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- •Preface
- •Contents
- •Contributors
- •Endovascular Aneurysm Repair
- •Clinical Applications
- •Aortic Procedures Planning
- •Performance Assessment
- •Future Prospects
- •References
- •References
- •Introduction
- •Medical Error
- •Traditional Training
- •Animal Simulation Labs
- •Virtual Reality Simulation
- •3: Radiation Safety
- •Introduction
- •Basic Radiation Physics Units
- •Personnel Dose Limits
- •Pregnant Personnel
- •References
- •4: Tools of the Trade
- •Needles, Catheters, and Wires
- •Vascular Access
- •Double Wall
- •Single Wall
- •Advantages/Disadvantages
- •Nonvascular Needles (Table 4.1)
- •Guidewires
- •Curved
- •Straight/Angled
- •Stiffness
- •Flexibility
- •Coating
- •Torqueability
- •Opacity
- •Catheters
- •Flush Catheters
- •Visceral Catheters
- •Multipurpose Catheters
- •Cerebral Catheters
- •Guiding Catheters
- •Microcatheters
- •Vascular Sheaths
- •Vessel Dilators
- •Accessories
- •Embolic Agents
- •Temporary Agents
- •Permanent Agents
- •Pushable Coils
- •Detachable Coils
- •Coiling Techniques (Fig. 4.48)
- •Vascular Plugs
- •Particulates
- •Liquid Embolics
- •Fogarty Balloons
- •Angioplasty Balloons
- •Drug-Coated Balloons
- •Vascular Stents
- •Balloon Expandable Stents
- •Self-Expandable Stents
- •Specialty Stents
- •References
- •Consults
- •Pre-procedure Evaluation
- •Consent
- •Code Status
- •Laboratory Testing
- •Antibiotic Prophylaxis
- •Anticoagulation
- •Antihypertensives
- •Contrast Allergy Prophylaxis
- •Procedure Plan
- •Post-procedure Management
- •Hospital Admission
- •Discharge
- •Follow-up Visits
- •IR Clinic
- •Conclusion
- •References
- •6: The IR Road Map: Vascular Anatomy Overview
- •Introduction
- •Imaging Modalities
- •Ultrasound
- •Computed Tomography
- •Magnetic Resonance Imaging
- •Cross-Sectional Anatomy
- •Chest
- •Segmental Lung Anatomy
- •Mediastinum
- •Pulmonary Arteries
- •Pulmonary Veins
- •Bronchial Arteries
- •Liver
- •Arterial Access
- •Double-Wall Technique
- •Common Femoral Artery Access
- •Kidneys
- •Ureters
- •Bladder
- •Uterus
- •References
- •Alternative Arterial Access Sites
- •Venous Access
- •Manual Compression
- •Closure Devices
- •Compression Devices
- •Topical Agents
- •Invasive Devices
- •References
- •9: Central Venous Access
- •Pathophysiology
- •Non-tunneled Central Catheters (NTCCs)
- •Tunneled Central Catheters (TCCs)
- •Implantable Ports
- •Peripherally Inserted Central Catheters (PICCs)
- •Clinical Indication
- •Conventional Therapy
- •Non-tunneled Central Catheters
- •Tunneled Central Catheters
- •Ports
- •PICCs
- •Interventional Therapy
- •Ports
- •PICCs
- •Pre-procedural Prep
- •History
- •Physical Exam
- •Imaging
- •Complex Venous Access
- •Post-procedural Management
- •Complications
- •Acute Complications
- •Long-Term Complications
- •Device Removal
- •Tunneled Catheter Removal
- •Port Removal
- •References
- •Pathophysiology
- •Clinical Indication
- •Conventional Therapy
- •Interventional Therapy
- •References
- •11: IVC Filters
- •Pathophysiology
- •Clinical Indication
- •Conventional Therapy
- •Interventional Therapy
- •IVC Filter Placement
- •VTE Prevention
- •Preprocedural Preparation
- •Complication
- •Access Site
- •Device-Related
- •Postprocedural Management
- •IVC Filter Retrieval
- •Advanced IVC Filter Retrieval Techniques
- •Conclusion
- •References
- •Pathophysiology
- •Arteriovenous Fistula
- •Arteriovenous Graft
- •Clinical Indication
- •Conventional Therapy
- •Interventional Therapy
- •AVG Angioplasty
- •AVF Angioplasty
- •References
- •13: Pelvic Congestion Syndrome
- •Pathophysiology
- •Clinical Indication
- •Conventional Therapy
- •References
- •14: Varicocele
- •Pathophysiology
- •Conventional Therapy
- •Interventional Therapy
- •References
- •15: Varicose Veins
- •Pathophysiology
- •Clinical Indication
