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Vascular 
Embolotherapy 



MEDICAL RADIOLOGY 
Diagnostic Imaging 



Editors: 

A. L. Baert, Leuven 

K. Sartor, Heidelberg 



3HRMAP 



J. Golzarian • S. Sun • M. J. Sharafuddin (Eds.) 

Vascular 
Embolotherapy 

A Comprehensive Approach 

Volume 1 

General Principles, Chest, Abdomen, 

and Great Vessels 



With Contributions by 

H.T. Abada ■ D. M. Coldwell ■ M. D. Darcy ■ L. Defreyne ■ A. Fauconnier ■ J. Golzarian 

D. Hunter ■ P. Lacombe 'A. Laurent ■ L. Machan ■ H. Mimura ■ T. A. Nicholson ■ J. P. Pelage 

J. S.Pollak-M. K.Razavi- J.A.Reekers- A. C.Roberts ■ G. T. Rosen ■ M. J. Sharafuddin 

G. P. Siskin ■ S. Sun ■ K. Takahashi ■ J. C. van den Berg ■ D. Valenti ■ R. I. White, Jr. 

J. I Wong 

Foreword by 

A.L.Baert 



With 171 Figures in 414 Separate Illustrations, 43 in Color and 33 Tables 



4y Spring 



er 



Jafar Golzarian, MD 

Professor of Radiology, Department of Radio 

University of Iowa Hospitals and Clinics 

Carver College of Medicine 

200 Hawkins Drive 

Iowa City, IA 52242 

USA 

Shiliang Sun, MD 

Associate Professor of Radiology 

University of Iowa Hospitals and Clinics 

Carver College of Medicine 

200 Hawkins Drive 

Iowa City, IA 52242 

USA 

Melhelm f. Sharafuddin, MD 

Department's ot Radiology and Surgery 

University ot Iowa Hospitals and Clinics 

Carver College of Medicine 

200 Hawkins Drive 

Iowa City, IA 52242 

USA 



Medical Radiology ■ Diagnostic Imaging and Radiation Oncology 

Series Editors: A. L. Baert ■ L. W. Brady ■ H.-P. Heilmann ■ M. Molls ■ K. Sartor 

Continuation of Handbuch der medizinisohen Radiologic 
Encyclopedia of Medical Radiology 



ISBN 3-540-21361-9 Springer Berlin Heidelberg New York 
ISBN 978-3-540-21361-1 Springer Berlin Heidelberg New York 



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io my parents 

a weLlspring of love and support without limit. 

I owe you everything. 

To my wonderful wife, Elham 
and my children Sina and Sadra 

Dr. Golzarian 

To my wife, Shuzhen, and daughter, Yue 
for their selfless support 



iomywifeL«9', and children Jacob and Evan 
Dr. Sharafuddin 



To all o 



Foreword 



Percutaneous image- guided treatment is now well recognized as an effective minimally 
invasive treatment modality in modern medicine. Its field of application is growing 
every year due to the availability of more and more sophisticated materials, tools and 
devices, but also because of the technical progress in reduction of the dose of ionizing 
irradiation incurred by both patient and radiologist during fluoroscopy. 

Vascular embolotherapy is now one of the main forms of endovascular percutaneous 
treatment of diseases of the vascular system. 

The editors of the two volumes of "Vascular Embolotherapy: a Comprehensive 
Approach", J. Golzarian, S. Sun and M.J. Sharafuddin, leading experts in the field, were 
successful in obtaining the collaboration of many other internationally renowned inter- 
ventional radiologists. I am particularly indebted to Professor Golzarian for his origi- 
nal concept for these books and his relentless efforts to complete the project in good 

I would like to congratulate the editors and authors on producing these well-written, 
superbly illustrated and exhaustive volumes covering all aspects of vascular embolo- 
therapy. The readers will find comprehensive up-to-date information as a source of 
knowledge and as a guideline for their daily clinical work. 

These two outstanding books will certainly meet with high interest from interven- 
tional radiologists and vascular surgeons. They - and therefore their patients - will 
greatly benefit from its contents. Also referring physicians may find these books very 
useful to learn more about the indications, possibilities and limitations of modern vas- 
cular embolotherapy 

I am confident that these two volumes will encounter the same success with readers 
as the previous books in this series. 

Leuven Albert L. Baeet 



Preface 



Therapeutic embolization has now become a major part of modern interventional prac- 
tice, and its applications have become an integral component of the modern multimodal- 
ity management paradigms in trauma, gastrointestinal hemorrhage and oncology, and 
the endovascular therapy of vascular malformations and aneurysms. The past decade 
has also marked the emergence of several new indications for therapeutic embolization, 
such as uterine fibroid embolization, and the widespread acceptance of embolization 
therapy as an effective non-operative management modality for major hepatic, splenic 
and renal injuries that once posed tremendous challenge to the trauma surgeon. Emboli- 
zation therapy has also become an integral facet of the modern oncology center, offering 
solid-organ chemoembolization, preoperative devascularization, hepatic growth stimu- 
lation prior to resection, and direct gene therapy delivery. 

Despite this remarkable growth, there are currently few references available to sum- 
marize this major field in vascular interventional therapy. The purpose of our two- 
volume book was to organize and present the current state of the art of embolotherapy 
in a comprehensive yet manageable manner. Our goal was to provide a user-friendly, 
well- illustrated, and easy- to -browse resource to enable both experts and novices in 
this field to quickly derive high-yield clinically relevant information when needed. In 
addition to standard applications of embolotherapy, we have also included a number 
of closely related applications that have become intimately associated with the field of 
therapeutic embolization, such as stent-graft placement and radiofrequency ablation. 
The two volumes constitute the combined experience of many of the leading experts in 
the field and have been generously supplemented with helpful tables, illustrations and 
detailed imaging material. We have also striven to include insightful discussions and a 
"cookbook" segment in each topic to provide a quick outline of procedural preparation 
and technique. We have included a chapter on monitoring and resuscitation of the hem- 
orrhaging patient that should be a "must-read" for the interventionist who is not well 
versed in surgical critical care. Readers will also find important coverage of pathophysi- 
ology and of diagnostic clinical as well as imaging workup. 

We hope this reference will meet the needs of physicians providing therapeutic embo- 
lization, whether they are trainees, recent graduates or even well-established interven- 
tionists who wish to refresh their memory or learn the opinion of some of the field's 
led experts before embarking on a difficult case or trying a new technique or 



Iowa City Jafar Golzarian 

Shiliang Sun 
Melhem J. Sharafuddin 



Contents 



leral Principles 1 

Embolotherapy: Basic Principles ;md Applications 

Melhem J. Sharafuddin, Shiliang Sun, and Jafar Golzarian 3 



Embolization Tools 

Jafar Golzarian, Gary P. Siskin, Melhem J. Sharafuddin, 

Hidefumi Mimura, and Douglas M. Colswell 

Controlled Delivery of Pushable Fibered Coils for Large Vessel Embolotherapy 
Robert I.White Jr. and Jeffrey S.Pollak 

Work-up and Follow-up after Embolization 

Jim A. Reekers 



5 Upper GI Bleeding 

Luc Defreyne 49 

6 Embolization for Lower GI Bleeding 

Michael Darcy 73 

7 Haemobilia and Bleeding Complications in Pancreatitis 

Tony A. Nicholson 87 

8 Balloon-occluded Retrograde Transvenous Obliteration ol Gastric Varices 
in Portal Hypertension 

Koji Takahashi and Shiliang Sun 99 

Gynecology and Obstetrics 105 

'■' Interventional Mana^nneni of l'^iparfuin Hemorrhage 

Hicham T.Abada, Jafar Golzarian, and ShilliangSun 107 

10 Fibroids 

Gary P. Siskin, Jeffrey J. Wong, Anne C. Roberts, Jean Pierre Pelage, 

Arnaud Fauconnier, Pascal Lacombe, Alexandre Laurent, and 

Jafar Golzarian 119 

10.1 Uterine Fibroid Embolization: Practice Development 

Gary P. Siskin 119 



Co:iTciits 

10.2 Pre -op Work- Up and Post-op Care of Uterine Fibroid Embolization 

Jeffrey J.Wong and Anne C.Roberts 125 

10.3 Fibroid Embolization: An.itomv nod Tedimoil Considi 
Anne C. Robe; 

10.4 Results and Complic 
Jean Pierre Pelage, Arnaud Fauconnier, and Pascal Lacombe 157 

10.5 How to Minimize Failure after UFE 

Jafar Golzarian and Jean Pierre Pelage 177 

10.6 Perspectives 

Alexandre Laurent, Jean Pierre Pelage and Jafar Golzarian 187 

Pelvic Congestion Syndrome 

Lindsay Machan 199 



Genitourinary 213 

12 Varicocele Embolization 

David Hunter and Galia T. Rosen 215 



13 Embolization Therapy for High-Flow i'nnpis 
Jim A. Reekers 



Aortic-Iliac 233 

14 Endoleak: Definition, Diagnosis, and Management 

David Valenti and Jafar Golzarian 235 

15 Internal Iliac Artery Embolization in the Stent-Graft Treatment of 
Aortoiliac Aneurysms 

Mahmood K. Razavi 253 



Respiratory System 261 

16 Bronchial Artery Embolization 

Jos C. van den Berg 263 

17 Pulmonary Arteriovenous Malformations 

Jean Pierre Pelage, Pascal Lacombe, Robert I.White, Jr., 

and Jeffray S.Pollak 279 



Subject Index 297 

List of Contributors 303 

Contents and List of Contributors of Volume 2 305 



General Principles 



1 Embolotherapy: Basic Principles and Applications 



Melhem J. Sha 



3 Sun, and Jafar Gol: 



Introduction 3 

The Ideal Vascular Occlusion Technique 4 

Cktssificilion of liiliavasaila; E:'.:h::i|i: Ageivis 

Essential Elements for Success in Successful 

Embolotherapy 5 

Go:y.pli:a:io:'^ of EaiLioloihe; .ipy J> 

Guidelines ii iio Te-:li:~ iq".ic-3 :■: Pieveni ai'.d Man 

Co:y.pli:;itions 6 

Guidelines and t': Ln t "jy!i-s i:' ^rJled ■ I- 1 j : '. i l" ,1 J 

Upper GI Bleeding 7 

Lower GI Bleeding 7 

Hem'.p".ysis/h:o:'.clual Artery Embolization 7 
Cookbook: (Materials) S 
Trauma 9 

Conclusion 9 



Introduction 

Embolotherapy is defined as the percutaneous endo- 
vascular use of one or more of a variety of agents 
or materials to accomplish vascular occlusion. The 
number of applications of embolotherapy continues 
to expand. This text provides a brief overview of 
the current applications of embolotherapy, current 
embolic techniques and some related general prin- 

Embolotherapy initially evolved as a minimally 
invasive means for arresting uncontrolled hemor- 
rhage in a number of clinical scenarios including 
upper gastrointestinal (UGI) bleeding resulting 
from ulcerative disease, malignancy, pancreatitis 



M.J. Shah afuddtn.MD 

Pepar: mints of K.; J -olo ay and Mirgery. "Jniversity of ioiva Hos- 
pitals and Clinics, 200 Hawkins Drive, Iowa City.IA 52242, USA 
S.Sun.MD 

Associate Professor ■:if Radiology, "University of ~.<:-\\\i Hospitals 
and Clinics, 200 Hawkins Drive, Iowa City, IA 52242, USA 

i. GOLZARIAN.MD 

!- : :o:essor .:■!" ti;id;o..:'ey '. ■ i : e l ; . : r, Vasaib: and laicirentional 
Radiology, University of Iowa Hospitals jnd Chnics, 200 
Hawkins Drive, 3957 JPP, Iowa City, IA 52242, USA 



and hemobilia [1-9]. Its efficacy was also described 
in lower gastrointestinal (LGI) hemorrhage due to 
tumors, diverticular disease, angiodysplasia [7, 10- 
14]. Embolotherapy was also determined to be a valu- 
able tool in the management of obstetric and gyne- 
cologic bleeding due to peripartum complications, 
and in benign and malignant gynecologic tumors 
[15, 16]. Bronchial artery embolization is also a well 
recognized and often the only effective modality for 
the management of severe hemoptysis in a variety 
of inflammatory lung conditions [17, 18]. It has also 
been described in spontaneous retroperitoneal hem- 
orrhage, as well as retroperitoneal and intraperito- 
neal hemorrhage due to vascular tumors [19]. 

Perhaps one of the most well recognized applica- 
tions of embolotherapy is traumatic hemorrhage, 
especially from pelvic fractures, and appendicular 
musculoskeletal injuries [20-23]. In recent years, 
embolotherapy has also become increasingly recog- 
nized as an excellent modality for the non-operative 
management of solid organ trauma, including the 
liver [24-28], spleen [26, 29-32] and kidneys [26, 33- 
35]. Embolization is also the leading modality in the 
management of iatrogenic solid organ and vascular 
injuries, especially those cause by percutaneous 
biopsy and laparoscopy [36]. Transjugular embo- 
lization in conjunction with TIPS [37], as well as 
direct percutaneous transhepatic embolization [38, 
39] of bleeding portosystemic varices are also effec- 
tive approaches in the management of UGI and LGI 
hemorrhage due to portal venous hypertension. 

With the current advances in technology allow- 
ing more accurate and controlled deployment of 
embolic agents, embolotherapy has now become the 
procedure of choice for the management of visceral 
and solid organ aneurysms [40-42]. In addition, 
embolotherapy has now arguably become the pri- 
mary facet in the management of vascular malfor- 
mations of all varieties, in the central nervous system 
and head and neck [43, 44], pulmonary circulation 
[45-48], viscera, trunk and extremities [49-54]. 

Embolotherapy is also an effective means for the 
management of symptomatic male varicocele [55], 



M. }. Sharafuddin 



vasogenic impotence, and priapism [56, 57]. Embo- 
lotherapy is also the main ef fee live modality for the 
management of the pelvic venous congestion syn- 
drome in women [58]. 

Embolotherapy has recently gained acclaim as 
valid tissue ablation and devascularization modal- 
ity. Portal vein embolization is becoming an increas- 
ingly well recognized tool for organ flow redistri- 
bution, to allow increased regeneration prior to 
planned hepatic resection [59-61]. It is also a prom- 
ising modality to enhance vector expression in gene 
transfer therapy aimed at the hepatocyte [62]. Pre- 
operative embolization of vascular skeletal metas- 
tases or vascular solid organ tumors was also rec- 
ognized as a useful application in the early days of 
Embolotherapy [63-65], Ablation of d ys functioning 
organs using various embolization techniques and 
regimens has also been well described for manage- 
ment of hypertension or protein wasting in end-stage 
renal disease [66, 67], hypersplenism, and immune 
disorders of the spleen [30, 68-70], and recently in 
Graves' disease of the thyroid [71]. The evolution of 
uterine fibroid embolization has established the role 
of embolotherapy as a viable alternative to hysterec- 
tomy, and undoubtedly revolutionized the manage- 
ment options in this very common disorder [72-74]. 
Chemoembolizalion has also become a key compo- 
nent of the modern multimodality treatment para- 
digms of primary and metastatic hepatic tumors 
P5-77]. 

The advance of endovascular therapy for aorto- 
iliac aneurysmal disease has also brought about yet 
another ( loiirisliii'iii application ol embolotherapy. 
Embolization of the internal iliac artery plays an 
important adjunct initial modality to allow endo- 
vascular treatment of aortic aneurysms with exten- 
sion into the common iliac arteries [78-80]. It also 
plays an crucial role in the secondary management 
of complications related to endoleaks [81-84]. 



The Ideal Vascular Occlusion Technique 

The ideal vascular occlusion technique is one that 
allows accurate guidance and delivery to the target 
with low risk of injury to normal structures. This 
characteristic is a function of various specific attri- 
butes: (1) radiopacity, radio-opaque markers or abil- 
ity to mix into radiopaque suspension, (2) simplicity 
of the delivery technique, (3) reliability of delivery 
mechanism, (4) ability to reach distal vascular beds, 



(5) amenability to trouble shooting/salvage in case 
of complications or device mjlfunct ion (for example 
ability to easily retrieve and preferably also rede- 
ploy the device in case of misplacement; (6} effi- 
cacy or the ability to result in rapid occlusion for 
a duration appropriate to the desired application; 
(7) being adaptable to allow selective occlusion of 
various vessel types and sizes; (8) biocompatible 
components, and (9) cost competit: 



Classification of Intravascular Embolic Agents 

Numerous devices or materials have been used to 
accomplish effective vascular occlusion and their 
specific details are beyond the scope of this brief 
summary. A broad classification and examples 
are listed in Table 1.1. Broadly speaking, embolic 
materials can be classified into different categories 
based on their physical and biological properties. 
It is important to note that the level of occlusion, 
which is primarily determined by the size of the 
agent, can also be affected by the occurrence of sec- 
ondary clumping of individual particles. Embolic 
materials and devices are now available that can 
allow the occlusion of anywhere from a large vessel 
to a distal arteriolar or capillary level. The major- 
ity of non-neurovascular embolization procedures 
are currently performed with coils, Gelfoam, par- 
ticles, and liquid sclerosants. There has also been 
increased interest in solidifying liquid mixtures and 
tissue glues. Mechanical embolic agents function 
by causing a direct mechanical obstruction of the 
lumen as well as providing a matrix for thrombus 
ioniianon ultimately resulting in occlusion. Certain 
agents can also incite an inflammatory reaction in 
and around the vessel, which further accentuates 
the occlusive effect. Liquid sclerosant agents such as 
absolute alcohol cause direct destruction and dena- 
turation of endothelial proteins. 

Of all the attributes and features of an embolic 
agent, the main factors influencing its selection in 
a specific application relate to the desired level of 
occlusion in the vascular tree and the desired per- 
manency of occlusion. For example, when dealing 
with traumatic or degenerative hemorrhagic condi- 
tions, small particulate and liquid agents should be 
avoided as they can reach the capillary level result- 
ing in significant non-target ischemia and infarc- 
tion. On the other hand, such agents may be per- 
fectly appropriate in conditions where hemorrhage 
is caused by a hypervascular tumor. 



Embolotherapy: Basic Principles and Applies 



Table 1.1. Broad classification of 



i' embolic agents pat. 



Proximal mechanical: 

• Coils: 

o Conventional Ciantuico cols ■: C . 3 5 inch) [110] 

o Microcoils (0.014-0.018 inch) [111] 

o Conventional Guglielmi detachable coil (GDC) [112, 113] 

o New 3D GDC [114] 

o Radioactive coils (Platinum coils implanted with 

radioactive 32P) [115] 
o Biodegradable coils [116, 1 17] 
o Mechanism of detachment: 

■ s'imt'le wire pusher 

■Electrically detachable (GDC) [118] 

■Mechanically detachable [104, 119] 

• Celfoam: Leve' of occlusion depends on size and prepara- 
tion i torpedoes, pled gels, starry, powder) 

• Detachable balloons [120] 

• Shape memory polymers [Ul ] 

• Cast forming materials: 

o N -butyl 2 -cya no a cry late [122, 123] 
o Ethylene-vinyl alcohol copolymer/di methyl sulfoxide/ 
micron j zed tantalum mixture (Onyx) 

Distal mechanical: small particular? agents: 

• Standard polyvinyl alcoitoi fPVA): nonuniform size, 



• Round PVA: calibrated uniform size. aggregating 

• Trisacryl gelatin riiicrospi'.eres ■: Embospherej: 
calibrated, flexible, non-aegivgr.i n'.ti 

■ Embogold: radiopaque microspheres 

• Ytlr;um-93 glass radioactive microspheres iTherasrri'.erei 
[124] 

Liquid iderositig liquids: 

• Absolute ethanol [51,52] 

• E:: hi bloc: biotiegradable rib ro sing agent [.-.i] 

• Hypertonic dextrose 

• Boiling contrast 

• Prcvicone iodine 

• sodium tetrad ecyl sulfate (Sotradecol) 

Citcmeembollzatton mixtures 

Miscellaneous techniques: 

• stem-assisted and hailoon-assisted coi. ivirto.reling iech- 
nique [in wide neck aneurysms! [1^6-129] 

• Direct fibrin acfiesive i:"i:ec:ic-:". .it; ring oalloon i nil at ion 
across neck [130] 

• Covered stents [131, 132] 

• Direct thrombin imection into aneurysms: [133, 134] 

• Flow directed balioon calheterization [135] 



Essential Elements for Success in Successful 
Embolotherapy 

Embolotherapy is a delicate balance between safety 
and efficacy. Therefore, all involved parties (includ- 
ing the interventionist, referring physician and the 



it or patient's family) need to be in agree- 
about expectations and risks before proceed- 
ing. The following criteria must always be satis- 
fied: (1) clinical appropriateness of embolization, 
(2) proper pre-procedural imaging studies and/or 
angiographic localization of the bleeding abnor- 
mality or target vessel(s), (3) accurate determina- 
tion of target vessel size, (4) accurate assessment 
of the status of collateral circulation, (5) appropri- 
ateness of embolic agent choice, (6) availability of 
modern angiographic equipment and a full array 
of diagnostic and interventional devices and sup- 
plies, and (7) technically skilled and experienced 
operator including knowledge of trouble shooting 
techniques. 



1.3.1 

Complications of Embolotherapy 

The complications oi emlvMotberapv .ire well 
described, but vary in their manifestations depend- 
ing on the affected end-organ [85, 86]. By nature, 
success depends on complete abolishment of vas- 
cular supply, be it normal or abnormal vasculature. 
This can often be accomplished but not without 
a risk of compromise to adjacent normal tissue. 
Moreover, aggressive pursuit of difficult vascular 
territories poses a risk for non-target emboliza- 

Embolotherapy is associated with the usual 
iodinated contrast related risk of nephrotoxicity 
and access related hemorrhagic and thromboem- 
bolic complications. However, the most signifi- 
cant complication of embolization is non-target 
embolization. It occurs when normal vessels are 
unintentionally occluded due to a technical failure 
of a device of or if the embolic material or device 
refluxes out of the embolized vessel into the parent 
vessel. Non-target embolization can affect the sys- 
temic arterial system, and can take the form of pul- 
monary embolization when working in the venous 
system or when the embolic material passes through 
an AV fistula. Many post embolization compli- 
cations are the results of inadequate technique, 
incomplete or suboptimal diagnostic angiography 
or inadequate evaluation of the vascular supply and 
collaterals before embolization. Adhering to metic- 
ulous technique and attention to details are crucial 
during the embolotherapy to minimize non-target 
embolization. Significant complications following 
embolotherapy can occur as a result of the use of 
an inappropriate embolic agent. Liquid sclerosant 



M. J. Sharafuddin 



agents and small particles such as very small PVA 
or Gelfoam powder should be used very carefully as 
they can cause occlusion to the capillary level with 
significant tissue infarction. 

Complex embolization procedures require pro- 
longed fluoroscopic exposure to the skin especially 
when using the same projection under magnifica- 
tion and without proper collimation [87]. The opera- 
tor needs to be cognizant of that risk and needs to 
reduce radiation exposure by using pulse fluoros- 
copy, minimizing magnification and periodically 
varying the angle of i luoroscopy beam. 

A spectrum of end-organ ischemic complica- 
tions can occur with embolo therapy. Bowel infarc- 
tion can complicate splanchnic embolization tar- 
geting bleeding or could result from inadvertent 
non-target embolization from an upstream source 
[88]. Gallbladder infarction or bile duct necrosis 
can complicate hepatic artery embolization or che- 
moembolization [89, 90]. Splenic abscess and over- 
whelming sepsis can occurs following splenic embo- 
lization [91]. Skin necrosis and nerve injury have 
been reported as a result of ethanol embolization of 
vascular malformations [53, 54]. Buttock muscular 
necrosis, buttock daudk'alion and sexual dysfunc- 
tion can occur as a result of internal iliac branch 
embolization, especially when distal or bilateral 
[92-95]. 

The "post-embolization syndrome" comprises 
a constellation of symptoms including pain, fever, 
nausea, vomiting, and leukocytosis due to ischemia 
or infarction of the embolized organ [85]. The post- 
embolization syndrome per se is almost expected 
sequelae of the procedure and should not be consid- 
ered a complication. It is much more common with 
a solid organ embolization and when sclerosant 
agents are used. Shock and cardiovascular collapse 
have also been rarely described during embolization 
with absolute alcohol [51]. 



Guidelines and Techniques to Prevent and 
Manage Complications 



In order to minimize the risk of compile 
during embolotherapy, experience, thorough knowl- 
edge of relevant vascular anatomy, proper plan- 
ning and execution using a well stocked modern 
inventory and availability of high quality fluoros- 
copy and digital subtraction angiograms cannot be 
overemphasized. In addition, safeguards have been 



ided to reduce the risk of complic 
during embolization, such as ultraselective tech- 
nique and the avoidance of pressor drugs [96]. The 
importance of correction of coagulopathy prior to 
embolotherapy cannot be overemphasized, with a 
number of studies demonstrating high failure rates 
noted in coagulopathic patients [97]. Conversely, 
in high risk embolization procedures not associ- 
ated with active hemorrhage, heparinization or 
treatment with ^Ivvoprotetn 1 lb/Ilia blo.l-.er; have 
been shown to reduce thromboembolic complica- 
tions [98]. When occlusion at a consistent level in 
the vascular tree is desired, some authors advocate 
using newer particulate agents such as Embosphere 
over conventional PVA; the inhomogeneity of PVA 
particle and their tendency to clumping may con- 
tribute to more proximal occlusion and lack of effi- 
cacy is cases where distal occlusion is desired [99]. 
Although Embosphere is reported to allow for more 
accurate and consistent occlusion at the desired level 
in patients undergoing uterine fibroid embolization 
(UFE) [100], the clinical outcome after UFE is not 
different between non-spherical PVA compared to 
Embosphere [101]. 

Familiarity with a variety of specific trouble 
shooting techniques is an important prerequisite 
to success in embolotherapy. When embolizing 
a large vessel, coil stability is essential. A study of 
the effect of sizing on stability suggests that a cer- 
tain degree of oversizing is essential to minimize 
the risk of dislodgement. However, this should be 
weighed against the negative effect of an elongated 
and incompletely formed coil on hemostasis. An 
oversizing ratio of around 15% has been suggested 
in arteries, although in veins more oversizing is 
required [102]. Some authors recommended the use 
of tightly packed nested coils to enhance hemostatic 
efficacy [103]. Newer detachable coil designs allow 
testing of stability before detaching the coil and may 
be preferred in high risk situations [104]. Occlusion 
balloons in high tlow situation or when using liquid 
agents are very useful to prevent non-target emboli- 
zation. Of all trouble shooting techniques, the abil- 
ity to quickly retrieve misplaced or migrated coils is 
a crucial skill [105, 106]. 

Finally, the injection technique of embolic par- 
ticles is of paramount importance. Flow-directed 
injection of the particles respects the physiology 
of the circulation. Forceful injection can result not 
only in vessels damage or reflux but also in some 
situation, may provoke the opening of the normal 
vascular anastomosis with subsequent non-target 
embolization. 



Embolotherapy: Basic Principles and Applic 



1.4.1 

Guidelines and Principles in Selected Clinical 

Scenarios 



agement of hemobili 
genie injury or tunic 



resulting from trauir. 
>[8]. 



1.4.1.1 

Upper Gl Bleeding 



;tiology of UGI bleeding requir- 
ing angiographic intervention is from ulcers non- 
responsive to endoscopic maneuvers [1, 4]. Gelfoam 
has been the favored material in the setting of upper 
GI bleeding. Oftentimes embolization of the left gas- 
tric or gastroduodenal artery is required. If a bleed- 
ing source is identified, a combination of gel foam 
slurry followed by larger pledgets can be used. How- 
ever, if superselective catheterization of the bleeding 
vessel is performed, coil embolization is the tech- 
nique of choice. If there is an associated pseudo 
aneurysm, embolization should be performed on 
both sides of the pseudo aneurysm with coils ("coil- 
sandwich" technique). Special care should be taken 
if the patient has a history of prior gastric or esopha- 
geal surgery. If collateral supply is compromised, 
a superselective embolization technique should be 
performed if at all possible. Duodenal embolization 
is technically challenging because of the dual blood 
supply to the duodenum from the celiac axis and 
superior mesenteric artery. 

Antegrade obliteration of the superior duode- 
nal branches via the gastroduodenal artery is often 
insufficient alone, as the bleeding points can be 
quickly pressurized via the rich anastomotic con- 
nections from the inferior pancreaticoduodenal 
arcade. In such cases, a "coil-sandwich" technique 
or alternatively direct obliteration of the bleeding 
segment or pseudoaneurysm by nested coils or a 
casting agent may be needed to prevent recurrence. 

When no bleeding site is identified angiographi- 
cally, some have advocated empiric embolization of 
either the left gastric artery of gastroduodenal artery. 
However, in our opinion this should be reserved as a 
last resort option. Aggressive non-selective emboli- 
zation in UGI bleeding can cause infarction, pancre- 
atitis, or severe gastroduodenal tissue ischemia and 
friability, which can markedly limit or complicate 
subsequent surgical options. When contemplating 
empiric embolization ol the lelt "astnc artery, .are 
must be taken to exclude the possibility of replaced 
left hepatic artery completely originating from the 
left gastric artery [107]. 

Hemobilia is a subset of UGI bleeding that is par- 
ticularly d iff icu It to manage by conventional means. 
Embolotherapy is a valuable modality is the man- 



1.4.1.2 

Lower Gl Bleeding 

Recent evidence suggests an important role for 
embolotherapy in the management of lower GI 
bleeding. A variety of agents including Gelfoam, and 
coils have all been described. Proximal emboliza- 
tion should be avoided, and selective micro cath- 
eter catheterization and micro coil embolization, 
ideally at the level of the arcade or vasa recta is 
preferred . Selective embolization maybe technically 
challenging in vasoconstricted shocky vessels or if 
vasospasm develops from repeated instrumenta- 
tions. Pretreatment with a calcium channel blocker 
or intraarterial administration oi a vasodilator may 
be beneficial. The use of vasopressin or other vaso- 
constrictors should be avoided following emboliza- 
tion because of the risk of intestinal infarction with 
this combination. Likewise, careful follow-up of the 
patient's symptoms and abdominal examination are 
crucial; should ischemic complications be suspected 
exploratory surgery should be performed to rule out 



1.4.1.3 

Hemoptysis/Bronchial Artery Embolization 

Bronchial artery embolization is the therapeutic 
modality of choice for severe hemoptysis in chronic 
inflammatory conditions of the lungs such as cystic 
fibrosis, and bronchiectasis. The traditional teach- 
ing is to perform unilateral embolization of the 
involved side. Bronchoscopy is helpful to localize 
the site of bleeding. Curiously, the patient can also 
accurately localize the side of bleeding. It is impor- 
tant to realize that one must not rely on the demon- 
stration of active extravasation from the bronchial 
artery to justify the bronchial artery embolization. 
Hypervascularity and/or enlargement of the bron- 
chial arteries are sufficient to proceed with embo- 
lization. Particulate agents, such as PVA, are the 
embolic agent of choice although some investiga- 
tors recommend the addition of Gelfoam plug into 
the proximal bronchial artery. Coils should not be 
used. One challenging aspect of bronchial emboli- 
zation is the need to avoid unintended emboliza- 
tion of a spinal artery that c 
from the bronchial artery. 



M. J. Sharafuddin 



Cookbook: (Materials) 



A. General Principles and Safeguards 

in Embolotherapy: 

1. Appropriateness: Discuss indications, risk/ 
benefits with referring physician, patient/ 

2. Establish clear procedure goals, priori- 
ties, acceptable endpoints, and alternative 
approaches. For example, in an unstable 
patient, procedural speed is paramount, and 
non-selective embolization should be pre- 
ferred over a lengthy selective embolization 
of difficult to reach bleeding site(s). 

3. Recognize high-risk situations for ischemic 
complications during embolization: 

■ Multiple -vessel embolization 

■ Altered collateral circulation: previous embo- 
lization, trail ma/iatro genie injury, atheroscle- 
rosis, shock, and pharmacological alteration 
(vasopressor therapy) 

4. Procedure planning: 

• Ensure availability of equipment and 
resources: Adequate fluoroscopy/DSA, avail- 
ability of catheters, guidewires, large inven- 
tory of coils and embolic materials. 

• Vascular access approach: retrograde versus 
antegrade, ipsilateral versus contralateral. 

• Choice of embolic material/method is para- 
mount and must be based on the target vascu- 
lar territory and the desired effect. Ability to 
reach distal vascular beds. For example, emer- 
gent non-selective embolization of a large 
vascular territory is best accomplished with a 
potentially temporary occlusive agent such as 
Gelfoam. 

• Be comfortable with a number of trouble 
shooting/salvage techniques in case of compli- 
cations/malfunction. For example, snaring or 
forceps retrieval a misplaced coil, deployment 
of a coil stuck in a catheter with a saline flush 
using a TB syringe [108]. 

• Go over available ;iimtomic studies (CT, angio- 
gram, scintigram). Active bleeding on the scin- 
tigram, enlarging hematoma, hematoma with a 
hematocrit level, and active contrast swirling or 
blush on contra st- e nil anced helical CT are all 
helpful signs for localizing active bleeding. 

• Avoid particulate agents if significant AV 
shunting is noted on the angiogram. 



• Be familiar with the normal and collateral 
vascular supply of target territory, and the vari- 
ant vascular anatomy especially if previously 
injured or compromised by trauma or prior 
embolization procedures. For example, when 
treating bleeding from a well-collateralized 
territory such as soft musculoskeletal tissue, 
liver, spleen, and the upper GI, using particles 
>500 urn is unlikely to cause significant isch- 
emia. On the other hand, even proximal coil 
embolization of the superior gluteal artery 
territory following severe crush injury to the 
buttocks may result in muscular necrosis. 

• Correct coagulopathy. Uncorrected coagulopa- 
thy is a significant cause of failure. 

5. Start with a nonselective regional angiogram, 
before proceeding to more selective injec- 
tions, with the uncommon exception of cir- 
cumstances the bleeding vessel is identified 
before the procedure (via imaging or endos- 
copy). 

6. After completion of the primary emboliza- 
tion procedure, it is important to check other 
potential collateral pathways. For example, 
profunda femoris and contralateral internal 
iliac arteries are injected following emboliza- 
tion of an internal iliac bleeding source. 

7. Avoid "burning bridges". For example, place- 
ment of proximal coils for a multifocal small 
vascular bleed will preclude a subsequent 
attempt to correct recurrent bleeding sup- 
plied from collateral anastomoses. 

8. Safety tips during embolization: 

• Maintain fluoroscopic monitoring (use pulse- 
flu oros copy). 

• If possible attempt to use an opacified 
embolic agent/ mixture, for example n-butyl 
cyanoacrylate can be mixed with Ethiodol 
[109]. 

• Carefully estimate volume of embolic material 
quantity to be used (excess leads to overflow 

• Beware of causes of reflux of embolic material 
which can cause non-target embolization: 

- Excess of embolic material quantity 

- Stagnation from prior embolic injections 

- Excessively forceful injection 

• Use frequent contrast injections to check 
residual flow rate/volume needed to fill the 
target territory without reflux. 



Embolotherapy: Basic Principles and Applic 



• Beware of signs of imminent backflow: 
stasis/near-stasis, obstruction of segmental 
branches. 

• Maintain tactile feedback during embolic 
material injection or coils deployment and 
void forceful contrast injections. 

• During embolization through occlusion bal- 
loon (always aspirate before balloon defla- 

B) Specific Trauma Embolotherapy Guidelines: 

• Embolize early when requested by the trauma 

• To avoid delays, have a reliable plan in place 
to provide prompt coverage in case of trauma 
bleeding emergencies. 

• Ensure procedural speed in unstable patient: 
non-selective embolization is preferred over 
lengthy selective embolization of multiple 
bleeding sites. 

• Realize that arterial embolization alone may 
not be sufficient in the following scenarios: 

■ Uncorrected coagulopathy 

■ Concomitant venous/bone marrow hemor- 
rhage (major venous injury, unstable pelvic 
fracture with marrow bleeding) 

• In patients with severe unstable pelvic bony 
injuries it is important pelvic fixation be first 
attempted (pelvic binder or external fixator} 

• Be cognizant of the fact that complications 
attributed to the embolization procedure 
may in fact be due to the trauma itself. For 
example, impotence/incontinence maybe 
the result of sacral plexus injury in iliosacral 
fractures, and muscle necrosis could be the 
result of crush injury in blunt trauma. 



(e) presence of an overwhelming contraindication to 
surgery, as in massive extraperitoneal hemorrhage 
from pelvic ring disruption; (f) continued bleeding 
following initial surgery, especially damage control 
laparotomy where visceral in}iirtes were packed. 

