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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

304
A. Uacker and A. H. Matsumoto
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2. Textor SC, Lerman LO. Paradigm shifts in atherosclerotic
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3. Textor SC.Renal arterial disease and hypertension. Med Clin North
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4. Parikh SA, Shishehbor MH, Gray BH, White CJ, Jaff MR. SCAI
expert consensus statement for renal artery stenting appropriate
use. Catheter Cardiovasc Interv. 2014;84:1163–71.
5. Textor SC, McKusick MM.Renal artery stenosis: if and when to
intervene. Curr Opin Nephrol Hypertens. 2016;25:144–51.
6. Messerli FH, Bangalore S. Renal denervation for resistant hypertension? N Engl JMed. 2014;370:1454–7.
7. Cooper CJ, Murphy TP, Cutlip DE, Jamerson K, Henrich W, Reid
DM, etal. Stenting and medical therapy for atherosclerotic renal
artery stenosis. The CORAL trial. N Engl JMed. 2014;370:13–22.
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Matsumoto AH.Stenting for atherosclerotic renal artery stenosis.
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9. Olin JW, Froehlich J, Gu X, Bacharach JM, Eagle K, Gray BH,
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GI Bleeding
MichaelDarcy
Pathophysiology
Gastrointestinal bleeding (GIB) can occur anywhere along
the GI tract with upper GI bleeding (UGIB) being that which
occurs proximal to the ligament of Treitz and lower GI
bleeding (LGIB) arising distal to that. While GI bleeding can
be either arterial in origin or the result of venous variceal
bleeding, this chapter will focus on arterial bleeding as variceal bleeding is covered in the chapters on TIPS (Chap. 38)
and BRTO (Chap. 39).
GIB is a very common problem with 100 cases of UGIB
and 21–27 cases of LGIB per 100,000 adults per year [1, 2].
GIB can occur in any age group and there are many causes of
bleeding. A study of 1929 patients showed that ulcers were
the most common cause of UGIB (34%) followed by varices
(33%), erosive esophagitis (8%), and Mallory-Weiss tear
(6%) [3]. LGIB sources of bleeding are more diverse which
vary depending on the part of the bowel involved, and an
exact etiology is often not dened. Table 27.1 shows the
pathology that was the source of bleeding in a series of 112
patients who underwent embolization for LGBI [4]. Most
often bleeding is the only actual symptom, although patients
may have some associated symptoms. Ulcers may present
with abdominal pain, and signicant vomiting or retching
may precede bleeding from a Mallory-Weiss tear. The type
of bleeding is not always a good way to distinguish UGIB
from LGIB.In a large study of UGIB patients [3], 55% presented with hematemesis, but 42% had melena alone, and
2% had hematochezia alone. For LGIB, the color of the
blood is also not very helpful to determine which part of the
bowel is bleeding.
M. Darcy (*)
Chief of Interventional Radiolgy, Mallinckrodt
Institute of Radiology, Washington University in St Louis,
St. Louis, MO, USA
e-mail: darcym@wustl.edu
27
Table 27.1 Percent of pathology causing bleeding in LGIB
Small bowel Colon Rectum
# of Pts 36 36 40
Diverticula 39%
GI anastomosis 25% 8% 5%
Post-endoscopic biopsy 22% 8%
Malignancy 6% 6%
Angiodysplasia/AVM 3% 8%
Unspecied 72% 25% 78%
Adapted from Ref. [4]
Hematochezia may indicate a more distal source such as
a rectal bleed, and melena is sometimes associated with a
more proximal source, however, if the bleeding is brisk
enough even an UGIB can present with hematochezia.
Given the wide range of pathology that can cause bleeding, the risk factors are also extremely variable, but one of
the most common factors encountered is abnormality of
coagulation parameters. Elevation of the INR due to medications or liver disease and low platelet count from a variety of
causes can precipitate bleeding from a lesion that otherwise
might not bleed.
Key Point
High INR and low platelets can precipitate bleeding
from a lesion that might not otherwise bleed.
