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230
Fig. 20.1 Classication of
traumatic aortic injury [12] (Reproduced from Azizzadeh etal. [12]. With permission from Elsevier)
GRADE I
Intimal Tear Intramural
Intima
Media
Adventitia
GRADE II
Hematoma
M. J. Hagar et al.
GRADE III
Pseudoaneurysm

Clinical Indication

Aortic transections predominantly occur in young males. In a recent study involving 63 consecutive patients with trau­matic aortic injuries, the mean age was 37.9years, the range was from 5 to 77years old, and the male-to-female ratio was 10:1 [13].
The clinical presentation of patients with aortic injuries varies depending on whether or not the aortic injury is con­tained and the severity of associated injuries. Some patients with a small tear in the aortic intima and minor associated injuries may be asymptomatic, while others with a complete aortic rupture, including the intima, media, and adventitia, may present with signs of shock and/or paralysis.
Common symptoms of aortic injuries include retrosternal or intrascapular pain, dysphagia, dyspnea, and stridor. An aortic injury should be suspected in patients with a fractured rst rib or ail chest. Additional physical exam ndings may include the presence of a precordial or midscapular murmur and differential blood pressures between arms or between the upper and lower body [6] (Table20.1).
Radiographic ndings indicative of aortic transections in decreasing order of frequency are included in Table 20.2. Although most of these ndings can be found in patients without aortic transections, the presence of two or more of these radiographic signs in the same patient is highly sugges­tive of an aortic injury [6] (Fig.20.2a).
Because of the general lack of specicity of radiography, patients with suspected aortic injuries usually undergo addi­tional imaging studies depending on their level of stability. CT angiography is the diagnostic test of choice for evalua-
GRADE IV
Rupture
Table 20.1 Signs and symptoms of acute aortic injury
Symptoms of aortic injury Signs of aortic injury
Retrosternal or interscapular pain Dyspnea or stridor Precordial or midscapular murmur Dysphagia Differential blood pressures between arms
Table 20.2 Radiographic ndings of aortic transections
Widened superior mediastinum greater than 8cm Indistinct or obscured aortic arch Rightward nasogastric tube deviation Rightward tracheal deviation Depressed left main stem bronchus Apical pleural cap Abnormal aortic contour Left hemothorax Obscured descending aorta Wide left paraspinal line Thick paratracheal line
Fractured rst rib or ail chest
or between the upper and lower body
tion of suspected traumatic aortic injuries [8] (see Fig.20.2b). Direct signs (Table 20.3) include active contrast extravasa­tion, contained rupture/traumatic pseudoaneurysm, intramu­ral thrombus, aortic dissection, and abnormality of the aortic contour/pseudocoarctation. Indirect signs of aortic injury include mediastinal or periaortic hematoma, retrocrural hematoma, or a small caliber of the aorta distal to the injury site. Transesophageal echocardiography (TEE) and intravascular ultrasound are useful adjuncts in stable patients with equivocal ndings on CTA [8]. There is evidence that
20 Traumatic Aortic Injury
231
Diagnosis of
Traumatic
Aortic Injury
Fig. 20.2 A 53-year-old male with traumatic aortic injury after being
struck by a car. (a) Pre-TEVAR anteroposterior view of chest showing widened superior mediastinum (10.2 cm in horizontal diameter), obscured aortic arch, abnormal aortic contour, rightward tracheal devia­tion, and thick paratracheal line. (b) Pre-TEVAR CTA showing direct signs of aortic injury such as contained aortic rupture, abnormality of the aortic contour and indirect signs of aortic injury such as mediasti­nal/periaortic hematoma, and small caliber of the aorta distal to the injury site
Hemodynamically
Unstable
Likely due to
aortic injury
Emergent
endovascular
repair
Fig. 20.3 Management algorithm for patients with blunt traumatic
aortic injury
Not likely due to aortic injury
Resuscitate
and search for
other injuries
Elective
endovascular
repair
Hemodynamically
Stable
Elective
endovascular
repair
depends on the stability of the patient. If the patient is stable, the patient should be resuscitated, and other potentially life­threatening injuries should be managed appropriately prior to endovascular repair. If the patient is unstable and it is felt that it is likely due to the aortic injury, urgent or emergent endovascular repair is preferred. If the patient is unstable and the hemodynamic instability cannot be explained by the grade of aortic injury, other injuries and causes for instability should be identied rst and managed accordingly [8, 15].