With pelvic trauma, the goal is to rapidly and tem- 
porarily reduce the pressure head with cessation of 
bleeding. Therefore, Gelfoam is the preferred agent 
initially, although coils can also be used. Prolonged 
attempts at subselective catheterization of bleeding 
sites are counter productive, and there should be 
no hesitation in embolizing the entire internal iliac 
artery, especially when multifocal bleeding from 
various branches of the internal iliac artery is pres- 
ent. The goal is to rapidly stabilize the patient before 
they become hypothermic and coagulopathic and 
the embolization should be performed in an expedi- 



Conclusion 

Embolization therapy has become a major arm of 
modern interventional therapy. Its applications 
have become fundamental cores in the multimodal- 
ity treatment paradigms in trauma, oncology, and 
endovascular therapy of vascular malformations 
and aneurysms. Knowledge of different techniques, 
materials and vascular anatomy and variants is 
essential to obtain good clinical outcome and mini- 
mize complications. 



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Radiology 1541:245 



2 Embolization Tools 



Jafar Golzarian, Gary P. Sis: 
and Douglas M. Coldwell 



Introduction 15 

Embolic Agents 15 

P-.n t : _ ii I Lt le Agents 15 

Polyvinyl Alcohol Particles 16 

Spherical Embolic Agents 18 

Gelfoam 21 

Other Resorbable Agents 23 

Liquid Agents 23 

Ethanol or Absolute Alcohol 24 

Cyanoacrylate 24 

Ethibloc 25 

Onyx 25 

Detergent-Type Sclerosants 26 

Coils and Metallic Embolization 26 

Coil Anchors 27 

Balloons 28 

Stent Grafts 28 

Micro catheters 28 

Conclusion 29 

References 29 



Introduction 

Embolo therapy is a major aspect of Interventional 
Radiology and, as such, there are an increasing 
number of indication;, ongoing research, and new 
developments. Numerous materials have been used 
for embolization and, recently, many new embolic 
agents, and devices have been developed. In this 
chapter we review the most common materials used 
in daily practice of most interventional radiologists. 
In this two-volume textbook, each chapter discusses 
separately the optimal embolic materials related 
to the corresponding clinical indications. We will 
also refer the readers to Chap. 10.6 in volume I, and 
Chap. 17 in Volume II, discussing future develop- 
ment in embolic materials. 



Embolic Agents 



J.G, 



,MD 



Professor of Riidioiogy. 1 lire; tor. Vascular and Interventional 
Radiology, University of Iowa, Department of Radiology. 
200 Hawkins Drive, 3957 JPP, Iowa City, IA 52242, USA 
G. P. Siskin, MD 

Associate Professor of Radiology iind CVostetrics and Gyne- 
cology, Department of Rac.iolcgy. Alo.uiy Medical College, 47 
New Scotland Avenue, MC-1 13, Albany, NY 12208-3479, USA 
M.J.Shahafuddin.MD 

Departments of Radiology and Surgery, 3JPP, University of 
Iowa Hospitals and Clinics, 200 Hawkins Drive, Iowa City, IA 
52242-1077,USA 
H.Mimt_-ra,MD 

Associate Processor of Radiof >gv. "University of iowi Hospitals 
and Clinics, Department of Radiology, 200 Hawkins Dr, 3957 
JPP, Iowa City, IA 52242, USA 
D.M. Coldwell, MD 

Professor of Radiology, University of Texas Southwestern 
Medical Center, 5323 Harry Hines Blvd. Dallas, TX 75390- 
8834, USA 



The key decision in the performance of any embo- 
lization procedure is the choice of agent. Based on 
their physical and chemical properties, embolic 
agents can induce mechanical occlusion of the ves- 
sels; provoke the formation of thrombus by inflam- 
matory reactions or destroy the endothelium lead- 
ing to thrombosis. In this section, we will discuss 
the particulate agents, liquid agents and metallic 
embolic materials. 



2.2.1 

Particulate Agents 

Particulate embolic agents are typically used for the 
embolization of tumor and tumor-related symptoms 
in addition to the treatment of certain hemorrhagic 
conditions. In general, these agents are adminis- 
tered from a selective position within the arterial 
vasculature of the target organ and are subsequently 



flow-directed Cowards the abnormal area being 
treated. This differs from coils and other mechani- 
cal agents which are administered directly into the 
abnormal blood vessels and are expected to cause 
their effect while they remain where they are admin- 
istered. Particulate agents tend to be classified as 
either absorbable or non- absorb able. This tends to 
pertain to the agent itself and not necessarily to the 
occlusion induced by the agent. 



2.2.1.1 

Polyvinyl Alcohol Particles 

Polyvinyl alcohol, which interventionalists know as 
the most commonly used particulate embolic agent, 
is also well known for its use in a variety of domestic 
and industrial products (Fig. 2.1). In particular, it 
has historically been used in cements, packaging 
materials, water-resistant adhesives (such as the 
backing of postage stamps), cosmetics, and house- 
hold sponges. In 1949, Grindlay and Claggett [1] 
established the biocompatibility of PVA by using 
it as filling material after pneumonectomy. Since 
then, it has been used as a skin substitute in burn 
patients [2], for support in patients with rectal pro- 
lapse [3], and for closure of a variety of congenital 
heart defects [4]. 

The preparation ot polyvinyl alcohol for use as 
an embolic agent first involves its conversion into 
absorbable foam that is subsequently compressed 
[5]. Once the compressed foam is dried, it retains 
its compressed shape but when placed into solu- 
tion, it resumes its original shape [5], The particles 
themselves are prepared by rasping or blending a 
compressed block of polyvinyl alcohol or punching 
out polyvinyl alcohol plugs [5-7]. The irregularly 
shaped particles that are formed from this process 
are passed through sieves with sequentially smaller 
holes to separate them into various size ranges. One 
potential problem with this method is the axes of the 
particles may be oriented in such a way that large 
particles may be able to pass through small holes 
depending on the orientation of the individual par- 
ticles as they pass through the sieves [6]. Some early 
reported problems with PVA were directly related to 
the variability in size of early particle preparations, 
before changes were made in the manufacturing 
process to ensure size uniformity [8]. 

Tadavarthy et al. reported the first use of PVA 
as an embolic agent in patients with cervical carci- 
noma, hemangiosarcoma of the liver, hemangioen- 
dothelioma of the neck and forehead, and an arte- 




Fig.2.1.PVA pj!l:dcs crdilieieiy. ^izes. (Courtesy of Cook inc.) 



malformation of the spine [5, 9]. Since 
then, PVA has been successfully used to embolize 
vessels in patients with a variety of disorders includ- 
ing head and neck arteriovenous malformations 
and tumors [10], lower gastrointestinal bleeding 
[11], bone metastases from renal cell carcinoma [12], 
hemoptysis caused by cystic fibrosis [13], priapism 
[14], and hemorrhage caused by pelvic neoplasms 
and arteriovenous malformations [15, 16]. Today, 
PVA is perhaps best known for its role in uterine 
fibroid embolization [17-20] and hepatic chemoem- 
bolization procedures [21-23]. 

One potential advantage of particulate agents in 
general is the potential to occlude a target vessel at a 
desired point along the course of that vessel (proxi- 
mal or distal) by selecting a particle size that corre- 
sponds to that diameter. Generally, the use of small 
particles will result in a more distal occlusion and 
larger particles result in a more proximal emboliza- 
tion. However, this is less reliable with irregularly 
shaped PVA particles than with newer, spherical 
embolic agents. The tendency of irregularly shaped 
PVA to clump together due to the surface electrostatic 
charge often makes the effective size of this agent 
larger than that of the individual particles, which 
may lead to an embolization that is more proximal 
than intended [24]. Dilution and slow infusion of 
particles during the embolization procedures may 
be technical factors that can reduce the tendency for 
particulate aggregation, which may subsequently 
lead to a more distal embolization [24]. 

Several studies have described the histologic 
effects of PVA particles on embolized blood ves- 
sels. Initially, PVA particles do not occupy the entire 
lumen of the embolized vessel [25, 26]. Insirnd, Ihev 



Embolization Tools 



tend Co adhere to the vessel wall, perhaps due to the 
irregular configuration of the particles, leading to 
slow flow in the vessel [27]. Slow flow ultimately 
leads to inflammatory and foreign body reactions, 
which results in platelet aggregation and thrombus 
formation within the intraluminal lattice of the PVA 
particles. These intlammatoi y changes can last for 
as long as 28 months after embolization [13]. These 
changes can result in thrombosis and focal angio- 
necrosis of the vessel wall [8, 28-33]. Angionecrosis 
tends to be localized to the points where particles 
directly contact the vessel wall and can potentially 
lead to perivascular extravasation of particles [13, 
30]. However, this finding has not been consistently 
observed [8]. 

PVA has been described as a non-absorbable or 
permanent embolic agent because it is not biode- 
gradable. Davidson and Terbrugge described the 
appearance of intravascular PVA in a specimen that 
was resected 8 years after embolization of a facial 
vascular m.il [•:■■] ninlion [31]. In this patient, particle 
fragments were found and the only change in par- 
ticle morphology was slight calcification. However, 
PVA particles are not consistently found in speci- 
mens obtained after embolization [32], either due to 
distal particle migration [8, 29] or to the use of H 
and E staining during the preparation of pathologic 
slides; polyvinyl alcohol particles are best seen with 
the Verhoeff-van Gieson stain [33]. 

While the permanence of PVA as an embolic 
agent is well established, it is also clear that the 
occlusion caused by PVA particles is not permanent. 
Some reports cite occlusions lasting for at least sev- 
eral months [5, 13, 28]. More persistent occlusions 
will occur with the organization of thrombus, disap- 
pearance of inflammatory infiltrate, and ingrowth 
of connective tissue into the particles, all of which 
can lead to extensive fibrotic changes [13, 28, 29]. 
Luminal recanalization after PVA embolization 
has also been reported [13, 16, 31, 34, 35]. Proposed 
mechanisms for recanalization have included angio- 
neogenesis and capillary regrowth caused by vascu- 
lar proliferation inside the organized thrombus [8, 
13] and resorption of the thrombus found between 
clumps of PVA in the lumen of an embolized vessel 
after the resolution of inflammation [8, 25, 30]. 
Recanalization does seem to occur in the portion 
of the vessel lumen previously containing thrombus 
and not in the portion containing polyvinyl alcohol 
particles [30]. 

To date, there have been no complications 
reported that have related directly to intravascu- 
lar polyvinyl alcohol. That is not to say that there 



have not been complications seen after emboliza- 
tion procedures utilizing polyvinyl alcohol as the 
embolic agent. These complications, however, relate 
more to the effects of occluding blood vessels in the 
target organ vasculature than to the embolic agent 
used. As described earlier, the inclusion of small 
particles in early preparations of PVA increased 
the risk for inadvertent end-organ injury. Specific 
complications have included facial nerve palsy after 
external carotid artery embolization [36], paralysis 
aiter bronchial artery embolization [a'7], bladder 1 or 
muscle necrosis and paralysis after pelvic emboliza- 
tion [38, 39], premature ovarian failure after fibroid 
embolization [40], and two infant deaths after the 
embolization of hepatic arteriovenous malforma- 
tions [41]. Both of the deaths were attributed to pul- 
monary hypertension, presumably caused by parti- 
cles passing through the malformation and into the 
pulmonary artery circulation. In response to these 
reports, manufacturing techniques were modified 
to minimize the number of particles smaller than 
the sizes specified for a given preparation of polyvi- 
nyl alcohol [6, 41]. 

2.2.1.1.1 

How To Use PVA 

PVA particles are available in different sizes from 
50 to 1200 u.. They are distributed dry or in solu- 
tion. To be used, they have to be mixed in a solu- 
tion ol contrast and saline. The proportion ot con- 
trast varies related to the concentration of iodine. 
We usually use a solution containing 40% contrast 
(Visipaque 300). Practically, the mixtures should 
provoke a suspension of the particles in the solu- 
tion to prevent flocculation (Fig. 2.2). To obtain 
a uniform suspension, different methods are uti- 
lized. First, the particles are placed in a sterile bowl 
and mixed with contrast and saline. A 10- or 20-cc 
syringe is used to aspirate the solution and will serve 
as a reservoir. It is connected to the middle hub of 
a stopcock and a 3- or 5-ml syringe connected to 
the end-hub is used to aspirate back and forth to 
mix the particles (Fig. 2.3). Another way is to use 
a 3-ml non-lower lock syringe. After aspirating the 
solution, the syringe is rotated continuously during 
the slow injection of the particle. This rotation can 
prevent precipitation of the particles. As stated pre- 
viously, the use of high dilution of the particles is 
essential to prevent catheter occlusion or clumping 
that may result in a proximal embolization (Fig. 2.4). 
We routinely dilute the particles in a 40-cc solution 
of contrast and saline. After the first syringe is used, 



H 



Kip. 2.2. I-'VA sn:;^ensio: 




Fig. 2.3. A 20-tX syringe used i 

three-way stopcock. The PVA solution is aspirated with die 

3-cc syringe and injected to the catheter 




Fig. 2.4. The .pi iv-; demons! ra:es the ,it 
particles occluding the catheter 



we usually add another 10-cc solution to the bowl 
to obtain a better dilution. Sometimes this dilution 
continues up to a final solution of 70-80 ml for a vial 
of 1 ml PVA particles. 



2.2.1.2 

Spherical Embolic Agents 

The recent interest in embolization procedures has 
led to the development of a new class of particu- 
late agent, the spherical embolic agent. The move- 
ment towards a spherical configuration has its basis 
largely in the previously mentioned disadvantage's 
of irregularly shaped PVA particles as an embolic 
agent. These include the size variability in par- 
ticle preparations, the tendency for PVA particles 
to aggregate potentially leading to more a proxi- 
mal embolization than intended, and anecdotal 
reports citing difficulty in injecting these particles 
through microcatheter. Any agent that addressed 
these difficulties with irregular PVA and resulted 
in an effective embolization along with a success- 
ful clinical outcome could be expected to become 
quickly accepted within the interventional radiol- 
ogy community which has been the case with spheri- 

2.2. 1.2. J 

Trisacryl Gelatin Microspheres 

In 1996, Laurent etal. reported on the development 
of a new, non- re sorb able embolization agent with 
a spherical configuration [42]. These spheres were 
made from a trisaciy! polymer matrix impregnated 
with gelatin that is hydrophilic, biocompatible and 
nontoxic (Fig. 2.5) [42]. The trisacryl polymer has 
been used for many years as a base material for 
chromatography media used to purify biopharma- 
ceuticals. The presence of denatured collagen on the 
sphere surface supports cellular adhesion onto the 
material [42, 43]. Even in this initial publication, 
the ability of these spheres to address the disad- 
vantages of irregularly shaped PVA particles were 
highlighted. In particular, these spheres can be more 
effectively separated by size with a sieving process 
than irregularly shaped PVA since they only have 
one dimension [42]. This leads to a narrow range of 
sphere sizes within a given preparation of spheres 
(± 20 to ± 100 u). In addition, these investigators 
describe the ability of these spheres to be admin- 
istered easily through most microcatheters [42]. 
Finally, they were shown to have no tendency to 
form aggregates, which theoretically would mini- 
mize the chance for an embolic occlusion to be more 
proximal than intended. It has been suggested that 
the hydrophilic interaction of these spheres with 
fluids and a positive surface charge, both contrib- 
ute to the reduced formation of particle aggregates 



Embolization Tools 




Fig. 2.5 a,b. Ti'JsacryL gel. it in microsphei'c-s ::t f ::".:"":■ -ph. etc': (loh nesy .:■!" K;.v sphere Meili.:.ilj. a TYis.icryl g. 
suspension.b Microscopic iT.;iee; : iiemo!";vii';i:ing the spheres 



[42, 44, 45]. In its original form, these spheres are 
clear, which make them somewhat difficult to see 
during the process of preparing them for us. Tri- 
sacryl gelatin microspheres stained with elemental 
gold are also available (EmboGold, Biosphere Medi- 
cal Inc., Rockland, MA) for easier visualization of 
the spheres during preparation. 

The initial clinical experience with trisacryl gela- 
tin microspheres was reported by Beaujeux et al. in 
105 patients with tumors or arteriovenous malfor- 
mations in the head, neck or spine [46]. From this 
experience, it was learned that the precise calibra- 
tion of these spheres enables interventionalists to 
have good control over the desired site of occlusion 
by appropriate size selection. In addition, the embo- 
lization were clinically effective, demonstrating that 
complete devascularization of the target pathology 
was often not possible but may not have been neces- 
sary to meet the goals of the embolization procedure 
[46]. 

To date, the use of trisacryl gelatin microspheres 
(Embospheres, Biosphere Medical, Rockland, MA) 
lit sever.il different clinical applications lias been 
reported. Bendszus et al. demonstrated that tri- 
sacryl gelatin microspheres are effective in the 
preoperative evaluation of meningiomas, produc- 
ing significantly less blood loss at surgery than 
irregularly shaped PVA particles [47]. Yoon has 
described its use in bronchial artery emboliza- 
tion for hemoptysis [48]. These spheres have also 
been utilized effectively in the treatment of uter- 
ine fibroids [49-52]. Pelage et al. have suggested 
that a limited approach be utilized with this appli- 
cation in an effort to reduce the extent of tissue 



necrosis associated with this procedure [49]. They 
have advocated this limited approach given the 
ability of these microspheres to precisely target 
certain vessels. The flow-directed nature of micro- 
spheres makes it likely that the embolic material 
is first directed into the hypervascular pathology 
being targeted for embolization. A r 
approach can therefore potent i all;' In: 
the target t 



■nit the effects 



of the emboliz 

mize unintended embolization of then 

surrounding the target pathology. 

As described, the ability to target the level ol occlu- 
sion with spherical agents such as trisacryl gelatin 
microspheres is one of the most appealing aspects 
of this class of agent. In animal studies, Derdeyn 
et al. demonstrated that for a given vessel and par- 
ticle size, trisacryl gelatin microspheres penetrate 
significantly deeper into the blood vessel than PVA 
particles [44]. If one selects spheres that are the same 
size as PVA particles, the spheres will travel more 
distal in the vasculature of the target organ. There- 
fore, if an interventionalist is seeking to occlude a 
vessel at a similar point in the vessel to PVA par- 
ticles, larger spheres will need to be selected, which 
was confirmed early on by Beaujeux et al. [46]. The 
ability to achieve a controlled arterial occlusion was 
highlighted by Pelage et al. in their work studying 
uterine artery embolization in sheep. They found 
that the proximal aggregates formed by PVA par- 
ticles cause the actual level of occlusion to be both 
proximal and distal and to correlate poorly with 
the size of the PVA particles [53]. Conversely, they 
found a significant correlation between the level of 
arterial occlusion and the diameter of the trisacryl 



gelatin microspheres used for embolization [45]. 
Therefore, large diameter spheres can be used if a 
proximal embolization is desired while small diam- 
eter spheres are recommended if a distal emboliza- 
tion is indicated. These findings were confirmed in 
humans by Laurent et al. [54], who appropriately 
called for additional research focusing on the opti- 
mal size spherical agent required for particular 
types of pathology since without this knowledge, 
the ability to size match the spheres with the target 
vessel cannot be fully utilized. 

Histologically, the initial work of Laurent et 
al. and Beaujeux et al. found that these spheres 
provoke a moderate giant cell and polymorphonu- 
clear inflammatory cell reaction [42, 46]. Siskin 
et al. found that at 7 days, the response to the tri- 
sacryl gelatin microspheres consisted of macro- 
phages and occasional lymphocytes and increased 
over time. When gold-colored microspheres were 
evaluated, the response consisted almost exclu- 
sively of lymphocytes, with occasional si.int cells 
noted [35]. 

There have been complications reported in asso- 
ciation with the use of trisacryl gelatin microspheres. 
De Blok et al. reported a case of fatal sepsis after 
uterine artery embolization performed with this 
agent. In this case, diffuse necrosis of the vaginal 
wall and cervix was found, attributed to distal pene- 
tration of spheres measuring 500-700 |i in diameter 
[55]. These authors agree with Pelage et al. that a 
more limited approach to embolization should be 
utilized when using this agent. Brown reported 
three deaths in patients with hepatocellular car- 
cinoma embolized with 40- to 120 u microspheres 
[56]. All three patients died after demonstrating pro- 
gressive, irreversible hypoxemia. Two of the patients 
had autopsy confirmation of microspheres in small 
pulmonary arteries. Signs felt to place patients at 
risk for this event included tumor extending high 
into the dome of the liver, a large adrenal metasta- 
sis with tumor thrombus extending into the inferior 
vena cava, and presence of a systemic draining vein 
[56]. Brown et al. theorized that the small size of 
these spheres was likely responsible for this compli- 
cation and that patients embolized with either larger 
spheres due to their size or PVA particles due to their 
tendency to aggregate are likely protected from this 
potential complication. Richard et al. reported on 
a series of patients with non-infective endometritis 
after uterine artery embolization performed with 
gold-colored trisacryl microspheres [57]. While it is 
not known if these clinical findings could be attrib- 
uted to the elemental gold in these microspheres, the 



manufacturer has recommended that only the non- 
colored microspheres be used for uterine fibroid 
embolization at the present time. 



How To Use Embospheres 

The particles are loaded in a syringe or in a vial. 
When loaded, the syringe containing the particles 
is connected to a three-way stopcock. Another 5-cc 
syringe with contrast material is also connected. 
The contrast is aspirated and after 3-5 min a uni- 
form suspension is obtained. The solution can be 
injected easily and slowly. There is no need to per- 
form the back and tor ill aspiration like for PVA par- 
ticles. This maneuver is not recommended since it 
might damage the spheres. In our experience, there 
is still some clumping with these particles so we 
usually use a 10- or 20-cc contrast solution to have 
a bigger dilution. 

2.2.1.2.2 

Polyvinyl Alcohol Microspheres 

Recently, microspheres consisting of polyvinyl alco- 
hol have been released and approved for use to treat 
hypervascular tumors (Fig. 2.6). These spheres were 
developed to address the shortcomings of PVA par- 
ticles, similar to the trisacryl gelatin microspheres. 
Histologically, PVA-based microspheres are associ- 
ated with a milder inflammatory response than both 
PVA particles and trisacryl gelatin microspheres 
[35]. The acute cellular response to embolization 
with PVA microspheres consists exclusively of Neu- 
trophils. At 7 and 28 days after embolization, the 
inflammatory response consists ot macrophages and 
occasional lymphocytes, which is different than the 
macrophages and giant cells seen after emboliza- 
tion with PVA particles. Siskin et al. have presented 
their preliminary success with PVA microspheres 
for uterine fibroid embolization. However, there 
are increasing concerns on the results of uterine 
artery embolization for fibroids using PVA micro- 
spheres. Recent reports (abstracts) demonstrate a 
higher rate of partial devascularization of fibroids 
with these particles (see the Chap. 10.5). Laurent et 
al. have also demonstrated that Contour SE particles 
are highly compressible [58]. This compressibility 
is associated to a change of the spherical shape of 
the particles becoming more oval. The failures may 
be explained by the higher compressibility of the 
particles and early proximal occlusion resulting to 
insufficient embolization. 



Embolization Tools 




Fig.2.6a,b. Spherical PVA (Beadblock i'.vdrogel spheres; courtesy ofTerumo). a Misprision of die Read Block particles, b Mici 
scopic im.ige showing the sphere 



2.2.1.3 
Celfoam 

Gelfoam, a water-insoluble hemostatic material pre- 
pared from purified skin gelatin (a non-antigenic 
carbohydrate), is frequently used as a biodegrad- 
able, absorbable embolic agent [59]. Correll and 
Wise [60] were the first to report the hemostatic 
properties of Gelfoam and its potential for use 
during surgery. It has been reported that in this 
setting, Gelfoam promotes hemostasis by hasten- 
ing the supporting thrombus development [61]. In 
1964, Gelfoam was first used as 
agent for occluding a traumatic carotid 
fistula [62]. Since then, Gelfoam has bee 
fully used as an embolic ayent for .) variety of ind: 
tions including renal cell carcinoma before: 
[63], bone cancers [64], gastrointestinal bleeding 
[65], hemobilia [66], and arterial injury caused by 
trauma [67]. In 1979, Heaston et al. [68] described 
the first use of Gelfoam in the pelvis for postpartum 
hemorrhage after bilateral hypogastric artery liga- 
tion. Since then, postpartum hemorrhage [69-71], 
postoperative hemorrhage [72], arteriovenous fistu- 
las [73], cervical ectopic pregnancies [74], and bleed- 
ing caused by pelvic malignancies [75] and uterine 
fibroids [76-79], have all been effectively treated 
with Gelfoam embolization of the uterine or internal 
iliac arteries. Pelvic embolization remains one of the 
most common indications for the use of Gelfoam as 
an embolic agent, primarily because of support in 
the medical literature demonstrating fertility pres- 
ervation after embolization [70-72, 77, 80, 81]. 

Histologically, Gelfoam initiates an acute full- 
thickness necrotizing arteritis of the arterial wall, 
with local edema and interruption of the elastic 



interna [63, 82]. Within 6 days after Gelfoam 
administration, acute inflammatory and foreign 
body, giant cell reactions have been observed [83]. 
These reactions induce thrombus formation, the 
residue of which can be found for several months 
[84]. However, Light and Prentice [83] noted 
that the cellular reaction initiated by Gelfoam 
abated by day 30 and no Gelfoam or thrombus 
was seen at day 45, which served as the basis for 
the premise that Gelfoam is a temporary embolic 
agent. Studies have revealed that the resorp- 
tion time for Gelfoam typically occurs within 7- 
21 days of embolization [84, 85]. However, when 
used for surgical hemostasis, unabsorbed gelatin 
sponges have been found in wounds 2-12 months 
after implantation [86]. 

Classically, the occlusion caused by a Gelfoam 
embolization has been considered "temporary" in 
that flow becomes reestablished to a treated vessel 
over time. The literature, however, provides support 
for both a temporary and permanent occlusion after 
Gelfoam embolization. In animals, the time to recan- 
alization after a Gelfoam embolization has ranged 
from 3 weeks to 4 months [84, 85, 87]. Bracken et 
al. [63] found arterial reca realization in two patients 
who underwent embolization for renal cell car- 
cinoma after 5 and 6 months. However, persistent 
occlusion after Gelfoam embolization has also been 
observed [63, 88]. Jander and Russinovich [88] 
found that the permanence of Gelfoam occlusion 
might be related to the amount of Gelfoam used, 
stating that if a bleeding vessel was densely packed 
with Gelfoam, the occlusion would be permanent. It 
has also been suggested that an aggressive inflam- 
matory reaction caused by introduction of Gelfoam 
into the vasculature may cause fibrotic and other 



changes in the vessel wall that result in a more per- 
manent occlusion. 

Ischemic and infectious complications have been 
reported when using Gelfoam as an embolic agent. 
Ischemic complications associated with the use 
of Gelfoam in the pelvis include buttock ischemia 
[68], lower limb paresis [38], and bladder gangrene 
[89]. These complications have been attributed to 
the small size of the embolic agent used, prompting 
recommendations that Gelfoam powder not be used 
in the nonmalignant setting [90]. Infectious com- 
plications, including at least three pelvic abscesses, 
have been reported after pelvic embolization with 
Gelfoam [72, 91, 92]. In addition, hepatic infections 
resulting in abscess formation have been reported 
when using Gelfoam during hepatic arterial che- 
moembolization procedures [93]. These infections 
maybe caused by the potential for Gelfoam to retain 
enough air bubbles to support aerobic organisms 
[86]. Because of this potential, early surgical articles 
recommended using as little Gelfoam as possible, 
avoiding prolonged exposure of Gelfoam to con- 



taminated air, and thoroughly compressing the Gel- 
foam so that large air bubbles are eliminated and not 
introduced into a patient [86]. 

Gelfoam is currently available in two forms: a 
powder containing particles ranging indiameter from 
4d to (i() |i or a ".lirei from wind] sections ol various 
sizes can be cut [59]. Gelfoam, like PVA, is not radi- 
opaque and is Ivpically mixed with contrast before 
injection. The small size of the particles in Gelfoam 
powder increases the risk for ischemia caused by distal 
artery occlusion [38]. The pledgets cut from a sheet 
of Gelfoam are typically larger and result in a more 
proximal artery occlusion than Gelfoam powder [59]. 
An additional technique is to create Gelfoam slurry 
by mixing pledgets between two syringes via a three- 
way stopcock. This method will decrease the size of 
the injected Gel loam and allow a more distal delivery 
than that achieved with pledgets. There are different 
ways to cut the Gelfoam sheet. One way is to use a 
blade and cut a thin layer of the Gelfoam. Then this 
layer is cut longitudinally and transversally to small 
pieces using scissors (Fig. 2.7). Other possibility is to 




Fig.2.7a-d. Gelfoam. a First cut the Gelfoam pi. 
scissors, c bach fragment is then cut to small c 



;i longitudinally wiih blade, b The pledget is then cut to size vertically using 
s. d The particles are soaked ;n contrast unci ready to be used 



Embolization Tools 



scratch the Gelfoam sheet carefully with the blade to 
obtain small size fragments (Fig. 2.8). The sizes of 
particles will be much less homogenous than the pre- 
vious approach. However, forceful mixing of the par- 
ticles with contrast can make it possible to obtain a 
jelly-form solution that can be injected easily. Finally, 
Gelfoam can be cut to long and tiny fragments also 
called 'torpedo". Torpedo fragments are usually used 
for obtaining a proximal vessel occlusion in major 
arteries or as a complementary embolization to pre- 
vent from rebleeding (Fig. 2.9). 




Fig. 2.S. Gel:oa:v. shiny. 7::e Geliojm pledge; . 

".he bfide a: ;i 4?' J angle. T::e shu ry i? mixed with the contr 

After -cve:\il back tad fi'o jspiraiions. J jelly-like solutio: 

obtained 



2.2.1.4 

Other Resorbable Agents 

2.2. 7.4. J 
Oxycel/Su xq icel 

Oxycel (Becton Dickinson, Franklin Lakes, NJ) is 
composed ot iibi'illar absorbable oxidized regener- 
ated cellulose. The basic functional unit of oxidized 
cellulose is the an hydro glucuronic acid. It is most 
commonly used as a local hemostatic agent in open 
surgical procedures by acting as a matrix for normal 
blood coagulation. It absorbs up to ten times its 
weight in blood. Oxycel is available in various forms 
and preparations: pads, strips, cotton, and powder. 
Although it was primarily used as a local hemostatic 
agents in open surgery to control oozing from raw 
tissues, its use in endovascular procedures has also 
been described both experimentally and clinically 
[94, 95]. 




Fig. 2.9. Gelfoam "torpedo'' 



As with Gelfoam, the main occlusion segments 
were recanalized by 4 months and no trace of either 
Oxycel remained, nor tissue reaction against either 
material [94]. Oxycel is highly effective in applica- 
tions where temporary occlusion is desired such as 
trauma and pre-operative vascular reduction [96, 
97]. Depending I'll the application and desired effect, 
Oxycel may be delivered as slurry suspended in a 
radiopaque mixture or in autologous blood through 
an angiographic catheter, or can be injected in its 
powdered form through a microcatheter [96-99]. 



2.2.1.4.2 

Avitene 

The agent is composed of a microfibrillar collagen 
preparation supplied in the form of a powder. It has 
been shown to be an effective particulate embolic 
agent in a number of experimental studies and clini- 
cal reports. In arteries embolized with Avitene sus- 
pended in saline moderate recanalization occurred 
by 2 weeks and total recanalization by 2 months. 
Arteries embolized with Avitene suspended in 
sodium Sotradecol remained occluded at 2 months 
with the longer occlusion duration attributed to 
increased inflammatory changes induced by Sotra- 
decol [100]. It is a useful agent for tumor necro- 
sis and organ ablation [101]. The agent is delivered 
through a microcatheter. 



2.2.2 

Liquid Agents 

Sclerosants permanently destroy the vascular endo- 
thelium through different mechanisms depending 
the type of agents: chemical (iodine or alcohol); 



osmotic effect (salicylates 
detergents (morrhuate s 



hypertonic saline); 
n, Sotradecol, polido- 



canol, and diatrizoate sodium) [102]. If injected in 
the artery, they can pass the capillar)' level allowing 
distal embolization. Their usage is thus much more 
challenging. They are mostly used in organ ablation 
such as tumors, veins or arteriovenous malforma- 
tions (AVM}. 



2.2.2.1 
Ethanol c 



1 Absolute Alcohol 



Absolute alcohol is a very effective embolization 
agent. It destroys the walls of the blood vessels by 
inciting a strong inflammatory reaction and causes 
an instant precipitation of endothelial cells proteins 
and rapid thrombosis. Ethanol can result in trans- 
mural vessel necrosis, and diffusion into the sur- 
rounding tissue. It can be used intravascular or 
through direct puncture of the lesion. Because of its 
lack of radio-opacity, inflow occlusion with the use 
of balloon catheters is important to prevent from 
untargeted embolization. If inflow occlusion i 
possible in case of AVMs, then outflow occlusior 
can be achieved with the use of orthopedic tour 
niquets, blood pressure cuffs or manual compres 
sion depending on the location of the lesion. Con 
trast is injected into the vessel in order to measurt 
the volume of alcohol. In case of AVM, cor 
is injected to the nidus during inflow occlusion 
until the draining veins are seen. This reflects the 
volume of alcohol needed to fill the nidus without 
spilling into the draining veins. Alcohol needs to 
be retained for several minutes within the lesion 
then drawn up. The balloon is then deflated and 
contrast injection should be repeated to evaluate the 
degree of vessel occlusion. In AVM embolization, 
the injection should be continued till the nidus is 
thrombosed. 

If the inflow occlusion is not possible, alcohol 
can be mixed to Ethiodol in an 8:2 or 7:3 ratios in 
order to become more radiopaque [103]. This mix- 
ture makes it possible not only to see the flow, but it 
also increases the distribution and embolic effect of 
alcohol [104]. 

It is important to consider the risk of necrosis of 
neighboring tissues and of the skin when using alco- 
hol by a percutaneous or endovascular route. The 
risk of systemic toxicity increases in doses above 
1 ml/kg or if a volume greater than 60 ml is used. 
Complications can be as high as 15% of patients 
treated with absolute alcohol (range: 7.5%-23%) 
[105]. Severe complications such as cardiac arrest 
and pulmonary embolism have been reported [106, 



107]. The mechanism remains unknown and may 
include pulmonary vasospasm, pulmonary embo- 
lism, and direct cardiotoxicity. Patients must be 
monitored closely, and some practitioners advocate 
the use of continuous pulmonary artery pressure 
monitoring during ethanol procedures. Most com- 
plications are self-limiting or may be successfully 
treated with skin grafting; in the case of skin necro- 
sis, however, neurologic complications can be per- 
manent. Ethanol blood levels correlate directly with 
the amount of ethanol injected, regardless of the 
type of malformation [102, 108]. General anesthesia 
should be used in children when using alcohol due 
to its possible local and systemic effects. 



2.2.2.2 
Cyanoacrylate 

The tissue adhesives or glue are fast and efficient 
non-resorbable, non-radiopaque embolic material, 
based on polymerization of the acrylate monomer. 
Cyanoacrylate is composed of an ethylene molecule 
with a cyano group and an ester attached to one 
of the carbons. Isobutyl 1 -cyano acrylate was used 
previously but its production has been stopped after 
detection of sarcomas in animals exposed to large 
doses. N-butyl 2-cyanoaa-ylate or glue (Histoacryl; 
B. Braun, Melsungen, Germany) is the most used 
in Europe. TruFill (Cordis Neurovascular, Miami 
Lakes, FL> is another N-butyl cyanoacrylate (NBCA) 
that has been approved by the FDA. Glue starts to 
polymerize on contact with anionic substances such 
as plasma, blood cells, endothelium or saline. When 
in contact of the vessel, glue provokes an inflamma- 
tory reaction resulting in fibrosis [109]. 

Special skill and experience are required to 
assess the proper dilution of N-butyl cyanoacrylate 
in iodized oil (Ethiodol or Lipiodol) to opacify the 
acrylate but also to control vascular penetration. 
Control of time and place ot polymerization depends 
onmanyfactorssuchas blood flow, caliber of vessel, 
dilutionof the acrylate, velocity of injection, etc. The 
speed of polymerization is affected by the concentra- 
tion of iodized oil. Thus, in a rapid or high flow situ- 
ation, pure glue or a solution with a lower concentra- 
tion of Ethiodol should be used. Incase of slow flow, 
a solution with a larger concentration of Ethiodol 
can be used (80%/20%). Tantalum or tungsten can 
be added to the solution before injection, to increase 
the radio-opacity of the agent. Embolization with 
glue is always performed through microcatheter. The 
micro catheter is typically changed after the injec- 



Embolization Tools 



Cion. It needs to be positioned as close as possible to 
the embolization target. The microcatheter maybe 
glued to the vessel. This is a potential complication 
that might occur in case of reflux, early polymeriza- 
tion or delayed removal of the microcatheter. This 
issue is less frequent wit li hydroplulk'-coated micro- 
catheters. In case this occurs, the microcatheter is 
simply cut off and buried in the groin so that it will 
endothelialized. 

