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First published online March 28, 2007
British Journal of Radiology (2007) 80, 331-336
© 2007 British Institute of Radiology
doi: 10.1259/bjr/34204483
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Full paper

Endovascular therapy in the management of moderate and massive haemoptysis

A Poyanli, Asst Prof., MD B Acunas, Prof. I Rozanes, Prof. K Guven, MD S Yilmaz, MD A Salmaslioglu, MD E Terzibasioglu, MD and R Çirpin, MD

Istanbul Medical Faculty, Department of Radiology, Capa 34390, Sehremini, Istanbul, Turkey

Correspondence: Arzu Poyanli, Assistant Professor, IU Istanbul Tip Fakultesi Radiodiagnostik ABD, Department of Radiology, Capa 34390, Turkey. E-mail: aopoyanli{at}hotmail.com


   Abstract
Top
 Abstract
Introduction
 Methods and materials
 Results
 Discussion
 References
 
The aim of this study was to retrospectively evaluate 140 patients with severe (97 massive, 43 moderate) haemoptysis treated by bronchial artery embolisation. Between January 1997 and April 2005, 140 patients (120 males and 20 females, aged 23–71 years) with severe haemoptysis considered surgically inoperable because of limited pulmonary reserve were treated by embolisation. The cause of haemoptysis was tuberculosis in 136 patients and malignancy in four. Embolisation succeeded in controlling haemoptysis immediately after the intervention in 138 patients (98.5%) and at 1 month in 126 patients (90%). Severe haemoptysis recurred in 11 patients with prior massive haemoptysis and 3 patients with prior moderate haemoptysis in a mean time of 3.7 months (1–7 months) after the last intervention. The bleeding source was detected during angiography and embolised in 12 of these patients. Two patients with malignant tumour died because of abundant bleeding, following an asymptomatic period of 30 days. There were no procedure-related major complications. Bronchial artery embolisation is a safe and effective palliative treatment alternative in moderate and massive haemoptysis.


   Introduction
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 Abstract
 Introduction
Methods and materials
 Results
 Discussion
 References
 
Massive haemoptysis is defined as 300–600 ml of bleeding in 24 h [1]. The cause of death is usually asphyxiation rather than exsanguination. Mortality risk in massive haemoptysis is reported to be between 50 and 85% with conservative treatment alone and death generally occurs during the first hour [1, 2]. Resection of the diseased lung has in the past been considered the definitive treatment for massive haemoptysis. Emergency surgery during active bleeding has a 17–35% mortality rate [3, 4]. Many patients are unfit for surgery because of a combination of the acute hypoxaemia and limited lung capacity due to diffuse and severe chronic pulmonary disease.

Angiographic detection and endovascular treatment of the bleeding source is reported to be an effective and safe palliative treatment alternative [1, 5]. Recent successful results have broadened the indications for endovascular treatment to include moderate (more than or equal to three episodes of 100 ml of bleeding per day within 1 week) and even mild (chronic or slowly increasing) haemoptysis cases [6].

In this study, we aimed to evaluate our experience with 140 patients with massive and moderate haemoptysis treated by bronchial artery embolisation.


   Methods and materials
Top
 Abstract
 Introduction
 Methods and materials
Results
 Discussion
 References
 
Between January 1997 and April 2005, 140 patients (120 males and 20 females, aged 23–71 years, mean 44.1 years) with severe haemoptysis considered surgically inoperable because of limited pulmonary reserve were treated by bronchial artery embolisation. History of massive haemoptysis was present in 97 (69.2%) patients and moderate haemoptysis in 43 (30.8%).

Haemoptysis was caused by tuberculosis in 136 (97.1%) patients and lung cancer in four (2.9%). Haemoptysis was massive in all patients with lung cancer. All patients diagnosed with tuberculosis were in the inactive stage of the disease.

Bronchoscopy findings were taken into consideration whenever they were available. We did not insist on this procedure in order not to delay the treatment. Bilateral bronchial angiography was performed in every case.