Table 20.3 Direct signs of aortic injury on CTA
Direct signs of aortic injury on CTA Active contrast extravasation Contained rupture/traumatic pseudoaneurysm Intramural thrombus Aortic dissection Abnormality of the aortic contour/pseudocoarctation
conventional catheter angiography may be unnecessary when CTA is indeterminate in blunt thoracic trauma [14].
Endovascular repair is preferred over open surgery for treatment of traumatic aortic injuries as it is less invasive and has been shown to have reduced early complication rates and hospital length of stay [8, 15]. The suggested management algorithm (Fig.20.3) for patients with blunt traumatic aortic injury based on the recommendations of Eastern Association for the Surgery of Trauma (EAST) Practice Work Group [8]

Conventional Therapy

Using imaging criteria, Azizzadeh etal. [12] classied trau­matic aortic injury (TAI) into four categories, ranging from intimal tear to rupture (see Fig.20.1). In their series, patients with grade 1 aortic injuries were interrogated with intravas­cular ultrasound to conrm CT ndings but were then man­aged medically. Grades 2 and 3 were treated with either open or endovascular repair. Grade 4 patients either died prior to imaging or they underwent thoracic endovascular aneurysm repair (TEVAR). The left subclavian artery was covered in 48% of the patients in the series. None of these patients required upper extremity revascularization post-TEVAR for arm ischemia. In the non-emergent setting, a left carotid to subclavian artery bypass would be performed prior to TEVAR to prevent arm ischemia.
232
M. J. Hagar et al.
Conventional or open repair of thoracic aortic injuries gen­erally involves a posterolateral access to the chest cavity. Open aortic repair can be performed with or without cardio­pulmonary bypass (CPB) [16] under general anesthesia, using double-lung intubation. Distal aortic perfusion can be obtained with CPB.The patient is generally anticoagulated with heparin. In most situations, the aorta is cross clamped proximal to the left subclavian artery. The aorta is then opened and explored. The proximal aorta is sewn to a woven Dacron graft. The distal anastomosis is created and the graft is ushed prior to unclamping. During open repair, signicant blood loss can occur. Open repair is shown to be associated with a 28% mortality rate and a 16% paraplegia rate [17, 18].

Interventional Therapy

Genesis ofIR Procedure
Kato etal. reviewed their experience with endovascular stent grafts in patients with thoracic aortic trauma in 1997 [19]. In this early experience, three patients had acute aortic injuries, while seven had chronic posttraumatic aneurysms. The authors reported a 100% technical success rate with thrombosis of the aneurysm sac in all patients, as seen on follow- up imaging. There was no aortic injury- or repair­related morbidity or mortality within the follow-up period.
Indications forChoosing IR Procedure
Many reports continue to support the high technical success rates of endovascular therapy in the setting of traumatic aor­tic injury [2025]. Technical success rates in several series are 100% with procedural complication rates varying between 0 and 8.3% [20, 24, 26]. Given the high periopera­tive mortality of open repair [2123, 25, 27], TEVAR is the preferred method of therapy in experienced trauma centers.
Results andData
Xenos etal. [28], in a meta-analysis, reviewed 17 retrospec­tive cohort studies. They reviewed 589 trauma patients with treated thoracic aortic injuries—369 patients by an open repair of thoracic aortic injury and 220 patients by endovas­cular repair. Despite higher injury severity scores, patients who underwent endovascular repair had signicantly lower procedure-related and 30-day mortality rates (Fig. 20.4).
Additionally TEVAR was associated with signicantly lower spinal cord ischemia rates, when compared to open repair. Long-term data is also available [29], suggesting durability of TEVAR in the trauma setting. None of the studies have more than 5years of follow-up; several authors [20, 22, 30
33] have raised concern about stent graft failure, migration,
and the need for repeat intervention in young patients.
Key Point
TEVAR is associated with a lower 30-day mortality and spinal cord ischemia rate compared to open aortic repair for traumatic aortic injury.