The use of glue in peripheral indications was not 
very popular. However, there is an increasing inter- 
est for using glue in peripheral indications. Glue 
has been used for AVMs, arteriovenous fistulae, 
GI bleeding from the GDA, portal vein emboliza- 
tion for tissue regeneration, bleeding \ 
in patients with portal hypertension, 
endoleaks and priapism [110, 111]. It might be used 
for distal flow directed embolization in GI bleed- 
ing or pseudo-aneurysms that are out of range for 
a sandwich technique occlusion. If the bleeding 
artery can be catheterized to the point of rupture 
(and eventually beyond into the bowel lumen), slow 
deposition of highly concentrated glue might be safe 
[112]. The catheter tip should be wedged proximally 
from the bleed ing point to achieve excellent control 
of the glue penetration. This technique can be par- 
ticularly useful in upper GIH bleeding to achieve 
occlusion of the bleeding vessel and the connection 
points with the collaterals. 

Deep and diffuse penetration can cause ischemia 
or even infarction of neighboring tissue. The use 
of an overly diluted solution can result in delayed 
polymerization with risk of distal artery or draining 
vein occlusion. A drip of glue can be attached to the 
microcatheter which can eventually be embolized 
to a non-targeted location during retraction of the 
catheter. 

With the introduction of Glubran2 (GEM, Italy) 
(a mixture of N-butyl 2-cyanoacrylate and meth- 
acryloxysultolane) the aaylate seems more stable 
in the mixture with Lipiodol and less "sticky", 
which, has improved the control over the polym- 
erization. 



2.2.2.3 
Ethibloc 

Ethibloc (Ethnor Laboratories/Ethicon Inc., 
Norderstedt, Germany) is not available in the US. 
This biodegradable solution is a mixture of zein 
(a water-insoluble prolamine derived from corn 
gluten), alcohol, poppy seed, propylene glycol oil 



and contrast medium. It polymerizes on contact 
with ionic fluids developing a consistency similar 
to chewing gum, and subsequently hardens fur- 
ther. Ethibloc provokes thrombosis, necrosis and 
a fibrotic reaction with a giant cell inflammatory 
reaction that may produce pain and fever. The 
product is available in a preloaded syringe. Pump 
flushing through a three-way stopcock can emul- 
sify the mixture; 10 ml of Ethibloc are mixed with 
0.5 ml of Lipiodol. This mixture does not dissolve 
catheters. The system must be primed with a non- 
ionic fluid, such as 50% glucose to prevent solidi- 
fication in the delivery device. It can be mixed 
with Lipiodol (Laboratoire Guerbet, Paris, France) 
to allow for improved visualization. The emboliza- 
tion endpoint is stasis of the injected substance. It 
is important to slowly retract the delivery device 
while injecting the mixture. No significant com- 
plication has been reported. Ethibloc seems safer 
than alcohol because of its fewer complication rate. 
Also, it is much less painful than alcohol during the 
injection and does not require general anesthesia 
[113]. 



2.2.2.4 

Onyx, (Micro Therapeutics, Irvine Ca), is a biocom- 
patible liquid embolic agent. It is an ethylene vinyl 
alcohol copolymer dissolved in various concentra- 
tions of dimethyl sulfoxide (DMSO) and opacified 
with micronized Tantalum powder. When this mix- 
ture contacts aqueous media, such as blood, the 
DMSO rapidly diffuses away, with resulting in situ 
precipitation and solidification of the polymer. It 
forms a soft elastic embolus without adhesion to the 
vascular wall or the catheter [114]. The polymeriza- 
tion process is time dependent and is mainly influ- 
enced by the amount of ethylene in the mixture, with 
less ethylene polymer becomes softer. Onyx is avail- 
able in several different concentrations; the higher 
lore viscous. Using a higher con- 
kes it easier to prevent the liquid from 
getting too far from the catheter tip. Since the poly- 
mer will solidify on contact with aqueous media the 
delivery catheter must be pre-f lushed with DMSO. A 
'DMSO- compatible* catheter is required; DMSO will 
degrade most currently available catheters. Onyx 
is non-adhesive, allowing for easy removal of the 
delivery catheter, and of the polymer itself. Unfortu- 
nately it is quite expensive. This agent is mainly used 
for intracranial aneurysms. In peripheral, Onyx has 



been successfully used for the 
[115]. 



2.2.2.5 

Detergent-Type Sclerosants 

The detergent- type sclerosants includes: aetoxi- 
sclerol (polidocanol l%-3%), sodium tetradecyl sul- 
phate (STS), sodium morrhuate, and ethanolamine. 
Theses detergents can be used in liquid or foam. 
They act specifically on endothelium provoking its 
maceration. Sclerosis therapy requires a contact 
between the endothelium and a highly concentrated 
agent to be successful. It is therefore more effective 
in lesions with little flow. If used in high flow situ- 
ations, the use of tourniquet or other compression 
techniques is of primary importance. They have 
been used in variety of indications in medicine 
including in GI bleeding, vascular malformations, 

2.2.2.5.7 

Polidocanol (Aetoxiscterol) iVX>-3%) 

This agent is used for the small venous malforma- 
tions and small venous varicosities [116-120]. Poli- 
docanol is effective by altering the endothelium and 
promoting thrombosis. In addition, it has strong 
tissue fibrosis effect after tissue damage. Polido- 
canol is a urethane anesthetic and unique among 
sclerosing agents in that it is painless to inject [116]. 
Basically, general anesthesia is not necessary. 

Injection volume and concentration of scle- 
rosant depend on the size of the lesion and the flow 
rate. Some authors used it as sclerosing foam by 
mixing sclerosant and C02 or air [117, 118] (see also 
Sect. 2.2.2.5.2). The German manufacture of polido- 
canol recommends a maximum daily dose of 2 mg/ 
kg [117]. Some authors described that the i 
recommended dose in the treatment of 
veins is 6 ml of 3% polidocanol [118]. This agent is 
associated with less severe allergic and inflamma- 
tory reactions [119]. Skin necrosis is rare. However, 
Cabrera reported skin necrosis in 6% of cases with 
venous malformations. One reversible cardiac arrest 
was reported [121]. 

2.2.2.5.2 

Sodium Tetradecyl Sulfate (Sotradecol) 

Sodium tetradecyl sulphate damages the endothe- 
lium resulting in thrombosis and fibrosis. This agent 



can be used in a liquid solution or by creating a foam 
with air. The main difference between liquid solution 
and foam is the long life of the foam in the vein and 
by the clear separation obtained between the blood 
and the sclerosant. Its injection is not painful. Usu- 
ally, the Sotradecol is mixed with Lipiodol and air 
(5 cc of Sotradecol, 2 cc of Lipiodol and 20 cc of air). 
Using two plastic syringes and a three-way stopcock, 
and a 1:4 or 1:5 ratio of sclerosant to air, a stable 
and compact roam is obtained [1 22 -124], There is no 
agreement on the maximum dose of Sotradecol. Skin 
necrosis is a well-known complication related to the 
use of this substance [125]. Percutaneous injection 
of STS has been reported to provoke thrombosis of 
localized vascular lesions, facilitating their surgical 
identification and removal [125], 

2.2.2.5.3 
Ethanolamine Oleate 

Ethanolamine oleate is a mixture of 5% ethanol- 
amine oleate (synthetic mixture of ethanolamine 
and acid oleic) and iodized oil (Lipiodol) (ratio 
5:1-5:2). It is a salt of an unsaturated fatty acid and 
has been used as a sclerosing agent because it has 
excellent thrombosing properties [126]. The oleic 
acid is responsible for the inflammatory response. 
The sclerosing action is dose-dependent, due to the 
diffusion of the solution through the venous wall, 
provoking mural necrosis, thrombosis, and fibrosis. 
The conjoint use of coils embolization as well as 
inflated balloons within the internal jugular vein 
in cases of cervicofacial venous malformations in 
order to prevent the systemic passage of the scle- 
rosant has been reported with a 92% success rate 
[127]. The complications include anaphylactic shock, 
temporary trismus, pleural effusion, pneumonia, 
and hemolytic reactions [128]. Approximately 50% 
of oleic acid combines with serum proteins within 
30 min that can cause renal toxicity in association 
with a marked intravascular hemolysis, hemoglo- 
binuria, and hepatotoxicity [126, 129]. 



2.2.3 

Coils and Metallic Embolization 

Chapter 3 of this volume will discuss the use of coils 
for peripheral embolotherapy in more detail. Accu- 
rate catheter or microcatheter placement is essential 
to the performance of coil embolization. A sizing 
arteriogram is first performed to insure that the 
coil is appropriately sized. The coil should be about 



Embolization Tools 



15%-20% larger Chan the imaged vessel in order 
Co prevent the distal migraCion of Che device. Coils 
have been commonly utilized in trauma or in cases 
where the occlusion of an artery greater than 2 mm 
is desired to accomplish the clinical end. When there 
are large vascular structures such as aneurysms that 
need to be occluded, the combinaCion of large coils 
and 30-cm sections of movable core j;u idewires with 
the cores removed have been reported to be uti- 
lized as fillers to take up the available space so that 
thrombosis will occur. A relatively new device, the 
Amplatz spider (Cook, Inc., Bloomington, IN} has 
been utilized to form the framework that will allow 
the placement of somewhat smaller coils into large 
vascular structures to occlude them (Fig. 2.10). 

Coils are available in a wide variety of sizes from 
2 mm to 15 mm in size and are made from either 
stainless steel or platinum and may have Dacron 
fibers placed at right angles to the long axis of the 
coil to increase the surface area and thereby to 
increase the speed and permanence of thrombosis. 
In practice, most coils utilized in mkrocathetersare 
platinum and those in 4- to 5-F catheters, stainless 
steel. It should be noted that all coils are permanent 
devices and should be utilized when the desired 
occlusion is permanent. Coils should not be used in 
combination with particulate embolization for the 
treatment of tumors, as they will occlude the access 
for further treatment. Coils may, on the other hand, 
be utilized with Gelfoam embolization in the treat- 
ment of pelvic bleedings allowing the hemorrhage to 
be halted quickly and permanently. 

It should also be noted that when larger vessels 
are occluded with coils, collateral arteries form 
relatively rapidly and the distal vascular bed is still 
perfused but at a lower pressure than before the 
embolization. This is the theory behind the proxi- 
mal occlusion of the splenic artery to halt splenic 
hemorrhage. The use of these coils presupposes 
the existence of collaterals. For example, emboli- 
zation of the renal artery will most likely not result 
in viable renal tissue as the kidney is an end-organ 
and will not have a collateral arterial system that 
will support the kidney. 

Other types of coils are those that have a con- 
trolled release either due to a mechanical release or 
that of electrochemical dissolution of an attachment 
joint. These GDC-type coils have the advantage that 
trial placement is used to accurately size the coil and 
the ill-sized coil can be removed without danger of 
distal embolization. The disadvantage is in their 
high cost which has prevented their widespread use 
outside of intra-cranial aneurysm embolization. 



2.2.3.1 

Coil Anchors 

These are devices used to allow the stable deploy- 
ment of coils into a large vessel with high flow or 
high wall compliance. Its main purpose is to allow a 
tight formation of coils to be deposited while main- 
taining a stable position in high flow vessels such 
as the aorta or iliac arteries or in highly compliant 
vessels such as large veins. These devices are also 
particularly useful for occlusion of large arteriove- 
nous fistulas in the lungs, and large portosystemic 
collaterals [130]. While many devices have been used 
to accomplish this goal such as modified stents or 
vena cava filters, a number of devices have been 
specifically designed for this application. 

2.2.3.1.1 
Amplatz Spider 

This device consists of a stainless-steel self-expand- 
ing spider shaped object which can be introduced 
through a guiding catheter or vascular sheath. 
The spider blocks the movement of steel coils and 
allows rapid occlusion of the vessel while minimiz- 
ing the risk of inadvertent non-target embolization 
(Fig. 2.10}. One modification allows the spider to 
be screwed onto a threaded guidewire before load- 
ing into the catheter allowing it to be retrieved 
and repositioned to ensure accurate placement. In 
some difficult applications multiple spiders may 
be deployed to provide a stable matrix for securing 
subsequent coils, sometimes in staged procedures 
[130-132]. 

2.2.3.1.2 
Coil Cage 

This is essentia llv a modi lied GianturcoZ stent mod- 
ified to function as a cage to trap the coils within 
it against the direction of blood flow, while also 
reducing the risk of proximal or distal coil emboli- 
zation. It is deployed through a long 8-F introducer 
sheath [133]. 

2.2.3.1.3 

Retrievable Coil Anchor 

This is a new design that offers the advantage of 
improved safety due to ability to retrieve and rede- 
ploy su bop tim ally placed devices. It is also intended 
to enhance the occlusive efficacy by allowing retain- 
ing a high density of occlusive material without 




Fig. 2.10. Spider Amplatz device. (Courtesy of Cook inc.) 



and are currently used in clinical practice. When 
using a stent graft, proper sizing and precision of 
deployment are critical for technical and clinical 
success. Balloon-expandable stent grafts are very 
useful as they can be placed very precisely with no 
shortening. An important drawback with most of 
available stent grafts is their larger profile, making 
their use much more difficult in tortuous vessels. 
The balloon expandable stent grafts, however, have 
a smaller prof ile than the self-expandable stent graft 
but they are less flexible. It is anticipated that future 
advances in material and engineering will result in 
lower profile and more flexible self-expanding s tent- 
graft systems that will pose comparable technical 
demands to bare stents. 



compromising the self-anchoring capability of the 
nested coils, which also enhances safety. This is 
important because of the high-risk locations where 
such devices are usually required to be deployed. 
Preliminary in vivo experience with one design in 
a swine model has shown promise [134]. 



2.2.4 
Balloons 

Detachable balloons were on the market in the US 
several years ago but were recalled due to both man- 
ufacturing problems and the difficulties in accu- 
rately placing the balloons. The use of these devices 
has been replaced by the GDC-type coils which allow 
the trial placement of a coil and its exchange for 
a not lie r size if ilie first is moor reel. 



2.2.5 
Stent Grafts 

Stent grafts or covered stents are not embolic materi- 
als. However, in some clinical indication of embo- 
lization, they can be very useful. Stent grafts are 
composed of a metallic frame covered by either 
native venous grafts or synthetic materials such 
ewn into the inner or outer 
c stent frame. These devices 
essel injuries, aneurysms, or 
resulting in an endolumi- 
eries of homemade devices, 
the Cragg endoprosthesis was the first stent graft 
that became commercially available. These Nitinol 
based stent graft was used in different clinical indi- 
cations. Many other self- expand able and balloon- 
expandable stent grafts have been since developed 



as Dacron or PTFE, : 
portion of the metalli 
can be used in large v 
arteriovenous fistulas 
nal bypass. After a s 



Microcatheters 

Microcatheters are commonly utilized to facilitate 
placement as they are more maneuverable and can 
be placed much more d is tally than the usual 4- or 5- 
F diagnostic catheter. One must insure that the guid- 
ing catheter can utilize at least a 0.035-in. guidewire 
so that the catheter can be reliably placed through 
it. A Touhy-Borst rotating hemostatic valve can be 
placed on the guiding catheter to allow a continuous 
flush of saline around the catheter and intermittent 
contrast injections to visualize the embolization. 
Microcatheters, like diagnostic catheters, come in 
a variety of sizes from the larger bore (outer d iam- 
eter 3 F) to standard size (2.7 F) to very small bore 
(2 F). The two largest bores are widely utilized when 
particulate embolization is performed, as the cath- 
eters do not become easily obstructed. The small- 
est bore is most often used in neuro interventional 
applications with either coil or liquid embolics. The 
mieroait liefer hns l\:> combine llexibility niul It;k la- 
bility to allow d istal catheterization of target vessels. 
There are many microcatheter dedicated to periph- 
eral indication combining these features and kink 
resistance as well as accepting high flow injection 
rate (Fig. 2.11). 

The wires utilized are similar to those in diag- 
nostic catheters but of 0.018, 0.016, 0.014, and 0.010 
in diameter. The ends of these wires are usually 
straight and need a45°-90° bend placed in it in order 
to select the desired vessels. This bend can be placed 
by pulling the wire against the thumbnail or the 
introducer in the package. As a practical matter, it 
is usually easier to place the bend in the wire after it 



Embolization Tools 



is initially loaded into the microcatheter. The micro- 
wires usually have platinum or gold at their tips to 
aid in visualizing the tip of the wire under fluoros- 
copy. Excellent fluoroscopy and digital imaging are 
necessary to fully utilize the microcatheters. 

Power injection through the largest bore micro- 
catheters Cist usually be performed with tlow rates 
of 3-4ml/s at a pressure limit of 300 psi. This 
depends on the viscosity of the contrast and the 
diameter of the microcatheter. With some current 
microcatheters, high flow rates can be given up to a 
pressure of 750 psi (Fig. 2.11). Good distal diagnostic 
angiography can be performed through these cath- 
eters. It is still important to continuously visualize 
the catheter tip during the embolization procedure 
since movement of the tip can result in non-target 
embolization. 

When using a microcatheter, care must be taken 
to avoid plugging the lumen with embolic agent, 
particularly with PVA or resin microspheres, by 
increasing the dilution of the particles. Emboliza- 
tion is usually performed using 3-ml syringes to 
achieve adequate pressure. If the catheter becomes 
completely obstructed, an attempt to pass a wire 
through the catheter to clear it may be made but 
such an obstruction usually necessitates removal of 
the microcatheter and its replacement. 

Flow-directed microcatheters are also good tools 
developed for treating distal brain AVMs. These 
catheters are more flexible and smaller than the reg- 
ular microcatheters. They can be carried distallyby 
flowing blood. Also, the use of a 2-cc syringe filled 
with contrast can help the progression of the flow- 
directed microcatheter. These catheters can be used 
in some peripheral clinical indications such as inGI 
bleeding. 

Microcatheters and -wires have revolutionized 
interventional radiology allowing the placement ot 




Polyurethane and PTFE 

polyethylene (Polytetraflouroerhylene) 



iciocathtter. (Courtesy or' Ten: mo) 



embolic agents in more distal locations 
more accurately so that normal tissues 
and the therapeutic effect is enhanced. 



Conclusion 

The use ot embolization to treat a myriad of differ- 
ing conditions and diseases will only accelerate due 
to the new devices being developed and the newly 
found acceptance of loco- regional therapy. 



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Embolization Tools 



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Embolization Tools 



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Intervent Radiol 28:228-241 



Controlled Delivery of Pushable Fibered Coils 
for Large Vessel Embolotherapy 



Robert I. White Jr. and J. 



Introduction 35 

Techniques 35 

Nes i in g/P.i eking Technique 37 

A l t -." 1 1 ■.: ■ j " Technique 38 

Scaffold Technique 39 

Guide Catheters 39 

Microcoil Technique 39 

Microcoi! Usage with New 0.027 Endhole 

Micro catheters 41 

Conclusions 42 

References 42 



Introduction 

Pushable fibered coils have been the material of 
choice for large vessel occlusion for the past 30 years, 
since their introduction by [1]. Their simplicity, reli- 
ability, and availability have led to their widespread 
acceptance by interventional radiologists through- 
out the world. 

A number of significant modifications to the 
original stainless steel coils with wool fibers were 
developed. It was realized early on that wool led to 
occlusion followed by an intense chronic inflam- 
matory reaction [2]. This led manufacturers to sub- 
stitute polyester (Dacron) for wool fibers. Dacron 
fibers proved to have excellent platelet aggregation 
properties without causing the marked inflamma- 
tory response associated with wool. Currently, the 
basic fibered coil consists of a length of guidewire 
with multiple polyester threads attached trans- 
versely along most of its length. Fibered coil emboli 
are preshaped into a variety of different configura- 



R.I.Whcte Js.,MD 

Yule University School of Medicine, I 'ep.utmeni of Diagnostic 

Radiology, 333 Cedar Street, Room 5039 IMP, New Haven, 

CT 06520, USA 

Jeffrey S. Pollak, MD 

Yule University School of Medicine, I 'ep.utmea: of I !j;;gnos1ic 

Radiology, PO Box 20842, New Haven, CT 06504-8042, USA 



tions, such as a helix, and then stretched out in a 
cartridge for delivery into a catheter (Fig. 3.1a,b). 

Since the introduction of pushable fibered coils, 
detachable balloons, both silicone and latex, were 
developed for large vessel occlusion and more recently 
the Grifka large vessel occlusion device and the Amp- 
latzer vascular Plug [3-7]. All of these devices were 
unique in that they were retrievable before detachment 
and animal studies proved that long term occlusion 
was possible as a result of cross sectional occlusion at 
the time of their placement. Detachable balloons are 
no longer available and the Gianturco- Grifka occlu- 
sion device has limited usage because of its size. 

Improvements were made to pushable fibered 
coils, including the introduction of platinum fibered 
0.035-0.038 standard and 0.018 in "microcoils" 
[8, 9]. These later developments, provided a softer 
and moreMRI compatible coil but without the radial 
force of the original stainless steel coils. In Europe an 
Inconelcoil, with excellent radial force, replaced the 
stainless steel coils and so high radial force and soft 
fibered platinum coils for vessel occlusion, became 
available in Europe. The Inconel, high radial force 
coil, is not yet available in the USA. 

For neurovascular use, the development of the 
Gugliemi detachable coil (GDC) without fibers was 
essential for treatment of intracerebral aneurysm 
[10]. This coil and subsequent variations remains 
the standard for occlusion of narrow neck aneu- 
rysms. Variations of the GDC coil continue to be 
developed for management of cerebral aneurysm 
and other narrow neck aneurysms throughout the 
body [11]. The downside to the widespread use of 
GDC type coils for occluding arteries and veins are 
their expense and lack of thrombogenicity [12]. 



As a result of treating a large number of patients 
with high flow fistulas of the lung during the past 



R. I. White Jr. and J. S. Pollak 




Fig. i.l. a C.C-.i? High radia. force stainless -tec!. Tornado, .mo Wster ./oik The stitin.css -tee! ;■:■-.[ iiifi) has .1 high radial force 
which is unique among coil m a ma fa ctu re rs (Cook Inc., Bioomington, IN). The Tornado coil is a soft platinum shorter coil. 
Comparable coils induce: Trulill i Co re is Corpora t ion inc., Miami, rl\ and Diamond and Vortex :C-ioston Scientific Corpora- 
tion, Natick, MA). 7 lie Xester .:<::l 1 ngiii) :s a long, sort, phi: i num. h he red coil with vai vmg diameters which compresses 10 1 cm 
in lenglh when cached into :t cCood vessel, b .-If f/vc lop, 0.01 B-:m Micro-Tornado coils (Cook inc.) of 4 and 8 mm are shown. 
L'lidr: neaih, C.C1 S-in. 4 and S mm diameter Micron esters are shown. The M:cro:trster :s a longer length col which is racked 
rj.sily into ,111 occ hiding nutss 1 cm in length. Often both coils are c.sed. After occluding 1; ; -cm Itngl:'. 0: a flood vessel with 
Micioi'.eslei s, one 0: two Micro-Toi nados nt :tv oe acdec if there is a short icsidual length of blood vessel rec:::: ing ■:>;■; 1 11 si on 




Fig. .1.2. Cross sectional ■. col.is:- ■:: itch i eve c bv packing 01 nest- Fig, .1..'. Coaxial technictie to prevent coil elongation. I 
ing soft platinum coils, image a: lite rop den: oust rates partially diagram, a 5-F guide catheter is placed into the vessel 
occ It: dec blood vessel with elongated co:l. Often the vessel wik occluded. A microcatheter is advanced lo the site of occlusion 



appear occluded because of associated spas 
recanalization will haw occurred. I 'e::se packing as shown ir 
the bottom image is necessary to achieve predictable long- 
term cross sectional occlusion 



and while holding :::e g:::de catheter con.stant, the microcatheter 
:s advanced and the microcoil c.eploved.Tae support "purchase" 
provided by the guide calhelei helps tire intci venticnakst to pack 
the microcoil into .: tight coil m.iss leading to permanent occh:- 
sion.The use of gt:id:ng catheters is the most important step 10 
.'leveming ul eiengatie.n .uid tincerlatn long tern: occlusion 



8 years, we have confirmed the following two prin- 
ciples: Initial cross sectional occlusion provides long 
term occlusion (Figs. 3.2 and 3.3}. Safety and con- 
trol during deployment of conventional pushable 
fibered coils is achievable with the use of 6- or 7-F 
guide catheters. Longer 4- or 5-F catheters are placed 
coaxially through the guide catheter for deploying 
0.035/0.038 in. coils. The shorter guide catheter pro- 
vides stable position ("purchase") in the artery or 



vein to be occluded. The same principle can be uti- 
lized when using pushable fibered 0.018-in. micro 
coils. In this instance a 4- or 5-F catheter is the 
guide catheter and a longer microcatheter is placed 
coaxially for deploying the microcoils (Fig. 3.3). In 
general the first coil selected has a diameter at least 
20% larger than the vessel to be occluded. 

Experience with follow-up angiograms of 
patients treated for PAVMs proved that when high 



Controlled Delivery of rusl'.aiMe hoered Ceils for Large Vessel Embolotherapy 



flow PAVMs were treated with pushable fibered coils 
that deployment of one or two coils often produced 
a temporary occlusion which recanalized over time 
(Fig. 3.4). It was soon appreciated that initial deploy- 
ment of the first one or two coils was associated with 
elongation of the coil and spasm. In simple terms, 
elongation of the coil during detachment through 
an endhole catheter was not always associated with 
long term occlusion. 



3.2.1 

Nesting/Packing Technique 

Cross sectional occlusion of the artery/vein is easily 
produced when coaxial catheters were used. The 
elongation of pushable fibered coils is avoided by 
advancing the coil through the inner 4- or 5-F cath- 
eter while holding the outer guide catheter stable 
in the artery or vein (Fig. 3.3}. In this way the soft 




with recanali: 
mgiogram through the guide and 
:s later. c,d Nesting "packing" of 
oss-sectional occlusion Id) 



llormalion iPAVM). a,b A selective pulmonary 
ght lower lobe pulmonary malformation is still patent, 
placed just proximal ;o ihe jvcanalized coils, produc- 



fibered platinum coils are weaved into a tight mass 
which occludes the vessel. Long term follow-up of 
our patients proved these two concepts [13]. 



3.2.2 

Anchor Technique 

Another benefit of using guide catheters and the 
improved control they provided when placing push- 
able fibered coils was the realization that in high 
flow fistulas in the lung, we could anchor the first 
2 cm of a long 14-cm coil in a side branch, close 
to the aneurysmal sac. Thus, by "anchoring" the 
coil, we avoided any chance of coil migration and 
deployment of the remaining coil could be con- 
trolled (Fig. 3.5}. This technique was very useful 
in avoiding the potential of paradoxical emboliza- 
tion of the coil through the PAVM. The "anchor" 
branch was as close to the aneurysmal sac as was 
possible. This prevented unnecessary occlusion of 
normal branches since a distal branch is usually 
sacrificed by whatever occlusion technique is uti- 
lized (Fig. 3.6). This technique, while developed for 
controlled delivery of pushable fibered 0.035 and 
0.038 coils for pulmonary arteriovenous malforma- 
tions (PAVMs), has application throughout the rest 
of the body when using embolization coils. 




Fig. 3.5. The "anchor'' technique."'/.^ t e C" J"u ". i .." '. : e i- : very valuable 
for providing safe and disial occlus.on when there is a question 
about instabililv o: pushahle tibered cols. Diagranimatically, 
the guide catheter is placed in the artery to be occluded and 
a 5-F inner catheter or micro catheter is advanced into a side 
branch nest to the site requiring occlusion. At least 2 cm of a 14- 
cm standard Nester or Micrortester .ire advanced into the side 
branch wincr. is norm;: I. v sacrificed. The res: o:' I he coil .s ihen 
deployed List proximal to- ihal side brunch and addition;:! coils 
are racked so th.it cro ,; s-se-."ii' nrl ■ ■cclnsion is obtained 




Fig.3.t>a-(.'. in ih is patient witr, a.g:i tiow pan notary i'a lent- 
venous malformation c( ;he riglu lower iooe.a number oi" distal 
sice branches are c em oust ra lee immediate!}" proximal to the 
uneurysmal sac and fistula. The mner 5-F catheter was advanced 
into a side branch and 1 cm o: the fust coil was deployed (bi and 
then the 5-F catheter was retracted and the remaining 12 cm c<( 
the coil wns packed mi:' a tight coil mass. One additional 4-mm 
col was also packer distal. v i : r_ ■ :::e r-mm coil, and ihe una! 
angiogram in ici demonstrates a very distal occlusion immedi- 
Hlely itdiacent to- the sac w-ilh preservation of most of the normal 
brunches. This technique is tiseo rotitinely tor pulmonary mal- 
formations, out is aiso usee' for other venous and arterial occlu- 
sions when there is concei r; aooul migr.ULan. Again, the support 
or "purchase" of the gu icing catheter is critical to allow packing 
of the coil into a tight occlusion mass 



Controlled Delivery of Vus:\:vAe hdered Ceils for Large Vessel Embolotherapy 



3.2.3 

Scaffold Technique 



Guide Catheters 



In very high flow fistulas with large arteries, this 
technique is used to achieve a stable matrix, avoid- 
ing migration. By first deploying high radial force 
fibered stainless steel or Inconel coils, a scaffold is 
formed and the remaining cross sectional occlusion 
is produced with fibered platinum coils which are 
"weaved" into the interstices of this "endoskeleton" 
(Fig. 3.7). 

The first, high radial force coils placed to form 
the scaffold are oversized by 2 mm, i.e. for a 10-mm 
feeding artery, 12 mm diameter stainless steel or 
Inconel coils are first placed. These first coils may 
be anchored as well if there is concern about fixation 
in the artery. Usually several small diameter high 
radial force coils are placed as well into the "endo- 
skeleton", followed by several softer platinum coils 
until cross sectional occlusion is achieved. 

In very high flow fistulas with large arteries, 
12 mm or larger in diameter, the first coils are often 
placed through a balloon catheter (Boston Scientific, 
Natick MA) which has been temporarily inflated in 
order to stop flow. Once ;i scaffold is formed the bal- 
loon catheter is deflated and exchanged for a stan- 
dard coaxial guiding catheter and the occlusion is 
completed with long fibered platinum coils (0.035 or 
0.038 Nester. Cook Inc., Bloomington, IN) (Fig. 3.8). 




Fig. 3.7. "Scaffold" ledin.qi.ie. This lechnieue is used for high 
flow vessels when ri'.ere is concern abooi migration of ,i softer 
coil. Initially in li'.is diagram a high :adia' force coil, with a 
diameter 2 mm larger Ilia: 1 , the arieiy or vein being occluded, 
is placed, several high radial force coils may be placed and 
the occlusion is compleled ■..sing Nester cols to tightly pack 
within the "scaffold" or "endoskeie:on" 



Integral to using pushable fibered coils to produce 
cross sectional occlusion is the use of coaxial or tri- 
axial guide catheter systems. For venous occlusions 
(varicocele and/or pelvic congestion) or occlusions 
of PAVMs, we use standard 7/5 combinations (Pul- 
monary, Cook) or gonadal (Cordis Inc., Miami FL) 
with inner 5-F endhole catheters (Fig. 3.9). 

For visceral occlusions we use 6-F RDC (Cordis) 
guide catheters. In Figure 3.10, a splenic false aneu- 
rysm is occluded using a 6-F RDC guide catheter 
placed in the celiac and proximal splenic artery. A 
4-F endhole catheter is placed coaxially for stan- 
dard coils (Fig. 3.10a). A microcatheter for plac- 
ing microcoils can be placed either through the 
4-F catheter, creating a triaxial system, or directly 
through the 6-F guide catheter (Fig. 3.10b). A coax- 
ial 0.021 lumen microcatheter (Renegade catheter, 
Boston Scientific) is positioned in the distal splenic 
artery just beyond false aneurysm and microcoils 
are placed distal and proximal to the origin of the 
aneurysm ("trap method" or "closing the back and 
front door"), thus excluding the point of arterial 
injury from antegrade or retrograde refilling. 



Microcoil Technique 

Controlled delivery of all pushable fibered Micro 
coils (Cook, Boston Scientific and Cordis) 0.018 in. 
is possible by using a coaxial guide (4-6 F) and 
microcatheters [14]. In order to achieve cross sec- 
tional occlusion of the artery or vein, the micro 
coils must be delivered into a tight coil mass. To 
achieve this, a 0.016 pusher wire (Boston Scientific 
or Cordis) is used and the same weaving "action" is 
performed during deployment in order to nest/pack 
the microcoil into a tight coil mass (Fig. 3.3). 

Also, the microcoils are deliverable by the 'Squirt' 
technique. The Squirt technique is suitable for deliv- 
ery of all pushable fibered microcoils (0.018 in.) 
through microcatheters with 0.016- to 0.027-in. end- 
holes. The microcoil is loaded into the microcath- 
eter and preferably a 3-ml luer lock syringe, filled 
with saline is attached to the hub of the microcath- 
eter. Under fluoroscopic guidance, the microcoil is 
delivered with small boluses of saline. Final adjust- 
ment ill the miaocoil is accompli <.hed by movim:, thr 
microcatheter before final deployment of the coil, if 



R. I. White Jr. and J. S. Pollak 




Fig. .'.8:1 I. This pai:eni j'.s; a verv lug:: how Iis1u!li v:lh moderate pulmonary hypei tension. The lea pulnii.-p.ai v angiogram 
(a and d) demonstrated a high flow fisuiln with a 12 -mm diameier artery in the lea lower lobe. Using tlic r=.;i j j-.i .-. i L i raiding 
oulhelr: ieohmque. :■ dis;al bio noli ibi anchoring was no I inline,".:. :te!y apparent. l:i order ;o- provioe a safe and eon I rolled ooolu- 
sion. :i 20-mm ooclusion balloon oaiheie: i oosio:i ^oienutio, Thliok, MA : was nhoed a no :n:la:ird. VVhLe aillv hepai inized, an 
inner 'so.;i:old" i ci was proouoed, using 15-, 12- and ! 0-mni dolmen: stainless si^el ools. The balloon oa:jie:ei vvas d^hated 
and removed : d :■ and oui standard guiding o:ilheter sv?:em was plaoro. The ooolusio:: was eoniple:ed ;d and e: usi:'.g I 2 -mm 
Nesie: eoTs :o produec oross-ScOliomil exclusion. A ibdovv-pp angiogram 8 mo::: lis hi:er i fi demo::s:raled perniap.r:;: oeol-ision 
'.■:' Ih:s la;ge high ]] ■. -iv lisuila vvilh preset vai ion .;■■:' noi nial pulmonary artei y branches 




Fig.35a-d. A standard 7-F gonaoai guide oa:heier roi oo:U;sion ot the ir:"t sperm a tie or ovarian vein (Cordis Inc., Miami, FL) 
is demonstrated in (a) and in i b) the 7.'? pu nnop.ai v gui..li::g o.tl:-te:" i:^ inner oa:li^:er :or ooolusio:: ot" pulmonary arteriove- 
no i.i s ma I formal ions js show::. Onoe ihe ov:;rian oi' i:::ermp sperm a lie vei:: are eaiheiepzed, any slanoard lOO-om o-F end hole 
multipurpose catheter is advaneed ovvr a jienison wire deep m:o the spernuuo or ova: :an \v:n where soi^rosants and coils are 
usually placed. A standard 6-F RDC (Cordis [no.. Mi.: mi, FI. :■ guide oiitheter foi v; : w:al ep.:pp:izaaon is demonstrated with a 
coaxial 4-F catheter in (c) and in (d), a Iriaxial svsleni :s o!enionst:a:ed with an inner 0.021 lumen microcatheter 



Controlled Delivery of rusriaole hoered Ceils for Large Vessel Embolotherapy 




Fig.3.10a-d. A huge splenic artery tVdse aneurysm is demonstrated neat ihe hihini of ".he spleen (a :. The ■■:•-¥ RDC ■."Litheter is 
advanced into ihe of ! rice of the splenic artery and a miciocalhelei is passed ;o ihe site of iniury in the distal splenic artery i b). 
The microcatheter is advanced distaLv beyond the site of trie communication wit:: trie :"a!se aneurysm. Vicronesler coils are 
r laced distal and proximal to the origin o: trie false anrtnysm 1 1 and di one ihe rina! angiogram demon si rates occ Vision ;:if the 
lower pole of the srieen wilt, preset vat ion :.': the upper pole 



the initial position of the partially delivered coil is 
distal to the site desired. 