- •Conventional Therapy
- •Interventional Therapy
- •References
- •16: Vascular Malformations
- •Pathophysiology
- •Hemangiomas
- •Vascular Malformations
- •Arteriovenous Malformations (High Flow)
- •Venous Malformations (Low Flow)
- •Lymphatic Malformations
- •Clinical Indication
- •Conventional Therapy
- •Interventional Therapy
- •High-Flow AVMs
- •Low-Flow Venous Malformations
- •Klippel-Trenaunay Syndrome
- •Lymphatic Malformations
- •References
- •Pathophysiology
- •Abdominal Aortic Aneurysm (AAA)
- •Thoracic Aortic Aneurysm (TAA)
- •Clinical Indication
- •Abdominal Aortic Aneurysm
- •Thoracic Aortic Aneurysm
- •Conventional Therapy
- •Abdominal Aortic Aneurysm
- •Thoracic Aortic Aneurysm
- •Interventional Therapy
- •Abdominal Aortic Aneurysm
- •Thoracic Aortic Aneurysm
- •Common Complications
- •Access
- •Contrast Nephropathy
- •Spinal Cord Ischemia
- •Postoperative Monitoring
- •References
- •18: Aortic Dissection
- •Pathophysiology
- •Clinical Indication
- •Conventional Therapy
- •Interventional Therapy
- •Preprocedure Work-Up
- •Post-procedural Management
- •References
- •19: Endoleak
- •Pathophysiology
- •Clinical Indication
- •Conventional Therapy
- •Interventional Therapy
- •Type II Endoleaks
- •Type III Endoleaks
- •Type IV Endoleaks
- •Type V Endoleaks
- •References
- •20: Traumatic Aortic Injury
- •Pathophysiology
- •Clinical Indication
- •Conventional Therapy
- •Interventional Therapy
- •Pre-procedural Prep
- •Pre-procedural Imaging
- •Post-procedural Management
- •Post-procedural Imaging
- •References
- •21: Bronchial Artery Embolization
- •Pathophysiology
- •Clinical Indication
- •Conventional Therapy
- •Interventional Therapy
- •Outcomes
- •References
- •Pathophysiology
- •Pulmonary Arteriovenous Malformation
- •Pulmonary Artery Pseudoaneurysm
- •Clinical Indication
- •Pulmonary Arteriovenous Malformation
- •Pulmonary Artery Pseudoaneurysm
- •Conventional Therapy
- •Pulmonary Arteriovenous Malformation
- •Pulmonary Artery Pseudoaneurysm
- •Interventional Therapy
- •Pulmonary Arteriovenous Malformation
- •Pulmonary Artery Pseudoaneurysm
- •References
- •23: Lymphatic Interventions
- •Pathophysiology
- •Clinical Indication
- •Conventional Therapy
- •Interventional Therapy
- •Pedal Lymphangiography (PL)
- •Intranodal Lymphangiography (IL)
- •Dynamic Contrast Enhanced MR Lymphangiography (DCMRL)
- •Thoracic Duct Embolization
- •Plastic Bronchitis
- •References
- •24: Mesenteric Ischemia
- •Pathophysiology
- •Acute Mesenteric Ischemia
- •Chronic Mesenteric Ischemia
- •Clinical Indication
- •Acute Mesenteric Ischemia
- •Arterial Occlusive Disease
- •Nonocclusive Mesenteric Ischemia (NOMI)
- •Portomesenteric Vein Thrombosis
- •Chronic Mesenteric Ischemia
- •Conventional Therapy
- •Acute Mesenteric Ischemia
- •Arterial Occlusive Disease
- •Nonocclusive Mesenteric Ischemia (NOMI)
- •Portomesenteric Vein Thrombosis
- •Chronic Mesenteric Ischemia
- •Interventional Therapy
- •Acute Mesenteric Ischemia
- •Chronic Mesenteric Ischemia
- •References
- •25: Visceral Aneurysms
- •Pathophysiology
- •Visceral Artery True Aneurysms (VATAs)
- •Visceral Artery Pseudoaneurysm (VAPA)
- •Clinical Indication
- •VATA
- •VAPA
- •Conventional Therapy
- •Interventional Therapy
- •Splenic Artery Aneurysms
- •Renal Artery Aneurysms
- •Hepatic Artery Aneurysms
- •Celiac Artery Aneurysms
- •Complications
- •Splenic Aneurysm
- •Renal Aneurysm
- •Hepatic Aneurysm
- •References
- •26: Renal Artery Stenosis
- •Pathophysiology
- •Clinical Indications
- •Conventional Therapy
- •Interventional Therapy
- •Post-procedural Care
- •Conclusion
- •References
- •27: GI Bleeding
- •Pathophysiology
- •Clinical Indication
- •Conventional Therapy
- •Interventional Therapy
- •Complications
- •References
- •28: Uterine Artery Embolization
- •Pathophysiology
- •Fibroids
- •Adenomyosis
- •Postpartum Hemorrhage