Clinical Indication
The presentation of GI bleeding can range from occult bleeding detectable only by testing the stool with a hemoccult test
all the way up to massive life-threatening bleeding. Physical
exam is often unrevealing but may provide some clues.
Hepatomegaly, splenomegaly, or scleral icterus could indicate liver disease and suggest a variceal rather than arterial
source. A rectal exam is important for patients with LGIB
since 40% of rectal cancers can be palpated on digital exam.
© 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_27
305

306
M. Darcy
Table 27.2 Advantages and disadvantages of the imaging modalities
used to detect GI bleed
Tagged RBC
scan CTA Angiography
Rate of detection 0.1cc/min 0.3cc/
Localization of bleeding
vessel
Radiation exposure Low Medium High
Poor Best Good
min
1.0cc/min
Imaging is rarely needed early in the evaluation of UGIB
as endoscopy detects the source of bleeding in the majority
of cases. For LGIB, the imaging approach depends on if it is
chronic minor bleeding versus major bleeding (bleeding
causing signicant drop in hematocrit or hemodynamic
instability). For chronic bleeding, if colonoscopy fails to
yield a diagnosis, CT can be used to further study the colon
and with reconstruction can provide a virtual colonoscopy.
The small bowel can also be looked at by CT or CT enteroclysis, which involves lling the small bowel lumen with
water or polyethylene glycol to provide contrast, which
allows identication of a lling defect [5].
Key Point
It is important to understand variceal vs. arterial GI
bleeding. Look for evidence of liver disease including
hepatosplenomegaly, scleral icterus, and abdominal
varices.
Tagged RBC nuclear medicine scans are the most sensitive tests for detecting bleeding (0.1cc/min); however many
feel that these are too sensitive (Table27.2). Angiography
usually requires 1cc/min of bleeding for visualization, so it
is fairly common to have a negative angiogram follow a
positive tagged RBC scan. A recent study with 84 positive
tagged RBC scans reported that angiography revealed
bleeding in only 20 patients and only 9 of those were able to
have successful hemostatic embolization [6]. An additional
problem with tagged RBC scans is that incorrect localization of the source of bleeding is common which may mislead subsequent angiographic interrogation. The primary
indication for tagged RBC scans currently is to try to localize slow or intermittent bleeding that is not localized by any
other test.
For more active bleeding, CTA is preferred. CTA detects
0.3cc/min of bleeding [7], so it is a more realistic predictor
of a positive arteriogram. Also the localization of the bleeding is better with CTA than tagged RBC scans [8].
Furthermore, it has the advantage of sometimes being able to
specically identify the pathology that is bleeding, which
allows both better triage and prediction of prognosis
Fig. 27.1 Abdominal CT in a patient with LGIB revealed a small
bowel tumor (arrow). Since the patient was not bleeding extensively,
she was able to be triaged to surgery rather than angiography
(Fig.27.1). Finally, CTA can provide detailed arterial anatomy
that often allows the angiographer to target the specic vessel
that is bleeding. However, once a CTA is positive, all efforts
should be made to perform the arteriogram expeditiously. If
performed within 90 min of the CTA, 88% of arteriograms
will be positive, but only 45% percent are positive when the
arteriogram is delayed more than 90min after the CTA [9].
GI bleeding will often stop spontaneously, so the patient
who is not massively bleeding should at least initially be
managed conservatively. Indications to treat include bleeding that causes a signicant drop in the hemoglobin/hematocrit, requires transfusions, or leads to hemodynamic
instability. Less severe but chronic bleeding may also require
treatment since it may cause anemia. The decision when to
treat has to be tempered by the clinical condition of the
patient. A young otherwise healthy patient can tolerate blood
loss much better than an older person with coronary or
carotid atherosclerotic disease in whom hypotension or
decreased oxygen carrying capacity of the blood could lead
to coronary ischemia or stroke.