Earlier experience with the Squirt technique, 
using a 1-ml syringe and vigorous force to propel 
the microcoil can result in the microcatherer 
moving opposite to the force of injection and the coil 
deployed proximally or, worse yet, into a non-target 
vessel. A 3-ml syringe is preferable for delivering 
microcoils by the squirt technique and of course 
if there is a fistula or if there is any concern about 
non-target embolization, a 0.016-in. pusher wire is 
utilized. The first microcoil placed for closing a fis- 
tula should always be placed with a pusher wire for 
maximizing control. 



Microcoil Usage with New 0.027 End hole 
Microcatheters 

The development of microcatheters with 0.027 
endholes (Renegade Hi-Flo, Boston Scientific, 
and Mass Transit, Cordis) enabled easier delivery 
of particulates for embolization of hepatocellular 
cancer and uterine fibroids. Un fortunately, the 0.016 
pusher wires will become trapped between the 0.018 
microcoil and the inner diameter of these larger 
lumen microcatheters. If coil delivery is desirable 
using a pusher wire, a Teflon coated standard 0.021 
wire is utilized. Our preference though is to deliver 



irough these large lumen microcath- 
eters with the Squirt technique using a 3 ml luer lock 
saline filled syringe. 

Of note though, the Squirt technique should not be 
used for deployment of the first microcoil for treat- 
ment of aPAVM or other fistula. In this instance the 
coil may pass directly through the fistula. 



3.6 

Conclusions 

Since the development by Gianturco of the first 
pushable fibered coils over 30 years ago, significant 
advances in coils and catheters have occurred. It is 
now possible to deliver pushable fibered standard 
0.035 and 0.018 microcoils inacontrolled and precise 
manner. Experience on a day to day basis with high 
flow fistulas of the lung has enabled us to develop a 
number of techniques which enable safe deployment 
and cross sectional occlusion of the vessel. 



1. Gianturco C, Anderson I H, Wallace S (1975) Mechanical 
devices tor arterial occlusion. Am I Roenlgenol 1 24:4JS— 
435 

2. Barth KH, Strandberg JD, Kaufman SL et al ( 1 978] Chronic 
vascular reactions to steel coil occlusion devices. Am J 
Roentgenol 131:455-453 

3. White RI Jr, Ursic TA, Kaufman SL et al (1978) Thera- 
peutic embolization with. detachable ba Loons: physi- 



cal factors inflr.enciijg peimaiieiit occlusion. Rnoiologv 
126:521-523 

4. Kaufman SL, Strandberg JD, Barth KH et al (1979) Ther- 
aoiriiuc em :-:A. ;tai..tn wtL: del.tcriace si.icot'.e baboons: 
long-term effects in swine, lures: Radio! 14:156-161 

5. Barth KH, White RI Jr, Kaufman SL et al (1979) Metriza- 
mio-e, the ide;'.l raaiopcque filing material :".:■[' delacr.aole 
silicone balloon embolization. Invest Radiol 14:35-40 

6.Grifka RG, Mullins CE, Gianturco C et al (1995) New 
Gianiurco-Grifka vascular occlusion device: initia' stud- 
ies in a canine model. Circulation 91:1840-1846 

7.Sharafuddin M, Gu X, Umess M et al (1999) The Niti- 
nol vascular occlusion plug: preliminary experimental 
evaluation in peripheral veins. 1 Vjsc Interveni R.uiiol 
10:23-27 

S.Kaufman SL, Martin LG, Zuckerman AM et al (1992) 
Peripheral trntiscatheter embolization with platinum 
microcoils. Radiology 184:369-372 

9. Morse SS, Clark RA, Puffenbarger A (1990) Platinum 
microcoils for therapeutic embolization: nonneuroradio- 
logic applications. Am I Roentgenol 155:401-403 

0. Guglielmi G, Vinuela F, Septeka I et al (1991) Electro- 
ihrombosis of saccular aneurysms via endovascular ap- 
proach. I. Electrochemical basis, technique. ami experi- 
mental results. I Neurosurg 75:1-7 

1. Klein GE, Szolar DH, Karaic R et al (1996) Extracranial 
aneurysm and arteriovenous fistula: embolization with 
the Guglielmi detachable coil. Radiology 201:489-494 

2. White RI Jr, Pollak JS, Picus D (2003) Are Guglielmi 
detachable coils necessary for treating pulmonary arte- 
riovenous malformations: Letter to the editor, kad.okgv 
226:599-600 

3. Pollak JS, Thabet A, Saluja S et al (2005) Clinical and 
..■.:..:' ■.;■....■. outcome aftei - 1 1 1 !"■ ■ ■ I f'.erapy pultr.onarv 
arteriovenous malformations. Accepieo, for preservation 
SIR 2005, NewOrleans, LA, in press I Vase Intervent Radiol 
2006 

4.0sugaK,WhiteRIIr (2003) Micronester: a new pushable 
foeied microcotl tor embololheraay. O.rdiovasc Inter- 
vent Radiol 26:554-556 



4 Work-up and Follow-up after Embolization 



General Work-up 43 

IV. ■fi-i.ij.i ["■ 'i Hjviiri fr-.'xy r\::ih ■.iz.i 

^mi-Emergency 44 

Elective Embolization 44 

Follow-up 45 

References 46 



General Work-up 

It is important to become tami liar with all aspects of 
the patient's clinical historv, as this will ultimately 
help to determine the appropriateness of the planned 
intervention and will also help optimize and guide 
the catheter-based intervention. For example, one 
should know if the patient is using anti-coagulant 
medication or other meditation, which might alter 
the clinical presentation .>! hemorrhaging patient 
or influence the efficacy oi the embolization pro- 
cedure. It is important to be informed about the 
patient's medical history and medication. A history 
of contrast allergy is important, as these patients 
should be pre-treated with corticosteroids. Since 
B-blockers might fully mask the hyperdynamic 
response of hypovolemic shock, appropriate pre- 
cautions should be taken in patients with elevated 
creatinine who are usinii Meuoi mm l.vtore contrast 
medium is given. Patients with renal insufficiency 
should be pre-treated with hydration, alkaliniza- 
tion and N-acetyl cysteine (600 mg dosing every 
6 h, preferably twice before the intervention). Oral 
anti-coagulants can reduce theprothrombotic el led 
of coil embolization and, whenever possible, should 
be stopped or reversed before embolization, or alter- 



J.A. Reekers, MD, PhD 

AondemL" Medial Centre. Uruwisr.y of Amsterdam. Depart- 
ment of Radiology, Gl-207, Meibergdreef 9,1105 AZ, Amster- 
dam, The Netherlands 



natively another embolization material should be 
used, such as occlusion balloon or glue. 

Before starting any elective embolization it is 
important to talk to the patient and obtain informed 
consent. In talking to the patient, emphasis should 
not only be on the advantages but also on the risks 
and complications of embolization therapy. Alter- 
native therapeutic options should be discussed. In 
both emergency and elective embolization there is 
no scientific proof that antibiotics should be given 
prior to embolization. Always work as a team with 
the referring physician, to have a back-up plan for 
possible procedure failure or complications. 

Needless to say, embolization should only be per- 
formed with ample experience and support. Optimal 
angiographic facilities and all necessary materials 
should be at hand. 



Work-up for Emergency Embolization 

Requests for emergency embolization are usually 
unexpected and often occur after hours, therefore 
logistical support must be optimized to provide 
trained personal who are available on a 24 h basis. 
In case of an emergency there is usually not much 
time for full diagnostic work-up. Undoubtedly a 
CT scan can be very helpful to guide the interven- 
tion. In traumatic bleeding essentials like hemody- 
namic monitoring and live-support should be avail- 
able. Some basic lab data should also be recorded 
(Table 4.1). Furthermore, typed and cross match 
packed red blood cells should be obtained imme- 
diately. Fresh frozen plasma and platelets also may 
be required to correct coagulopathies that develop 
in severe hemorrhagic shock. Intravenous access 
and fluid resuscitation are standard. However, this 
practice has become controversial. For many years, 
aggressive fluid administration has been advocated 
to normalize hypotension associated with severe 
hemorrhagic shock. Recent studies of urban patients 



with penetrating trauma have shown that mortal- 
ity increases with these interventions; these find- 
ings call these practices into question. Reversal of 
hypotension prior to the achievement of hemostasis 
may increase hemorrhage, di^kidee pa it ially formed 
clots, and dilute existing clotting factors. Findings 
from animal studies of uncontrolled hemorrhage 
support these postulates. These provocative results 
raise the possibility that moderate hypotension may 
be physiologically protective and should be permit- 
ted, if present, until hemorrhage is controlled. 

For a hemodynamic;! I ly unstable patient with, for 
example a pelvic bleeding, timely embolization may 
be the patient's only chance for survival. Although 
some of the literature may disagree, it has been our 
experience that any delay in embolization therapy 
to allow the application of external or internal 
pelvic fixators can result in deadly delays. Patients 
with acute hemodynamic instability do not die in 
the angio suit, as modern anesthesia can almost 
always keep them alive during the procedure. They 
die, however, from the sustained shock and blood 
transfusions which will lead to multi-organ failure 
(MOF) days after the initial procedure. There is a 
direct relation between the amount of blood trans- 
fusions and the chance to leave the hospital alive. On 
the other hand, recently available Velcro-type pelvic 
binders offer a rapid and effective alternative to time 
consuming orthopedic fixation procedure in pelvic 
fractures and may allow stabilization of the patient 
without delaying indicated angiographic emboli- 
zation procedures. It is therefore paramount to get 
the patient to the angiography suite as promptly as 
possible. It has been the experience in some major 
trauma centers that an angiography suite next to 
the trauma bay is a very helpful arrangement. It is 
important for the interventionist to be present at the 
emergency department when the patient gets in and 
to start the preparation for the embolization proce- 



Medication history 

Prodi IV' i lib m dine. acirv.ued partial L'.iomboi^asdn time, 

.111.:. p: aielets count 

Heiiiodo^iii/heiiiiit:/:!]: 

A:' teri.il blood gase?, base deficit; a no lactate levels i reflect 

acid-base and perfusion status) 



ized on CT, especially newer multi-detector scan- 
ners, allowing the angiographer to zoom in on the 
likely site of major bleeding without a proceeding 
exhaustive angiographic search. In hemodynami- 
cally unstable patients, a focused ultrasound exami- 
nation of the abdomen while the patient is being 
prepared for the angiogram can sometimes localize 
a pelvic or intra-abdominal tin id collection and help 
guide the intervention. Therefore, we believe that 
cross-sectional imaging in some form should be per- 
formed as a work-up whenever possible. 

Other forms ot bleeding localization can also be 
used. In a patient with GI bleed ing who was first seen 
by an endoscopist, as is usually the case, application 
of a clip to the bleeding site can guide a possible sub- 
sequent catheter intervention. Having a good under- 
standing with the endoscopist on this is important. 
Similarly, in patients presenting with hemoptysis, 
bronchoscopy can be of great help to determine the 
bleeding site, along with a cross-sectional imaging 
study. Again, blood, plasma and at least two large 
caliber running intravenous lines should always be 
available. In addition, we have also found that, in 
these semi-acute patients, professional monitoring 
by an anesthesiologist is highly advantageous. 



4.4 

Elective Embolization 



Elective embolization can be performed for many 
4.3 indications as will be presented in other chapters 

Semi -Emergency in this book. Different indications have different 

appropriateness criteria and require different work- 
If there is an acute indication for embolization up and preparations (Table 4.2). For example, prepa- 



therapy, but if the patient is hemodynamic stable, 
spiral CT can be very beneficial to help planning the 
intervention. A pseud oaneurysm of a visceral vessel 
certainly will target the intervention. A retroperito- 
neal hematoma will suggest potential bleeding sites. 
Active extravasation can also sometimes be visual- 



l for a uterine fibroids embolization procedure 
varies greatly from preparation for a varicocele 
embolization. Work-up and preparation includes a 
focused history with physical examination, evalu- 
ation by an appropriate allied clinical specialist 
(for example, a gynecologist in the case of uterine 



Work-up and Follow-up after Embolizatio 



fibroid embolization), and a proper imaging and 
laboratory evaluation. Patient education is a crucial 
part of the preparation procedure, as some of these 
elective embolization procedures can result in sig- 
nificant complications. The patient needs to be well 
informed of the indications, alternatives, and the 
risk of complications. 



Follow-up 

The follow-up should be focused on the possible 
complications and clinical outcome (Table 4.3). In 
the acute and immediate post-procedural phase, 
special attention should be directed to the early 
detection of sequelae of non-target embolization, 
which can often result in major complications. It 
is a good practice to routinely conduct a telephone 
interview with the patient no later than a week after 
the procedure. Modern interventionists are clini- 
cal providers and an interventional clinic follow- 
up at an appropriate period of time following a 
major embolization procedure is not an option but 
a required minimal standard of practice. 

After embolization of a uterine fibroid clinical 
follow-up might be sufficient. However, to pre- 
vent an early recurrence, early MR controls might 
be necessary. Pain control following embolization 



of a congenital vascular malformation can often 
be effectively accomplished done with oral anal- 
gesics, such as acetaminophen or non-steroidal 
anti-inflammatory drugs. However, in the case 
of embolization of a solid organ or tumor, special 
care should be taken to the management of post- 
embolization pain that can be severe. In some 
instances, for example uterine fibroids or kidney 
tumor embolization, opiates or epidural anesthesia 
maybe required. The interventionist should always 
check the patient personally as post-embolization 
pain can sometimes be unpredictable, and may be 
the source ol significant anxiety and negative per- 
ception by the patient. Fever, usually below 38.5°C 
but sometimes as high as 39°C, and nausea are also 
often seen after embolization due to tissue necrosis. 
Fever above 39°C is suspect lor intect ion or abscess 
formation. CT scan guided percutaneous sampling 
and drainage might be mandatory in some of these 
cases. Surgical consultation for debridement and 
drainage may also be needed in extreme cases. 
Wide spectrum empirical antibiotic therapy should 
be started whenever infection is suspected. In some 
embolization applications, like embolization of 
the splenic artery, there is a higher predilection to 
abscess formation, which can be treated with anti- 
biotics and percutaneous drainage. It is mandatory 
to document all of the details surrounding post- 
operative adverse effect and their management in 
the medical record. 



Table 4.2. Preparation for elei 


tive embolization 






Application 


Wo: k-up 




Procedural risks 


V'iiscu.ar makoniijiio;: 


MRI/MRA 




Necrosis 


Uterine fibroids 


MRI/MRA, US 




:• ep: ice:" 1 ,! i a/pain and lever 


Spermatic vein 


US 




kec.iirtii'."; 


-IK'Oleiil'.S 


Spiral CT, MRI, ang 


iography, duplex US 


Recurrence/no;;- large; embolization 


Primary liver tumors 


CT, angiography 




Necrosis/lever/ sepsis /recurrence 


Metastatic renal cell tumor 


CT, angiography 




Necrosis/ fever/pain 


Benign bone tumors 


CT 




Pain/recurrence 


Tumor in general 


CT/MR 




Necrosis/ fever/pain 



is of therapeutic embolization 

jmtIt: i-.il 



Tissue necrosis 

}iowl/p-ireiic:',viii.i ischer 



Plastic surgeon 
Surgeon 

[n let vent Ana! rjdiologi 
jnei u-iKkiia. rodn -\o'j.. 



Managemcni 

Skin g:,il'^/skin transplants 

CT scan/laparotomy 

Antibiotics/drainage 
NAIDS/morphine 



Take Home Points: 

• Work-up and follow-up of embolization patients 
should be specifically tailored to the patient, 
and the indication for intervention. 



be obtained from the 



■ Vital informati 
patient's medical history. 

• The doctor who performs the embolization pro- 
cedure should be responsible for the follow-up. 

■ Proper pain management is important after 
embolization. 

• Proper medical documentation is very impor- 
tant. 

■ A team approach is important. 



References 

Agnew Sij ! 1994: i-iemooyni'.nuo'.llv unstable pelvic fractures. 
Orthop Clin North Am 25:715-721 

Beers MH, Berkow R (eds) (1999) Hemostasis and coagulation 
disorders. In: Bens M!-!, Kerkow K feds: The Merck manual 
of diagnosis .uid :he:jpy. : 7th eon. HerrL, USA 

Ben Menachem Y, Coldwell DM, Young JW, Burgess AS (1991) 
Heiiio;:h:'.ge associated with pelvic fractures: causes, 
diagnosis, and emngeiji maii.igenie:"n. Am I koenogen.ol 
157:1005-1014 

Moore H, List A, Holden A, Osborne T (2000) Therapeutic 
ei)iL""'jii..nioii for acute h.ir::'.o:rhage in t!ir .:."■..'■. :'.".-ii :.:.d 
pelvis. Australas Radiol 44:161-168 

Simons ME liOOl ) Peiopher.u vascul.'.r nialforniations: diag- 
nosis ..inc. .•iricutaiiirous :v.a:':igr:::riil Can Ass.;,- Kaoio. I 
52:242-251 

Spies IB, Pelage JP (eds) (2004) Uterine artery embolization 
.mo gynecologic e:v.Lio!oihe;apv. Lippencolo USA 

Wilkins RA, Viamonie M !eds! f]9S2) Interventional radiol- 
oyv. 4|a.-kwel., ;!'xro:d 



Gl 



5 Upper Gl Bleeding 



Introduction 49 

Epidemiology 49 

[ndiojiions :-i[ Artenogrophy 50 

Ai iei iogiLiohy Verms Surgery 50 

Timing of Arteriography 50 

Gosno-duodeno! Aite::og:orhic Anatomy 51 

I 'iiignosti." At tenography 52 

Aketu.itiws to. !':og:'.o;:ic Catheter 

At iei iogiaphy 54 

Therapeutic Arteriography 56' 

Eir.oojzotion 56 

General Technical Aspects 56 

Specific Technical Aspects 57 

Particulate Embolization 58 

God Embolization 60 

Gelfoam Embolization 61 

Glue Embolization 65 

Other Embolic Agents 66 

Complications 67 

Outcome 68 

Perspectives 68 

Conclusion 68 

References 69 



Introduction 

The first attempts to arrest non-variceal upper gas- 
trointestinal hemorrhage (GIH) by transcatheter 
embolo therapy were undertaken in the early 1970s. 
As a low-invasive alternative for the high risk-bear- 
ing surgery, embolization had a bright future [1-5]. 
However, the endoscopic revolution pushed both 
embolization and laparotomy into the background. 
From the mid 1980s on, endoscopy had assumed its 
role of first-line hemostasis, leaving laparotomy for 
about 10% of refractory bleedings. Unlike in lower 
GIH, endoscopy rendered diagnostic arteriography 
in upper GIH redundant. Only at the turn of the cen- 

L.DEFHEYNE,MD,PhD 

Deportment of Vnsciihi:' one ]; , .:erve:::io: , .al Radiology, Ghent 
University Hospital, De Pintelaan 1 BS, 9000 Ghent, Belgium 



tury, interest in embolotherapy revived. Microcath- 
eter systems and the embolic agents became more 
efficient and safe. Growing confidence in endovas- 
cular techniques contributed to the revival, result- 
ing in an increasing number of promising scientific 
papers [6-10]. 



Epidemiology 

With an incidence of 50-100/100 000 and a mor- 
tality of 10%-14%, acute upper GIH is recognized 
world-wide as a clinically significant and expensive 
health-care issue [11-13]. 

Acute upper GIH may present as hematemesis 
(bloody or coffee ground), melena or in rare cases 
as hematochezia. When a nasogastric tube is placed, 
aspirate should be blood red. Soon after the initial 
presentation, a combination of these bleeding mani- 
festations usually occurs. 

Over 90% of acute upper GIH are non-variceal 
[11-13] with peptic ulcer accounting for about 50% of 
causes. Other major etiologies include erosions and 
mucosal inflammation such as oesophagitis, gas- 
tritis or bulbitis (20%-25%), neoplasms (5%-10%) 
and vascular malformations such as angiodyspla- 
sia, Dieulafoy, aorto-enteral fistula (10%). Despite 
general availabilitv and vigorous use of endoscopy, 
10%-20% of acute upper GIH remain without a doc- 
umented cause [12, 14]. 

Although bleeding ceases spontaneously in a 
high number of cases, there is a consensus that all 
acute upper GIHs should be investigated by endos- 
copy [15]. Emergency endoscopic intervention is 
compulsory in high-risk groups identified by pre- 
endoscopic stratifications models for rebleeding 
[16, 17] and mortality [18-21]. In low risk groups, 
the patients may be held under short observation 
to undergo endoscopy on a more elective basis. 
Gombined endoscopic injection therapy and ther- 
mal coagulation are able to control about 90% of 



L Perreyne 



acute bleedings, thereby significantly reducing 
the mortality rate [15, 22]. However, 10%-20% 
of upper GIHs recur or continue to ooze after 
initial bleeding arrest. In peptic ulcer bleeding, 
proton pump inhibitors [23, 24] combined with 
eradication of Helicobacter pylori [25, 26] have 
contributed to a reduction in rebleeding rates. 
Other endoscopic strategies such as adjunctive 
prokinetics (erythromycin 250 mg intravenous 
bolus to induce gastric emptying and improve 
visibility [27, 28]), hemoclipping and cryotherapy 
[29-32], aggressive treatment of non-bleeding risk 
stigmata [33] and scheduled second therapeutic 
endoscopy [34-37] seem promising or are still 
under investigation. 

Despite these advances in medical treatment and 
endoscopic intervention, mortality in acute upper 
gastrointestinal bleeding varies between 10% to 
15% and seems not to have declined for more than 
a decade [12, 38]. Besides age and severe co-morbid- 
ity, endoscopic failure to stop upper GIH and post- 
endoscopic rebleeding are highly associated with 
mortality [12]. 



Indications for Arteriography 



on individual parameters and each case discussed 
with the involved physicians [■■!■■!. -15]. When a patient 
is in a frail condition or when surgery has already 
failed, it is wise to decide for a less invasive arte- 
riographic exploration with the option of emboliza- 
tion. In peptic ulcer bleeding, elderly patients with 
a high cardiovascular risk and coagulation disor- 
ders are likely to profit from embolization [10]. In 
this study, surgery rescued patients with a lower 
risk profile and outcome in both therapy groups 
was similar. However, the study was a retrospec- 
tive survey which requires cautious interpretation 
[10]. In an own 10-year retrospective (unpublished) 
survey, we found that bleeding peptic ulcers visual- 
ized at endoscopy were five times more likely to be 
rescued by surgery. In other cases, the endoscopists 
did not trust surgical exploration of unclear acute 
upper GIH. They might be right, since Cheng et 
al. [46] demonstrated that 50% of the diagnostic 
failures at endoscopy will remain unclear after 
surgical rescue. These ultimate diagnostic failures 
were significantly associated with higher morbidity 
and mortality [46]. Besides clinical factors, angi- 
ographic equipment and expertise in embolization 
techniques are decisive for interventional radiol- 
ogy to be accepted as a valid option in refractory 
upper GIH. 



When facing an endoscopic refractory upper GIH, 
two practical questions arise. Firstly, should we rec- 
ommend rescue arteriography in every case or, if 
not, which cases should be reserved for surgery or 
which ones for embolization? Secondly, what is the 
optimal timing of a diagnostic arteriography? Both 
issues are controversial and have not yet received a 
definite answer. 



5.3.1 

Arteriography Versus Surgery 

If the endoscopic arid surgical literature are to be 
believed, arteriography hardly plays a role in sal- 
vage of endoscopically unmanageable upper GIH 
[39-42]. On the contrary, enthusiastic interventional 
radiologists stated that every uncontrollable upper 
GIH should be an indication for arteriography and 
embolization [8, 43]. The involved disciplines seem 
to indulge in navel-gazing. As is so often the case, 
the truth lies somewhere in the middle. For lack 
of scientific evidence (no randomized prospective 
studies available), decision making should be based 



5.3.2 

Timing of Arteriography 

Rapid fall in hemoglobin (Hb) or hematocrit (He) 
blood levels, high transfusion requirements (more 
than 4 U of packed cells in 24 h) [47-49] and low 
systolic blood pressure with tachycardia [50] have 
been postulated as indicators of active bleeding. 
However, patients will be resuscitated during or 
after endoscopy and often demonstrate hemody- 
namic stabilization and/or normalization of Hb and 
He values when they arrive in the angio-suite. In 
the heat of the fight against shock, the number of 
transfused blood products may not always reflect 
the actual severity of bleeding. In an own study, 
we found a positive arteriography in 36% of GIH 
episodes with less than 4U of packed cells trans- 
fused. Moreover, 40% of these patients bled actively 
on arteriography but had no blood transfusion or 
even shock therapy [51]. In our as well as others' 
experience, the alertness of the endoscopist facing 
an intractable bleeding and the rapidity of decision 
making are crucial to catch the patient while actively 
bleeding [52]. 



Upper GI Bleeding 




Fig. 5.1. DSA of celiac trunk with a 5-F Cobra catheter. Left Fig. 5.2. DSA of the hepatic artery with a 5-F Cobra catheter, 

gastric artery ( wlnfc iTitjh), splenic artery iiUioithcadsi. G as trod uodeiia I artery: ;■, iidciiii-:: heads), r.ghi gastroepiploic 

common hepatic cillery i n/urr tjnvwIiL'iiii). gastroduodenal artery : black iinoulicaits), i iglu gastric artery ( ir/rifc .7' r ( i n.) 

artery initall v.hdc iinen 1 !. right gastroepiploic artery (small branching from the left hepatic ar;e:y, arcade r.;hi!c i;ptcii>) 

white arrowheads), left (small dire if j -.inc. right i double small connecting : ighi and ^:l gastr ic artery {black arrows) 
iiriiiir) hepatic artery 



Gastroduodenal Arteriographic Anatomy 

The gastrointestinal tract is supplied by the unpaired 
visceral arteries branching from the abdominal 
aorta: the celiac trunk (Fig. 5.1), superior and infe- 
rior mesenteric artery. 

Each segment or organ of the gastrointestinal 
tract receives its blood from different so-called 
organ specific arteries, which are interconnected by 
arcades. 

The stomach is irrigated by the gastric arteries 
(left and right), the gastroepiploic arteries (left and 
right) and the short gastric arteries (from the distal 
splenic artery) (Fig. 5.2}. 

Between the left and right gastric artery (com- 
monly branching from the left hepatic artery), 
there is a small anastomotic arcade delineating the 
small curvature. Connections between the inferior 
esophageal and cardiac left gastric branches maybe 
observed occasionally during left gastric arteriog- 
raphy or by direct injection of a lower esophageal 
branch (Fig. 5.3). 

The right gastroepiploic artery is the continu- 
ation of the gastroduodenal artery running along 
the major curvature and becoming the left gastro- 
epiploic artery when approaching the splenic hilus. 
Here one can find constant collaterals to the splenic 
artery. The fundus of the stomach is supplied by 
several short gastric arteries branching from the 
distal splenic artery. Finally, multiple connections 







> ? 




' - y J 


■ 


v\ 









Fig. 5.3. DSA with a 5-F Cobra catheter of an inferior esopha- 
geal artery (jirrpir! showing anastomoses with cardiac 
branches {arrowheads) of ihe .efl gastric artery (arrows) 



between the tributaries of the major gastric arteries 
complete the anastomosing network. 

The duodenum is supplied by the pancreaticoduo- 
denal arteries, consisting of two, sometimes three or 
more trunks bridging the gastroduodenal and superior 
mesenteric artery. One pancreaticoduodenal arcade is 
located anteriorly (mostly as a continuation of the gas- 
troduodenal artery) and one posteriorly, with multi- 
ple anastomoses between them and other pancreatic 
building a rich collateral plexus (Fig. 5.4). 



L Pefreyne 




Fig. 5.4. DSA of the gas:roc:uodenai artery with a 5-F Cobra 
catheter ( n ■ /; .7 l" iii 101; si. Anterior i bhick -jn^nliciuis] and pos- 
terior (white iifrpv--l)Lii:is) pancreaticoduodenal arcades origi- 
nating with superior and inferior common trunks. Multiple 
interconnected mur;! arteries (niiiiil bi-.ick -.n rswhciuli] build 
loops Uniall winte ■.irmwhiiiiis) between the upper and the 
lower arcade, completing :he dual duodenal supply. Superior 
mesenteric artery {black arrows) 



Diagnostic Arteriography 

In stable and cooperative patients, the diagnostic 
arteriography is performed under local anesthe- 
sia via a transfemoral access and in the classical 
Seldinger technique. Celiac trunk and the supe- 
rior mesenteric artery (SMA) are catheterized 
with preshaped single-use 4- or 5-F catheters of 
the "Cobra" or "side-winder" type. Iodinated non- 
ionic iso-osmolar contrast medium (25-35 ml at a 
rate of 4-6 ml/s} is injected by a power injector into 
the celiac trunk and SMA. In patients with renal 
insufficiency, contrast allergy or hyperthyroidism 
gadolinium chelates (MRI contrast medium) have 
been suggested as a substitute for iodinated contrast 
medium [53], but reports on its use in the visceral 
arteries are still awaited. 

The arteriograms of the celiac trunk and supe- 
rior mesenteric artery should completely map the 
gastroduodenal blood supply. Anatomical vari- 
ants should be searched for (esophageal, phrenic, 
hepatic arteries branching from the aorta, direct 
origin of the left gastric from the aorta, etc.). If all 
territories are visualized and no bleeding source 



is found, hemobilia and wirsungorrhagia are 
excluded, the investigation should be completed 
with an abdominal aortography to trace an aor- 
toduodenal fistula. Furthermore, we generally 
finish the arteriography with a repeat study of the 
most suspected region. 

Using X-ray equipment, the passage of the con- 
trast medium in the arteries, the parenchymal stain- 
ing and the portal-venous return are recorded in one 
series by successive shots. In the digital subtraction 
technique, the contrast-filled vessels are automati- 
cally subtracted from the background. At this point, 
it becomes of utmost importance that the empty 
"background" mask remains spatially matched with 
the "filled" images. Therefore, the patients are asked 
to stop breathing and not to move during the record- 
ing. Moreover, bowel gas and peristalsis should be 
anticipated by the administration of 20-40 mg of 
butylhyoscine. When the patient's condition does 
not allow co-operation, general anesthesia should 
be readily available. 

After each series, the images are examined on the 
display to look for extravasation of contrast medium 
or a pseudoaneurysm. When bowel movement is 
di.itml.iin;;, images slu'iild a.lso t>e examined in the 
non-subtraction mode. Since Nusbaum and Baum 
investigated gastrointestinal bleeding in a canine 
model, it has been generally accepted that extrava- 
sation of contrast medium becomes visible when the 
blood loss exceeds 0.5 ml/min [54-56]. 

Only the demonstration of contrast medium 
extravasation provides proof of the site of vessel 
rupture. The detection of an aneurysm provides 
strong evidence, contrary to other structural abnor- 
malities, which are potential bleeding sources. In 
Table 5.1, we have summarized the angiographic 
findings in upper GIH and correlated them with the 
most commonly involved diseases. 

GIH is often intermittent and of varying rates, 
accounting for a considerable number of negative 
angiographic studies [57]. In recent large retrospec- 
tive studies the diagnostic yield hardly exceeded 
50% [7, 8, 49, 51, 58]. If no contrast extravasation 
is detected, provocation of bleeding with intra- 
arterial or intravenous injection of vasodilators, 
heparin or even fibrinolytics has been proposed, 
albeit with inconsistent success [59-61]. Occasion- 
ally, more selective catheterization may provoke 
bleeding and visualization of contrast extravasa- 
tion (Fig. 5.5). 

Carbon dioxide has been proposed as an alter- 
native (negative) contrast medium for arteriogra- 
phy of GIH. Carbon dioxide has a very low viscos- 



Upper GI Bleeding 



Table 5.1. Angiographic findmgs and cniiicooaihologic correlatio: 



Angiographic finding 

Co lit 1.1 SI 

Aneu rysiii 



Focal/spot-like mucosal hyper 



Segmental mucosal hyper 



Neovascularisution/extramucosal 
hyperemia 



Arterial wall alterath 



Clinical correlation 

Active bleeding (> 0.5 ml/min) 

iatrogenic trauma i post-operative, post-bile duet 

inter vent i on. post- liver biopsy) 

Ace. dental trauma 

Pancreatitis (proteolysis, pseudocyst ; 

Mycotic 

Arteriitis (polyarteriitis nodosa etc.] 

Collagen tissue disorder (Ehler Danlos etc.] 

Dieulafoy lesion 

Arteriovenous malformation ano. fislua] 
Rendu -Weber- Osier (HTT) telangiectasia 

Ulcer 

Small arteriovenous malformation 
Rendu -Weber- Osier (HTT] telangiectasia 

Post-opera live (anastomotic, stomal) 

Gastroduodenitis 

Hypei tensive gastropaihv 

Tuberculosis/granuloma (sarcoidosis] 

Benign tumor (leiomyoma etc.) 

Majgnaitt tumor ; care in ■ j n -.i , lymphoma e;c.) 

Metastatic tumor (renal cell cancer etc.) 

Malignant, metastatic tumor 
Cavernous/capillary hemangioma 

Tuberculosis 

Tumor infiltration and erosion 
Proteolytic erosion (pancreatitis] 
Atheromatosis 




Fig.5.5a-c.A fo-year-old male with known live: cirrhosis and no: ta! hyp^i tension, presetting wiili ; Helena. Endoscopy re 
gastroesophageal varices Grade '.'.. bill without oieeding sligmata. ;-.!■. ■:■■! inundated duodenum did not .-How adeqttat 
a DSAof the common hepatic artery with a 5-F Cobra catheter whhoul evidence of con Ira si medium extravasatit 
eurysm. Note (he i educed liver size with ,11 lenalizati on. b Selective i :SA of the gaslroduodenal it: tery stiddenly ciemonstralrs 
exti itva sat 1011 (iinroi jica.isj, most pro? ably causae, by erosion of the main ii uitk Oinoir.i). c Control USA of the hepatic artery 
after sandwich embolization of the gaslroduodenal ai lerv with O.O.'S-in. ( ? mm diameter. 5 cm length! stainless ste^i coils 
: iirroii/iLii:/.'). tieliveiec. through the :■-:-' catheter. The ga slic-duodena I ai terv is occluded distal 10 the origin 0: (he superior pan- 
creaticoduodenal arte'y. The hepauc artery i.iwiw.v) aberrantlv originated from the superior mesenieric artery [double iin-oii'l. 
Control endoscopy conlii med d tied era I ulcer with ad it e rent ciol. No reblerciing, bin paii^itt coed of mu hi -organ failure 



ity allowing detection of much smaller amounts of 
extravasation [62]. However, the few clinical reports 
on carbon dioxide in GIH are casuistic and not con- 
vincing [63, 64]. Furthermore, the initial enthusi- 
asm was damped by the dill ion hies and side effects 
encountered with the administration of C02 into 
visceral arteries [64-66]. 



Alternatives to 

Diagnostic Catheter Arteriography 

Nuclear medicine became involved in detection 
of gastrointestinal bleeding in the late 1970s. 
Two competing imaging tracers were developed: 
Technetium (Tc-99m) sulfur colloid [67] and Tc- 
99m labeled red blood cells (RBC) [68]. Although 
Tc-99m sulfur colloid scintigraphy should detect 
bleeding rates as low as 0.05-0.1 ml/min, it is rap- 
idly cleared from the blood pool in the reticuloen- 
dothelial system (half time of 2.5-3.5 min) limiting 
its applicability to the active bleeding period. To 
prolong the level of radioactivity, in vivo labeling 
of RBC with Tc-99m was developed, with slightly 
lower bleeding detection rates of 0.2 ml/min [68, 
69]. Timing of scanning sequences is optimized 
to detect extremely rapid bleedings (immediate 
"radionuclide angiogram"), intermittent bleed- 
ings (every 30 s for 60-90 min digitally compiled 
in a "movie mode"), as well as low-grade bleedings 
(delayed scanning up to 24 h) [70]. In delayed bleed- 
ings occurring during a reduced level of radioactiv- 
ity, injection of a second dose of radio-labeled RBCs 
can be helpful [71]. 

Most of the work with Tc-99m labeled RBC scin- 
tigraphy has been carried out for detection of lower 
GIH with the rationale to avert blind bowel or 
colonic resection. However, investigators still disa- 
gree on the usefulness of radionuclide methods to 
detect and localize bowel bleeding, guide surgery or 
screen patients for arteriography [72-77]. 

Contrast-enhanced computer tomography angi- 
ography (CTA) is n i/li;illc-nj;in£ modalitv to local- 
ize contrast extravasation in acute bleeding with- 
out catheterization. In GIH, multislice CTA seems 
promising for detection of acute small and large 
bowel bleeding. A preliminary report calculated 
a CTA sensitivity of 62.5% (15 of 24 patients) for 
locating the bleeding site [78]. Moreover, in 41.7% of 
the cases, CTA disclosed the nature of the bleeding 
lesion [78]. In upper GIH, detection of the bleeding 
by enhanced CT scan might be less relevant, but is 
nevertheless possible (Fig. 5.6a,b). 