Pre-procedural Prep
Generally, consultation from the trauma services is prompted once the patient’s mechanism of injury is understood and imaging is obtained. Large trauma centers may employ an “aorta alert team” consisting of cardiovascular/vascular sur­gery, anesthesia, andpreferably interventional radiology to be on hand during the arrival of an unstable patient with clinical concern for aortic injury at the scene of the accident. Once informed or emergent consent is obtained, the patient should be urgently brought to the Endovascular Suite or hybrid operating room. Frequently the poly-trauma patient has been intubated in the eld or in the emergency depart­ment. Close, multidisciplinary communication is essential as associated injuries may need to be addressed rst or at the same time as TEVAR.
Pre-procedural Imaging
Generally, these patients receive CTA from the thoracic inlet to the femoral bifurcations. This will allow the intervention­alist to plan on what size and number of stent grafts will be used. Ideally, this is done on a 3D workstation. Close atten­tion should be paid to the access vessels. Though rarely obtained in emergency setting, CTA of the head and neck is helpful to determine if the left vertebral artery communicates with the basilar artery. Generally, in the emergency setting, it is thought that the left subclavian artery can be covered empirically. However, selective catheter angiography can also be performed during the TEVAR.
AMABILE 2004
Study name Odds ratio and 95% Cl
ANDRASSY 2006 BROUX 2006 BUZ 2007 CHUNG 2007 COOK 2006 DOSS 2005 KASIRAJAN 2003 KOKOTSAKIS 2007 KUHNE 2005 LEBL 2006 MCPHEE 2006 OTT 2004 PACINI 2005 RIESENMAN 2007 ROUSSEAU 2004
Favours TEVAR
OPEN REPAIR
210
20 Traumatic Aortic Injury
Odds
ratio
0.810 0.904
0.667
0.591
0.333
0.145
0.960
0.280
0.250
0.429
0.427
0.667
1.333
0.323
0.341
0.254
0.204
0.447
Fig. 20.4 Forest plot showing lower 30-day mortality after TEVAR in comparison to open repair of traumatic descending aortic rupture [28]
(Reproduced from Xenos etal. [28]. With permission from Elsevier)
p-Value
0.683
0.583
0.135
0.201
0.957
0.432
0.280
0.564
0.580
0.762
0.835
0.488
0.478
0.095
0.296
0.005
0.1
0.2
0.5 1
Favours
5
233
The How To
Here’s what you expect to see in the interventional
suite:
1. Thin-slice CTA with multi-planar reconstructions
vessels adequately during device positioning. Ideally, the imaging is obtained on breath hold, with rapid, 6 frames/sec digital subtraction acquisition; anesthesia can suspend breathing temporarily to aid with image acquisition. With satisfactory pre- procedure imaging, sometimes
graft are also determined prior to the procedure.
2. Patient is brought to interventional suite or hybrid OR and placed supine on the table (arms by the side in most cases as upper extremity injuries are common).
3. After the review of a pelvic CTA, either “pre­close” techniques (employing common femoral access under ultrasound guidance followed by deployment of two suture-based closure devices) or surgical exposure of the femoral artery is employed. (Refer to Chap. 8 for further informa­tion on closure techniques.)
4. Contralateral femoral access for diagnostic angi­ography is also obtained. The ascending aorta is
catheter advanced from the contralateral groin.
5. 20.5a) is obtained in approximately 45° left anterior oblique (LAO) position (exact view determined from CTA).
stent graft already in position. Angiography can be obtained from upper extremity or, most com­monly, contralateral groin access.
6. TEVAR is generally performed over a stiff wire. These wires can be traumatic to the aorta and should be delivered through a 5F catheter that has already catheterized the ascending aorta utilizing softer angiography wires.
7. The stent graft is advanced expediently from the
the risk of iatrogenic iliac injury if the device does not follow the wire.
8. Occasionally patients with poor access vessels may require the use of balloon re-collapsible sys­tems or the creation of so called endo conduits to allow safe passage of the stent graft systems.
(continued)
234
9. Patients can generally be systemically anticoagu­lated with heparin, with a target ACT of greater than 250, although this may be reduced in the set­ting of intracranial or solid organ injury.
10. Once the landing zones proximal and distal to the
tioned appropriately, the stent graft is deployed
20.5b, c).