Conventional Therapy
Endoscopy should usually be the rst step for UGIB.It can
both localize the source of bleeding and identify the pathology in the majority of cases. Additionally the bleeding can
often be treated with a variety of endoscopic techniques
including injection of vasoconstrictors or sclerosants, thermal
or electrocoagulation, or by application of constrictive clips
or clamps. Additionally, gastric acid suppression through the
use of intravenous proton pump inhibitors is recommended

27 GI Bleeding
307
as they have been shown to reduce the rate of rebleeding and
mortality [10].
Surgery is indicated in several situations, the rst being if
bleeding is massive and life-threatening and immediate control
is needed. This, of course, requires that the source of bleeding
has been identied so that the surgeon knows which vascular
pedicle to control or what part of the intestinal tract needs to be
resected. Another reason for surgical treatment is if the bleeding pathology is something that will not respond well to embolization. Examples include diffuse bleeding from a non-focal
pathology such as inammatory bowel disease or if the bleeding is likely to be venous bleeding as with a bowel tumor. Also
while embolization can stop bleeding, if the pathology is something that requires a curative resection, then it may make sense
to triage the bleeding patient to surgery. Studies show that
angiographic embolization and surgery demonstrate comparable control of bleeding, but embolization is associated with
lower morbidity and mortality [11, 12]. Thus, if there are no
specic indications for surgery, patients more often are referred
for the less invasive interventional radiologic option.
Interventional Therapy
In the early years of interventional therapy, bleeding was often
controlled by intra-arterial infusion of vasopressin to constrict
the arteries feeding the bleed. The problems with this are that
it required prolonged arterial catheterization (24–48 h) and
recurrent bleeding was high (often up to 40% of the time) after
the infusion was stopped [13]. The rst embolization procedure to stop GI bleeding was reported by Baum etal. in 1974
[14]. Since that time arterial embolization has expanded to
become one of the dominant tools for managing GI bleeding
because of renements in angiographic imaging as well as the
catheters and embolic agents used for embolization.
For UGIB, the usual indication for angiography is inability to control the bleeding with endoscopic techniques or
rapid recurrence after endoscopic therapy. Rarely, a patient
may be referred to angiography without rst undergoing
endoscopy. However, if the endoscopist feels that the bleeding is so massive that they will not be able to visualize the
bleed, angiography is performed.
Key Point
Indication for UGIB angiography:
• Inability to control the bleeding with endoscopy
• Rapid recurrence after endoscopic therapy
Indication for LGIB angiography:
• First-line therapy for bleeding
• Bleeding demonstrated on tagged RBC scan or CTA
LGIB is harder to evaluate with endoscopy because of
blood owing toward the scope. One study of urgent colonoscopies showed that even with water-jet pumps and suction,
complete colonoscopy to the cecum was possible in only 69%
of patients and a source of bleeding was identied in only
39% of patients [15]. Therefore, in many institutions, angiographic embolization will be the front-line therapy. Which
technique is utilized rst will depend in part on the local
expertise of the interventional radiologists versus the endoscopists. Typically, the indication to proceed with angiography
for LGIB is demonstration of bleeding on either a tagged
RBC scan or a CTA.If bleeding is not demonstrated on either
of those screening tests, then it is usually not indicated to proceed with angiography since those tests are 3–10 times more
sensitive at detecting bleeding than angiography.
For UGIB, technical success (occluding the target artery)
ranges from 69% to 100%, while clinical success (clinical
evidence that bleeding stopped) ranges from 63% to 97%
[16]. Clinical success is lower than technical success
because some patients continue to bleed despite successful
occlusion of the artery. If the vessel suspected to be the
source of bleeding cannot be identied on angiogram,
empiric embolization may be performed, although this is
still up for debate. Typically, empiric embolization is guided
by prior identication of the bleeding source by endoscopy.
The success rate for empiric embolization is comparable to
embolizing a vessel that is seen to be extravasating on angiography [17].