Fig.5.6a-n.A43-year-cki nun scflVriiiga svncopeand melena. 
He had taken a X'-AiP tor .i lice- like ma I. use I day previously. 
Endoscopy showed a spurting artery adjacent to die papilla. 
Two attempts at i a i eel ion and sclerotherapy were unsuccessful, 
a Enhanced CT scan showed extravasal ion ihhick arrow) at D2, 
without identifiable cause. Anterior i iWi/rv arro.'. ) and poste- 
rior pancreaticoduodenal arcade i ir/i/re iitron-hoad) are indi- 
cated, b Emergency PSA of: he superior mesenteric artery (5-F 
Cobra catheter) confirms exlravasation at P2 i.arro^lioads). 
Although anterior (double arro'.v) and posterior {arrow) pan- 
creatoduodenal arcades are fully visualized, the bleeding 
artery can not be different lated. Noie ilow reversal in the gas- 
troduodenal artery because of celiac "a urn-, stenosis, c Selective 
PEA of the common origin >A the inferior pancreaticoduode- 
nal arteries: contrast rxtravasates ■:,nioir/iC;i,7) from a mural 
artery I ana ir) branching from die anterior pancreaticoduode- 
nal arcade (double arrow: ,\\ the transition from the lower to 
the upper course, d Sapers elective I )SA of the mural branch 
at its origin with a 2.7-1- micro catheter, con firming rupture of 
as distal segment [arrowheads'. However, the bleeding vessel 
can not be followed ot\e to ref exive bowel contractions, e After 
a 5-min wait, bowel movements ceaseol and the course of the 
mural artery becc'ines visible agaia. Tip o: the microoatheter 
(arrow) and extravasation 'arrowheads). I Control PSA after 
miection of 3.2 ml o\ PVA 1 ."0-2.-0 u. shows occlusion of the 
cast a I segment. Clue was noi a good opt. on as lite supplied area 
is too large. P la I i mini microcoils wou.d occlude too proximally 
id lowing distal collaieralizanon. !- in ally, a more distal catheter- 
ization of this small ami tortcous branch was not attempted 
to avoid vasospasm and less of free flow, g Control DSA of 
the common inferior pancreaucodiiodenal trunk reveals per- 
sisting contrast extravasation iijnvat heads), probably from a 
mural branch of the posterior pancreaticoduodenal arcade 
(arrow). Anterior arcade [double ariv.v). h iiSA of the celiac 
trunk with a 5-E Simmons-1 catheter shews contrast dilution 
in the common hepatic artery ; anoirsi due to flow reversal in 
the gastroduodenal artery. The 2.7-E m i croc a theter was intro- 
duced into the gust re-duodenal artery and all side-branches 
were "blindly" investigated until the one with a distal rupture 
was found. If we had keci the catheter in the mesenteric artery 
and had performed a contralatera. puncture and catheteriza- 
tion of the celiac trunk, microcatrieterizatioa. guidance would 
have bren easier, i Tip of lite at. c re c.i die I rr :. auail arro n ) posi- 
tioned in front of the rupture site i anoiri: contrast medium 
escapes immediately into the duodenal lumen [arroulieads). 
An ultimate site-branch of the ruptured mural artery is indi- 
cated [small [nil.:: head). Embolization was performed with 
0.6 ml of 1/3 diluted glue (Gluebran2/lipiodol). j Control DSA 
of the superior mesenteric artery no longer demonstrates con- 
trast extravasation. Most of the polymerized glue is located in 
the bowel lumen, adherenl to the duodenal wall iarroulieads). 
During embolization visibility was blurred due to piling up 
of the extravasated glue in the duodenal lumen, accounting 
for the unusualiv large amount required to stop the bleed- 
ing, k Duodenosce-py immediately after eaioo.izatioa reveals 
clean and blood free duodenum with adherent glue pellet 
(iirroiWii'iTifs). I Endoscopic view of ["'2 after intensive flush- 
ing and washing shows a craternorm mucosal lesion (anvrivs) 
with a shape similar to that of the extravasated contrast depot 
in (aj. The glue plug was hosr.:. ami was.iec awav ■■-.lido 
arrowheads), m Pigilal iiv..:ge posi endoscopy confirms dial 
the glue (arrowheads) was dislodged from the bleeding wall 
defect ( land marked by t!ir arterial ekie cast, small arrows) and 
moved downwards ait;: the duodenum, n Retrospectively, one 
single PSA sequence already revealed tiiat lite a.eeding (luee 
arrow) was located on a mural loop connecting both embol- P* 



Upper GI Bleeding 




opacified uii'ir-wiiciiiti), the posterior mural artery 
ismiill line i; si is faintly visible due to backrlow in 
the posterior paiicieaticoduocena. arcade iiloid'lc 
■.iitpvli-jii-.is). No i ee'eed ing. !-Ji, ".csc op ic com:'.-, 
the next day and I week la:er showed uneventful 

ig of the mucosa! erosion. Com me: 1 .;: In 
of the patient's young age. n on -compromised ciini- 
cal status and the technical diiiKT.ities encountered 
during embolization, surgical salvage would have 
been a reasonable al;e: native, i Endoscopic images 
courtesy by Prof, i ■<:. Isabelle Colie. gastroenlerolo- 
gist at the Ghent University Hospital i 



Therapeutic Arteriography 

There are several ways to stop gastrointestinal 
bleeding by catheter intervention: infusion of vaso- 
constrictive drugs (vasopressin), embolization and 
intentional induction of vasospasm. 

Vasoconstriction mid local vasospasm are physi- 
ological defenses against exsanguinations. When 
the bleeding has ceased and no extravasation is vis- 
ible, focal vasospasm at arteriography sometimes 
indicates the bleeding site. 

Therapeutic vasopressin infusion into the main 
arterial trunks induces visceral vasospasm, enhanc- 
ing the physiological vasoconstrictive reaction 
against bleeding. Initial enthusiasm about vaso- 
pressin infusion ebbed away because of less favora- 
ble results compared to embolization [79-81], and 
the systemic side effects [82]. Vasopressin infusion 
has been shown more effective in lower than in 
upper GIH. 

Proximal vasospasm induced by manipulations 
of the diagnostic catheter in the main branches or 
arcades was a major problem in the early days of 
visceral catheterization [83]. Modern diagnostic 
catheters have smaller diameters (4-5 F compared 
to the older 6-7 F) and softer tips. Proximal cath- 
eter induced vasospasm is less frequently encoun- 
tered. In contrast, distill vasospasm often occurs 
during superselective catheterization due to micro- 
guidewire manipulations. Iatrogenic vasospasm 
is irritating as it may once and for all preclude 
entering of the spurting artery [6, 84, 85]. Because 
iatrogenic vasospasm frequently results in instant 
bleeding arrest, some have induced it intentionally 
to stop extravasation in lower GIH [86]. Although 
preliminary results are promising (93% of bleed- 
ing stopped), the durability of this haemostatic act 
should be confirmed in other studies, also dealing 
with upper GIH. Nevertheless, we should be less 
alarmed when iatrogenic vasospasm of the previ- 
ously bleeding artery limits further catheterization. 

Embolization goes beyond vasospasm and aims 
at definitive occlusion of the bleeding artery. 



Embolization 

Superselective embolization is the endovascular 
analogue to surgical vessel clipping. The technical 
success of embolization is determined by the ability 



of superselective vessel catheterizatio 
of appropriate embolic agents. 



5.8.1 

General Technical Aspects 

All efforts should be made to obtain assessable arte- 
riographic images of the upper GI tract. In hemody- 
namically unstable patients or in patients who are 
unable to cooperate, tracheal intubation and general 
anesthesia are mandatory. At our institution, the 
angiography protocol for acute bleeding includes a 
request for anesthesiologies! assistance. 

The primary goal of arteriography is to locate the 
bleeding site. Revealing the nature of the bleeding 
lesionwillbemoredittii.il It md, in planning emboli- 
zation, is of subordinate importance. Arteriographic 
results might be subdivided into three categories: (1) 
normal findings, (2) contrast medium extravasation 
proving active bleeding and (3) structural arterial 
abnormalities. In each of these situations, the tech- 
nique of embolization will differ. 

If no abnormalities are detected, one should con- 
sider blind [48] or so-called "prophylactic" [87] or 
"empiric"[49] embolization of the left gastric or gas- 
troduodenal artery (Table 5.2). Blind embolization 
was first applied with poor success by Reuter et al. 
in 1975 [2], reinvigorated by Lang et al. in 1992 [87], 
criticized by Dempsey etal. in 1999 [48] and recently 
highly advocated in larger retrospective studies by 
Ania et al. [7] and Schenker et al. [8]. Blind embol- 
ization is tempting because of its technical simplic- 
ity and safety (see 5.8.2.3 Gelfoam embolization). 
However, one should keep in mind that effectiveness 
of blind embolization has not been proved against a 
control group. In view of the considerable number of 
spontaneous bleeding arrests that may occur after 
non-therapeutic artenographv [?1], the outcome of 
such a comparative study might be quite unpredict- 
able. In daily practice however, '.ve agree with Lang 
et al. to recommend deliberate use of blind emboli- 
zation only when there is definite prior identifica- 
tion of a lesion in the vascular territory [87]. 

If contrast medium ext i 'avas.ition is demonstrated, 
the location on the arterial tree determines the tech- 
nique of embolization (Table 5.2}. If blood spurts 
from a main artery such as the gastroduodenal, then 
embolic hemostasis should be performed at the site 
of rupture to be effective and safe. If the bleeding 
point cannot be reached, embolization by injection of 
Gelfoam "from a distance" might be safe yet uncer- 
tain as the bleeding might stop only temporarily. 



Upper GI Bleeding 

Table 5.2. Contra si ex^rava^ation/aneurys::'. in upper C-IH: lech.aio.ie o: embolization according tc 



sandwich embolization - 
(coils) (Figs. 5.5 and 5.9) 



coil embolization and . 
rogr.ide cathet 



cello-am embolization - 

injection, to provoke 

.i^ospasm or to call for 

ree nd oscop y/s u rgery 




sandwich r:v.oo.^a:i'::'. 
(platinum microcoils) 
(Fig. 5.11) 

embolization and retrograde 
catheterization (Figs. 5.6, 5.10) 

glue embolization 

(or particulates) 
(Figs. 5.12, 5.14, 5.15) 



if bleeding point is close to 
main artery consider sandwich 
technique coiling (Fig. 5.1 1 ) 



Glue embolization of major arteries is very effective 
but contains a high risk of ischemic complications. 
Thus if, in major artery rupture, the bleeding point is 
beyond the range of catheterization, alert the gastro- 
enterologist to get a control endoscopy or, even wiser, 
get a surgeon for a definitive salvage. 

If the bleeding is located on a mural artery or its 
tributaries, then we have more options (Table 5.2). 
The mucosal area supplied by a mural artery is 
delimited. Branches from adjacent mural arteries 
contribute to a more or less extended dual supply. 
Therefore, ischemic complications after emboliza- 
tion in the mural tree are assessable. Flow directed 
remote inject ion of particulates or even glue is a valid 
technique if the rupture site cannot be reached. 

Any aneurysm detected on the arterial tributar- 
ies located in the bleeding area should be considered 
as a pseudoaneurysm and therefore treated as a con- 
trast medium extravasation. 

If structural abnormalities such as vascular 
malformations, hvpei vascular tumors, vessel wall 
irregularities suggesting erosion etc., are visualized, 
then we may try for a palliative embolization with 
Gelfoam or particulates. Rarely, curative emboliza- 
tion of an arteriovenous malformation or fistula is 
achievable with non- re sorb able agents, such as glue 
or detachable balloons. 



5.8.2 

Specific Technical Aspects 

Embolic agents can cause permanent or tempo- 
rary occlusion. According to their behavior in the 
bloodstream, embolic agents maybe categorized as 
mechanically either proximally or distally occlusive 
and distally flow-dependent occlusive. In case of 
a (pseudo-)aneurysm, endosaccular embolization 
might be an option, similar to coiling of intracranial 
aneurysms (Table 5.3). 

Properties of the microcatheters and micro- 
guidewires we use are listed in Table 5.4. Most com- 
panies offer adequate coaxial systems. We do not 
adhere to specific brands and have used all kinds 
ot microcaiheters and microti] ide'.vi res over the 



II vasospasm due to nikrocatheter mauiptila- 
patience is required; eventually w ith- 
manipu- 



draw the catheter a little. Sup. 
lations often irritate the bowi 



ill, which thei 
iring the vessel course. Intravenous 
butylhyoscine may reduce wall reactivity, but even 
better is taking a rest and the opportunity to study 
the arteriogram, while flushing the microcatheter 
(Fig. 5.6d,e). 



Table 5.3. Embolic agents, 



i:id applicability in upper GIH 



Embolic agents/ 




Mechanical 


Mechanical 


Flow dependent 


Endo- 


Apol.c- ."'i.irc 


e:::bolisaiion Tc-jh moii-e 




ivoxnr.al 


distal 


distal 


saccula: 


in upper 






: :■ c l: 1 u s i c- :i" ' 


occlusion 3 


occlusion" 


occasion 


GIH 


Particles 














Non -calibrated PVA 




_ 


+ 


++ 


_ 


Yes 


Calibrated PVA or gelatin 


spheres 


" 


" 


+++ 


" 


f 


Gelatin sponge 














Plugs (> 2mm) 




++ 


+ 


+ 


- 


Yes 


Powder 




" 


+ 


+++ 


" 


(Yes) 


Coils 














Macrocoils (0.035-0.038 ii 


ich) 


+++ 


+ 


- 


++ 


yes 


Microcoils (0.013 inch) 




- 


+++ 


+ 


-M- 


Yes 


Detachable microcoils 




++ 


+++ 


- 


4-++ 


1 


Liji.iiils 














N-butvl 2- cvanoacrvbte 




- 


+ 


++ 


+ 


Yes 


Et;'.vlene polvvinvi alcohc 


1 


- 


+ 


++ 


-M- 


r 


Ethanol/polidocanol 




- 


- 


+++ 


" 


No 



' "':■■. -.v :. ■::... — !-■ ■ !-" .:■-.' 
""Flow dependent" 
-, Not applicable; - 



:o the point ■.■: clr-iv-iy. 
i- ihj e j i i b ■."■■ ] i c" agcm w.ll be carried bv -he bL:'.-ds:ie:iin k 
aoi typical to very characteristic ad ion; :. no exiviier.c 



e from Ihe catheter rip. 



5.8.2.1 

Particulate Embolization 

Particulate embolization is an option when contrast 
extravasates and the bleeding branch is beyond the 
reach of superselective catheterization (Fig. 5.7). 
Non- calibrated polyvinyl alcohol particles (PVA) in 
sizes of 150-250 u to 250-350 u. or even larger should 
be used. The amount of particles should be kept as 
low as possible to avoid ditluse distal embolization. 
After each injection of 0.1-0.2 ml (up to a maximum 
of 1 ml) of a dilution of PVA, control arteriogra- 
phy should verify that the bleeding point has been 



occluded. If extravasation is no longer visible, injec- 
tion should be stopped and occlusion confirmed 
after 10-15 min (Fig. 5.6f). 

Bleeding from hypervascular tumors, such as 
duodenal metastasis of renal cell carcinoma, can 
be stopped by palliative particulate embolization 
(Fig. 5.8), although other authors preferred Gelfoam 
[88, 89]. 

• Mechanism of action; flow-directed distal 
embolization, shunting of particles to the point 
of least resistance (rupture site), cluttering and 
plug formation of particles (no deep penetra- 



Table 5.4. Cookbook 


: Properties of catheters and guid 


Bwires used in upper GIH embolization 






Configuration 


Caliber 
(French/inch) 


Length 

(cm) 


Hydrophilic 
coating 


Radiopacity 


Sheath 


Straight 


4-5 


10 






Catheter 


Cobra I/sidewinder I or II" 


4-5 


60-1 00 h 


Optional 


Distal part 


Guidewire 


J-tip 


0.035 


150-170 


Yes 


Yes 


Micro catheter 


Straight (steam shapeable) 


2.4-3.0= 


130-150 


Yes 


Tip marker 


Microguidewire 


J-tip ^"-gO") or straight if 


0.01 4-0.02 l d 


150-180 


Yes 


Yes 



a For a transbrachial approach, also consider a vertebral or he 
° For transbrachial approach. 

e Only in rare occasions ive resorted to s mailer French-size mi 
■' Some companies offe: ir.ico 'Cathetei-nucrogiiidewire sets. 



rely use guiding caterers. 



Upper GI Bleeding 




Fig.?. 7a -i. A 52 -year -old man with hcip.atemrsis aftet j suicide a tieir.pt will" i'0 no jive lluicl. C:'. gastrosccpy no visualization ot' 
a [c-sion due to massive bleeding, a Celiac trt:nk l"'5A demonstrating contra si medium exiravasation 1 iWi.tp iifiyiri from a distal 
branch of the lef; gastric artery iiinciii7);'i?;/ri. Nole the cotirsr of the right gastric artery pranchnrg off :he left hepatic at tery 
i ir/iift' iiiii.'; iic .hi), b S elective Pi A of the letl gastric artei y with a 2.7- r microcatheter \,u * ■:■■.: i;c;iit): route to the rup trued artery 
; i/.wiWe .-im: n i too tortuous fo: supciseleciive catheter izariop.. Proximal coil emb- 'lization would obviously allow inflow via the 
collateral arcace to the right gasn ic artery (small iIptou). Therefore, flow d tree tec! embolization with small amounts 10.5 ml) o( 
l-VA particles { I 50-250 l; i was pei formed, c Post-emb' 'ligation I' 1 tSA sh- 'W'iirg distal occlusion of the b. ceding artei v : ititoii) and 
a c. a ceiit mural arteries. Reverse liow into the tighi gasti jc artery ■: : ,r lon'ti^iJ-i. No rebleec.mg uniil 2 weelss I a lei ■ 'Ozmg from a 
smalt ulcer at the same location was easilv treated by sclerotherapy. The paliem died S mo:'.: lis later of a gastrii 




Fig. 5 .tin d. :■: "■'■■■■-.. ■ .d .v. -.I.:, w I: ■■ . :.c-\ Writl ■ .e:f pirp.t: tC !■ ■ill 1 ." :>: i riiti. cell cancer I ye-.i i previously n >w prese:r:s with 
melena from bleeding d ;i ■:■■.! e j- ,i I metastases, a I ';>A of I he o ■in in ■.: ■ : : hepatic artery showing hvpeivasculai tumoi bf.ish iitironj) 
.n lite cur dent:: p. sr: coiiec bv hyper rrophied duocenal bra itches ■.::' tne gastroc.r.odep.a! at tei y. b,t Stipe [selective v:st:a!izair 'it of 
two diffeivitt tumor compartments [arrows) with a 2.7 -F microcatheter [aire-:; iiidiis). d Control i :SA afler inieoiion of several 
miililitres oi PVA I 50-250 u and 250-255 li in four tumor leedei s itwo o'i them shown here;, confrrmip.g uimor devasculai iza- 
tion. After each injection of 0.5-1 ml of PVA. superseleciive I ' SA was performed to control flow arrest and prevent reflux of 
particulates. Patient stopped bleecntg fir aboul 7 monihs and was then retreated 



» Major disadvantages: proximal occlusion due to 
cluttering of particles may leave major collaterals 
and distal circulation patent. Late recanalization 
after PVA embolization is described but is not a 
matter of concern in acute GIH. 

» Adverse effects: low risk of ischemic complica- 
tions when the guidelines for size and injected 
volume of particles are respected. 



» Future perspectives: calibrated particles of pol- 
yvinyl alcohol or gelatin penetrate deeper into 
the vascular system due to lower viscosity. Risk 
of ischemia is probably higher, but no clinical 
experience reported. Palliative tumor emboliza- 
tion might be more efficient with calibrated par- 
ticles, in analogy with uterine fibroid emboliza- 



5.8.2.2 

Coil Embolization 

Large-caliber stainless steel or so-called Gianturco 
coils are coated with strands of Dacron. They are 
compatible with most 4- to 5-F diagnostic catheters 
(0.035 or 0.038 inner diameter). They are used to 
embolize in large size arteries (left gastric, gastrodu- 
odenal or hepatic arteries) (Fig. 5.5) [90]. Under 
favorable anatomical conditions, a small bleeding 
branch of the pancreaticoduodenal arcade can be 



entered with a diagnostic 5-F catheter and eventu- 
ally occluded by a small (1-2 mm) stainless steel 

Platinum microcoils have a core of 0.018 in. and are 
compatible with 2.7- to 3.0-F microcatheters. Differ- 
ent manufacturers provide coils in different shapes 
(straight, helical, complex, crescent, omega etc.) and 
lengths (1 to several cm). Ideally, the ruptured vessel 
segment should be endovascularly "ligated" by plac- 
ing microcoils on each side of the rupture point, 
averting retrograde collateralization (Fig. 5.9). 




Upper GI Bleeding 



To perform this so-called sandwich technique, 
the bleeding point must be crossed, which in small 
mural arteries might be difficult if not impossible. 
In such cases, direct proximal occlusion might also 
work (Fig. 5.10). Microcoils are pushed into and out 
of the microcatheter by a flexible guidewire with a 
stiff and flattened tip ("coil pusher"). Alternatively, 
short, straight micro toils can be pushed and ejected 
by contrast medium injection. With this latter tech- 
nique, one can try to "shoot" the coils more distally 
in the bleeding artery (Fig. 5.10). Moreover, always 
check that all pancreaticoduodenal arcades are 
visualized to exclude dual supply of the ruptured 
segment. Eventually, sandwich embolization can 
be accomplished by approaching from both sides 
<Fig.5.6 E ). 

If, due to small caliber or tortuosity, the mural 
artery cannot be catheterized, sandwich technique 
occlusion of the main artery might be a solution 
(Fig. 5.11), provided the bleeding point is very near 
to the branching point and no collaterals are visible. 
However, even if angiographically not apparent, the 
distal tract of the ruptured artery will be patent in 
many cases, allowing collateral retrograde re-per- 
fusion. If embolization has not occluded poten- 
tial anastomoses, early post-embolization endos- 
copy to ensure sustained hemostasis is mandatory 
(Fig. 5.11). 

For treatment of upper GIH, stainless steel coils 
and platinum microcoils were found to be more 
effective if combined with Gelfoam or PVA [7, 87]. 

In lower GIH, platinum microcoils placed in or 
near to the bleeding artery have served as a land- 
mark for surgical exploration. In upper GIH, there 
is little indication of such guidance, as gastroduode- 
nal anatomy does not present particular difficulties 
dining laparotomy. 

Microcoils can be used to protect the distal cir- 
culation by blocking and reversing the bloodstream 
when flow-directed particulate or glue embolization 
is considered (Fig. 5.12). 



> Mechanism of action: local mechanical obstruc- 
tion of blood flow and promotion of thrombus 
formation (Dacron strands). 

■ Major disadvantage: Flow may be restored if coil 
embolus is loose (thrombus organization} or 
patient has a coagulation disorder (tailing throm- 
bus formation). Therefore, coil embolus should be 
as compact as possible by filling up the dead space 
between the large diameter coils with smaller 
ones. Angiographic flow arrest is no guarantee 
that occlusion will be permanent. 

■ Adverse elfecfs/complicafions: Coils delivered at 
the rupture site may perforate the vessel wall (or 
pseudo-wall in case of an aneurysm) and aggra- 
vate the bleeding. Coil placement may also pro- 
voke or increase vasospasm. 

• Future perspectives: Detachable coils can be 
repositioned until a focal and compact mechani- 
cal obstruction is achieved. Detachable coils may 
be covered with small Dacron strands to pro- 
mote thrombus formation or with an expanding 
hydrogel to minimize dead space between the 
coil loops. Although dedicated detachable coils 
are available for intracranial aneurysm emboli- 
zation, the high cost of these coils precludes its 
routine use in non-neurointerventional indica- 



5.8.2.3 

Gelfoam Embolization 

Introduced as early as 1975, surgical gelatin or Gel- 
foam is still widely used for embolization of upper 
GIH because of its availability and easy handling 
combined with quick and so-called safe occlusion 
[2, 91]. Gelfoam is an absorbable non-radiopaque 
non-permanent embolic agent consisting of dry 
gelatin. Control angiogram performed several days 
to weeks after embolization will demonstrate reca- 
nalization of the occluded trunk [92]. Practically, 



Fig.55a-f. A 04 ■ iv.o ■ ■ .-.: [.'.ceo.; widi liemaleniesis. Ga ;l:oscopic fieco-sia-as of bleeoiag ocibo./aiodenal n leer toiled as wel. 
a~ enie:gencv ■air^riv. keo.eeding afier 4 days wirli shoe!-*, a-e Coalmen hepolic PSA sao-ws vasospastic sasrroduocena! orrery 
I/iU'jJl" linen 1 ! brondiiiig from die r.gii: hepoi:c arrerv [mult in-iHr.:. Contrast in ed; lira exaavasalion from die disail diird of 
die a j si rod nod en a I artery hecoaaes slowly vis:ble dinau /icii/si. d because of die vasospasm I lie op: ion was [.:■ o.ith.elej :ztr die 
gasrroduoaenai orlery with a 2.7-F nicrocatheter [jsitili ijnvvs) instead of w:th the ?-!- diagnosis Colt.i catheter (iin-flirl. 
Raptare of die main vessel is demoa.sa'aled [iiir;.-. i;,:,:i<i). e Aloer plugging tee ga:a:od::ode::ol artery wi;]i several platinum 
aiicrocoils iiirri;: s) in sandwich :ec !inique : die extravasanon siops. f Control '. is A of riie super. or a: es enteric ai ie:y excludes 
:v:rogrode coba:eraazauon of die gastroduoo.enal ar:e:y, which :s oconidec. [iii :■:■:: sj. Siiadow o: coils is risible din-aii'/icii/sl. 
^ersisiea: shock wit; - . :eo I ceding Icon: gastr.c lesion 5 -r,ys .a:er, ueoieo agaai w.lc .e:l gasiric artery emholizal :on. f'oueiii d;ed 
in septic shock 7 days later 





Fig.5.10a-g. A 67-ivji-old male live: t:anso2;nl recipient Willi ntrlena and hemato- 
chezia.Threed'.iodeit:;! ulcer:;! ions are k:'cw : :t rrcm prevj. .us endc'SCO'pv. Lower gastroin- 
testinal bleeding w : as susoected. kuieiv. was lefeired i:: emergency wiihoul colonos- 
copy 01' giisiroduodirnoscopv. a I oA ■ o' iJie supeiiei mesenteric .ulery showing contrast 
medium extravasation i'iir.';'ii7vci7;fs) but without clear difrVrenliauon between colonic 
and tiuodenai bleeding. l> Selective PSA of the intei ior pancreaticoduodenal artery 
( : r r .■ : ■ 1 1 : suggests bleecing from a dtiodcital mural artery l -Jottih: iinoni. ExtravasLtiion 
iiifiviirfioi'ijj). c Sr.perse lee live no:'-st:blr.:cteo I is A of the anterior pancreaticodtioden.tl 
a sonde uimiii/s) with a 2.7- r microca Iheter ; uliit-: .ino-. h,:.:i:i>j: bleeding {at ivi; hcinis) 
from a mural biaitcn i ut'/irc ■ r ■ .■ l 1 i i ■ s :■ of the licd/ont.;! diu idriu! segment: Note the dis- 
crepancy between '.lit supersede live oioluie and the ovei views: lite cotirse of the artery 
might have been altered bv petiStLtlsisoi lite htiliajv suspect mural artery is not involved. 
H| dDSA of the bleeding mura! arterv demcnstiatiiigexiiav.istiiioii i.irrouiiead) and intra- 
H mural (arrows) contrast medium due to the wedged catheter position, e Three straight 
^J platinum microccols (2 mm by 10 mm: ■: I. 'tig .it to-.-, si were pkicec bv injection, f Control 
^ DSA in non-subtracted reco:' struct ion: cittern bleeding mur.il a: lery {arrowheads) with 
' distal stop caused by the platinum micro coils uinow:). g Control PSA of the pancrea- 
ticoduodenal trunk: contrast extravasation :s no longer observed. 'Coils (arrowheads). 
Control duodenoscO'pv the next day: no bleeding in I '3, no lesion observed 



Gelfoam fragments, cubes, plugs or pledgets are 
manually cut to stripes of variable sizes from flat 
blocks of branded surgical sponge. These "torpe- 
does" are back-loaded into a 1- or 2-ml syringe after 
removing the plunger. A small amount of contrast 
medium is sucked in just to soak the torpedo for 
radio-opacity [3]. The pledget is then injected into 
the 4- to5-F diagnostic catheter. Other investigators 



prefer the dry method of loading and lancing the 
Gelfoam torpedo [93]. Under fluoroscopic control, 
the Gelfoam pledget is expelled by force into the 
target vessel. The first pledget will be drawn into the 
main trunk and stuck at the point of vessel tapering 
or at the first bifurcation. The next torpedoes will 
pile up proximally to the first one. The pledgets 
should be sized according to the diameter of the 



Upper GI Bleeding 




Fig. 5.1 I ii -'I. A .ic-vear-olo rem ..lie iimierwent terminal :leo:=:i:--:"y for bowel com plica I ions arler laser llienipy for endomeiriosis. 
- : osi opera live bleeding froin gr-.slr. ■; tr.oe and fal. .11 hematocrit. il.as.:roscopy revea.e;i large organized clot at die major car- 
viiture. a Contrast meoiur.'. extri'.vas.dion iunvwlii-.iii) on celiac :nink !>SA. Let: gasaric artery f iu _ r\i n- }; splenic artery [J^iti-li 
iirrrtir). b USA of [he let"; ga?: lie artery: extravasation ■: irwir/.'L'iiifj! from a dny s id e-Li ranch near its origin unroii). ttv -.ipted 
for .'. sandwich embolization of Hie T.am vessel. c Superseded ive calheler.zauon with, a 1.7 -V microc:idie:er of rhe in an; irnery, 
oosil loning rhe lip liin-ovltdhii distallv :o the origin or' die nipt.: re bra noli :. .inoirl. d Pos:-e:"r'.bolizauo:i PSA shows plai.iiv.im 
niicrocoils dr-nuii 1 .' i pi'oxi cm I ly ail;: distallv from the bleeding oomt. preventing backtiow liii'i'na-liciiiis) j\~\*i potenlial reper- 
fvision. No retrograde opacification of the tiny r'aplured arrerv was observed. Conli'X gastrosc.opv ai d.'.y I po stem hoiizai ion: 
coherent do:; at day 2 arterial oozing treated with adrenaline iniecrion and b.pola: coagnlat-on with permanent hem os ".a sis. 
Progressive re nog race col lateralization of the 11 leer artery was the .ikr.v cause. Nowadavs, we wou'd have injected .; droplet of 
glue (or PVA) after p.acing the disra. cods, occ hading I he tiny side branch as well 



vessel to occlude. Usually, to occlude the main trunk 
of the left gastric artery three or four torpedoes of 
2-3 mm by 1-2 cm are sufficient. After each injec- 
tion, a control angiogram should verily that flow 
has stopped (Fig. 5.13). Applied in this way, Gelfoam 
remains very appropriate for proximal occlusion of 
the left gastric artery and gastroduodenal artery if 
no contrast extravasation is visible [87, 92]. Until 
the plug is resorbed, blood pressure distally will 
be lowered, enabling clots to be formed and organ- 
ized. Moreover, if bleeding recurs, a possible con- 



trast medium extravasation in the same territory 
might still be suitable for embolization, since the 
main trunk might be opened again [92]. 

• Mechanism ot action: mechanical proximal occlu- 
sion with thrombus formation. 

• Major disadvantage: Flow will be restored within 
days or weeks after resorption of the gelatin and 
organization of the clot. 

• Adverse effects/complications: Overly small gel- 
atin pledgets may cause diffuse distal emboliza- 
tion and subsequently ischemia. For the same 




a-f.A 58-year-old female live: r jli :"Lfp Llt jii recipient with massive uppei GIH. Ai ieiial Needing from preantral ulcer with 

attempt of endoscopic ."lipping, a PSA ol' celiac trunk confirming tontr-.isl medi'.im e\;ravasat:on L.nioi\ , h:'j..li from a side- 
bra nch '.:' Ike : ign: ga ; I roes.. •..:■.■: ar.ery ioi ;■: ■!■> i. I 'onor hep-rue ,11 terv : ■.!■:■ u tic iIitonj shows ii'.irafiep.itic veal, nregclai iiies. 
I 'isloca;ed heinockp from previous endoscopic intervention ; :■, hitc iinou). b Non- subtracted I 'SA demonstrates extravasation 
i,i 1 IV- 1! !ic..i,h) and potential collateral; 10 Ike 1 uplured branch : iir loirs), t Non-subt:ac;ed I ' 5A skow : ing exiiavjsation iiin-flir- 
lici-.l). As Ike an;ra; ranch (jitcui) might he too small for su perse lee l;ve calkelei izati on. we first performed a coil block of 
ike g-.isi:'. -epiploic artery i-.lonbh: inrcni ) distal to ike brand) ((tJicn j. Hilker a particulate embolization from the main artery 
or gJiic- iniection was then considered, d Non-subtracted PSA.: die bleeding branch is emereo over a few millimeters witk ihe 
J.7-F microcatheter iilcublc. iinoiri ano vasospasm (■■.i"on , hcti..li has developed. No further catkelerizalion possible. VvWge 
a:":g. g: jpky deiv.o 11st rates collaterals I iinvirs). e No n-subtrac tec. image of glue cast : iiitousi after injection of a 1 ::■ diluted 
Glt;ehraii2.'i_ipiodol 'Jr mixr.ire. f Non- subtracted 1 ' ' : A shows d ^vascular! zed antral aiva i-.v lOH'iicad; 1. Also visible is a small 
llnor.bus [double tin <■■■--■ i) due to reflux of glue into ike epiploic ai leiy f : e r ivithdi awing Ike microcatheter. Flow in Ike epiploic 
artery distally to the safety coils is reversed I black arrows) 




Fia.r.i .iii.1). A ?'. -vear-o!d male willi iiernntemesis .iiiJ iiem.: ■rrliaeic : : h.. :■:!■.. 3 torn ;'.■.":'. fided with fresh olood blurring die endc- 
s-".:-pic view. <i ?-F Cobr.i o^t'ietej' in the let: gastric artery ; !iwirsi: i' ! SA reveals .1 hypervasanar e.: moral lesion iij.'reii'/rciiis; 
m die fundus, b Control DSA .iiiJ noii-subrr.'.cted image after imection ::if four so-T.ewhat unoersized Gelfoam torpeooes 
f svisikeo iv i ill conm! st medium. i^f:'ii /.■ L - .■ j : / > :■ co 11 lirrr. ins occlusion 0: die 111:11:1 trum-. of the >tl gasrnc and die maior t mil or 
artery. Tumor blush ls no longer visible. An alter mi live bin in ore elaborate op I ion was sr.oe is elective paructdaie embolization 
of the tumor. We c noose a oroyimal Gelfoam rmfo-.izatioii to avoid any risk of iscitemia and necausr surgery was p. aimed afirr 
patient's stabilization, f'alieni did ::oi re'raieed bin unfortunately J.ed troni mudi-organ failure 



Gelfoam particles o 
• Future perspecth 



product innovation in this field 



idvise the use of scraped 
Gelfoam powder for blind 



5.8.2.4 

Glue Embolization 

The tissue adhesive N-butyl 2-cyanoacrylate or glue 
(Histoacryl) is a fast and efficient 110 n- re sorb able, 
non-radiopaque embolic material, based on polym- 
erization ofthe acrylate monomer. Special skill and 
experience are required to assess the proper dilution 
of N-butyl cyanoacrylate in lipiodol (Lipiodol-UF, 
Guerbet, oily contrast medium) to control vascular 
penetration and avoid ischemia. Therefore, it is not 
surprising that reporting on the use of glue in the 
gastrointestinal tract is scarce [4, 94]. Glueing ofthe 
microcatheter, once a classical problem, is no longer 
an issue due to its hydrophilic coating. Glue might 
be used for flow-directed permanent distal emboli- 
zation in extravasation or pseudo-aneurysms that 
are out of range for a sandwich technique occlusion 
(Fig. 5.14). 