Angiography was performed via femoral access in all patients. Embolisation was performed with high brachial puncture in four cases because the feeders originating from the subclavian artery could not be catheterized via femoral access. A 5F vascular sheath was used in all cases to facilitate catheter changes. 4F cobra or Simmons-1 catheters were used for selective catheterization. A microcatheter was used when necessary to ensure safe catheterization.

Assessment included selective bronchial angiography in every case. Additional angiography of the intercostal, subclavian or inferior phrenic arteries was performed depending on the location of the disease in the lung (Figure 1Go). Further flush angiography of the aortic arch and thoracic aorta was performed if the source was not identified. Pulmonary angiography was not routinely performed.


Figure 1
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  		Figure 1. Endovascular treatment was performed in a 61-year-old male patient with massive haemoptysis due to tuberculous bronchiectasis. (a) Left intercostal bronchial trunk, (b) right bronchial artery, (c,d) branches of right internal mammary artery. (e) A branch of the right costocervical trunk and (f) right fourth, and (g) fifth intercostal arteries causing parenchymal staining and pulmonary venous shunts were embolised after selective catheterization. (h) Post-embolisation image, intercostal artery injection. This patient had no recurrent bleeding during a follow-up period of 8 months.

 
Extravasation of contrast medium, thrombosis, hypertrophy or tortuosity of the vessels, pseudoaneurysms, parenchymal staining and arteriovenous shunting were considered positive angiographic findings.

After selective catheterization of the bleeding source in the bronchial artery or non-bronchial systemic vessels, embolisation was performed under fluoroscopic control using 250–350 µm and 350–500 µm sized polyvinyl alcohol (PVA) particles (Contour; Boston Scientific, Natick, MA) suspended in contrast medium. 350–500 µm PVA particles were used in patients with bronchopulmonary shunts and large bronchial arteries. Embolisation was terminated when antegrade flow was observed to stagnate or terminate.

Two 5 mm/10 mm and 3 mm/4 mm sized coils (Cook, Bjaeverskov, Denmark) were used to embolise the bleeding source originating from the main trunk supplying the apical and posterior branches of the right superior lobe artery in one case.

In patients with recurrent bleeding, additional bronchial artery, aberrant bronchial artery and abnormal non-bronchial systemic and pulmonary supply were investigated with angiography.


   Results
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 Abstract
 Introduction
 Methods and materials
 Results
Discussion
 References
 
Bronchoscopy was performed prior to angiography in 119 patients (85%). Bronchoscopy lateralized the side of bleeding in 73 patients (61.3%), but failed in 46 patients (38.7%).

Angiography findings are summarized in Table 1Go and the distribution and number of embolised arteries in Table 2Go.


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  		Table 1. Angiographic findings

 

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  		Table 2. Distribution and number of arteries which were embolised

 
Nine arteries (2.9%) in six patients not initially detected during selective injections were identified in the thoracic aortography performed immediately after embolisation. One was one right bronchial, and the other eight were intercostal arteries. All were embolised successfully.

The immediate success rate after bronchial artery embolisation, defined as no recurrence of bleeding within 24 h, was 98.5% (138 of 140 patients). Additional left bronchial artery supply, not detected in the first session, was detected and embolised during repeat angiography in two patients who had 150 ml of bleeding during the first 24 h. There was no recurrence at 3 months and 6 months follow up.

Control of haemoptysis at 1 month was observed in 126 patients (90%). 86 of these patients had massive and 40 had moderate haemoptysis and there was no recurrence during a mean follow up period of 33.6 months (1–90 months).

Severe haemoptysis developed in 11 prior massive and three prior moderate haemoptysis cases during an average time of 3.7 months (1–7 months) following the last intervention. There was systemic collateral supply from the costocervical trunk and abrupt termination of the segmentary pulmonary arterial branch in 1 case, and bronchial artery and systemic collateral development (not present in the previous session) in 11 cases. The bleeding sources or sources in these patients were embolised following selective catheterisation. Two sessions of endovascular treatment were performed in ten and three sessions were performed in two patients with recurrent haemoptysis. All of the recurrences were moderate. No haemoptysis was reported after the last embolisation during a mean follow up period of 46.6 months (16–86 months). Two of the cases with malignancy died during abundant bleeding following an asymptomatic 1 month period before any intervention could be performed.