For LGIB, several series on embolization have shown
good technical success (89–100%) and slightly lower clinical success (68–96%) [18–23]. This good technical success
is primarily because modern micro-catheters allow the
emboli to be delivered very close to the bleeding site, often
in the vasa recta in the wall of the bowel (Fig.27.2). More
specically for LGIB, the efcacy depends on the location in
the bowel and the etiology of the bleeding. Lesions with a
focal blood supply (like a diverticular bleed) are more effectively treated than lesions that have multiple vessels feeding
it. Examples of the later include angiodysplasias, tumors,
and inammatory bowel. A meta-analysis of 25 studies of
embolization for LGIB reported that the rate of recurrent
bleeding after embolization was only 15% for diverticular
bleeds but 45% for angiodysplasias and other lesions [24].
Regarding location, embolization tends to be less successful
in the small bowel (because of a richer collateral network)
and cecum (because bleeding in that location is often due to
angiodysplasia) [25]. Another series reported that rebleeding
rates were 15% in the large bowel versus 60% in the small
bowel [26]. Empiric embolization is rarely performed for
LGIB due to the risk of ischemic bowel.
The results of embolization for both the UGIB and LGIB
also depend on coagulation status and the type of embolic
agent used. Some emboli like coils do not actually occlude

308
Fig. 27.2 (a) SMA arteriogram shows active extravasation (arrow) into the ascending colon. (b) Arteriogram done after embolization with micro-
coils shows the coils (arrow) in the vasa recta in the bowel wall and no further bleeding
M. Darcy
ow and rely on formation of thrombus on the coils. If a
patient has a coagulopathy, embolization with coils alone is
associated with a higher rate of rebleeding. Multiple studies
have shown that n-butyl cyanoacrylate glue (super-glue) can
more effectively occlude vessels in the face of coagulopathy
[27–29]. However, safe use of glue requires considerable
expertise. Coils are usually able to be placed very precisely
and tend to be used more frequently.
Pre-procedure management starts with the initial consult.
The goals during that patient evaluation would be to determine
if the patient is bleeding enough to warrant an arteriogram, if
they have any severe contraindications to an arteriogram (such
as history of life threatening contrast reaction), and if they
have other medical conditions that could complicate an arteriogram or the sedation. If the patient has a severe cardiac or
respiratory condition that would not allow safe performance of
an arteriogram with conscious sedation, then enlisting the
assistance of an anesthesiologist should be considered.
Anesthesia support can also be invaluable if the patient needs
ongoing resuscitation during the arteriogram. During the
consult, the procedure and its risks need to be discussed in
detail in order to obtain informed consent from the patient.
Baseline hemoglobin and hematocrit levels are important
not only to assess the initial degree of bleeding but for
comparison to assess the results of therapy. Platelet count,
PT, PTT and INR are necessary to determine if there is an
underlying coagulopathy or to see if a patient is excessively
anticoagulated. Correction of coagulopathy is important
since that alone may stop the GI bleeding but also because
embolization is less effective in the coagulopathic patient.
Serum creatinine must be checked since diagnostic
angiography and interventions involve a high contrast load.
Renal failure is only a relative contraindication to angiography
since embolization may be lifesaving.
The patient must be kept NPO since the procedure will
typically require sedation. If there is a history of contrast
reaction, steroid premedication should be considered; an
emergency premedication may be administered in the lifethreatening situation.
Post procedure, the patient has to be kept at bed rest with
the leg straight to allow the femoral puncture site to seal and
to avoid bleeding. Vital signs must be monitored for several
hours post-angiogram to look for hypotension or tachycardia
which might indicate bleeding. The groin and peripheral
pulses must be checked with each vital sign check to make
sure there are no puncture site complications. Monitoring to
see if the intervention successfully stopped the bleeding is of
utmost importance. This includes following the hemoglobin
and hematocrit, transfusion requirements, and output of blood
(hematemesis or melena). The later can be difcult for lower
GI bleeds since the colon is a large reservoir and the patient
can continue to have bloody bowel movements long after
embolization has actually stopped the bleeding. If the patient
has any preexisting renal dysfunction, a serum creatinine
should be checked a day or two after the angiogram to look
for contrast nephropathy.