Massive bleeding from duodenal ulcers might 
be treated with glue embolization ofthe gastrodu- 



odenal artery or muscular/mural branches, as 
suggested by Lang [94]. However, this technique 
entailed an increased risk for acute bowel infarction 
and chronic stenotic complications [94]. If the bleed- 
ing artery can be catheterized to the point of rup- 
ture (and eventually beyond into the bowel lumen), 
slow deposition of highly concentrated glue might 
be safe [95]. However, in such cases, glue might 
escape immediately into the bowel lumen blurring 
the view on the arterial site (Fig. 5.6i,j). If possible, 
the catheter tip should be wedged proximally from 
the bleeding point to achieve excellent control of the 
glue penetration. This technique can be particularly 
useful in upper GIH bleeding to achieve occlusion of 
the bleeding vessel and the connection points with 
the collaterals (Figs. 5.12 and 5.15). 

Arterial devasai la nz.itioti of n small area (usually 
less than 1 cm2) is well tolerated in the stomach and 
duodenum due to the rich dual collateral supply and 
healing capacities ofthe mucosa. Ischemic effects of 
penetration or reflux of glue might be anticipated 
by placement of protective microcoils (Fig. 5.12) [95, 
96]. 

• Mechanism of action: Rapid polymerization after 
contact with ions in blood to create an elastic and 
adherent plug. 

• Major disadvantages: Control of time and place of 
polymerization depends on many factors such as 




I : ig.:".]-!a -ii. A i>S - ye .1 1 -■. ■ Id male wit:: massive Neec.i:'g from duodenal Pet;e: drain -.ir.e: ,1 uiiiiphcj.tnl gastrectomy for ,y<- 
plastic LLcer. a I '?A ■.:' :lie inle: ioi a:::e :ior :~ ;i r.t re-:', lit o i : .: c-d e:'.a J a::ery reread exiravasaiion ur.'c '\!:,:-.iJ) from ,1 :" u:al ar;ery 
handling !':■.::: the upper segment of the arcade, b Late arterial phase shows accumulation of contrast in a pseudoaneu- 
rvsm iiTiTiUi/jCii:/:. 7 lie gasiroduodenal ,n lei v is very short itirro-; } and there is reflux in;o the hepatic artery iiionbli: di 101; ). 
c ^:pers elective i 'SA of the mural artery with a 2.7 -Y microcatheter dinoi; ) shows extravasation or staining of a psrudoan- 
eurysm (dnonh,:aJi) d Control D5A of the arcade after injection of C.l cc of I to 3 diluted glue demonstrates occlusion oi 
the :::ti:al artery with, glee cast \iu i-hi/ilJi/s). Superior a:::ei io: i ,im ■.'■■■. i a::d pos:ei io: arcade [iioubic anvw) aic ■ 'pacilied. No 



blood flow, caliber of vessel, dilution of the acr- 
ylate, velocity of injection etc.. The microcatheter 
may be glued in the embolus. 

■ Adverse effects/complications: Deep and diffuse 
(>1 cm2) penetration can cause ischemia or even 
infarction. 

■ Future perspectives: With the introduction of Glu- 
bran2 (GEM, Italv) (mixture ot X-biityl 2-cyanoacr- 
ylateand meTh.u ryloxysiiliolane) the acrylate seems 
more stable in the mixture with lipiodol and less 
"sticky", which, in our opinion, has improved the 
control over the polymeri 



5.8.2.5 

Other Embolic Agents 

Sclerotic agents such as ethanol and polidocanol are 
pure liquids which penetrate into the capillary bed, 
causing coagulation necrosis [97] and therefore are 
not suitable for transarterial embolization. Detach- 
able balloons are very helpful in the rare case of an 
arteriovenous fistula [98]. 

• Future perspectives: Superselective intraarte- 
rial infusion of platelets has been successful in 
patients with GIH suffering refractory thrombo- 



Upper GI Bleeding 




Hg . it . I ;"> a -- f. A 74-year-old female wiiJi h e : j"k. I e j ti ^ -^ l s after aortic vaive replacement. Massive bleeding on endoscopy withotil 
visible lesion, li PS A of the common hep a lie artery revealing conn a si medium extravasation dinr. irji.w.i;) from ".he i ight gasti i: 
n riery iiir-rcir:, branching from I lie let", hepatic artery (doid'hj ,n ioi; s). b Selective PSA at the left hepatic n fiery with a 2.7-F 
itu en. ■catheter ninon-ii: d lsi.i1 excravasatron from a pyloric branch '.hinnir/ii'iii/i o: die right gastric artery idonbii iinnrrs). 
c Superselective catheterization, of trie sm.ill tortuous right gastric artery results in wedging trie catheter tip iiinmi's) in a 
proximal pyloric branch. Contrast medium pai 1 1. illy rerieti ates into the pyloric wall : iin-niWiciifi. d Non-subn acied PSA after 
withdrawing the microcatheter {<wir-\vliaiiti\ into the mai:'. right gasnic artery uin-yirj: ruptured site i.i.' i\-nii,:..i,l) ,;s well us 
".he i ight -to- left gastric arcade i-.i-iali:' -.jrivwi are clearly visualized. Because of the tortuosity and siii.il I dimensions, \ve decided 
co perform a Mow directed distal occlusion to prevent nackward tilling via the gastric arcade or the proximal pyloric artery. 
e Pigital image of the glue case (iini'ir.O. The ];S diluted glee penetrated into the ruptured artery to lite point of extravasation 
i id ioii/ilJi/;. and into the gastric arcade, f Post -emoolizat ion PSA of the hepatic arte: v ■::■ nil rming occltisr 'it ct the right gas- 
tric a rtery. Shadows of the glue cast i.i. 1 :\. ,ii',v,i,'s i. Left hepatic ai leiy remains patent i iinonj;. No rebleeding ar.d no ischemic 
complication at endoscopy 



cytopenia [99, 100]. Ethylene/vinyl alcohol co- 
polymer or Onyx (MTI, USA) is used as an alter- 
native for glue in embolization of intracranial 
AVMs. Because penetration of the copolymer 
into the AVM nidus can be accurately monitored, 
this liquid embolic plastic has the potential of 
improving target arterial devascularization in 
the GI tract. 



Since the introduction of the microcatheter s) 
ischemic complications or infarction are 



encountered in upper GIH embolization. Prudence 
is called for when arterial supply has been altered 
by previous surgery or by arteriosclerotic narrow- 
ing or occlusions. Back flow or reflux of Gelfoam 
into the hepatic or splenic artery may cause organ 
infarctions, which fortunately are seldom clinically 
relevant [7, B]. Overdosing the amount of particu- 
lates or glue can occlude too many collateral vessels 
and hence provoke irreversible ischemia. Also, over- 
dosing may result in reflux of embolic agents into 
adjacent non-involved territories. Chronic duodenal 
stenosis has been described as a late complication of 
glue embolization of the gastroduodenal artery or its 
muscular side-branches [94]. 

The contribution of contrast medium overload 
to renal complications is not well documented, but 



L Perreyiie 






appears low. Renal insufficiency is multifactori;illy 
related to hypovolemic shock or concomitant dis- 
eases and mostly transient [7, 8]. 

Intimal damage during (micro-)catheteriza[ion 
with subsequent dissection and flow arrest can 
occur after forced entry in tortuous trun 
branches. Although rarely reported, every i: 
tionist should be prepared for it, since it may pn 
elude any hemostatic action [8, 10]. 



5.10 
Outcome 

Devascularization of the target area, confirmed 
by angiographic cessation of extravasation or flow 
arrest in the vessel believed to supply the bleeding 
source, is achieved in 90%-95 % of cases [6-9, 58]. 
In 15%-25% of primary vessel occlusions, major col- 
lateral flow to the bleeding site will persist, requir- 
ing a second or third vessel embolization [6-8, 49]. 
Proximal anatomical obstacles, such as celiac trunk 
stenosis or occlusion, maybe the cause of technical 
Imhii'es. 

Primary clinical success, defined as cessation 
of bleeding within 30 days of embolization, ranges 
from 58%-78% [7-10, 51, 58, 97, 102]. After second- 
ary rescue by repeal endoscopv. surgery, re-emboli- 
zation or a combination of interventions, bleeding 
can be controlled in about 90% of patients [7, 51, 
58]. 

The mortality rate after embolization for refrac- 
tory upper GIH varies between 25%-35% [7, 8, 10, 
51]. Mortality is associated with underlying disease, 
multi-organ failure and rebleeding after emboliza- 
tion. Schenker et al. [8] calculated that patients 
with a clinically successful embolization were 13.3 
times more likely to survive, independently of their 
clinical condition. 



5.11 
Perspectives 

In several studies, attempts have been made to 
explain the high primary failure rate. The use of 
coils as the only embolic agents was found to be 
associated with rebleeding [7]. Other investigators 
did not confirm an association with procedural 
parameters. Coagulopathy [7, 8, 102], multi-organ 
failure or shock [6, 8] and corticosteroid use [6] are 



clinical risk factors for recurrence of bleeding after 
embolization. 

All associated parameters counteract intrinsic 
hemostasis and induce rebleeding when emboliza- 
tion does not permanently plug the vessel at the site 
of rupture. During devascularization of the target 
area, the embolic agent often does not enter the 
ruptured segment. Although contrast extravasation 
may disappear, the abundant collateral circulation 
will get an opportunity to re-supply the unplugged 
hole in the ruptured artery. In blind or proximal 
embolization, which essentially relies on the effect 
of pressure drop and clot formation, this mecha- 
nism of failure is even more relevant. Because asso- 
ciated clinical factors may be difficult to correct, 
refinement of the technique is a key to improving 
clinical success of embolization. In our experience, 
if a "spot weld" embolization cannot be achieved, 
the embolic agent should be pushed into the target 
area to penetrate the rupture site. For this purpose, 
minimal and adequately diluted glue has proved to 
be efficacious. It may be that other liquid or par- 
ticulate embolic agents (ethylene/ vinyl alcohol, 
calibrated PVA or gelatin particles, thrombin etc.) 
may achieve the same goal, but experience has not 
yet been reported. If this technique is anatomically 
impossible or unsafe and another occlusive method 
has to be chosen, early endoscopic control is another 
key to preventing failure. 



5.12 
Conclusion 

Transcatheter embolization has the potential to fur- 
ther reduce mortality in acute non-variceal upper 
GIH, provided we continue our efforts to optimize 
the occlusive technique and enhance the haemo- 
static effect. Furthermore, increasing angiographic 
sensitivity, which in our opinion depends much 
on the alertness of the involved endoscopist, will 
reduce the need for non-targeted blind emboliza- 
tion. Whether transcatheter techniques can replace 
surgical salvage in upper GIH remains to be estab- 
lished by prospective randomized studies. 



Upper GI Bleeding 



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102. Encarnacion CE, Kadir S, Beam CA, et al. (1992) Gastroin- 
testinal bleeding: treatmenl with gastrointestinal arterial 
embolization. Radiology 183:505-508 



6 Embolization for Lower Gl Bleeding 



Michael Darcy 






6.5.1 

6.5.2 
6.5.3 



73 



73 

Lhidcj lying Principles 73 
Type of Lesion 74 
Clinical Considerations 75 
Anatomy 75 
Technique 77 

Initial Mesenteric Catheter 78 
Micro catheters 79 
Embolic Agents 79 
Alternative Therapies 81 
Results 82 
Technical Success 82 
Clinical Success 82 
Recurrent Bleeding fo 
Complications 83 
Future Development and Researcl 
Conclusion 84 
References 84 



in the recent literature, this is actually not a new 
concept. Embolization to treat LGI bleeding was 
first described in 1974 [1]. These authors reported 
three cases of small bowel embolization followed in 
1978 by a report of two cases of colonic diverticular 
bleeding embolized with autologous dot [2]. There 
were several initial reports of high rates of clinical 
success, terminating bleeding in 80%-96% of cases 
[3-5]. 

Unfortunately, the early attempts at LGI embo- 
lization were hindered by an unacceptable rate of 
colonic infarction which was as high as 10%-20% 
in some series. Thus for LGI bleeding, embolization 
was largely abandoned in favor of vasopressin infu- 
sion which is usually reversible if the therapy results 
in bowel ischemia. Since the early 1990s, techno- 
logical advances both in microcatheters as well as 
embolic agents have considerably altered the tech- 
nique so that embolization is now a safe and viable 
option for managing LGI hemorrhage. 



Introduction 



Whereas endoscopic therapy can often be used to 
manage upper gastrointestinal bleeding, these tech- 
niques are difficult to apply to lower gastrointesti- 
nal (LGI) bleeding. Thus angiographic techniques 
assume greater importance in managing LGI hem- 
orrhage. For many years the primary interventional 
technique utilized was vasopressin infusion. With 
the development of microcatheters and embolic 
agents that can be used with them, embolization has 
assumed a more prominent role and in our practice 
and has become the procedure of choice. 

Although embolotherapy in lower gastrointes- 
tinal (LGI) tract has been a topic of great interest 



M. Darcy, MD 

Professor of jv.tdiobgy . : nd y.:jgei v. Mallnii'krodt Institute of 
Radiology, Washington University School of Medicine, 510 S. 
Kii'.g-high.w.-y Blvd., Si. Louis, MO 63110-1076, USA 



Physiopathology 

6.2.1 

Underlying Principles 

Vasopressin infusions and embolization differ fun- 
damentally in the mech.intsm by which they work. 
With vasopressin infusion the goal is to decrease 
the head of pressure to the bleeding site and allow 
stable clot to form. Vasopressin infusions diffusely 
constrict all the arteries leading to the bleeding site 
and the specific vessel that was bleeding is not really 
targeted by this therapy. This mechanism allows the 
treatment to be carried out by simple selective cath- 
eterization of the main trunk of the visceral artery. 
Thus the difficulty of the catheter manipulation 
is usually minimal. Even with the older forms of 
embolization using autologous clot and gelfoam, the 
treatments targeted more central vessels and relied 



on decreasing the arterial pressure to the general 
region of the hemorrhage rather than specifically 
targeting the actual site of bleeding. 

A major disadvantage of vasopressin therapy is 
that vascular constriction occurs only during the 
infusion. Once the infusion is stopped the vasocon- 
striction quickly dissipates Thus in order to provide 
time for stable clot to form at the bleeding site, the 
infusion catheter must be maintained in the artery 
for a day or 2. Catheter-related complications such 
as peri-catheter bleeding, thrombosis, or dissections 
can result from this prolonged catheterization. Also 
since the vasoconstriction ends when the infusion 
is stopped, the incompletely healed lesion is soon 
subjected to normal arterial flow. This is likely what 
accounts for the high rate of recurrent bleeding (up 



to 50%) that 
pressin also ca 
lar beds and c 
leading to angi 
With model 



I he 



after vasopressin therapy. Vaso- 
;s vasoconstriction in other vascu- 
i cause coronary vasoconstriction 
and even myocardial infarction, 
embolotherapy, however, the goal 
hifted towards direct mechanical blockage of 
pecific branch vessel from which the bleed- 
rises. This is accomplished by super-selective 



catheterization. While this technique does require 
a higher level of skill to achieve the more selective 
catheter position, the modern super-selective tech- 
niques sometimes allow the catheter to be advanced 
right up to the actual point of extravasation in the 
bowel wall (Fig. 6.1). This eliminates many of the 
problems associated with vasopressin infusion and 
should lead to both fewer systemic effects and less 
effect on the surrounding normal bowel. An added 
benefit to a very peripheral embolization is that this 
should decrease the potential for collateral flow 
to the defect in the artery where the extravasation 
originates. Theoretically one would expect that this 
would lead to improved efficacy. 



6.2.2 

Type of Lesion 

While technology changes have altered the patho- 
physiologic approach underlying the therapy, the 
type of lesion from which the bleeding originates 
also has important pathophysiologic implications. 
In some conditions like a bleeding colonic diver- 



ii 


b 

/ 



nogra 



witho 



the splenic flexure. 
l> More selective contra?: 
iiiiecliC'ii done throng:-. 
a micro catheter in the 
middle colic artery, c The 
microcritheter h.rs t'een 
maneuvered to within 
a few millimeters of 
the point of extravasa- 
tion, d Arteriogram .^osi 
embolization showing 
the microcoil out beyond 
I lie ::".;i rg.n.i. artery and 
occlusion of only the 
specific branch that war- 

NeedlC 



Embolization for Lower GI Bleeding 



ticulum or a focal ulcer, the lesion is small and con- 
sequently the vascular anatomy tends to be simple. 
The bleeding will often arise from a single small 
branch. 

Other conditions like inflammatory bowel dis- 
ease or tumors often affect larger areas and multiple 
arterial branches may supply the bleeding site. The 
bleeding may be a diffuse ooze rather than a focal 
source of extravasation. In this setting, it is less likely 
that one could occlude all the branches feeding the 
bleeding site without compromising a significant 
number of branches and risking bowel ischemia. 

Although angiodysplasias are usually small, 
they also have an increased number of small arte- 
rial branches that intercommunicate and make it 
difficult both to embolize very focally but also to 
effectively terminate the bleeding. Several authors 
have implicated angiodysplasias as the cause of 
clinical failure despite technical success at deposit- 
ing embolic agents in the target vessels. Bandi et al. 
[6] noted that rebleeding occurred in 50% (three of 
six) of angiodysplasias treated with embolization. 
While it can be argued that angiodysplasias are a 
pathologic condition not suitable for embolization, 
there are some reports of embolization providing 
successful control of angiodysplasia bleeding [7-9]. 
Also, even if definitive bowel resection is still war- 
ranted, embolization may control bleeding long 
enough to allow a patient to be medically stabilized 
and undergo a bowel prep prior to resection. 



Clinical Considerations 



Prior to all interventional procedures, a careful 
assessment of the patient is crucial. As with all angi- 
ographic procedures, a history of contrast allergy or 
renal dysfunction should be sought. If present, the 
arteriogram may need to be delayed in order to allow 
adequate pre-treatment. However, the decision to 
delay needs to be tempered by the magnitude of the 
bleeding. For patients with massive hemorrhage, the 
need to stop the bleeding may out-weigh the need for 
a prolonged course of steroids or hydration. 

When contemplating LGI embolization there are 
some unique aspects of the history that need to be 
investigated. Knowing the past surgical history is 
important since prior intestinal surgery may have 
disrupted potential arterial collateral pathways 
and will increase the risk of an ischemic complica- 
tion. If the patient has had radiation therapy to the 



i, the risk of ischemic complications may 
ice radiation therapy may obliterate 
small arterioles that cnii potentially provide collat- 
eral flow to maintain the viability of an embolized 
segment. Although one may be planning to utilize 
embolization, sometimes the initial arteriogram 
will reveal that the lesion is not amenable to embo- 
lization. It then becomes important to know if vaso- 
pressin infusion is a reasonable alternate therapy. 
Thus a history of coronary disease should also be 
sought since this is a relative contraindication to 
vasopressin infusion. 

The pre-procedure evaluation should also include 
assessment of the patient's coagulation parameters 
and bleeding history. Any coagulopathy or throm- 
bocytopenia should be corrected ifpossible since the 
clinical efficacy of LGI embolization is significantly 
diminished in patients with clotting abnormalities 
[10, 11]. In one small series [10], LGI hemorrhage 
was controlled by embolization in all patients with 
a normal coagulation profile. However, all three 
patients with coagulation abnormalities suffered 
recurrent bleeding. 

Finally, it may be useful to have a surgical evalu- 
ation simultaneously during the interventional 
radiologic pre-procedure evaluation. Fortunately, 
complications requiring surgical correction are 
quite rare; however, if bowel infarction does occur 
and surgical correction is not an option, then this 
complication could very well lead to death. Having a 
surgeon consult at the front end allows better coor- 
dination of care should surgical intervention be 
required. Also, if the patient is deemed to not be a 
surgical candidate, then the irreversible nature of an 
ischemic complication assumes greater significance 
during the consent process. 



Anatomy 

The superior mesenteric artery (SMA) supplies the 
entire small bowel, cecum and colon usually up to 
the splenic flexure. As such this is the vessel that 
is commonly studied first if there are no clues that 
the bleeding is coming from the inferior mesenteric 
artery (IMA) distribution. The primary branches of 
the SMA have numerous interconnections both in the 
mesentery and via the arcade along the mesenteric 
margin of the bowel. This communication between 
mesenteric branches may provide more than one 
pathway to reach a site of extravasation (Fig. 6.2). 




6.2. a SMA arteriogram with early ^Miavasaticn in the hepatic flexure 
). The microcatheter w : as initially advanced through, ".he high 
right colic branch [black an\->: ). b The microcatheter could not be advanced 
into the specific branch union i dial u-as bleeding because of unfavorable 
angles, c The bleeding brai'.ch was easily c-.uheterized after re-approaching 
the area through the middle colic artery, d A microcoil has been deposited 
right at the point of bleeding, e Final arte! iogi-.ini shows cessation of bleed- 
ing but good preservation ji ;he arterial arcade along the mesenteric border 
o: t lie bowel 



The IMA supplies colon distal to the splenic flexure 
including the descending colon, sigmoid colon, and 
rectum. When embolizing rectal branches off of the 
superior hemorrhoidal branch of the IMA, one must 
remember the rich collateral network around the 
rectum with middle hemorrhoidal branches arising 
from the internal iliac arteries. The internal iliac 
arteries should be studied after embolizing a rectal 
branch to exclude the possibility of collateral flow 
to the bleeding site. 

Although the celiac artery is rarely considered 
when dealing with LG1 bleeding, there is an uncom- 



natomic variant in which portions of the 
colon can be supplied by a branch arising 
from the splenic artery or its pancreatic branches. 
This can be suspected when comparison of the SMA 
and IMA arteriograms reveals a relative lack of 
perfusion in the left half of the transverse colon. A 
celiac arteriogram will demonstrate a branch to the 
left transverse colon that supplies the bowel in the 
gap between the SMA and IMA distributions. 

TheLGI tract is quite long and there is significant 
diversity in the peripheral aspects of the different 
arteries. In the small bowel, particularly 



Embolization for Lower GI Bleeding 



the jejunum, there are a great number of intercon- 
nections between arterial branches in the mesen- 
tery. In the colon, there is communication along the 
marginal artery but fewer branches in the mesen- 
tery leading up to the marginal artery. Thus there 
are fewer potential collateral pathways (Fig. 6.3). 
However, in the rectum the potential for collateral 
flow increases again since the rectum also receives 
arterial supply from the middle and inferior hemor- 
rhoidal arteries. 

Lesions in the LGI segments that have increased 
collateral potential are probably more prone to 




Fig.6.3.a SMA iirtenogr.im showing 

tions in the meseniciv between lite sm.ill bowel branches. 

b IMA arteriogram showing :hoi aside from the marginal 

artery, there are relatively few potential 

between the major IMA branches 



recurrent bleeding due to greater collateral per- 
fusion around the embolic agents. This has been 
implicated as a possible explanation for the higher 
rate of clinical failure in some anatomic segments. 
Peck et al. [12] reported that rebleeding was more 
common after embolizing jejunal and cecal lesions. 
The higher incidence in the jejunum was felt to 
relate to better collateral perfusion in that area. The 
higher incidence of rebleeding in the cecum was not 
felt to relate to the vascular supply but rather was felt 
to reflect the higher incidence of angiodysplasias in 
the cecum. 

Differences in segmental arterial supply prob- 
ably also impact on the risk of infarction. The 
rectum is likely to tolerate embolization better than 
other regions since it has a dual blood supply with 
the superior hemorrhoidal artery off of the inferior 
mesenteric artery and middle hemorrhoidal arter- 
ies arising from the internal iliac circulation. This 
translates into increased potential for collateral 
blood flow and thus decreased risk of ischemia. The 
cecum may be more prone to ischemia since there 
is not a well developed arcade along the mesenteric 
border of the cecum and instead there are separate 
anterior and posterior cecal branches. The tissue 
supplied by these individual branches may be more 
susceptible to ischemia and in fact infarction of the 
cecum (even after microcatheter embolization) has 
been reported [13]. 



Technique 

An access sheath is a useful adjunct and usually 
automatically placed when starting a LGI hemor- 
rhage case. The sheath will decrease the friction 
between the angiographic catheter and the arte- 
rial wall at the entry site and will allow better con- 
trol over the manipulation of the catheter. When 
performing embolization a sheath also helps pre- 
vent loss of arterial access if the catheter should 
become plugged by the embolic agent and need to 
be removed. This is less of an issue with modern LGI 
embolization since a microcatheter is typically used 
coaxially through the outer 5-F angiographic cath- 
eter. If the microcatheter becomes occluded by the 
embolic agent, it can be removed through the outer 
5-F catheter with out losing arterial access. Usually 
a 6-F sheath is used even though the initial catheter 
used to engage the visceral arteries is most often 
5 F. This allows slightly easier manipulation of the 



catheter plus the sheath can be more easily flushed 
to prevent thrombus formation around the catheter. 
A 5-F catheter occupies so much of the lumen of a 
5-F sheath that IV fluids attached to the sheath side 
port often will not flow well. 



6.5.1 

Initial Mesenteric Catheter 

Typically the procedure starts with a 5-F angio- 
graphic catheter which is used to select the main 
trunk of the visceral artery. This is used both for 
performance of the diagnostic arteriogram as well 
as to provide a conduit to direct the microcatheter 
into the visceral artery. The choice of the initial 5-F 
catheter depends greatly on personal preference but 
also depends on the particular shape of the target 
artery the target artery. 

For an SMA, the primary catheter chosen is 
most often a cobra or a Sos Omni (Angiodynamics, 
Queensbury, NY) re-curved catheter. Which one 
will perform best depends on the orientation of the 
proximal segment of the SMA. If the proximal SMA 
has a downward course, then a recurved catheter 
like a Sos or Simmons 1 will most easily seat down 
into the SMA trunk. When the SMA is oriented so 
that the proximal trunk comes straight off the aorta 
at a right angle, the Sos or the cobra will likely work 
equally well. Occasionally the proximal SMA actu- 
ally heads cephalad before turning in a caudal direc- 
tion. For this type of SMA a cobra works better. 

The cobra shape has one advantage for work in the 
SMA in that it can be advanced well beyond the SMA 
origin. It can even be used to engage individual small 
bowel or colic branches. This can be advantageous in 
two situations. First, if the SMA trunk is capacious 
and the branch you need to go out arises from the 
SMA at an acute angle, micro catheters (which are 
exceedingly floppy) will sometimes just buckle in 
the main SMA rather than go around the corner into 
the desired branch. In this setting, it may be neces- 
sary to engage the first order branch with the cobra 
itself before trying to advance the microcatheter. 
Secondly, if the more peripheral branches are very 
tortuous and the microcatheter needs to be pushed a 
little harder, it will sometimes start to buckle in the 
main SMA. Advancing the cobra closer to the first 
order branch will provide additional support for the 
microcatheter and decrease buckling (Table 6.1). 

Compared to the SMA, the IMA origin tends to be 
more constant and almost always is directed acutely 
downward immediately after it originates from the 



Tabled.]. iVlaierials cookbook to:' rii'.boazanon of SMA bleeding 

First line tools: 

Standard 6-F access sheadi 

0.035-in. Bent son g'jidewin? 

5-F Sos Omni catheter : Aisg.odynamicsl to engage SMA 

\iassT:ansil microcalb.eler wiih imrgrated wire to advance 

in case of failure to engage SMA trunk: 

5-F Cobra or Simmons type II to seat into SMA 

4-1" Glide Cobra for particularly small or acute. v angled SMAs 

0.035-in. glidewire (Terumo) to help engage or seat into SMA 

in case of J iff i cull advancement cut into pei ipheral branch.es: 
Allei naie wire: Trail sead vo:e i Bosioa. Scienafic'i 
Alternate microcathccer: Rea.egace i Boston Scientific] 



aorta. However, the aorta is also smaller in dia 
here compared to the level of the SMA. For this reason 
a Sos catheter often is not the best choice despite the 
caudal orientation of the proximal I MA. The smaller 
aortic caliber will sometimes compress the curve of 
the Sos and keep the catheter tip from engaging the 
IMA origin. A catheter that works more consistently 
to engage the IMA is the RIM (Roesch Inferior Mes- 
enteric, Cook Inc., Bloomington, IN). Once the RIM 
engages the IMA origin, the catheter is pushed mini- 
mally into the body to seat the catheter tip slightly 
into the IMA trunk (Table 6.2). 

These general catheter trends maybe altered by the 
presence of large atherosclerotic plaques in the aorta. 
Sometimes this will distort the vessel origin such 



Table 5.2. Materials cookbook :or emholizaiion o: IMA bleeding 

First line tools: 

Standard 6-F access sheadi 

0.035-in. Bentson g'jidewire 

5-F RIM catheter (Cook Inc.) 

\!assT:ansii microcalb.eler wiih imrgraled w.re io advance 

in case of failure to engage [MA trunk: 
5-F Sos Simmons type II to seat into IMA 



in case of difficuli advancement ou I into peripheral branches 
Alternate wire: Trail seed ivire i Boston Scienafic! 
Alternate microcathe:er: Rea.egace i Boston Scientific] 



Embolization for Lowe;- i..| Bleeding 



Chat the usual catheters will not work. Large plaques 
around the IMA origin can distort the ostium suffi- 
ciently that a cobra or even a straighter catheter like 
an MPA (Cook Inc., Bloomington, IN} have occasion- 
ally been needed to engage the IMA ostium. When 
the usual catheters fail to engage the IMA ostium, a 
brief flush aortogram may be needed. This not only 
confirms that the IMA is actually patent but will also 
delineate the location and orientation of the IMA 
origin. This is best performed with the flush cath- 
eter positioned down near the lower half of the 3rd 
lumbar vertebral body to avoid tilling SMA branches 
that might overlap and obscure the IMA origin. A 
15 -20 degree right anterior oblique projection is 
useful to profile the IMA origin since the vessel usu- 
ally courses in a left anterolateral dh 



6.5.2 

Micro catheter 5 

Once the 5-F catheter has been seated in the origin 
of the target vessel, a microcatheter is then advanced 
further out towards the site of extravasation. Modern 
microcatheters are typically complex constructions 
that have a stiffer larger section (usually about 3 F) 
closer to the hub and this stiffer section provides 
good pushability. Towards the tip of the catheter, 
it generally becomes smaller (2.7 F) and more flex- 
ible to aid maneuvering the catheter through small 
tortuous arterial branches. 

The catheters themselves have no torque con- 
trol and thus high torque guidewires are used to 
steer the catheter through the tortuous turns in 
the mesenteric arteries. These wires are typically 
0.018-0.014 in. in diameter in order to readily pass 
through the microcatheter and tiny peripheral ves- 
sels. An example of such a wire is the Transend wire 
(Boston Scientific, Natick, MA). 

While these specialized devices are critical, it 
is also vital to have a high quality imaging system. 
Because the goal is a super-selective embolization, 
it is necessary to precisely localize the bleeding site. 
Multiple small tout i asl ■ injections done as the catheter 
is advanced more selectively and viewing in multiple 
obliquities both make it easier to identify the specific 
branch that is bleeding. High quality fluoroscopy is 
essential to be able to visualize these small injections 
as well as the manipulation of these micro-devices. 
Digital road-mapping also helps facilitate directing 
the catheter into the appropriate branch. 

The optimal level of embolization has not been 
conclusively determined. One study proposed that 



embolization at the level of the marginal artery is 
less effective than embolizing out in the vasa recta 
[14]. They were able to stop bleeding in all patients 
when the microcoils were placed beyond the mar- 
ginal artery, but when the microcoils were placed 
in the marginal artery itself half of the patients 
rebled. A critical comparison of two studies pro- 
vides additional insight [15]. This letter noted that 
while in both studies [12, 16] initial bleeding was 
controlled in 71%-86% ol patients, the long-term 
clinical success varied. When emboli were depos- 
ited at or proximal to the marginal artery [12] 
52% of the patients developed recurrent bleeding. 
However, when emboli were deposited beyond the 
marginal artery [16] their recurrent hemorrhage 
rate was 0%. Another recent study though reported 
moderate recurrent hemorrhage despite embolizing 
at the level of the vasa recta [6]. Plus at times it may 
not be technically possible to embolize distal to the 
marginal artery (Fig. 6.4). Thus the optimal level of 
embolization has not clearly been defined and larger 
clinical trials are needed to clarify this point. 



6.5.3 

Embolic Agents 

Polyvinyl alcohol (PVA) particles have been used in 
a number of series [6, 10, 17-20]. The particles need 
to be suspended in iodinated contrast since PVA is 
not intrinsically radio-opaque otherwise it is not 
possible to fluoroscopically monitor the emboliza- 
tion. Because the PVA is flow directed, delivery of 
this embolic agent is less precise than with coils and 
more subject to local hemodynamics. If the catheter 
is obturating the feeding artery, the particles will 
not flow away as readily. Also as the vessel starts to 
become occluded by the PVA, the resistance to flow 
increases and hence the potential for reflux to non- 
target segments of bowel will increase. 

PVA size is an important consideration. The par- 
ticles should be at least 300-500 u.m. Kusano et al. 
[21] demonstrated that using smaller particles led to 
a high rate ot intarclion. Smaller particles occlude the 
arterioles too peripherally which decreases the poten- 
tial for collateral flow which in turn is important to 
maintain enough perfusion to keep the bowel viable. 

Probably the more common embolic agent 
used for LGI embolization is the microcoil. Both 
microcoils and PVA have been used successfully in 
reports of LGI embolization and while there have not 
been any trials to determine if one embolic agent is 
superior; microcoils do have several advantages over 




j Later phase of an IMA arteriogram 

si'.cwing bleeding i-irciiir) in [he low descend- 
ing colon, b Contrast imecdcns out in the mar- 
gin:;, aitejv fai>o to identiiv ti'.e specific vasa 
recta from which the Needing '.iiginiued. c Coils 
{iiiivitj were deposited in the marginal artery. 
Kletci.ng stopper a no ::o ischemia developed 



PVA. They are highly visible at fluoroscopy and this 
allows tor precise control over their deployment. 

Another advantage is the mechanism of deploy- 
ment. Unlike PVA which relies on flow direction, 
microcoils are precisely placed by pushing them out 
of the microcatheter. Simultaneously this is also a 
disadvantage of microcoils. in order to achieve this 
precise placement, the microcatheter needs to be 
maneuvered right to the desired point of coil depo- 
sition. If the vessels are small or tortuous this can be 
challenging. If the catheter can not be manipulated 
out into the specific vessel that is bleeding, PVA may 
be a better choice in that situation (Fig. 6.5). 

Precise coil deployment also requires careful 
selection of coil size. If the coils are sized appropri- 
ately they will form into a loose coil spring at the tip 
of the catheter. Using a coil that is too large for the 
target artery will cause the coil to not form properly 
and this can cause the catheter to back out into the 
feeding vessel. This can lead to occlusion of a larger 
branch than was intended and increase the poten- 
tial for ischemia. This is particularly a problem with 
super-selective LGI embolization. Since the microcoil 
is often being deposited in a tiny vasa recta, there is 
often not sufficient space to allow the n 



i the smallest 2-r 
n elongated stretched out shape. 



up properly. Thus e" 
will often assume ai 

Some manufacturers of micro catheters also r. 
duce coil pushers designed to push coils through the 
microcatheter. However, some of the micro catheters 
have lumens with a diameter around 0.025 in. or larger. 
When using microcoils which are often 0.018 through 
a microcatheter with a larger internal diameter, it is 
possible for the usual coil pusher to wedge along side 
of the coil. This not only may prevent advancing the 
microcoil out of the catheter, but as the pusher is pulled 
back it may also pull the trapped microcoil with it. 

A 0.025 in hydrophilic wire (Boston Sdenttlic, 
Natick, MA) is a nice alternative to use instead of the 
coil pusher. The larger lumen prevents wedging along 
side of the microcoil. The hydrophilic coating of the 
glidewire allows the wire to more readily pass around 
the tortuous curves that the microcatheter may be 
forced to take. 

ill get stuck in the 

not be pushed out into the 

ire. In that setting the coil 

of the microcatheter with 

injection. This can 

lock syringe. This 



Sometimes the i 
microcatheter s 
artery even with a glidei 
canusually be flushed oi 
a firm but short controlled salir 
be achieved by using a 1-cc Lui 



Embolization for Lowe:' ul Bleeding 




Fig.6.;'. a SKI A jrlci ■.■guii! with blearing; iru-cn-i in ih e ile'.im.b More selective s:udy shows m 
Lie fore trie level of thrvasn recta. In addition, the arteries leading to tire extravasation : liniifi are smal^r :ban die microca:he:ei. 
c '. ' esoiie liberal use of nitroglycerin boluses, the ci; the lei tip (<incjiri was able re be advance:: on iy a In lie closer to the Needing. 
A small voainic ■ if fKiC-7'JO Lint f'VA pai ucies were invcted a: that point, d Emai i;rteriogra:r. sbow : s cessaiion o:' bleeding and 
minimal devasculnriz.il ion of tiie bowd. Tiie patient had iv:- symptoms of ischemic bowel 



generates sufficient force to push the coil out of the 
catheter but the volume is small enough to prevent 
significant catheter recoil or vessel damage. 