Mild chest pain developed during and after the process in 67 (47.8%) cases. It resolved spontaneously in 2–7 days.

There were no major procedure related complications.


   Discussion
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 Abstract
 Introduction
 Methods and materials
 Results
 Discussion
References
 
Severe haemoptysis occurs most commonly in patients with a history of chronic inflammatory pulmonary disease. In the non-Western world, pulmonary tuberculosis –including tuberculous bronchiectasis – is the most common underlying cause in severe haemoptysis [7]. Despite the increase in human immunodeficiency virus (HIV) associated tuberculosis in the West, malignancy, cystic fibrosis and other non-tuberculous causes are still the most frequently reported causes [8]. In this study group including 140 patients with severe haemoptysis, tuberculosis was the aetiology in 97.1% of cases and lung cancer in 2.9%.

It is reported that bronchoscopy helps to detect the bleeding site in a lung or lobe in patients with diffuse pulmonary disease [9]. However, in patients with severe haemoptysis, the airways are filled with large volumes of blood restricting the use of bronchoscopy and similarly rendering endobronchial treatment ineffective [7]. Hsiao et al reported that bronchoscopy was not a prerequisite in the treatment process considering the risk of airway compromise from sedation, delay in definitive treatment, hypoxaemia and high cost [10]. In this study, bronchoscopy findings were taken into consideration whenever they were available. Not having performed a bronchoscopy did not affect our endovascular treatment progress. Bronchoscopy findings have not altered the course of angiography and endovascular treatment in any of our patients. In our experience, there was no need for emergency bronchoscopy during active severe bleeding.

CT has diagnostic superiority over bronchoscopy and chest radiograph for demonstrating underlying pathology and the site of bleeding in haemoptysis, especially in bronchiectasis, bronchogenic carcinoma and aspergilloma cases [8, 11]. Vascular pathologies such as arteriovenous malformation or aneurysm, which are rare causes of haemoptysis, are also depicted very clearly in contrast enhanced CT examinations [12]. With recent developments in multidetector CT technique it is now possible to scan the whole thorax with very thin slices (1.25 mm) in a very short time (12–15 s) [13, 14]. Both the lesion causing haemoptysis and the bronchial and non-bronchial systemic feeding arteries are detected during the same study using 80–100 ml of contrast medium. In angiography controlled studies, 86–87% of the pathologic vessels detected by angiography are reportedly demonstrated with CT angiography (CTA) as well [13, 14]. The road map thus prepared for the interventional radiologist by CTA is thought to shorten the examination time in critical patients.

The source of severe haemoptysis is the bronchial circulation in 90% of cases [15]. Significant bleeding from the pulmonary circulation is rare (5%) and is usually secondary to erosion of a pulmonary arterial branch by chronic inflammation. It is recommended to investigate the pulmonary circulation for a bleeding source following systemic arterial embolisation, in patients with recurring haemoptysis due to fibrocavitary tuberculosis [5]. In a minority of cases (approximately 5%) severe haemoptysis may originate from the aorta (e.g. aortobronchial fistula, ruptured aortic aneurysm) or non-bronchial systemic pulmonary arteries [16, 17]. Intercostal arteries, thoracic arteries originating from axillary and subclavian arteries in the upper and inferior phrenic artery in the lower zone disease should be investigated during the initial session, particularly in cases with chronic infection and pleural disease because non-bronchial systemic artery supply is the most important cause of early recurrent haemoptysis after successful bronchial artery embolisation [5]. Since history of chronic infection was present in the majority of patients in this study, systemic vascular supply was investigated in all sessions.

Chun et al reported that they found and embolised 29 additional arteries (14.5%) which were identified on post-embolisation thoracic aortography. They stressed that inferior phrenic artery and intercostal arteries could be overlooked when thoracic aortography was not performed. It is known that the bronchial arteries do not have a constant origin and that they originate from the inferior aspect of the aortic arch in up to 15% of the population [19]. Regarding these findings, we injected the aortic arch and thoracic aorta after searching for bronchial artery and systemic vascular supply.