27 GI Bleeding
309
Fig. 27.3 (a) Celiac arteriogram in a patient with bleeding from a duo-
denal ulcer. The GDA (arrow) is faintly seen, because of poor penetration of the x-rays due to the patient’s obesity, but no extravasation is
seen. (b) Selective catheterization and arteriogram in the GDA now
clearly show the extravasation (arrow). (c) Coils (large arrow) were
The How To
1. Prior to starting make sure there is adequate IV
medication infusion (such as vasopressors).
2. Arterial access is most often from a femoral artery
approach via the Seldinger technique (refer to
Chap. 8 for further information).
3. A sheath is placed to allow easy introduction of
catheters but also to maintain access in case the
angiographic catheter should become occluded by
the embolic material.
4. Initial selective arteriography is done with a 5 Fr
catheter positioned in the trunk of the visceral vessels. Which vessel to start with depends on your
suspicion of what part of the GI tract the bleeding
placed in the GDA distal to the site of bleeding to avoid back-bleeding
from collaterals. Extravasation of contrast (small arrow) is still seen
because the bleeding originates proximal to the coils and close to the
origin of the GDA. (d) Arteriogram after embolizing more proximally
up to the GDA origin (arrow) shows bleeding has stopped
27.3a
suspected small bowel or right colon bleeding.
to arise distal to the transverse colon.
5.
arteriograms should be performed. Which vessel
is selected depends on the suspected site. For
example, the gastroduodenal artery would be subselected for a suspected duodenal bleed (see
27.3b).
6.
into the target vessel that is bleeding. With gastroduodenal or left gastric bleeds, this may be done
with the 5 Fr angiographic catheters, but usually a
(continued)

310
micro-catheter is advanced through the 5 Fr catheter in order to super-select the bleeding vessel.
Micro-catheters are essential for LGIB because
here the catheter has to be advanced as close to the
vasa recta as possible to avoid bowel ischemia.
7. After selecting the bleeding vessel, the vessel is
occluded with the embolic material of choice. In
some vessels it is important to start beyond (distal
27.3c).
8. After embolization, repeat angiography is done
27.3d).
9. Other vessels that might provide collateral blood
supply to the bleed then need to be angiographically interrogated. For example, after a GDA
embolization via the celiac trunk, the SMA needs
to be injected because the inferior pancreaticoduodenal artery arising from the SMA can provide
collateral supply to a GDA bleed.
10.
that vessel is catheterized and also embolized.
11.
stopped, catheters are removed and the arterial
access is closed with a closure device or by manual compression. If there is concern that the patient
may acutely rebleed (in patients with non-focal
diffuse blood supply or patients with coagulopathy), a sheath may be left in place to allow rapid
access back into the arterial system for repeat
arteriography.
M. Darcy
Complications
Complications common to any angiographic procedure
include occlusion, bleeding or hematoma at the access site,
and contrast-induced nephropathy or allergic reactions. The
main embolization-related complications include bowel
ischemia or infarction and nontarget embolization.
Bowel ischemia is rare after embolization for UGIB
because of the robust collateral supply to the stomach and
duodenum. The risk of ischemia is increased if the patient
has had any prior surgery on these organs since surgery may
have disrupted some of the potential collateral pathways. For
LGIB, the rate of signicant ischemia is around 5% or lower
[4, 19, 22]. Although the collateral supply is less robust,
modern micro-catheter techniques allow for very focal
embolization with emboli being deposited often as far as the
vasa recta. However while a focal bleeding source like a
diverticular bleed might be controlled by embolizing a single
vasa recta, more diffuse bleeding may require embolizing
several branches increasing the risk for bowel ischemia.
Animal studies have shown that the chance of ischemia signicantly increases if four or more vasa recta are embolized
[30]. Ischemic changes can range from asymptomatic mucosal abnormalities identied only at endoscopy all the way to
complete infarction of the affected bowel which requires
surgical resection if death is to be avoided.