Alternative Therapies 

Ifit isnotpossible topass the en theterselectively enough 
Co permit safe embolization, alternate approaches need 
to be considered. The initial approach may be to fall 
back to the well established methods of vasopressin 
infusion. Some of the main benefits of a vasopressin 



infusion are that it does not require super- selective 
catheterization, it is fairly effective at stopping bleed- 
ing, and the infusion can be stopped if symptoms of 
ischemic bowel develop. However, the rebleeding rate 
is very high after stopping the vasopressin infusion and 
this treatment can not be readily applied to patients 
with significant coronary vascular disease. The rela- 
tive benefits and risks of vasopressin therapy versus 
embolization have been recently reviewed [22]. 

An alternative to diffusely constricting the whole 
mesenteric vessel is to purposefully induce local vaso- 
spasm by means of catheter manipulation. This tech- 
nique was discovered fortuitously in some patients 
in whom spasm was induced accidentally during 



attempted catheterization for embolization [23]. 
Although this prevented doing the embolization, some 
of these patients stopped bleeding as a result of the 
spasm alone. With this technique the initial maneuver 
is to wedge the catheter as close to the bleeding as pos- 
sible and let it sit there for several minutes occluding 
the vessel. If that alone iails to induce spasm, then the 
catheter and wire are moved rapidly back and forth 
to induce spasm. With this technique they were able 
to initially stop bleeding in all 15 patients in who they 
attempted this procedure. One patient (6.7%) had 
recurrent bleeding within 24 h. Complications were 
minimal. They did have two patients who had dissec- 
tion of their proximal IMA artery, but no patients had 
clinically evident bowel ischemia or infarction. 

Instead of inducing spasm, another recently 
described technique that may not require super- 
selective catheterization is intra-arterial platelet 
infusion. This has been described in a few cases 
where bleeding was too diffuse to allow safe emboli- 
zation [24]. In oneLGI case, diffuse colonic bleeding 
was terminated by infusing 4 units of platelets into 
the proximal SMA. Presumably infusing platelets, 
which are normally present in the blood, should 
carry little risk of causing ischemia but both the 
safety and efficacy of this technique needs to be vali- 
dated in larger series. 

If the patient is a surgical candid ate and embo- 
lization is not technically feasible, another option 
is to mark the bowel to localize the lesion and aid 
resection. The main benefit of this technique is that 
it will aid identification of lesions, such as angio- 
dysplasias, that can not usually be palpated by the 
surgeon. Marking the bowel allows precise localiza- 
tion of the bleeding lesion which in turn insures that 
the proper segment of bowel is resected and that the 
amount of bowel removed can be more limited. 

There are two ways to mark the bowel. One is to 
deposit a coil in the mesenteric branch leading to the 
bleeding lesion [25]. During the operation, the sur- 
geon should be able to palpate the coil. If it can not 
be palpated, an abdominal radiograph will reveal the 
location of the coil. The surgeon then resects the seg- 
ment of bowel supplied by the artery containing the 
coil. Localization can also be done with methylene 
blue dye. In this technique, the microcatheter is placed 
close to the bleeding site and the patient is transported 
to the operating room with the microcatheter in place. 
Once the bowel has been surgically exposed, methy- 
lene blue is injected through the catheter. This brightly 
stains the bowel allowing the bowel segment contain- 
ing the lesion to be easily identified. Ag;iin this insures 
resection of the correct bowel segment. 



Results 

When discussing the results of LGI embolization 
one must understand the difference between techni- 
cal and clinical success. The successful deposition 
of embolic material in the intended target artery, 
with occlusion of flow and termination of contrast 
extravasation is the general definition of technical 
success. Clinical success on the other hand is suc- 
cessful termination ot bleeding as evidenced by no 
further bloody output, stable vital signs without 
pressors, and a stable hematocrit. 



6.7.1 

Technical Success 

Technical success for LGI embolization is quite high, 
generally around 80%-100%, in most series [5, 10, 
12, 16, 26-28]. Vessel tortuosity or spasm preventing 
catheterization of the target vessel are the most com- 
monly cited causes of technical failure. This statistic 
has not changed much over the past 30 years despite 
improvements in technology. However this likely 
reflects the changing goals of LGI embolization. In 
early stud ies.flowdirected emboli were injected from 
a less selective position than is currently required 
for placement of microcoils. However, modern inter- 
ventional radiologists advance catheters far more 
peripherally into the artery before embolizing. For 
example, embolization was considered to be techni- 
cally successful in only 73% ol cases reported in one 
study [6]; however.theydidnot embolize if they could 
not advance the catheter into the vasa recta beyond 
the marginal artery. Thus in recent series the defini- 
tion oftechnic.il success may just be more stringent 
and more difficult to achieve. This may explain why 
the technical success rates have remained unchanged 
despite improved technology. 



6.7.2 

Clinical Success 

Clinical success (the successful termination of bleed- 
ing) depends on more than just the deposition of 
embolic agents. Some pathology such as inflamma- 
tory conditions or tumors, do not have a focal blood 
supply and may be fed by multiple branches. In that 
setting, bleeding may continue even after successfully 
occluding a feeding vessel. Collateral supply around 
may also result in continued bleeding if 



Embolization for Lowe;- i..| Bleeding 



the coil is placed too proximally. As mentioned earlier, 
coagulopathy also makes clinical failure more likely. 
This is because microcoils may not completely occupy a 
vessel lumen and successful occlusion actually depends 
partially on formation of thrombus around the coils. 
Clinical success therefore occurs at a slightly lower rate 
than technical success. In modern series clinical suc- 
cess is achieved in 71%-100% [10, 12, 16-19, 26, 29]. 



6.7.3 

Recurrent Bleeding 

After LGI embolotherapy, the literature reports 
that anywhere from 0% to 52% of patients will have 
recurrent hemorrhage [6, 12, 16, 17, 19, 29, 30]. This 
wide range is partially due to different lengths of 
follow-up since shorter follow-up may lead founder- 
estimation of the rebleeding rate. 

In a recent study [6], twelve ol 35 (3 4 ,J o) patients 
rebled a mean of 74 days (range 2-603 days) after the 
initial embolization. Perhaps bleeding occurring 
603 days after embolization should be considered a 
separate discreet event instead of recurrent hemor- 
rhage and in fact three of the 12 patients were docu- 
mented by angiography to be bleeding from sources 
different from the original site. However, half of the 
patients were bleeding from the same site that was 
originally embolized. In the remaining patients the 
site of bleeding was not determined. In other series, 
recurrent bleeding was reported to originate from 
a site different from the one originally treated in as 
many as 50%-66% of the cases [10, 19]. 



Complications 

Like other vascular interventions, LGI emboliza- 
tion procedures have potential for puncture site 
and catheter related complications. Clinically sig- 
nificant puncture site bleeding, hematoma, or occlu- 
sions occur in around l%-2% of cases. Dissection 
of the target vessel is possible but rare. 

The most feared complication is bowel ischemia, 
but this is the area where we have seen the greatest 
change between modern embolization techniques 
and those used in the 1970s and 1980s. In the early 
series, infarction occurred in 10%-20% of cases 
and this was the primary reason why embolization 
for LGI bleeding was largely abandoned. Since the 
development of microcat he ters and suitable embolic 



agents, the reported rates of major ischemic compli- 
cations in most series have dropped to close to 0% 
(range 0%-5.9%) [6, 10, 17, 19, 20, 31]. 

While overt infarction is very rare, overall com- 
plications in the modern series have been reported 
at an average rate of 21% with the range being as low 
as 5% up to 70% [10, 12, 16, 18, 19, 26, 29]. While 
this seems unacceptably high, one must realize that 
the vast majority of the complications are not clini- 
cally significant. Examples ol these insignificant 
complications include self-limited abdominal pain 
that resolved without therapy or minor patches of 
ischemic mucosa that were asymptomatic and dis- 
covered only on endoscopy done for other reasons. 
These types of "ischemic complic.it ions" have rarely 
required any kind of therapy. 

One unanswered question is if these minor isch- 
emic insults could lead to delayed complications such 
as stricture formation. Bandi et al. [6] reported no 
clinically significant complications in their group of 
48 patients with follow-up out to 10 years. They had 
ten patients with clinical iol low-up and 25 with objec- 
tive post-procedure evaluation (endoscopy or surgi- 
cal pathology). No patient had any symptoms oi an 
ischemic complication including six patients who had 
minor signs of ischemia identified at endoscopy. 

In another study of 14 patients [30], one patient 
had circular muscular fibrosis identified on histo- 
logical exam and the authors postulated that this 
might become an occlusive bowel stenosis. How- 
ever, this patient also had an extensive emboliza- 
tion procedure with numerous gelfoam pledgets 
being injected from the proximal arcade of theSMA. 
Thus the technique used in this case was really not 
a modern super-selective embolization and was 
probably more analogous to the older methods of 
embolization used 20-30 years ago. Thus when 
using modern super-selective techniques, the risk 
of significant ischemic complications is now so low 
that embolization should be considered a reasonable 
first-line therapy for LGI hemorrhage and should 
not be avoided because of fear of infarction. 



Future Development and Research 

One of the ongoing needs is to continue to improve 
the ability of microcatheters to track out into very 
small peripheral branches. Since vessel tortuosity 
and spasm are the main causes of technical failure, 
improving catheter characteristics should improve 



M. IKircy 



technical success. Alternatively, future research 
could seek to develop better embolic agents. An agent 
that could be positioned as precisely as a microcoil 
without having to get the delivery catheter all the 
way out to the bowel wall could be another way to 
overcome the tortuosity and spasm problem. 

Another area that needs investigation is to fur- 
ther define She results of embolization stioilified 
by anatomic location within the bowel and type of 
lesion. Mosl studies bave pooled different tvpes ot 
pathologic conditions. Only a few case reports have 
focused only on specific pathologic lesions such as 
angiodysplasias [7, 9]. While these studies mostly 
report success, the follow-up is generally short and 
their results are contradicted by other small series 
that suggest that angiodysplasias are prone to 
rebleeding after embolization [6, 12]. 

The vast majority of studies to date have also 
lumped together bleeding from both small bowel 
and colonic sources. The differences in vascular 
anatomy with greater potential for collateral flow in 
the jejunum and rectum make it unlikely that bleed- 
ing in these regions can be terminated as effectively 
as in regions like the descending colon that have 
more limited collateral potential. The preliminary 
work by Peck et al. [12] has suggested that regional 
differences in etticacv will occur but given that this 
study had only a few patients in some anatomic 
regions, larger studies are clearly needed. 

Regional anatomic differences may also alter the 
risk of complications. Gerlock et al. [13] pointed 
out the lack of a good arterial arcade in the cecal 
region and that there tend to be independent anterior 
and posterior cecal branches. They reported a case 
of cecal infarction and suggested that the unique 
anatomy in this region may lead to a higher risk of 
infarction. They cautioned against embolization of 
the terminal portions of these terminal branches 
ileocolic artery. Again larger series are needed to be 
able to stratify risk by anatomic region. 

Evaluation of the long term effects of emboliza- 
tion is another area where additional research is 
needed. The length of follow-up in modern series is 
quite short. Although this proves short term safety 
and efficacy, there is little data on longer term 
rebleeding rates. This will be a difficult task since it 
may be hard to determine if delayed hemorrhage is 
coming from the original lesion that was embolized 
or a different lesion. Although short term safety has 
been well documented, longer term studies are also 
needed to determine if these patients will develop 
more chronic complications such bowel stricture. 
Finally, it will be important to better define what 



role embolization has in patients that are surgical 
candidates. In these patients it will be important to 
better document that LGI embolization (for either 
pre-operative stabilization or as definitive therapy) 
provides a survival benefit compared to just surgi- 
cally removing the offending bowel segment. 



6.10 
Conclusion 

Although for many years embolization was felt to 
be contra indicated in the LGI tract because of the 
risk of infarction, modern technologic advances 
in microcatheters have significantly decreased the 
risks of LGI embolization. Given the advantages of 
this technique, LGI embolization is rapidly gaining 
acceptance. While the results to date have been very 
good, considerable work is needed to better define 
in what regions, for which lesions, and under what 
circumstances is LGI embolization best suited. 



References 

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c;idie:er he:': ost, rsis of gz*i\'-MriW*li:-.'i\ bleeding using 
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2. Bookstein ]], Naderi MJ, Walter JF (1978) Transcatheter 
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3. ChuangVP, Wallaces, Zornoza J, Davis LJ (1979) Trans- 
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8. Tisnado J, Cho SR, Beachley MC, Margolius DA (1985) 
Tiansca:he-er embolization o: .ingio dysplasia of the 
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9. Tadavarthy SM, Castaneda-Zuniga W, Zallikofer C, 
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Embolization for Lowe:' '..■! Bleeding 



Massive lower gastroiniestmal hemorrhage from the sur- 
gical anastomosis in patients with multiorgan trauma: 
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Alcohol particle's. Cardiovasc Intervent Radio] 2^:461 - 



(1987) Low-dose particulate polyvinylalcohol emboli- 
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467 

11. Encarnacion CE, Kadir S, Beam CA, Payne CS (1992) 

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. Curzon IL, Nicholson AA,Dyet]F, Hartley J (1996)Trans- 
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. Nicholson T, Ettles DF (1999) Embolization for life-threat- 
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. Guy GE, Shetty PC, Sharma RP, Burke MW, Burke TH 
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20. Defreyne L, Vanlangenhove P, de Vos M, Pattyn P, 
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21. Kusano S, Murata K, Ohuchi H, Motohashi O, Atari H 



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23. Cynamoni,AtarE,SteinerA,Hoppenfe!d BM, Jagust MB, 
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24. Madoff DC, Wallace MJ, Lichtiger B, Komanduri KV, 
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for focal lower gastrointestinal hemorrhage. Acta Radiol 
44:334-339 

31. FunakiB,KostelicJK,LorenzI,HaTV,YipDL,Rosenblum 
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colonic hemorrhage. A)R Am I Roentgenol 177:829-836 



Haemobilia and Bleeding Complications 
in Pancreatitis 



¥ A. Nicholson" 



Introduction 87 

Haemobilia 87 

Clinical, Pathophysiological and Anatomical 

Considerations 87 

Imaging and Technical Considerations 88 

Endovascular Management and Results 90 

Complications 91 

Bleeding Complications in Pancreatitis 91 

Clinical, Pathophysiological and Anatomical 

Considerations 91 

Imaging and Technical Considerations 91 

Endovascular Management and Results 94 

Percutaneous Ultrasound or CT Guided 

Embolization or Thrombin Injection 95 

Complications 97 

Summary 97 

References 97 



tis is 5%-10% [5, 6]. Such aneurysms are caused by 
the actions of pancreatic enzymes such as elastase 
on adjacent blood vessels released in the course of 
pancreatitis. 

Though spontaneous thrombosis of such aneu- 
rysms has been reported [7] mortality from con- 
servative management is said to be more than 90% 
[8, 9]. The reported mortality when such aneurysms 
are treated surgically ranges from 12.5% to 40% 
[10]. Importantly re-bleeding can occur in 6%-10% 
of patients who survive initial surgery [11]. The first 
report of successful embolization in this condition 
was in 1982 [12]. Since then there has been a plethora 
of articles describing the diagnosis and endovas- 
cular treatment of pancreatitis associated visceral 
aneurysms [8, 13-15]. 



Introduction 



Haemorrhage into the biliary tract is called haemo- 
bilia. It was first described in 1654 [1], but the con- 
dition was not termed 'haemobilia' until 1948 [1, 
2]. The majority of cases are due to trauma (50%), 
operative trauma accounting for 15% [2], though 
this incidence may have increased with the intro- 
duction of laparoscopic biliary surgery [3]. Pancrea- 
titis is a rare cause of haemobilia. 

The majority of patients who develop signifi- 
cant bleeding as a complication of pancreatitis do 
so because of associated upper gastrointestinal 
ulceration and inflammation. Occasionally portal 
vein thrombosis can lead to variceal bleeding [4]. 
Neither of these pathologies is within the remit of 
this chapter. The estimated incidence of visceral 
aneurysm development in patients with pancreati- 



T.A.NiCHOL50N,KSc-M,Sc-.MKChB,FRCR 
Consultant Vascular Radiologist and Senior Lecturer, Leeds 
Teaching Hospitals NHS Trust, Great George Street, Leeds 
LSI 3EX, UK 



7.2.1 

Clinical, Pathophysiological and Anatomical 

Considerations 

The classical triad of gastrointestinal bleeding, right 
hypochondria! pain and jaundice suggest haemo- 
bilia [2]. However it can be difficult to diagnose 
and if bleeding is of low volume may present as 
anaemia of unknown cause. Bleeding can also be 
massive and life threatening. The commonest cause 
as already stated is blunt and penetrating trauma 
in 35%. Iatrogenic haemobilia is a complication of 
all forms of biliary surgery, percutaneous biliary 
procedures (4%-14%) including stent insertion [16] 
and biopsy (3%-7%) [17]. In addition an aberrant 
papillary artery, found in approximately 20% in 
cadaveric studies, can bleed following endoscopic 
sphincterotomy [18], Other causes include gallstone 
induced cholecystitis, halothane induced liver necro- 
sis, varices secondary to severe portal hypertension, 
primary and metastatic" malignancies of the liver 



T. A. Nicholson 



and biliary tract, arteriovenous malformations in 
the liver or pancreas and infections and infestations 
including ascariasis, hydatid and amoebic abscess, 
and mycotic aneurysms due to any organism [17]. 

Haemobilia is almost always due to damage to the 
hepatic artery. As this supplies only about one third 
of the liver's blood supply it can usually be tied off 
or embolized with impunity. However if the portal 
vein is occluded interruption to the hepatic arterial 
supply may lead to liver infarction. This is not invar- 
iable as the hepatic arteries can backfill around the 
portal triads. This latter feature also means that a 
proximal tie or embolization may not be effective. 
Therefore embolization is best done proximal and 
distal to the pseudoaneurysm or bleeding point. 



7.2.2 

Imaging and Technical Considerations 

Although ultrasound and ERCP can confirm the 
diagnosis of haemobilia in a few cases, CT is more 
sensitive, contrast enhanced CT (CECT) diagnos- 
ing active blood loss or haematoma and its site of 
origin in almost 100% of cases . In occult cases 
increased attenuation of bile in the gall blad- 
der and ducts confirms the diagnosis [17]. Good 
quality selective and super-selective angiography 



remains the diagnostic procedure of choice, as it 
not only confirms the diagnosis, but also localises 
the site accurately and allows immediate treatment 
by embolization (Fig. 7.1). It is essential prior to 
definitive treatment to make sure that the portal 
vein is patent and this must be imaged on CECT 
or indirect portography. 

Catheterisation of the hepatic artery is usually 
performed from the femoral artery. The radial or 
brachial approach may be preferred especially where 
the patient is thin and the angle with the aorta very 
acute. A 4- or 5-F Cobra Glidecatheter (Terumo) and 
hydrophilic wire will usually suffice to diagnose and 
cross the bleeding point in the hepatic artery. If it 
is very peripheral, proves difficult or is stenosed or 
in spasm, a co-axial system will almost always do 
so. Occasionally patients have a series of intermit- 
tent large haematemeses. Though the diagnosis of 
haemobilia is obvious from their history, ERCP and 
perhaps CT findings, no pseudoaneiiiysm or bleed- 
ins site ran be see it at anyiogiaphv. Invariably there 
will be spasm somewhere associated with the tem- 
porarily sealed bleeding site or occult pseudoan- 
eurysm. Usually local contrast injection will reveal 
this but in any case the area should be embolized. 
This usually requires a coaxial system to negotiate 
the narrowed segment (Fig. 7.2). 

For a list of technical requirements see Table 7.1. 



Table 7.1. Cookbook 



AH. 



- imaging available especially 



1. Buscopam 20-40 mg 

2. Maxalon and Atropine should be avail- 
able in case of vomiting or bradycardia 



Comments 



1. If acute rupture may be Should not be attempted without 
no previous imaging full nursing and technical support 

2. GA with full anaesthetic 
support 

'.j-'jcjgon 1 ugrm 



Catheters 


1. 5-F appropriate fern orovisc era! glide- 


1. 5-F Sos type catheter or 


4-F fern orovi see ral catheters 




catheter e.g. Cobra 1 or Sidewinder 1 or 


_ Wo It man loop often useful 


;c:qiiaKe than 5-F 




2. Coaxial catheters are often very useful in large diameter aortas 






if superselective or distal embolization i 


s 2. Multipurpose or Beren- 






necessary 


stein catheters useful if am 
approach 




Wires 


Glidewire (Terumo) 


Other hydrophih'c wire 




Embolic 


Steel coils 


1. Glue 


Unless the haemorrhage is in 


material 


Platinum microcoils if co-axial system 


2. Thrombin 


diad'ly life -hreatening (see !- 




used 


3. Long detachable coils or 


do not use: 






detachable balloons it i:u 


Particles 






aneurysm must be pa., a J 


Crelfbam 
.V_Ii>!<i|ji>un blood 



Haemobilia ami Bleeding C implications in Pancreatitis 




Fig.7.1a,b. Coeluc angiography i:'. J palien; With life threatening haemo- 
bilia 24 h post ch- 'lecystectomy revealed a large hepatic pseudoaneurysm 
(a] treated successfully ay proximal artd distal coil embolization (b) 





Fig. 7.2a-c. Coeliac angiography or. ,1 53 -yen j -eld patient post 
laparoscopic cholecystectomy who suffered three large hae- 
matemeses in the set i opens Live pel sou. The initial angiogram 
ia) wns thought to be normal anc :'.o further procedure whs 
carried out. However. :'.ote die spasm ;n the segment 6 artery 
iJiTjii iiciJiii). 24 h later after two more major episodes of 
l'!eed;ng during which die palient became unstable, repeal 
aiigiogi-.iphv ibi revealed the area of spasm to be due to a 
pseudoaneurysm iitnvwln'-.iiij). This was successfully emboi- 
ized with steel coils (c) 



T. A. Nicholson 



7.2.3 artery from where the pseud oaneurysm arises. In 

Endovascular Management and Results post surgical cases this nearly always involves the 

hepatic artery proper (Fig. 7.1a) but in post biopsy or 

Haemobilia requires treatment as spontaneous reso- PTC cases the pseudoanetirysm usually a rises from a 

lution is exceedingly rare and the mortality from right hepatic branch and themainhepaticarterycan 

ruptured pseudoatieurvsms is in excess of 90%. be preserved (Fig. 7.3). In acute cases of penetrat- 

Technically endovascular management is relatively ing injury the bleed may be quite distal and where 

simple and involves the proximal and distal emboli- bleeding is immediately life threatening particles ot 

zation, with tightly packed steel coils, of the hepatic 500-1000 urn diameter can be used (Fig. 7.4). 




Fig.7.3a,b. Hepatic aneiiogiam in a 26-year-old nun with a small inoperable neuroendocrine tumour in the head of his 
p ,ino reus. The papilla oi" V'ater coil J nol be accessed a: HRCf 1 an J he underwent a peiciiraneous stent ing procedure .it which 
two se:f-e\p. ; ;:di:;g sients we:e inserted u.-nvr ,::ioi:iii,i,l;\ apparently side by side (ai. ]2 hours late: repeal ERCP ; eve .tied a 
sign hi cam haeiv.oirhage : i ■. ■ ni I he papilla. The ang.ogiam revealed a segment 4 .uteri;;. pseiiooane-irysm ■: ;>pp-:' iUi\'wh<\iJ.i) 
which was embolized success.rully with coils (b) 




Fig.7.4a,b. This pa tie:'.: was ad milled in haeniodyiianiic shock after a knife wound to the right hypochononum. hir.ei giritcv 
hepatic angjograpj'.y revealed a segmem s haemon juige ;a). As ti'.e patiem had an unrecoidahle o a. -:-.\ pressure a: the time 
7(i(.. 000 |.im !-VA pai tides were iniecied selectively : b : wit:: i immediate improvement in haciv.odvnamic stains, iiie pa tint; was 
discharged within 5 days ■:■: the procednre 



!-!;i ei 11 obi J.; jiii; ; . Rleediijt; O/inph.: 



a !-';i :ii" re J titii 



If the portal vein is occluded and the bleeding site 
is in the hepatic artery proper or at the gastroduo- 
denal artery origin, as is sometimes the case after 
surgery for pancreatitis or pancreatic carcinoma, 
treatment decisions become very difficult. Surgery 
maybe possible but has a very high mortality. Pack- 
ing the aneurysm itself with long detachable coils or 
detachable balloons has been described [19]. How- 
ever in the author's experience, whilst this is effec- 
tive in the short term, the aneurysm may recanalize 
due to clot re tract ion and rebleeding may take place. 
This is maybe fatal especially if the patient has been 
discharged after initially successful embolization. 
If further elective surgery is definitely contraindi- 
cated, proximal and distal hepatic artery emboliza- 
tion is the safest option relying on collateralization 
of the distal hepatic artery branches in the liver. The 
use of thrombin, which is described in the next sec- 
tion, has not, to the author's knowledge been used to 
treat a hepatic pseudoaneurysm causing haemobilia. 
However it may well be that this will be an effective 
treatment option. 

The results of embolization for haemobilia nre 
reported as being 95%-100% effective [3] even on 
an intention to treat basis and it should be the treat- 
ment of tirst choice. 



7.2.4 
Complications 

These are very rare. Clearly all the complications relat- 
ing to arterial catheterization at any site and for what- 
ever reason can occur. Non-target embolization should 
not happen in the experienced hands of a well trained 
operator. It is said thai Imtgal abscesses are commoner 
after hepatic arterial embolization [3] but there is no 
real evidence for this and most patients have had sur- 
gery or a penetrating injury prior to the embolization. 
Liver infarction as described abo\ 
a rise in liver enzymes is often observed [3]. 



Bleeding Complications in Pancreatitis 

7.3.1 

Clinical, Pathophysiological and Anatomical 

Considerations 



Pancreatif 

caused by the action of proteolytic enzymes, released 



from the necrotic pancreas, on vessel walls and are 
often associated with pseudocysts. Patients are usu- 
ally extremely ill with Ranson scores above 3. Prior 
to rupture most aneurysms are either asymptomatic 
or cause pain by pressure on local structures that 
may mimic the pain of pancreatitis. Imaging is 
therefore vital to their early diagnosis and treat- 
ment. The splenic artery is most commonly involved 
followed by the gastroduodenal and pancreaticodu- 
odenal arteries, although all peripancreatic arteries 
can develop aneurysms and pseudoaneurysms [20], 
Their natural history is to increase in size and ulti- 
mately rupture into the upper GI tract, abdominal 
cavity or the pancreas itself [21]. Occasionally they 
can erode into the aorta or adjacent venous struc- 
tures though the latter does not preclude emboliza- 
tion (Fig. 7.5). 



7.3.2 

Imaging and Technical Considerations 

Ultrasound is useful for many aspects of pancrea- 
titis but has a sensitivity of less than 73% for vis- 
ceral pseudoaneurysm in the condition, whereas 
contrast enhanced computer tomography (CECT) 
has a sensitivity of almost 100% [22]. CECT is also 
very useful in terms of endovascular treatment as 
it can indicate what type of aneurysm has formed, 
which artery it has formed from and whether there 

Angiography was formerly the procedure of 
choice for identifying the site of visceral aneurysm. 
It is certainly true that where ultrasound, CECT and 
endoscopy have failed to diagnose a source of active 
bleeding, angiography can occasionally do so. In 
one study angiography identified 90 out of 93 arte- 
rial pathologies [8]. However, it is the author's expe- 
rience that some aneurysms within pseudocysts 
are not associated with a specific named artery and 
even when obvious on CECT, cannot be diagnosed 
accurately by angiography (Fig. 7.6). It is probable 
that such aneurysms are either the result of erosion 
within the arteriolar or capillary bed or have a sig- 
nificant venous contribution. 

Catheterisation of coeliac and superior mesen- 
teric arteries is usually performed from the femoral 
artery. The radial or brachial approach may be pre- 
ferred especially where the patient is thin and the 
angle with the aorta very acute. A 4- or 5-F visceral 
curved Glidecatheter (Terumo) and hydrophi lie wire 
will allow more distal catheterisation which maybe 



reqmr 



i the ; 



uiysr 



: . A. Nicholson 




l : ig.7.;"a il. A 76-year-old man w : i;h acme on chronic pancreadlis secondary to alcohol abuse was ac: imt.eci Willi abdominal 
p i L j j . A.ocio::'.jna! ^m:. :'.:.ik. I i^.i i suggested a p. ::iaiiie epigasnic mass coo. liiii'.ecl by CHCT anc aiigio'giaphv to be a Iaige fas- 
ti od nod ena I arieiy pseucoar.r : .ii ys:n (a). It was ciear ;ha: this had eroded into the inferior and siiperio: mesenteric veins wi:h 
a oat en l poi la I win I a,b). 7 lie- Gastroduodenal ano inferior pa nc real icoo'.iodena I arteries were coil em noli zed I c) with a good 
result continued by a 24-h CI scan which also demo:;s:rated patency of the mesenteric and porta! wins. Xole the persistent 
layered contrast in the psemioanr-irysm sac which should no; oe mistaken tor persistent patency (d) 



pseudoaneurysm. If it is very peripheral, proves dif- 
ficult due to tortuosity or is stenosed or in spasm, a 
co-axial system will almost always do so. The CECT 
semi shoti Id i [id ic ;.ite the origin of the ;-meurvsin and 
selective catheterization of the appropriate artery 
may immediately confirm the CT findings. If the 
CT scan is not specific for origin, then start with the 
celiac trunk and follow with the SMA. Coil embo- 
lization should be proximal and distal with tightly 
packed coils (Figs. 7.1, 7.2, 7.4, 7.5, 7.7). If the aneu- 
rysm is not seen on either of these selective exami- 
nations then superselective catheterization should 



be performed according to the CT approximation of 
site in the following order: 

a. Splenic artery 

b. Hepatic artery 

c. Gastroduodenal artery 

d. Gastroepiploic artery 

e. Superior pancreaticoduodenal artery 

f. Dorsal pancreatic and pnticiciticn magna arteries 

g. Left gastric artery 

h. Right and left hepatic arteries 

i. Inferior pancreaticoduodenal artery 

j. Jejunal arcade 



Haemobilra and Bleeding Coi 




Fig.7.6ii--il. A 4S-ve;;r-o!d n;..in with lIi:'o:uc p;;ncrea:ii;s developer furdier abdominal aain. CHCT revealed ;; pseiidoaneurysiii 
:n his lesser sac (a). Selective a:id super selec:ive angiography faded 10 demons! rare ;;ny source for the pseud. ^aneurysm !b :. [i 
wjf riierefore LTi.rnl.-. ne-. ■;isJy punctured with ;; 1 1 -G;;uge need;e i e; ;;nd dirombosed will; 1 000 u:ii:s of a;nologo;is dironibin. 
CECT at 1 week demonstrated occlusion of the pseud caiiecrysm id) 



: . A. Nicholson 



T 




Fig.7.7a,b. Front and back door embolization of a splenic 
artery pseudoaneurysm in! secondary to acute on chronic 
pancreatitis with, a good result (b). This patient is alive and 
well with no recurrence at 52 months 


^■ffiwif.liMi' 



If after this, an aneurysm, diagnosed at CT, is 
not found or fills slowly from no named artery at 
superselective angiography, do not assume that that 
the CT scan is incorrect, that the aneurysm does not 
exist or is unimportant! Check the angiogram for 
areas of arterial spasm (Fig. 7.2) and if not found, 
consider percutaneous CT or ultrasound guided 
autologous thrombin injection. 

Post embolization, immediate check angiography 
is indicated. It is important to perform pre and post 
contrast enhanced CT initially as the aneurysm will 
still contain contrast from the initial embolization 
for up to 4 weeks post procedure (Fig. 7.5d). Further 
CECT scans at 24 h, 1 week, 1 month and 3 months 
are indicated. CECT should also be performed any- 
time where there is recurrent pain or haematemesis. 

If the aneurysm does recur, repeat angiography 
and embolization is indicated if there is still access 
and recanalization or recruitment of other arteries 
has occurred. CT guided percutaneous thrombin 
may also be used but it may be that open surgery is 
the only alternative. See Table 7.1 for details of tech- 
nical requirements. 



7.3.3 

Endovascular Management and Results 

There is still some controversy in this area. There 
are some who believe that "there are several situa- 
tions in which angiographic management is appro- 
priate. However, because the pseudoaneurysm may 
be supplied by collaterals which would form rapidly 
after embolization, a definitive operation should be 



performed as soon as possible" [23]. However, the 
literature would suggest that embolization is an 
effective treatment in its own right (Fig. 7.7). Critics 
would argue that the bulk of the literature consists 
of case reports and small case series. In the largest 
published series of 104 cases, compiled by postal 
survey, Boudghene described positive angiography 
in 90 cases of which 32 were embolized [8]. Angiog- 
raphy was therefore negative in 14 cases and there 
is no explanation as to why embolization was not 
performed in the other 68 cases. Of the 32 cases that 
were embolized 12 re-bled and five died. The results 
published by Boudghene are therefore almost as bad 
as the published surgical results. The question that 
needs answering is why some patients rebleed after 
apparently effective embolization or surgery? 

This author's experience over a 3-year period is 
of 16 patients all of whom had a definitive diagno- 
sis of visceral pseudoaneurysm at CECT but where 
the aneurysm was only imaged by selective or super 
selective angiography in nine cases. All nine were 
embolized using coils and there was no re-bleed or 
reformation of the aneurysm at between 6 months 
and 5 years. However, in seven cases pseudoaneu- 
rysms could not be seen at angiography (Fig. 7.6) or 
filled very slowly at super selective catheterisation. 
All seven of these pseudoaneurysms were within 
cysts intheomentalbursa.Inonly one of these seven 
cases was endovascular embolization attempted. In 
this partial la r case though embolization was clearlv 
initially effective the pseudoaneurysm reformed 
within 7 days. A second embolization was again 
effective but again the aneurysm reformed (Fig. 7.8). 
Subsequent embolization was not possible, as all the 



Haemobilia and Bleeding ; . ! implications in Pancreatitis 




Fig.7.8. Gastroduodenal arteriogram in a patient who had 
r.nueigone two previous coil embolizations for a slow filling 
pseudoaneurysm that rilled nom small GPA and pancreati- 
coduodenal branches. In this laie phase [he pseudoaneurysm 
has recurred from numerous small duodenal collaterals. Fur- 
thei embolization was noi possible 

main arterial access points had been embolized. 
This patient subsequently died at surgery. 

It would appear therefore that two different types 
of visceral aneurysms are possible in the patient with 
pancreatitis. The first is a true aneurysm (Type la) 
(Fig. 7.9) or a pseudoaneurysm (Type lb) (Fig. 7.7) 
arising directly from an eroded major named artery. 
These canbe treated by embolotherapy with coils. The 
second type of pseudoaneurysm (Type 2} (Figs. 7.6 
and 7.8) cannot be seen at angiography or fills very 
slowly with no major named arterial source. Such 
aneurysms occur within the omental bursa and are 
probably formed by the erosion of the arteriolar and 
capillary bed possibly with a venous contribution. 
It is possible that such aneurysms account for the 
rebleeding encountered after surgery and embolo- 
therapy in a significant number of patients. Attempts 
at embolizing these are likely to fail and a different 
strategy is necessary. The other six such pseudoaneu- 
rysms, described above, were treated by percutane- 
ous thrombin injections under CT guidance. 



7.3.4 

Percutaneous Ultrasound or CT Guided 

Embolization or Thrombin Injection 

The direct puncture percutaneous approach 
creatic aneurysm einholii'jtion was first dt 




i a recent history of 

admitted with further abdomi- 
nal pain. A CECT :<L.^n suggested an aneurysm of uncertain 
ongin.Aiigiogiaphy revealed a ".rue (Type I a ! aneurysm of an 
aberrant right hepatic artery (a). CiiZT had revealed a patent 
portal vein and so proximal and distal coil embolization was 
performed lb i. There were no farther complications and the 
patient is alive and well at 36 months 



by in 1992by CAPEKet al. who used coils after punc- 
turing an aneurysm within a pancreatic phlegmon 
at open surgery [23]. There have been other descrip- 
tions of the technique to treat non pancreatitis asso- 
ciated visceral aneurysms [24]. Subsequently Lee 
et al. described the use of thrombin to occlude an 
iatrogenic aneurysm caused by a percutaneously 
inserted drainage catheter [25]. Tins lend to reports 
of its use to treat true pancreatitis associated pseu- 
doaneurysms [26, 27]. 