It has been suggested that the artery of Adamkiewicz will arise from the right intercostobronchial artery in up to 10% of the population, but it is generally believed that the true incidence is considerably lower [20]. Embolisation distal to the origin of artery of Adamkiewicz is the ideal treatment method in these cases, especially with the modern angiography equipment making distal navigation possible. However, in some cases, a thin spinal branch may appear after initiation of embolisation resistance is increased in the vascular bed. In animal studies, particles larger than 200–250 µm were found to be too large to reach the spinal arteries and were considered safe when spinal arteries were not visualized [21]. In another experimental study, bronchopulmonary anastomoses in human lung were found to be 325 µm in diameter; therefore, the use of smaller particles could cause pulmonary infarction [22]. In this study, 250–350 µm and 350–500 µm sized PVA particles were used. 350–500 µm PVA particles were preferred in patients with bronchopulmonary shunts and large bronchial arteries. No spinal arteries were observed in selective injections prior to or during embolisation in any of the cases, and there were no neurological complications. Furthermore, no pulmonary infarction developed in any of the cases with bronchopulmonary shunts.

Currently, PVA particles are the most commonly used agents for bronchial artery embolisation worldwide. PVA particles are biocompatible and non-biodegradable and are considered to be a permanent embolic agent. However, unpredictable proximal vessel occlusion and catheter blockage caused by clumping or aggregation of irregular-shaped PVA particles have been reported [23]. Recently, the interest in spherical agents has grown, to overcome the drawbacks of PVA. Trisacryl gelatine microsphere (Embosphere; Biosphere, Rockland, MA; Contour SE; Boston Scientific, Boston, MA) is a new embolic agent that is increasingly used for uterine fibroid embolisation. In vivo and in vitro studies have shown that these particles clearly have better sizing and penetration characteristics than PVA [24, 25]. Vinaya et al reported a myocardial infarction followed by stroke in a patient with haemoptysis due to spontaneous passage of particles through the bronchopulmonary shunts with 500 µm sized embospheres [26]. It is obvious that further clinical and experimental studies investigating the effectiveness and safety of bronchial artery embolisation with these particles are needed.

Acute control of haemoptysis with endovascular treatment can be achieved in 73–98% of the patients with massive haemoptysis [27–29]. However, haemoptysis can recur with a frequency of up to 20%, especially in cases with chronic tuberculosis, aspergilloma and neoplasia [30–32]. Recurrent bleeding during the first 6 months after the embolisation procedure is usually due to undetected bronchial and systemic collaterals caused by diffuse pulmonary disease [5]. Late recurrent bleeding (after 6 months) usually develops due to disease progression. In this study, haemoptysis recurred in 1–7 months (mean 3.7 months) after the first intervention in 14 cases (10%). Haemoptysis following re-embolisation was encountered in two cases after 1 month and 6 months and a repeat endovascular treatment was performed. No haemoptysis was reported in the mean 46.6 months (16–86 months) follow-up period after the last embolisation until today. Two of the cases with malignancy died because of abundant bleeding after an asymptomatic 1 month period.

The successful results achieved with endovascular treatment in the control of massive haemoptysis have also brought up the idea of embolisation of moderate and chronic recurrent, mild haemoptysis compromising the life quality of the patient. Barben et al reported the results of bronchial artery embolisation in 46 bleeding episodes in 20 patients with cystic fibrosis. There were 22 massive, 10 moderate and 14 chronic recurrent bleeding episodes [33]. They observed that immediate success was achieved in 95% of the cases, whereas recurrent haemoptysis occurred in 55% of the cases after a mean period of 4 months. Yu-Tang et al reported the success rate as 81.5% in their study group consisting of 103 patients embolised for moderate to massive haemoptysis [34]. They stressed that in 15.5% of cases re-embolisation would be necessary and that endovascular treatment should be repeated whenever haemoptysis could be controlled by this method. In this study, moderate haemoptysis comprised 30.8% of the cases and successful results were achieved with endovascular treatment in these patients similar to those with massive haemoptysis (haemoptysis control at 1 month; 93% and 88.6% control with repeat session(s); 7% and 9.2% respectively, in moderate and massive haemoptysis cases).