11. FDA-approved stent grafts for blunt thoracic aor­tic injury are Cook Zenith Alpha, Gore, C-TAG, and Medtronic Captivia Valiant. Placement preci­sion, deployment-related migration, and the con­formability of stent grafts have improved steadily with each generation of device.
12. Generally, because of the short landing zones in trauma patients, the origin of the left subclavian artery
20.5c). Revascularization of
the left subclavian artery can be considered on a case­by-case basis depending on the patient’s overall con­dition. This only rarely needs to be done urgently.
13. ­sidered, due to the urgent nature of the procedure.
M. J. Hagar et al.
Table 20.4 Complications
Short term Mid/long term Access site injury Graft fracture or migration Stroke Endoleak Great vessel or cardiac perforation Left arm ischemia Paraplegia Vertebrobasilar insufciency Endoleak
-
Retrograde aortic dissection
a
Endoleak. Because aortic arch curvatures can be more acute in the young trauma patient, it is possible that proximal seal isn’t achieved with TEVAR (Refer to Chap. 19 for further information)
b
Retrograde aortic dissection. Because sizing can be challenging for a patient in shock, a grossly oversized stent can cause shear injury upon the aortic wall and result in retrograde dissection into the arch and ascending aorta
a
b
Device infection Fistula [34]
pressure goal should be approximately 80–100mmHg. The patient should be monitored for post-TEVAR complications such as access site hemorrhage, paraplegia, and stroke. The prognosis of the patient is often more dependent on the out­come of other injuries sustained by the patient.
Key Point
Post-TEVAR goal MAP is 80–100mmHg.
Key Point
Urgent indications for left subclavian artery revascu­larization in trauma TEVAR
• Left vertebral artery terminates in a posterior­interior cerebellar artery without communication with the basilar artery
• Poor collateral ow to left subclavian artery
Complications (Table20.4)
Post-procedural Management
If the seal obtained post-TEVAR was satisfactory and the patient has no other active sites of hemorrhage, mean arterial
Post-procedural Imaging
Post-procedural imaging includes chest X-ray which can be helpful to ensure the stent graft is well expanded (see Fig.20.5d). Ideally CT angiography should be obtained prior to discharge. The patient will then require lifelong monitor­ing of the stent grafts. Many endovascular specialists advo­cate imaging with CT at 1, 6, and 12 months and then annually thereafter for TEVAR, although the very long-term imaging requirements of TEVAR for trauma need to be bet­ter dened. Imaging may need to be performed more fre­quently if an endoleak is identied. Non-contrast CT or MR angiography can be used as an alternative in patients that cannot receive iodinated contrast.
20 Traumatic Aortic Injury
235
Fig. 20.5 A 53-year-old male with traumatic aortic injury secondary to
pedestrian versus motor vehicle accident. (a) Arch aortogram, obtained in approximately 45° LAO position, with ush catheter and wire in the ascending aorta. (b) Aortogram demonstrating advancement of col­lapsed stent graft under uoroscopic guidance with landing zones of

References

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2. Fabian TC, Richardson JD, Croce MA, Smith JS Jr, Rodman G Jr, Kearney PA, et al. Prospective study of blunt aortic injury: multicenter trial of the American Association for the Surgery of Trauma. JTrauma. 1997;42(3):374–80. discussion 380-3.
stent graft proximal and distal to aortic injury (red arrows). (c) Aortogram demonstrating deployed endovascular stent graft. The left subclavian artery origin was covered by the stent graft (yellow arrow). (d) Post-TEVAR LAO spot lm ensuring well-expanded stent graft
3. Cardarelli MG, McLaughlin JS, Downing SW, Brown JM, Attar S, Grifth BP.Management of traumatic aortic rupture: a 30-year experience. Ann Surg. 2002;236(4):465–9. discussion 469-70.
4. Smith RS, Chang FC.Traumatic rupture of the aorta: still a lethal injury. Am JSurg. 1986;152(6):660–3.
5. Svensson LG. Descending thoracic and thoracoabdominal aortic surgery. In: Sabiston and Spencer’s surgery of the chest. 7th ed. Philadelphia: Elsevier Saunders; 2005.
6. Cohen AM, Crass JR.Traumatic aortic injuries: current concepts. Semin Ultrasound CT MR. 1993;14(2):71–84.
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7. Javadpour H, O'Toole JJ, McEniff JN, Luke DA, Young VK.Traumatic aortic transection: evidence for the osseous pinch mechanism. Ann Thorac Surg. 2002;73(3):951–3.