- •Clinical Indication
- •Conventional Therapy
- •Fibroids
- •Adenomyosis
- •Postpartum Hemorrhage
- •Interventional Therapy
- •Fibroids
- •Adenomyosis
- •Postpartum Hemorrhage
- •AV Fistula
- •References
- •29: Prostate Artery Embolization
- •Pathophysiology
- •Benign Prostatic Hyperplasia
- •Prostate Cancer/Hematuria
- •Clinical Indication
- •Conventional Therapy
- •Interventional Therapy
- •References
- •30: Aortoiliac Disease
- •Pathophysiology
- •Blue Toe Syndrome
- •Leriche Syndrome
- •Fibromuscular Dysplasia
- •Clinical Indication
- •Conventional Therapy
- •Interventional Therapy
- •Abdominal Aorta
- •Aortic Bifurcation
- •Common Iliac Artery
- •External Iliac Artery
- •Internal Iliac Artery
- •Blue Toe Syndrome
- •References
- •31: Infrainguinal Disease
- •Pathophysiology
- •Claudication (Rutherford Categories 1–3)
- •Critical Limb Ischemia: Rest Pain (Rutherford Category 4)
- •Critical Limb Ischemia: Skin Lesions (Rutherford Categories 5–6)
- •Acute Limb Ischemia
- •Clinical Indication
- •Conventional Therapy
- •Interventional Therapy
- •Percutaneous Transluminal Angioplasty
- •Stents
- •Acute Limb Ischemia
- •References
- •Pathophysiology
- •Spleen
- •Liver
- •Kidney
- •Clinical Indication
- •Spleen
- •Liver
- •Kidney
- •Conventional Therapy
- •Spleen
- •Liver
- •Kidney
- •Interventional Therapy
- •Spleen
- •Pre-procedure
- •Post-procedure
- •Liver
- •Pre-procedure
- •Post-procedure
- •Kidney
- •Pre-procedure
- •Post-procedure
- •References
- •Pathophysiology
- •Pelvic Fractures
- •Extremity Fractures
- •Clinical Indication
- •Conventional Therapy
- •Interventional Therapy
- •References
- •34: Transarterial Chemoembolization
- •Pathophysiology
- •Clinical Indications
- •Conventional Therapy
- •Medical Management
- •Surgical Management
- •Interventional Therapy
- •Post-procedure
- •References
- •35: Transarterial Radioembolization (TARE)
- •Introduction
- •Pathophysiology
- •Clinical Indication
- •Conventional Therapy
- •Interventional Therapy
- •Primary Liver Cancers
- •Hepatic Metastatic Disease
- •References
- •36: Liver Ablation
- •Pathophysiology
- •Liver Cancer
- •Liver Metastases
- •Liver Cysts
- •Clinical Indication
- •Conventional Therapy
- •Liver Cancer
- •Liver Metastases
- •Liver Cysts
- •Interventional Therapy
- •References
- •Pathophysiology
- •Lung Cancer
- •Renal Cell Carcinoma
- •Bone Lesions
- •Clinical Indication
- •Lung Cancer
- •Kidney Cancer
- •Bone Lesions
- •Conventional Therapy
- •Lung Cancer
- •Kidney Cancer
- •Bone Lesions
- •Interventional Therapy
- •Radiofrequency Ablation (RFA)
- •Microwave Ablation (MWA)
- •Cryoablation
- •Irreversible Electroporation (IRE)
- •Lung Cancer
- •Kidney Cancer
- •Bone Lesions
- •References
- •Pathophysiology
- •Conventional Therapy
- •Ascites
- •Varices
- •Interventional Therapy
- •References
- •Pathophysiology
- •Etiology
- •Clinical Indication
- •Conventional Therapy
- •Medical Management
- •Surgical Management
- •Interventional Therapy
- •Post-procedural Management
- •Complications
- •References
- •40: Biliary Drainage
- •Pathophysiology
- •Clinical Indication
- •Conventional Therapy
- •Interventional Therapy
- •Conclusion
- •References
- •41: Biopsy Techniques
- •Introduction
- •Clinical Indication
- •Interventional Therapy
- •Needle Selection
- •Biopsy Techniques
- •References
- •Introduction
- •Pathophysiology
- •Ascites
- •Clinical Indication
- •Ascites
- •Conventional Therapy
- •Ascites
- •Interventional Therapy
- •Ascites
- •References
- •43: Obstructive Uropathy
- •Pathophysiology
- •Clinical Indication
- •Conventional Therapy
- •Urolithiasis
- •Infection
- •Urothelial Carcinoma
- •Neurogenic Bladder
- •Interventional Therapy
- •References
- •Pathophysiology
- •Clinical Indications
- •Percutaneous Radiologic Gastrojejunostomy (PRGJ) Tube
- •Percutaneous Jejunostomy (PJ) Tube
- •Conventional Therapy