In summary, effective palliation with endovascular treatment is achieved in the majority of moderate and massive haemoptysis cases after a single intervention. If necessary, the procedure may be repeated as long as the haemoptysis can still be controlled by this method. Endovascular treatment performed by an experienced staff with sufficient technical back-up is an effective and safe choice in the control of primary and recurrent haemoptysis. We believe that bronchial artery embolisation should always be considered for treatment of moderate to massive hemoptysis.

Received for publication June 14, 2006. Revision received July 18, 2006. Accepted for publication August 15, 2006.


   References
Top
 Abstract
 Introduction
 Methods and materials
 Results
 Discussion
 References
 

  1. Mauro MA, Jaques PF. Transcatheter bronchial artery embolization for inflammation (hemoptysis). In: Baum S, Pentecost MJ, editors. Abrams' angiography interventional radiology. Philadelphia: Little, Brown and Co., 1997:819–28
  2. Longefait H. Les hemoptysies dramatiques et leur traitement chirurgical. Rev Fr Mal Respir 1976;4:759–76.
  3. Conlan A, Hurwitz S, Krige L, Nicolaou N, Pool R. Massive hemoptysis. Review of 123 cases. J Thorac Cardiovasc Surg 1983;85:120–4.[Abstract]
  4. Magilligan DJ, Ravipati S, Zayat P, Shetty PC, Bower G, Kvale P. Massive hemoptysis: control by transcatheter bronchial artery embolization. Ann Thorac Surg 1981;32:392–400.[Abstract]
  5. Marshall TJ, Jackson JE. Vascular intervention in the thorax: Bronchial artery embolization for hemoptysis. Eur Radiol 1997;7:1221–7.[CrossRef][Medline]
  6. Antonelli M, Midulla F, Tancredi G, Salvatori FM, Bonci E, Cimino G, et al. Bronchial artery embolization for the management of nonmassive hemoptysis in cystic fibrosis. Chest 2002;121(3):796–801.
  7. Jean-Baptiste E. Clinical assessment and management of massive hemoptysis. Crit Care Med 2000;28:1642–7.[CrossRef][Medline]
  8. Hirshberg B, Biran I, Glazer M, Kramer MR. Hemoptysis: etiology, evaluation, and outcome in a tertiary referral hospital. Chest 1997;112:440–4.[CrossRef][Medline]
  9. Dweik RA, Stoller JK. Role of bronchoscopy in massive hemoptysis. Clin Chest Med 1999;20:89–105.[CrossRef][Medline]
  10. Hsiao EI, Kirsch CM, Kagawa FT, Wehner JH, Jensen WA, Baxter RB. Utility of fiberoptic bronchoscopy before bronchial artery embolization for massive hemoptysis. AJR Am J Roentgenol 2001;177:861–7.[Abstract/Free Full Text]
  11. McGuinness G, Beacher JR, Harkin TJ, Garay SM, Rom WN, Naidich DP. Hemoptysis: prospective high-resolution CT/bronchoscopic correlation. Chest 1994;105(4):982–3.
  12. Picard C, Parrot A, Boussaud V, Lavole A, Saidi F, Mayaud C, et al. Massive hemoptysis due to Rasmussen aneurysm: detection with helicoidal CT angiography and successful steel coil embolization. Intens Care Med 2003;29(10):1837–9.
  13. Remy-Jardin M, Bouaziz N, Dumont P, Brillet PY, Bruzzi J, Remy J. Bronchial and nonbronchial systemic arteries at multi–detector row CT angiography: comparison with conventional angiography. Radiology 2004;233:741–9.[Abstract/Free Full Text]
  14. Yoon YC, Lee KS, Jeong YJ, Shin SW, Chung MJ, Kwon OJ. Hemoptysis: bronchial and nonbronchial systemic arteries at 16-detector row CT. Radiology 2005;234(1):292–8.
  15. Remy J, Remy-Jardin M, Voisin C. Endovascular management of bronchial bleeding. In: Butler J, editor. The bronchial circulation. New York, NY: Dekker, 1992: 667–723