8. Nagpal P, Mullan BF, Sen I, Saboo SS, Khandelwal A. Advances in imaging and management trends of traumatic aortic injuries. Cardiovasc Intervent Radiol. 2017;40(5):643–54.
9. Svensson LG.Traumatic injuries of the aorta. In: Svensson LG, Crawford ES, editors. Cardiovascular and vascular disease of the aorta. Philadelphia: WB Saunders; 1997. p.184–91.
10. Rabinsky I, Sidhu GS, Wagner RB. Mid-descending aortic trau­matic aneurysms. Ann Thorac Surg. 1990;50(1):155–60.
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13. Chen SW, Wang SY, Liao CH, Huang YK, Liu KS, Lin PJ, etal. Timing of intervention in blunt traumatic aortic injury patients: open surgical versus endovascular repair. Ann Vasc Surg. 2015;29(8):1559–66.
14. Sammer M, Wang E, Blackmore CC, Burdick TR, Hollingworth W, Indeterminate CT.Angiography in blunt thoracic trauma: is CT angiography enough? AJR Am JRoentgenol. 2007;189(3): 603–8.
15. Fox N, Schwartz D, Salazar JH, Haut ER, Dahm P, Black JH, et al. Evaluation and management of blunt traumatic aor­tic injury: a practice management guideline from the Eastern Association for the Surgery of Trauma. J Trauma Acute Care Surg. 2015;78(1):136–46.
16. Jamieson WR, Janusz MT, Gudas VM, Burr LH, Fradet GJ, Henderson C.Traumatic rupture of the thoracic aorta: third decade of experience. Am JSurg. 2002;183(5):571–5.
17. Cowley RA, Turney SZ, Hankins JR, Rodriguez A, Attar S, Shankar BS.Rupture of thoracic aorta caused by blunt trauma. A fteen­year experience. JThorac Cardiovasc Surg. 1990;100(5):652–60. discussion 660-1.
18. Ott MC, Stewart TC, Lawlor DK, Gray DK, Forbes TL.Management of blunt thoracic aortic injuries: endovascular stents versus open repair. JTrauma. 2004;56(3):565–70.
19. Kato N, Dake MD, Miller DC, Semba CP, Mitchell RS, Razavi MK, et al. Traumatic thoracic aortic aneurysm: treatment with endovascular stent-grafts. Radiology. 1997;205(3):657–62.
20. Bell RE, Taylor PR, Aukett M, Sabharwal T, Reidy JF.Results of urgent and emergency thoracic procedures treated by endoluminal repair. Eur JVasc Endovasc Surg. 2003;25(6):527–31.
21. Czermak BV, Fraedrich G, Perkmann R, Mallouhi A, Steingruber IE, Waldenberger P, et al. Endovascular repair of thoracic aor-
tic disease: what we have learned. Curr Probl Diagn Radiol. 2004;33(6):269–82.
22. Iannelli G, Piscione F, Di Tommaso L, Monaco M, Chiariello M, Spampinato N.Thoracic aortic emergencies: impact of endovascu­lar surgery. Ann Thorac Surg. 2004;77(2):591–6.
23. Scheinert D, Krankenberg H, Schmidt A, Gummert JF, Nitzsche S, Scheinert S, et al. Endoluminal stent-graft placement for acute rupture of the descending thoracic aorta. Eur Heart J.2004;25(8):694–700.
24. Wellons ED, Milner R, Solis M, Levitt A, Rosenthal D. Stent­graft repair of traumatic thoracic aortic disruptions. J Vasc Surg. 2004;40(6):1095–100.
25. Lachat M, Pfammatter T, Witzke H, Bernard E, Wolfensberger U, Künzli A, etal. Acute traumatic aortic rupture: early stent-graft repair. Eur JCardiothorac Surg. 2002;21(6):959–63.
26. Morishita K, Kurimoto Y, Kawaharada N, Fukada J, Hachiro Y, Fujisawa Y, et al. Descending thoracic aortic rup­ture: role of endovascular stent-grafting. Ann Thorac Surg. 2004;78(5):1630–4.