- •Interventional Therapy
- •Percutaneous Radiologic Gastrostomy (PRG)
- •Post-procedural Management
- •Percutaneous Radiologic Gastrojejunostomy (PRGJ)
- •Percutaneous Jejunostomy (PJ)
- •References
- •45: Stroke
- •Pathophysiology
- •Clinical Indication
- •Conventional Therapy
- •Interventional Therapy
- •Complications
- •Post-procedure Management
- •References
- •46: Cerebral Angiography: Aneurysms
- •Pathophysiology
- •Clinical Indication
- •Conventional Therapy
- •Interventional Therapy
- •Pre-procedural Preparation
- •Post-procedural Management
- •Complications
- •References

230
Fig. 20.1 Classication of
traumatic aortic injury [12]
(Reproduced from Azizzadeh
etal. [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 37.9years, the range
was from 5 to 77years 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] (Table20.1).
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 specicity 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 8cm
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 identied 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 etal. [12] classied 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 conrm 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, signicant 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 ofIR Procedure
Kato etal. 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 forChoosing IR Procedure
Many reports continue to support the high technical success
rates of endovascular therapy in the setting of traumatic aortic injury [20–25]. 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 [21–23, 25, 27], TEVAR is the
preferred method of therapy in experienced trauma centers.
Results andData
Xenos etal. [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 signicantly lower
procedure-related and 30-day mortality rates (Fig. 20.4).
Additionally TEVAR was associated with signicantly 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 5years 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, andpreferably 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 etal. [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 insufciency
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 80–100mmHg. 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 80–100mmHg.
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 (Table20.4)
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 dened. Imaging may need to be performed more frequently if an endoleak is identied. 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
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Part V
Thoracic Interventions

Bronchial Artery Embolization
LeonardoI.Valentin andT.GregoryWalker
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 denitions may vary, the former is commonly
dened as hemoptysis that is greater in volume than 250cc
in 24h, while the latter is often dened as three or more episodes of hemoptysis, with volumes greater than 100cc in
24h over 3days in 1week [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 inammatory diseases, infections, neoplasms, and trauma. Of the
inammatory 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 ≥250cc/24h.
• Major hemorrhagic hemoptysis = hemoptysis ≥3/
week with ≥100cc/24h
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 conrmed 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 inammatory 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 etal. (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 conguration, 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 conguration, 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 identication of any component of
the arterial supply to the spinal cord that may arise from a
bronchial artery, specically 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
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