  16. Macintosh EL, Parrott JCW, Unrhu HW. Fistulas between the aorta and tracheobronchial tree. Ann Thorac Surg 1991;51:515–19.[Abstract]
  17. Pearse EO, Bryan AJ. Massive hemoptysis 27 years after surgery for coarctation of the aorta. J R Soc Med 2001;94:640–1.[Free Full Text]
  18. Chun HJ, Byun JY, Yoo SS, Choi BG. Added benefit of thoracic aortography after transarterial embolization in patients with hemoptysis. AJR Am J Roentgenol 2003;180(6):1577–81.
  19. Cauldwell EW, Siekert RG, Lininger RE, Anson BJ. The bronchial arteries: an anatomic study of 150 human cadavers. Surg Gynecol Obstet 1948;86:395–412.[Medline]
  20. Kardjiev V, Symenov A, Chankov I. Etiology, pathogenesis and prevention of spinal cord lesions in selective angiography of the bronchial and intercostal arteries. Radiology 1974;112:81–3.[Medline]
  21. Boushy SF, Helgason AH, North LB. Occlusion of the bronchial arteries by glass microspheres. Am Rev Respir Dis 1971;103:249–63.[Medline]
  22. Pump K. Distribution of bronchial arteries in human lung. Chest 1972;62:447–51.[Medline]
  23. Derdeyn CP, Moran CJ, Cross T, Dietrich HH, Dacey RG. Polyvinyl alcohol particle size and suspension characteristics. AJNR Am J Neuroradiol 1995;16:1335–443.[Abstract]
  24. Laurent A, Beaujeux R, Wassef M, Rüfenacht D, Boschetti E, Merland JJ. Trisacryl gelatin microspheres for therapeutic embolization, I: development and in vitro evaluation. AJNR Am J Neuroradiol 1996;17:533–40.[Abstract]
  25. Derdeyn CP, Graves VB, Salamant MS, Rappe A. Collagen-coated acrylic microspheres for embolotherapy: in vivo and in vitro characteristics. AJNR Am J Neuroradiol 1997;18:647–53.[Abstract/Free Full Text]
  26. Vinaya KN, White RI Jr, Sloan JM. Reassessing bronchial artery embolotherapy with newer spherical embolic materials. J Vasc Interv Radiol 2004;15(3):304–5.
  27. Ramakantan R, Bandekar VG, Gandhi MS, Aulakh BG, Deshmukh HL. Massive hemoptysis due to pulmonary tuberculosis: control with bronchial artery embolization. Radiology 1996;200:691–4.[Abstract/Free Full Text]
  28. Mal H, Rullon I, Mellot F, Brugiere O, Sleiman C, Menu Y, et al. Immediate and long-term results of bronchial artery embolization for life-threatening hemoptysis. Chest 1999;115:996–1001.[CrossRef][Medline]
  29. Kato A, Kudo S, Matsumoto K, Fukahori T, Shimizu T, Uchino A, et al. Bronchial artery embolization for hemoptysis due to benign diseases: immediate and long-term results. Cardiovasc Intervent Radiol 2000;23:351–7.[CrossRef][Medline]
  30. Mossi F, Maroldi R, Battaglia G, Pinotti G, Tassi G. Indicators predictive of success of embolisation: analysis of 88 patients with haemoptysis. Radiol Med 2003;105(1–2):48–55.
  31. Hayakawa K, Tanaka F, Torizuka T, Mitsumori M, Okuno Y, Matsui A, et al. Bronchial artery embolization for hemoptysis: immediate and long-term results. Cardiovasc Intervent Radiol 1992;15:154–9.[Medline]
  32. Katoh O, Kishikawa T, Yamada H, Matsumoto S, Kudo S. Recurrent bleeding after arterial embolization in patients with hemoptysis. Chest 1990;97:541–6.[CrossRef][Medline]
  33. Barben J, Robertson D, Olinsky A, Ditchfield M. Bronchial artery embolization for hemoptysis in young patients with cystic fibrosis. Radiology 2002;224:124–30.[Abstract/Free Full Text]
  34. Yu-Tang Goh P, Lin M, Teo N, En Shen Wong D. Embolization for hemoptysis: a six-year review. Cardiovasc Intervent Radiol 2002;25(1):17–25.



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