27. Reed AB, Thompson JK, Crafton CJ, Delvecchio C, Giglia JS.Timing of endovascular repair of blunt traumatic thoracic aortic transections. JVasc Surg. 2006;43(4):684–8.
28. Xenos ES, Abedi NN, Davenport DL, Minion DJ, Hamdallah O, Sorial EE, et al. Meta-analysis of endovascular vs open repair for traumatic descending thoracic aortic rupture. J Vasc Surg. 2008;48(5):1343–51.
29. Martin C, Thony F, Rodiere M, Bouzat P, Lavagne P, Durand M, etal. Long-term results following emergency stent graft repair for traumatic rupture of the aortic isthmus. Eur JCardiothorac Surg. 2017;51(4):767–72.
30. Orford VP, Atkinson NR, Thomson K, Milne PY, Campbell WA, Roberts A, etal. Blunt traumatic aortic transection: the endovas­cular experience. Ann Thorac Surg. 2003;75(1):106–11. discussion 111-2.
31. Bortone AS, De Cillis E, D'Agostino D, Schinosa Lde L. Stent graft treatment of thoracic aortic disease. Surg Technol Int. 2004;12:189–93.
32. Cambria RP, Brewster DC, Lauterbach SR, Kaufman JL, Geller S, Fan CM, etal. Evolving experience with thoracic aortic stent graft repair. JVasc Surg. 2002;35(6):1129–36.
33. Fattori R, Napoli G, Lovato L, Russo V, Pacini D, Pierangeli A, et al. Indications for, timing of, and results of catheter-based treatment of traumatic injury to the aorta. AJR Am J Roentgenol. 2002;179(3):603–9.
34. Saratzis AS, Fillipou D, Melas N, Kiskinis D.Endovascular stent­graft repair of an Aortobronchial Fistula: case report and review of the literature. EJVES Extra. 2005;9:123–5.
Part V
Thoracic Interventions

Bronchial Artery Embolization

LeonardoI.Valentin andT.GregoryWalker
21

Pathophysiology

Bronchial artery embolization (BAE) is a minimally invasive procedure that is frequently used in the management of mas­sive hemoptysis or a major hemorrhagic hemoptysis event. While exact denitions may vary, the former is commonly dened as hemoptysis that is greater in volume than 250cc in 24h, while the latter is often dened as three or more epi­sodes of hemoptysis, with volumes greater than 100cc in 24h over 3days in 1week [1]. Massive hemoptysis can be a life-threatening emergency. Continuing hemorrhage into the airway results in both hypovolemia and asphyxiation, with the patient drowning in his own blood, which can have a mortality of 50–85% if managed conservatively [2]. Pathologic processes that affect the airways and pulmonary parenchyma are the most common underlying etiologies that result in hemoptysis (Table 21.1). These include inamma­tory diseases, infections, neoplasms, and trauma. Of the inammatory etiologies, bronchiectasis is most frequently associated with massive hemoptysis which can result from a variety of diseases that include cystic brosis, chronic lung disease, and sarcoidosis. Pulmonary parenchymal infections such as aspergillosis, tuberculosis, and chronic pneumonia may also lead to massive hemoptysis, as can certain rheu­matic and immune disorders.
L. I. Valentin · T. G. Walker (*) Massachusetts General Hospital, Division of Interventional Radiology, Boston, MA, USA e-mail: leonardo.valentin@mgh.harvard.edu;
tgwalker@mgh.harvard.edu
Key Point
• Massive hemoptysis=hemoptysis 250cc/24h.
• Major hemorrhagic hemoptysis = hemoptysis 3/ week with 100cc/24h
Massive hemoptysis, in the vast majority of cases, is related to an underlying abnormality that involves the sys­temic arteries that supply the bronchial tree, namely, the bronchial arteries. By contrast, the pulmonary arterial sys­tem is rarely the culprit cause of massive hemoptysis, although this can occur in certain circumstances. Most schol­ars agree that Leonardo da Vinci rst described and illus­trated the bronchial arterial anatomy [2]. Viamonte performed the rst selective bronchial arteriogram in 1963 [3]. Initial understanding of the role of the bronchial arteries in the underlying pathophysiology of hemoptysis was largely empirical, based on early experiences in the 1970s [4, 5]. This pathophysiological knowledge has since been con­rmed using animal and human data [6]. Another important empirical nding that advanced the management of hemop­tysis was the demonstration that intentional occlusion of the bronchial arteries (via embolization) produced little or no signs of ischemia of the bronchial airway system but was successful in controlling hemoptysis. This allowed endovas­cular catheter-directed transarterial embolization to become one of the most accepted and widely used methods of man­aging massive hemoptysis.