Nontarget embolization refers to migration of the embolic
device or material from the intended target artery into an
undesired artery that you don’t want to occlude. This can be
the result of reux of injected particles or a mechanical
device backing out during placement (Fig.27.4). If the nontarget emboli are in a non-critical vessel, they can be left in
place, but if occlusion would lead to organ ischemia, then
retrieval of the errant embolic device should be attempted.
Key Point
Which vessel to select rst on angiography:
• Celiac rst for suspected UGIB
• SMA rst for suspected bleed of the small bowel or
right colon
• IMA rst for suspected bleed distal to the transverse
colon
Key Point
Risk factors for embolization:
• Bowel ischemia
• Bowel infarction
• Nontarget embolization

27 GI Bleeding
Fig. 27.4 (a) Celiac
arteriogram demonstrating
massive extravasation
(arrows) from the GDA. (b)
Common hepatic arteriogram
showing persistent
extravasation (arrow) from the
GDA proximal to the coils.
(c) After attempting to pack
coils all the way to the GDA
origin, the last coil backed out
and is sitting in the proper
hepatic artery (arrow)
311
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Uterine Artery Embolization
NicoleA.Keefe andZivJHaskal
Pathophysiology
Fibroids
Uterine broids, also known as leiomyomas or myomas, are
tumors that arise from the uterine smooth muscle.
Historically, references of broids date back to the time of
Hippocrates, when they were referred to as “uterine stones.”
Furthermore, ancient Egyptian female mummies show evidence of calcied pelvic masses suggestive of broids [1].
Fibroids affect up to 80% of women of reproductive age
with the majority of cases diagnosed in their 30s and 40s [2].
Fibroids are benign however rarely (0.1%) undergo sarcomatous degeneration [3]. They can become problematic as they
grow and cause both pressure and bleeding problems. They
can range from 1 cm up to 20 cm [4]. Fibroids can cause
heavy or prolonged menstrual bleeding, leading to anemia
(Table28.1). In postmenopausal women, vaginal bleeding is
atypical and should prompt further evaluation for endometrial cancer before attributing it to broids. Fibroids also lead
to “bulk” symptoms due to pressure on various structures.
Reproductive and environmental factors inuence a
woman’s risk of developing broids. Nulliparity is associated with an increased risk [5]. Both early menarche before
the age of 10 and the use of combined oral contraceptive pills
before the age of 16 increase risk [6]. Fibroids tend to regress
after menopause, emphasizing the hormonal relationship.
The risk of broids is also genetic, with rst-degree relatives
having a 2.5 times increased risk of developing broids [7].
Fibroids can be classied into four types based on the
location: submucosal, subserosal, intramural, and peduncu-
28
Table 28.1 Symptoms of uterine broids
Abnormal uterine bleeding,
metrorrhagia
Pelvic pressure Constipation, bloating
Back pain Infertility
Increased thromboembolic
disease
Sciatica pain Dyspareunia
Key Point
Fibroids grow with hormonal inuences and shrink
with menopause.
lated (Figs. 28.1 and 28.2) [2]. Diffuse broids within the
uterus are referred to as uterine leiomyomatosis.
• Submucosal broids are located beneath the
endometrium.
• Subserosal broids are located beneath the serosal
surface.
• Intramural broids are located within the thick
myometrium.
• Pedunculated broids grow on a stalk connecting them to
either the outer wall of the uterus in which they project
into the peritoneal cavity or to the inner wall of the uterus
in which they project into the endometrial canal.
Adenomyosis
Urinary frequency, difculty
urinating or retention
Increased rate of miscarriage
N. A. Keefe (*) · Z. J Haskal
University of Virginia School of Medicine, Department of
Radiology and Medical Imaging, Interventional Radiology
Division, Charlottesville, VA, USA
© 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_28
Another uterine pathology that causes menorrhagia is adenomyosis (Fig.28.3). This is characterized by endometrial glands
and stroma arising aberrantly in the uterine musculature.
Instead of having a “bumpy” uterine shape characteristic of
313
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