fat (arrows). (b) On a left subclavian angiogram, a tortuous, enlarged internal mammary artery (solid arrows) and its branches are seen to supply a hypervascular lesion in left upper lobe. A hypertrophic lateral thoracic artery (open arrows) also supplies the hypervascular lesion.
|
|
View larger version (152K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 22a. Prediction of nonbronchial systemic arterial supply. (a) Contrast-enhanced CT scan demonstrates diffuse pleural thickening at the upper thorax (solid arrows) and tortuous, enhancing vascular structures within a hypertrophic extrapleural layer of fat (open arrows). Hypertrophic bronchial arteries are also seen in the aortopulmonary window. (b) Selective intercostal angiogram shows tortuous hypertrophic vessels with systemic artery-pulmonary artery shunting (arrows).
|
|
View larger version (193K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 22b. Prediction of nonbronchial systemic arterial supply. (a) Contrast-enhanced CT scan demonstrates diffuse pleural thickening at the upper thorax (solid arrows) and tortuous, enhancing vascular structures within a hypertrophic extrapleural layer of fat (open arrows). Hypertrophic bronchial arteries are also seen in the aortopulmonary window. (b) Selective intercostal angiogram shows tortuous hypertrophic vessels with systemic artery-pulmonary artery shunting (arrows).
|
|
|
Conclusions
|
|---|
Massive hemoptysis constitutes a significant and often life-threatening respiratory emergency. Bronchial and nonbronchial systemic artery embolization is a safe and effective nonsurgical treatment for patients with massive hemoptysis. Knowledge of bronchial artery anatomy, together with an understanding of the pathophysiologic features of massive hemoptysis, are essential for performing BAE. The pulmonary artery can be the source of massive hemoptysis in a minority of cases, and pulmonary arterial disease should be considered in cases of recurrent hemoptysis. CT is useful in diagnosing the disease that causes massive hemoptysis, localizing the bleeding site, and selecting vessels to be embolized. In addition, CT may be helpful in predicting the presence of nonbronchial systemic collateral vessels, which can be a significant source of recurrent hemoptysis after successful BAE.
|
Footnotes
|
|---|
Abbreviations: BAE = bronchial artery embolization,
FOB = fiberoptic bronchoscopy,
ICBT = intercostobronchial trunk
|
References
|
|---|
- Haponik EF, Fein A, Chin R. Managing life-threatening hemoptysis: has anything really changed? Chest 2000; 118:1431-1435.[Abstract/Free Full Text]
- Najarian KE, Morris CS. Arterial embolization in the chest. J Thorac Imaging 1998; 13:93-104.[Medline]
- Marshall TJ, Jackson JE. Vascular intervention in the thorax: bronchial artery embolization for hemoptysis. Eur Radiol 1997; 7:1221-1227.[CrossRef][Medline]
- Fernando HC, Stein M, Benfield JR, Link DP. Role of bronchial artery embolization in the management of hemoptysis. Arch Surg 1998; 133:862-866.[Abstract/Free Full Text]
- Remy J, Voisin C, Ribet M, et al. Treatment, by embolization, of severe or repeated hemoptysis associated with systemic hypervascularization. Nouv Presse Med 1973; 2:2060-2068[French].
- Wholey MH, Chamorro HA, Rao G, Ford WB, Miller WH. Bronchial artery embolization for massive hemoptysis. JAMA 1976; 236:2501-2504.[Abstract]
- Remy J, Arnaud A, Fardou H, Giraud R, Voisin C. Treatment of hemoptysis by embolization of bronchial arteries. Radiology 1977; 122:33-37.[Abstract]
- Uflacker R, Kaemmerer A, Neves C, Picon PD. Management of massive hemoptysis by bronchial artery embolization. Radiology 1983; 146:627-634.[Abstract/Free Full Text]
- Uflacker R, Kaemmerer A, Picon PD, et al. Bronchial artery embolization in the management of hemoptysis: technical aspects and long-term results. Radiology 1985; 157:637-644.[Abstract/Free Full Text]
- Keller FS, Rosch J, Loflin TG, Nath PH, McElvein RB. Nonbronchial systemic collateral arteries: significance in percutaneous embolotherapy for hemoptysis. Radiology 1987; 164:687-692.[Abstract/Free Full Text]
- Hayakawa K, Tanaka F, Torizuka T, et al. Bronchial artery embolization for hemoptysis: immediate and long-term results. Cardiovasc Intervent Radiol 1992; 15:154-159.[Medline]
- Ramakantan R, Bandekar VG, Gandhi MS, Aulakh BG, Deshmukh HL. Massive hemoptysis due to pulmonary tuberculosis: control with bronchial artery embolization. Radiology 1996; 200:691-694.[Abstract/Free Full Text]
- Mal H, Rullon I, Mellot F, et al. Immediate and long-term results of bronchial artery embolization for life-threatening hemoptysis. Chest 1999; 115:996-1001.[Abstract/Free Full Text]
- Kato A, Kudo S, Matsumoto K, et al. Bronchial artery embolization for hemoptysis due to benign diseases: immediate and long-term results. Cardiovasc Intervent Radiol 2000; 23:351-357.[CrossRef][Medline]
- Jean-Baptiste E. Clinical assessment and management of massive hemoptysis. Crit Care Med 2000; 28:1642-1647.[CrossRef]
Top
Abstract
LEARNING OBJECTIVES