Even after a successful bronchial artery embolization, the underlying pathophysiological process that originally caused hemoptysis might not be affected, and additional bleeding episodes may continue to occur at a later time. This is due to the underlying inammatory process involv­ing the lungs and bronchi that promotes hypertrophy of
© Springer International Publishing AG, part of Springer Nature 2018 N. A. Keefe et al. (eds.), IR Playbook, https://doi.org/10.1007/978-3-319-71300-7_21
239
240
Table 21.1 Common causes of massive hemoptysis
Tuberculosis Sarcoidosis Aspergillosis Chronic lung disease Cystic brosis Interstitial pneumonitides COPD Malignancy
bronchial or even non- bronchial collateral systemic arterial pathways; this may eventually result in recurrent hemopty­sis that then requires repeat treatment [7].
When one is considering performing a bronchial artery embolization, it is extremely important to be familiar with the bronchial arterial anatomy. The bronchial arteries most commonly arise from the T3 to T8 levels, with the majority arising from the T5 to T6 levels. In addition to supplying the trachea and bronchi, these arteries also provide blood supply to the esophagus, the vagus nerve, the visceral pleura, mediastinal lymph nodes, and the vasa vasorum of the tho­racic aorta and pulmonary arteries [8].
Key Point
The bronchial arteries most commonly arise from the T3 to T8 levels, with the majority arising from the T5 to T6 levels.
L. I. Valentin and T. G. Walker
When the bronchial arteries arise in the normal fashion from the proximal descending thoracic aorta, these are termed orthotopic, while bronchial arteries that originate elsewhere from the aorta or from other vasculature are termed ectopic. In at least 20% of patients, the bronchial arteries might arise from sites other than the thoracic aorta (e.g., subclavian, internal mammary, thyrocervical, superior intercostals, pericardiophrenic and inferior phrenic arteries, the abdominal aorta, and even a coronary artery). In fact, recently a CT angiographic study showed that only 64% of patients had orthotopic bronchial arteries, and the remaining 36% had at least one ectopic bronchial artery, most com­monly originating from the undersurface of the thoracic aor­tic arch [9]. Additionally, multiple variations in the branching patterns of the bronchial arteries have been described [10] with the most common patterns, depicted in a famous series by Caldwell etal. (Fig.21.1).
Right-sided bronchial arteries typically arise from a shared trunk with an intercostal artery that supplies the uppermost intercostal musculature; this is termed an inter­costobronchial arterial trunk. In addition to this intercosto­bronchial artery conguration, a right bronchial artery may have its own distinct origin, especially when more than one right bronchial artery is present. On the left side, the bron­chial arteries usually have their own individual origin, with­out an intercostal association.
Fig. 21.1 Diagram shows normal variants in the bronchial arterial
anatomy as described by Caldwell. The most common pattern of bron­chial arterial anatomy, Type I, occurring in roughly 40% of individuals, is that of a single right intercostobronchial artery trunk and two left bronchial arteries, each with their own separate origin. The second most common conguration, Type II, which occurs in about 21%, also has a single right intercostobronchial artery trunk, but there is only one left bronchial artery. Type III anatomy occurs with similar frequency to Type II and has a right intercostobronchial artery trunk and an additional right bronchial artery with its own origin, along with two left bronchial arteries. In Type IV anatomy, which occurs in about 10% of individuals, there are paired right bronchial arteries, one of which has an intercosto­bronchial artery trunk, and there is a solitary left bronchial artery
Figure 21.2 demonstrates representative angiographic
appearances of orthotopic and ectopic bronchial arteries.
A crucial consideration when performing bronchial artery embolization is the identication of any component of the arterial supply to the spinal cord that may arise from a bronchial artery, specically the anterior spinal artery. This is important, as the inadvertent nontarget embolization of the anterior spinal artery during a bronchial artery emboliza­tion can result in paraplegia, a devastating complication. Several arterial branches can supply the anterior spinal