The author has used percutaneous CT guided 
thrombin injection in six patients where pancrea- 
titis associated aneurysms could not be seen at 
selective angiography. The technique is relatively 
simple, the aneurysm being punctured with a 
21-Gauge saline flushed needle under CT guidance 



T. A. Nicholson 



and 1000-5000 units of thrombin injected down the 
needle until resistance is felt. It is important not to 
aspirate blood into the needle and to rely on the CT 
image for position. If there is uncertainty about tip 
position, and aspiration of blood necessary, then 
the needle must be re-flushed with saline prior to 
thrombin injection. 

Initially human thrombin obtained from the 
blood transfusion service was used. However, 
although immediate thrombosis of the aneurysms 
was observed, recurrence occurred at follow up 
CECT (Fig. 7.10). This is not surprising in patients 
with on going pancreatitis. Repeat thrombin injec- 
tions were required - in one case on three separate 
occasions. Though eventually permanent occlusion 
was obtained and the patients are still alive and well, 
subsequent patients were treated with autologous 
thrombin prepared from 50 cc of their own venous 
blood. This was done to avoid potential anaphylaxis. 



which has been recorded with repeated human or 
bovine thrombin injections. The technique for pre- 
paring autologous thrombin is described in the lit- 
erature [28]. The results have been good in all six 
patients with permanent occlusion of the aneurysm 
confirmed by subsequent contrast enhanced CT at 
6-18 months. However four patients have required 
one repeat procedure and two patients two, within 
the first 3 months. Such patients may previously 
have accounted for the rebleed and death rate post 
embolization or surgery. 

There is one further indicrit ion tor III i ombin occlu- 
sion of pancreatitis associated visceral aneurysms. 
Where the portal vein has occluded as a complication 
and the patient has a proximal splenic or gastroduo- 
denal aneurysm, the proximal and distal coil emboli- 
zation of which could compromise the hepatic arterial 
supply to the liver causing liver infarction, thrombin 
injection may be a safer technique [29]. 




Fig.7.10a-e. A 3d -yen r- old wom.li! with an occr.ll lesser sac pser.doanearv.:;:-. c.v.gr.oseJ :.: ■IH'TT afiei :\n ,:cair on chronic 
episode <:■'< pancreatitis :. a;. Angiography revealed a stove liking r/seudoaiieiirvsm .n pancreaticoduodenal territory but il was 
not tilling t:o:i; any major ariery. It was therefore punctured percuianeocsly under CT gc.ioan.ce with a i:-gaugc needle !l>) 
and Thrombosed with 3?00 11111:? of ar.iologou;: ih.ro 111b in with a good result at 24 h (c). However, the aneurysm riao recurred 
at 1 month follow-in 1 CECT Id ) and trie procedare was repeated. CECT a: nionlhs demons: rated thromboses of the aneurysm 
(e) and :he patient is wek with no recurrence al '■) months 



!-!aemobija ami Bleeding Coiupl;.:. 



7.3.5 
Complications 

The complications of embolization for pancreatitis 
associated visceral pseudoaneurysms are the same 

;.is tor tlii? tre.umeii! of linemobilin. In addition and 
as mentioned the repeated use of bovine or human 
thrombin can lead to anaphylaxis and though rare, 
autologous thrombin is recommended. 



7.3.6 
Summary 

Aneurysms and pseudoaneurysms causing haemo- 
bilia or associated with pancreatitis are potentially 
fatal. Imaging, particularly CECT, is vital to their 
diagnosis. Conservative therapy is a poor option and 
treatment, which was formally via open surgery, is 
now best carried out by ans'ios'iMphy mid percutane- 
ous coil embolization in haemobilia and for Type la 
and b pancreatitis associated pseudoaneurysms. 
Percutaneous CT guided thrombin therapy is indi- 
cated for Type 2 aneurysms. 



Sa :'. Jb. '.■:•.'. P ( 1 ''4S: rtarmoiihage in to the biliary tract fol- 
lowing trauma: 'trauma: i.: harmohlia'. Surgery 24:571-86 
Green MHA, Duell RM, Johnson CD. Jamieson NV (2001 ) 
Haemobilia. Br I Surg 88:773-786 

Nicholson A, Travis S,EttlesDFet at (1999) Hepatic artery 
aitg. ■■:■£:' a pi vy and emriotizatiori for haemobil.a following 
laparoscopic cholecystectomy. CVIR 22:42-47 
Kiviluto T, Kivisaari L. Kivilaakso E (1989) Pseudocysts 
1:1 chrome pancreatil.;: surgical res : .:it ■: in '. 32 consecul ive 
patients. Arch Surg 124:204-243 

Canai-i^alelioglu L, Gurkan A (1996) The management 
."'.reding from a pancreatic pseudocyst: a case report. 
Hepato Gastroenterology 43:278-281 
Woods MS. TraversoLW.KozarekRAetal (1995) Success- 
ful tie;'. I ment o: meeding pseud o aneurysms of chronic 
pancreatitis. Pancreas 10:22-30 

V.;:' i.angenhove P. I>ef<eyne L, Kunnr:'. iVl (1999) Spon- 
taneous thrombosis of a pseudoaneurysm complicated 
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Boudghene F, L'Hermine C, Bigot GM (1993) Arterial 
compjeations o: pancreantis: diagnostic and therapeutic 
aspects in 104 cases. J Vase Interv Radiol 4:551-558 
Woods MS, Traverso LW, El Hamel A, Pare R, Adda G 
(1991) o.eeding pseud orysts ,m.:. psetiooanetnysms in 
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Woods MS. Balthezar EG, Fisher LA (2001) Haemorrhagic 
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. Frey CF (19/?i Pancreatic psetioocyst-operanve strategy. 
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. Uflacker R. Diehl JC (1982) Successful embolisation of 
a blei'.'.i../ y.'i'-ii sr'iry [iiei: .'..'.,. .eurysm secondarv to 
nec.rc .;'. p ui..ri.-i>ri:is : i..>i-f. r.'i -t Radiol 7:379-382 

. HuizinjiJ WK. Kahdeer- JM, Hryer |V (1984) Control of 
maio- i- .'■■■■-■': pancreatic pseudo- 

cysts ■;. i' iriM^lhtls" ,!'ir • c*-oolisation. Br f Surg 
71:131 136 

. Morii? h Mji.i N. <<:: iv;ivtr M tt al (1991 ) Successful 
transcalhclc: emholisationof pst'jdoaneurysm associ- 
ated with :■ in.rcsi.; ;."vl'UiI:i;vsi Am ] Gastroenterol 
86:1264-1267 

. Savastano S. Feltrin GP, Antonio T et al (1993) Arterial 
complications of pancreatiiisidiagnoslic and therapeutic 
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. Rai R, Rose ], Manas D (2003) Potentially fatal haemobilia 
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. Cardella )F, Vuiic I, Tadavarthy SM et al (1997) Vasoac- 
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Wilkins. Baltimore, p 243 

. Yamaguchi H, Wakiguchi S, Murakami G (2001) Blood 
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. Block S, Miae RW, Bittener R et al (1986) Identification 
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26:312-315 



Balloon-occluded Retrograde Transvenous 
Obliteration of Gastric Varices in Portal Hypertension 



Introduction 99 

Balloon-occluded Retrograde Transvenous 

Obkterntion 99 

Clinical Consideration and Pathophysiology 

of Gastric Varices 99 

Technique of BRTO 100 

Results of BRTO 100 

Conclusion 102 

References 1 02 



Introduction 

The major aims of interventional procedures for 
portal hypertension are prophylactic and emergent 
treatment of variceal bleeding, control of hepatic 
encephalopathy, and treatment of refractory ascites. 
Hypersplenism associated with hematological disor- 
der is an add it ional clinical problem in patients with 
portal hypertension. At present, the main primary 
embolo therapies available for portal hypertension 
are balloon-occluded retrograde transvenous oblit- 
eration (BRTO) and partial splenic embolization 
(PSE). In Japan, BRTO has recently been applied for 
gastric varices instead of either endoscopic treat- 
ment or transhepatic intrahepatic portosystemic 
shunt (TIPS) procedure, and numerous studies have 
reported that this method has an excellent success 
rate. Its efficacy for control of hepatic encephalopa- 
thy has also been demonstrated. 



Balloon-occluded Retrograde Transvenous 
Obliteration 

8.2.1 

Clinical Consideration and Pathophysiology of 

Gastric Varices 

Gastric varices are seen in approximately 30% of 
patients with portal hypertension. Although the 
risk of bleeding from gastric varices has been 
reported as relatively low, it differs depending on 
the site of the varices, being much higher in gastric 
fundal varices (nearly 80%) than in cardiac varices 
(nearly 10%-40%) [4]. Generally, control of gastric 
varices is more difficult than control of esophageal 
varices, and the mortality rate of ruptured gastric 
varices is as high as 45%-55% [3]. There are sev- 
eral treatment options for gastric varices, including 
endoscopic sclerotherapy, endoscopic ligation, sur- 
gery, and TIPS. However, in gastric fundal varices, 
endoscopic injection sclerotherapy is not effective 
due to their fast blood flow, and endoscopic liga- 
tion is technically difficult due to their large size. 
Poor hepatic functional reserve prohibits surgery in 
most patients with gastric varices. TIPS is a widely 
accepted procedure for refractory varices bleeding 
in portal hypertension. Although its success rate 
in gastric varices has been reported as 90%, the 
rebleeding rale is approximately 30% [1, 2]. Aggra- 
vation of hepatic encephalopathy is seen in 20% 
of patients after TIPS, and poor primary shunt 
patency is also a problem in patients undergoing 



K. Takahashi, MD 

Department of K;"iC.i.:i!ogy, As,iliik;iw;i Yedicul College, 2-1-1-1 
Midorigaoka, Asahikawa, 078-8 SI 0, Japan 
S. Sun, MD 

Associate Professor of Radiology. University of Iowa Hospi- 
tals and Clinics, 200 Hawkins Drive, 3957 JPP, Iowa City, Iowa 
52242, USA 



llir 






Recently, BRTO as an alternative has been widely 
applied for the treatment ot gastric varices in Japan, 
and favorable results - i.e., a success rate of greater 
than 90% and recurrence rate of less than 10% - have 
been reported. BRTO can be performed in patients 
with poor hepatic function reserve or hemorrhagic 
disorders. And because it is less invasive than other 
procedures, BRTO is expected to get more accep- 
tances for treatment of gastric varices in the future. 



[v.Tokar.ash: oild S. Sill 



The major inflow vessels of gastric varices are 
the short gastric and posterior gastric veins. Gastric 
fundal varices in particular receive a large portion 
of their blood supply from these veins, while the left 
gastric vein supplies cardiac varices. Gastric vari- 
ces drain into the gastrorenal shunt in 80%-85% of 
cases, and drain into the inferior phrenic vein, which 
joins with the inferior vena cava (IVC) just below 
the diaphragm (gastro-caval shunt}, in 10%-15% 
of cases. The inferior phrenic vein also joins with 
the pericardiacophrenic vein or intercostals vein. In 
rare casen, gastrin varices hove both :;oslroienal ami 
gas! rot: aval outflow shunts [8] (Fig. 8.1). 



Technique of BRTO 

Prior to the BRTO procedure, we obtain a contrast 
enhanced CT image with 3-to 5-mm slice thickness 
to evaluate the location and extent of gastric varices 
and their feeding and draining veins. Gastrorenal 
and/or gastrocaval shunt vessels can be well dem- 
onstrated on serial axial CT images with appropri- 
ate contrast enhancement. We can also evaluate the 
size and tortuosity of these shunt vessels. The scle- 
rosant agent consists of a mixture of the same dose 
of 10% ethanolamine oleate (Oldamin; Mochida 
Pharmaceutical, Tokyo, Japan) and 300-350 mgl/ 
ml non-ionic contrast medium. The amounts vary 
depending on the size and number of varices. Before 
and during the procedure, 4,000 units of human 
haptoglobin (Green Cross, Osaka, Japan) are admin- 
istered to prevent hemolysis and subsequent acute 
renal failure. 

A 6-F balloon catheter (Clin: 
Japan) is inserted from either the 
ular vein or the right femoral vei 
advanced via left adrenal vein in 
shunt vessel and wedged into plai 
balloon. Then, a retrograde left adrenal venogram 
is obtained to evaluate the volume and collateral 
vessels of gastric varices. Hirota classified gastric 
varices into five grades according to the degree of 
progression and the number of collateral veins [4]. 
The presence of collateral veins may interfere with 
the complete tilling of gastric varices with sclerosant 
and result in inadequate embolization. Collateral 
veins that are small and few in number are throm- 
bosed during retrograde injection of sclerosant 
through the wedged balloon catheter, but those 
that are medium-to-large in size require selective 
embolization by an embolic coil or ethanol using 



cal Supply, Gifu, 
right internal jug- 
n. The catheter is 
to the gastrorenal 
e by inflating the 




Fig. 8.1. Diagram of una to my of the gastric varices and col- 
lateral vessels. A-.iV, adrenal vein; S,iC balloon catheter; CV, 
coronary vein; IpV. inferior phrenic vein; IVC, inferior vena 
cava; G-R'j-, gasrro-renol shunt: ■:.? V. gasify" vo rices; MC, micro- 
catheter; PrV, pericardiacophrenic vein; PG\~. posterior gastric 
vein; PV, porta! vein; KV, renal vein; SGV. short gastric vein; 
Sp, spleen; SpV, splenic vein 

a 2.9-F microcatheter system. The sclerosant agent 
is injected slowly or in a stepwise fashion through 
either a microcatheter [12] or a balloon catheter until 
the varices are completely filled, and then is left in 
the varices for 1-2 h. After the procedure, residual 
sclerosant is withdrawn through either a microcath- 
eter or a balloon catheter. To evaluate the effect of 
the treatment, contrast-enhanced CT is performed 
1 or 2 weeks after the procedure. In cases with inad- 
equate thrombosis of varices, a second or third pro- 
cedure is generally needed within an interval of a 
few weeks. Multiple procedures are more commonly 
needed in cases with many large collateral veins or 
a very large gastrorenal shunt with rapid blood flow 
(Fig. 8.2; Table 8.1). 



8.2.3 

Results of BRTO 

Excellent initial success rates of BRTO of 90%- 
100% and low recurrence rates of 0%-10 % have 
been reported [4, 5, 9]. Complete thrombosis of 
gastric varices has been identified on the follow- 
up CT scan. In addition to prophylactic treatment 
for gastric varices at high risk of bleeding, a high 
success rate of 82% has also been obtained in gas- 
tric varices with bleeding [7]. Some authors have 
reported an improvement of hepatic function and 
hepatic encephalopathy after BRTO [3, 6, 10]. How- 
ever, additional, longer-term studies will be needed 
to clarify the efficacy of BRTO on hepatic function 



Balloon -occluded Relrograde Transvenous ;!'bale:atioa of Gastric VV.rLtes in Portal Hypertension 




Fig.8.2a-f. Bahoon-oocluded retrograde iiansvenoiis obliteration for gastric varices, a The porlal venous .'base of the splenic 
I'.rteriogr.nV. shows gastric varices sttpplieo ay posterior nin ;■■■■-■ ) .uvi shorl gaslric iiin:n , !i<:<.ni) vein:;, b A left adrenal venogram 
obt.;.ned w.litoi.it L" . . I .:■■:■ n ■ ochivr.-:: sriOAvs .>nteg:ade 'kvv lo i.'.e Irfi ren.il veil; ^n ■-,■ ir; : aad inferior vena c.va (i;n:iuiV,ii/> :■, 
c A lefi adrenal venogram oataaied ua.de: ba.looa ii-clJu sio:i dioiv gastric varices . . r j ■■. ■ n-- .. a few small .:■.-.[.■ ieiv.1 vesse.- : . . - 1 1 ■ H 
esophageal varices i, -i.'i ■:'■■. /rcii/;. d bolero?, ml is iaiecieo ay..: the gaslric varices through a microcaraeier. e A contrast- en it a need 
CT nmtge before KK.TO shows tortuot.s gastric fund;;! varices iiiiTpirj!. f A contrast -nth an. red CT iiaage obtained : cavs after 
B-RTO shows thrombosis of the gastric varices 



, hemothoi 
d intravascular coagulation wi 
Aggravation of esophageal 



[4] 
16%-30%of 



i.nid hepatic encephalopathy. BKTO has also been tion, pulmonary ed 
used successfully to treat ruptured duodenal varices 
[11] (Fig. 8.3). 

Hemoglobinuria is seen after the procedure in 
nearly all cases, but usually disappears within a few 
days. Renal dysfunction is rare. One article reported 
a transient increase in serum creatinine level in 13% 
of cases, which returned to baseline within one 
week [7]. Minor symptoms such as mild fever and 
epigastric pain usually appear after the procedure 
but resolve within a few days or 1 week. Rare but sig- 
nificant complications, such as anaphylactic reac- 



: also reported 



fter BRTO due to occlusion of the 



Table 8.1. Cookbook: Yiiterir^s for aalloon-occluded rt 
gride transwa.ous obliteration 

- 7-F,25-cm Sheath (Terumo) 

- 6-F Balloon catheter (clinical supply) 

- Glidewire, 0.035-0.038 in. (Terumo] 

- Renegade or FAS tracker microcathete, 2.9 F 



Iv.TokaJ'.ash: and S. Puj 




Fig.8.3a-c. Biillooji-o j;Jud ed retrogiode kansvenous oblit- 
for duodenal varices, a A varicogron; obtained by 
iniection of 5C ler::':;;ujl throng:; a ;-'.ic.roco.theler advanced into 
die pjncreaticoduooien.'.l rein shows duodenal varices (iirrDir- 
heads). A balloon catheter :s inserted into the right ovarian 
>).b A contrast-enhanced CT obtained before BRTO 
shows duodenal varices dim; it), c A contrast-enhanced CT 
obtained 7 days after B-RTO shows thiombosis of the duo- 



outflow tract of varices. This is especially 
in patients with preexisting esophageal varices 
gastric varices with afferent flow from the left 
trie veins. However, these esophageal varices 
largely controllable endoscopically. 



of complications of portal hyper 



Conclusion 

BRTO has been proven clinically effective and safe 
in treatment of isolated gastric varices secondary to 
portal hypertension. More randomized perspective 
studies may be necessary to evaluate its usefulness 
in a worldwide scope and its relationship with other 
;h as endoscopic therapies and TIPS 



. horange K, yeron [M et al. (199'H I'ranijujjular :nlrahe 

pa:ic portosystemic shunt in tht iren'rnur.! ••' rcfrj. 

tory bleeding from ruptured ga-'n, va-ices. llepa;i>!oj{y 

30:1139-1143 
. Chau TN, Patch D et al. (1998. "Salvage" rransjugular 

i:i;ro:'.ep.'.t:c portosystemic shu ■ 

pared with esophageal variceal i'ieedm} 1 ,. <iailroer:;er;ii 

ogy 114:981-987 
. FukudaT, Hirota Set al. (2001) l.ong term results iiftia! 

loon -.'!■; citioed relrotrade ".rai'.sw.. -n- ■■.n.ci.uimmi.-. mc 

treatment of gastric varices ,m.:. hepatic encephalopathy. J 

Vase Interv Radiol 12:327-336 



Balloon -occluded Relrograde Transvenous Obliteration, of Gastric VV.:'ii:es in Portal Hypertension 



. Hirota S, Matsumoto 5 et al. (1???! Retrograde transve- 
:;■ '.r; ot ; iteration ..I" gastric varices. Rjdiology J ! i :.U L ">- 
356 

. Kanagawa H, Mima S et al. (]99(.j Treatmenl of gastric 
fundal varices by balloon- occluded retrograde transve- 
nous obkteral ion. I Gastroemerol Hepatol '.'.;••] -f S 

. Kato T, Uematsu T et al. (2001) Therapeutic effect of 
bikloon-occluceci retrograde transvem.-i.is .■ "■I.i-r.i. n 
of portal-systemic encephalopathy in paiienls with liver 
cirrhosis. Intern Med 40:688-691 

. Kitamoto M, Imanr.ira M et al. {l.i.ili Bit [loon- occluded 
reiro grade Iransvenous objuration ofgaslric fundal var- 
ices with hemorrhage. AiR Am ; Roentgenol 17S:1167- 

. Kiyosue H, Mori H et al. (2003) Transcatheter obliteration 
of gastric varices. RadioGraph 23:911-920 



9. Koito K, Namieno T et al. (1996) Balloon-occluded ret- 
rograde iransvenous obliteration for gastric varices with 
gaslroreital or gastrocaval c-.j I lateral:;. AIK Am I Koenlge- 
nol 167:1317-1320 

10. Miyamoto Y, Oho K et al. (2003) Balloon-occluded retro- 
grade iransvenous co. iteration improves live: function in 
patients with cirrhosis a no portal hypertension, i Gastro- 
enterol Hepatol 18:934-942 

11. Sonomura T, Horihata K et a I. (2002 I Ruptured duodenal 
varices successfully treated with balloon-occluded ret- 
rograde transvenoi.s obliteration. A"R Am ' Roentgem:-. 
181:725-727 

12. Takahashi K, Yaraada T et al. (2001) Selective balloon- 
occluded retrograde sclerosis of gastric varices using 
a coaxial microc.ttheter system. AIR Am i Roentgeno-. 
177:1091-1093 



Gynecology and Obstetrics 



Interventional Management of Postpartum 
Hemorrhage 



Introduction 107 

Clinical Considerations 107 

Definitions 107 

Clinical Evaluation 108 

l-';i: Iii'-'i'ivsi,;-.:. igv iOS 

Anatomy 108 

Nonr.al Anatomy 198 

Variants 109 

Etiology and Risk Factors 109 

Vaginal Delivery 109 

Cesarean Delivery 110 

Treatment 111 

Rlfod Transfusion II J 

Embolizalion Procedure 111 

Angiography and Embolization 

:-vr>m:'.<il lechnique 112 

Surgical Treatments 113 

Results lit 

fertility and Pregnancy 114 

Vrophylachi Approach 115 

Com plications 116 

Conclusion IIS 

References 116 



Introduction 

Postpartum hemorrhage (PPH) is a severe, life- 
threatening clinical event. It has been reported that 
at least 150,000 women per annum bleed massively 
during or immediately alter labor [1]. High obstet- 
ric morbidity and mortality secondary to PPH are 

H.T.Abada, MD 

Department of Imaging and Interventional Radiology, Centre 
le de l'lle de Fran 



!-\^pil.iLei Rene I '".if' 
Ccigy-l-'. .moist, r ranee 

J. GOLZARiAN, MD 

Professor of Radiology, Direc 
Radiology, University of Io' 
200 Hawkins Drive, 3957 IPP, 
S.Sun.MD 

Associate f rixessor of ji-.id [■:■!■ >gv. Univei^itv of !o\va Hc-^pit, 
and Clinics, 200 Hawkins Drive, Iowa City, IA 52242, USA 



reported in both developed and developing coun- 
tries. Indeed, the mortality rate due to PPH ranges 
from 13% to 40% [1]. In the United States, the mor- 
tality rate is 13%; however, France, with 414 deaths 
reported over a 4-year period has the highest rate 
of death related to PPH in Europe [2-5]. PPH repre- 
sents the most common cause of blood transfusion 
after delivery. 

The role of the interventional radiology in the 
management of PPH has gained wide acceptance in 
the obstetric-gynecologic community [6, 7]. This 
management requires a multidisciplinary approach 
that involves the obstetrician, intensive care physi- 
cian and interventional radiologist. Selective trans- 
catheter techniques for the treatment of intractable 
bleeding after delivery was first reported in 1970 by 
Brown [8, 9]. Despite the fact that several published 
series have proven the safety and effectiveness of the 
procedure, it remains an underused modality for 
PPH compared to uterine artery ligation or hemo- 
static hysterectomy [10, 11]. 

This chapter will describe the role of embolo- 
therapy for the control of PPH as an alternative 
approach to surgery. We will focus on anatomy and 
on the embolization techniques that are required for 
safety and optimal outcomes for the procedure. The 
clinical and physiological aspects are also discussed 
to provide a better understanding of the potential 
adverse effects that might complicate such a proce- 
dure in otherwise healthy young women. 



Vascular and Interventional 
Department of Radiology, 
■a City, IA 52242, USA 



Clinical Considerations 

9.2.1 
Definitions 

PPH is defined as blood loss of more than 500 ml 
after vaginal delivery or 1000 ml after cesarean 
delivery [12]. This definition is subjective since the 
quantification of bleeding is generally difficult to 



determine. Another approach to estimating blood 
loss is 10% or more drops in hematocrit value [13]. 
The concept of massive postpartum hemorrhage 
was recently defined to include blood loss (more 
than 1500 ml), a drop in hemoglobin concentra- 
tion (>4 g/dl), and an active massive transfusion 
(>4 units of blood) [11]. 

Blood loss that occurs during the first 24 h is 
known as primary PPH; secondary PPH is charac- 
terized by blood loss occurring 24 h to 6 weeks after 
delivery. 



9.2.2 

Clinical Evaluation 



One of the most catastrophic accidents occur- 
ring after delivery is DIC related to amniotic fluid 
embolism (AFE). This condition manifests with an 
acute onset of respiratory failure, circulatory col- 
lapse, shock, and thrombo hemorrhagic syndrome. 
In the United States, DIC accounts for about 10% of 
all maternal deaths. Exaggerated uterine contrac- 
tion caused by oxytocin, caesarean section, uterine 
rupture or premature separation of the placenta are 
risk factors for AFE. Pathophysiology of AFE may 
be related to lacerations on the membrane from the 
placenta that provides a portal entry for amniotic 
fluid into the maternal venous sinuses in the uterus 
[161. 



PPH diagnosis is often obvious when bleeding is 
visible and generally correlates with symptoms of 
hypovolemic shock. On the other hand, a clinical 
underestimation of visible blood loss is possible by 
as much as 50%. In addition, most pregnant women 
are healthy, and this physiologic condition can 
compensate for the blood loss. Hypovolemic shock 
occurs after a deep depletion of blood volume [14]. 
Early diagnosis of PPH is crucial for initiating 
appropriate management as early as possible. Man- 
agement includes restoration of the blood volume 
and identification of the underlying cause. Delay and 
inappropriate management are the leading causes of 
maternal death after delivery. 



Pathophysiology 



Pregnancy causes an increase in maternal blood 
volume by approximately 30%, reaching a volume 
of 4-6 1. The main benefit of this increase is to allow 
the body to respond to perfusion intake of the low 
resistance uteroplacental unit in order to handle the 
blood loss that occurs at delivery [13]. 

The uterus retains its proper physiological con- 
trol of postpartum bleeding. Contraction of the 
myometrium induces compression of spiral arteries 
resulting in hemostasis. The condition that predis- 
poses and worsens intractable bleeding after deliv- 
ery is uterine atony, which inhibits the mechani- 
cal process of hemostasis. In such circumstances, 
bleeding might alter hemostatic status, leading to 
hemorrhagic shock. Endothelial damage resulting 
from the shock causes disseminated intravascular 
coagulation (DIC) [15]. 



Anatomy 

9.4.1 

Normal Anatomy 

A thorough knowledge of vascular anatomy of the 
pelvis is essentialto ensure the safety and effective- 
ness of embolization in overcoming the intractable 
bleeding. The main pelvic blood supply during PPH 
is the uterine artery that arises from internal iliac 
artery (HA) (please refer to Chap. 10.3 for more 
details). The II A divides into an anterior and pos- 
terior branch. The anterior division gives rise to 
the visceral branches. The uterine artery generally 
originates from the medial aspect of the anterior 
trunk. Other branches include the superior vesi- 
cal, middle hemorrhoidal, inferior hemorrhoidal 
and vaginal arteries. The arcuate arteries are 
branches of the uterine artery that extend inward 
into the myometrium, and also have a circumfer- 
ential course around the myometrium. The arcu- 
ate arteries give rise to radial arteries that are 
directed toward the uterine cavity to become the 
spiral arteries in the endometrium (Fig. 9.1). The 
venous plexus runs parallel to the arteries. It is 
generally seen on the late phase of angiograms. Its 
recognition is important and should not be mis- 
diagnosed with contrast media extravasation. The 
vascular network of the female pelvis in pregnancy 
is extensive and provides numerous communica- 
tions between the right and left IIAs. There are 
also many anastomoses communicating with the 
branches of the IIA, such as the inferior mesenteric 
artery, lumbar and iliolumbar, and sacral arter- 
ies. A collateral pathway from the external iliac 



Interventional Mamisemeiii of Postpartum Hemorrhage 




Fia.°.!. Aiitioer.iiii of t':.c rigJn .ire: ine .utery oemon-n;a; ing Fie. 9.2. Seleaive ans^ogr.uii o: :igi'.t ovarian unerv feeJmi: 
spiral arteries the right side of the uterus 



artery provides anastomosis with iliolumbar and 
gluteal arteries. An unusual case of massive bleed- 
ing originating from the epigastric artery, which 
was responsible for embolization failure after the 
occlusion of both internal iliac arteries following 
n delivery, was reported [17]. 



9.4.2 
Variants 



myomata [24]. The role of this artery in PPH was 
previously documented during angiography [25] 
(Fig. 9.3). 

A personal case of anatomic variant was found 
during postpartum hemorrhage embolization in 
which the inferior mesenteric artery was the feeding 
vessel to the uterus (Fig. 9.4). 



Apart from the classic pattern in which the uterine 
artery arises from the medial aspect of IIA, there 
are many other variants that have been identified 
(please see Chap. 10.3). It may also arise from its 
anterior or lateral aspect of the IIA [18]. The origin 
of the uterine artery from the main IIA itself or from 
the aorta has also been described [18]. A common 
trunk between the uterine artery and vesical artery 
is another important variant that might lead to 
inadvertent vesical ischemia in cases of non-tar- 
geted embolization [19]. The uterine artery may also 
duplicate as illustrated by Redlich et al. [20]. The 
ovarian artery represents the second main vessel 
for PPH [21, 22]. The ovarian artery that partici- 
pates in uterine blood supply could represent the 
major feeding vessel to the uterus as demonstrated 
in UFE literature [23] (Fig. 9.2). Recently, Saraiya 
et al. illustrated uterine artery replacement by the 
rou n.i ligament artery during embolization lor leio- 



Etiology and Risk Factors 

9.5.1 

Vaginal Delivery 

A recent randomized trial 
the increased risk of PPH 
induction and augmentatio 
chorioamnionitis, and ma 
[26]. 

A report of 37,497 wome 
UK in 1988 showed that it 
known risk factors to majc 
risks were obesity, a large baby, and 
ified initially as 



the US highlighted 
patients with labor 
ligher birth-weight, 



who delivered in the 
addition to the well- 
PPH, other potential 
:d pla- 
"[27]. 
The most common cause of PPH is uterine atony. It 
; in 2%-5% of deliveries. However, the major- 
managed by conservative measures. Other 
of PPH are retained products of conception, 




Fig.9.3a,b. Rigi'.i iliac a:'.g og:am -howed ." i ."■■-. .1 1 y 1 ;liu\iy: : j"i .:■ n: ilir 1 .n le;v iiii'']vi:'.g ;he 1 ■. ■ 1 1 n ..". Iigaiv.ent afier c-:r. j>.:-.izn :i '.■:'. 
of both right internal UiaC and uterine arteries 




ig.9.4a,b.A 31-year-old worn 


an with PPH ( 


olic artery supplying the titer 


B («mnw),l»E 


eeds exclusively the uterus (a 


7DW).(C0Urt«! 



Sc^ctive Lii]gi-igi":;iti of l lie niredo: :i:esenteiic .uteiy : IMA 1 showed the !c-:l 
ly phase of selective angiogram of the )\'A shows that the second left division 
of Patrick Garance) 



placental abnormalities, uterine rupture, lower gen- 9.5.2 

ital tract laceration and coagulopathies. In a study Cesarean Delivery 

of 763 pregnant women who died of hemorrhage, 

l9°o bad placenta! abruption, 16% uterine rupture, A case-controlled study for risk factors of PPH 

15% uterine atony, 14%coagulopathies. 7% placenta following cesarean among 3052 cesarean deliver- 

praevia, 6% placenta accreta, 6% uterine bleeding, ies was performed by Combs et al. [29]. The major 

4% retained placenta, and 10% other or unknown factor was found to be related to general anesthesia 

causes [28]. (OR 2.94), followed by amniotitis (OR 2.69), pre- 



Interventional Management of Postpartum Hemorrhage 



eclampsia (OR 2.18), protracted active phase of labor 
(OR 2.40), and second (OR 1.90). 

On the other hand, maternal age represents an 
independent risk factor of blood loss irrespective of 
the mode of delivery. Indeed, a maternal age equal 
or superior to 35 years had an OR of 1.6-1.8 [3D]. 



Treatment 

Postpartum hemorrhage is an emergent clinical 
scenario and requires immediate medical attention. 
Mu Itidiscipli nary collaboration among the inten- 
sive care physician, obstetrician and interventional 
radiologist is crucial for optimal management. 
Interventional radiologists play a significant role 
in the treatment of massive or intractable bleeding. 
In the setting of ongoing bleeding after the deliv- 
ery, conservative management is the first approach. 
Measures include vaginal packing, uterine massage, 
intravenous administration of uterotonic medica- 
tions such as oxytocin or methylergonovine, curet- 
tage of retained placenta, fluid replacement and 
blood transfusion. These measures successfully con- 
trol the bleeding in most situations. Embolotherapy 
should be considered when these measures fail. 



9.6.1 

Blood Transfusion 

Blood transfusion represents a major component 
during the medical management of severe postpar- 
tum hemorrhage. A transfusion may be initiated in 
patients who continue bleeding, developing shock 
despite aggressive medical management. However, 
blood transfusion constitutes a risk of contamination 
by human immunodeficiency virus or hepatitis B and 
C [31]. The contemporary obstetrician's practice is to 
develop measures to reduce blood transfusion. Indeed, 
blood transfusions dropped from4.6% in 1976 to 0.9% 
in 1990. In a recent study, Reyal et al. confirmed these 
data with a transfusion rate of 0.23% on a cohort of 
19,138 deliveries over a 7-year period [32]. 

Our unpublished data in a retrospective study 
showed that embolization following PPH might pre- 
vent blood transfusion when close medical manage- 
ment and rapid evaluation of the emergency status 
is performed. These findings probably highlighted 
an additional advantage o( emboli/.mion procedures 
after delivery. 



9.6.2 

Embolization Procedure 



9.6.2.1 

Angiography and Emboliz 



When embolotherapy is indicated, the patient is 
transferred to an angiographic suite. Intensive care 
physicians should be present during the procedure. 
Right femoral artery access is obtained, and a 4- 
or 5-F sheath is inserted. Additionally, left femoral 
venous access may be obtained to be used by the 
intensive care physician if no other central access is 
available for supportive therapy. 

Catheterization of bilateral uterine arteries is 
mandatory. A cobra-shaped catheter is the best 
catheter to use for easy insertion into uterine arter- 
ies. The cobra catheter is available in three different 
types, each according to the degree of opening of the 
curve. The medium sized catheter (C2) is the one 
most commonly used. When using a 4-F catheter, 
one should make sure that the lumen of the cath- 
eter is able to accept 0.038-in. guidewire for possible 
microcatheter use. The contralateral internal iliac 
artery is catheterized first and can be reached by 
pushing the cobra. In some difficult cases, a curved 
catheter, such as SOS or sidewinder, could be handy 
to cross the aortic bifurcation. 

The ipsilateral uterine artery access is obtained 
using the Waltman loop. When the angle of aortic 
bifurcation is too tight, again the use of a sidewinder 
allows for easy catheterization. 

Aiiyioa :ipliy can detect contrast medium extrav- 
asation; however, this is not seen in the majority of 
cases. Contrast media extravasations were observed 
in 18% of patients in a recent study [33]. Even with- 
out extravasation, bilateral uterine artery emboliza- 
tion needs to be performed. 

The preferred embolic agent is a material that is 
resorbable. The one most widely used is Gelfoam. 
Gelfoam can be cut into different sizes depending 
on the target vessel diameter. The Gelfoam can also 
be cut in torpedo and inserted into a 1-ml syringe. 

Finally, an aortogram is performed to demon- 
strate the effectiveness of the procedure and the 
course of ovarian arteries that might be embolized 
secondarily in cases of rebleeding (Fig. 9.5). One 
must pay attention to collaterals from ovarian arter- 
ies during such embolization procedures because 
they may be responsible for delayed bleeding. Even 
though we routinely perform abdominal aortogram 
after embolization, we never embolize ovarian arter- 
ies to prevent possible delayed rebleeding. While we 




Fig. 9.5. Final sonogram sbowec! complete seclusion of uter- 
ine arteries. The patenl ovarian .uteries were d em cms tin led 



did not observe contrast extravasations from ovar- 
ian arteries during the abdominal aortogram in 
our data, one must be aware that it could happen. 
Indeed, Oei et al. demonstrated persistent bleeding 
following hysterectomy for intractable PPH related 
to a left ovarian artery that was embolized second- 
arily [34]. 

The patient leaves the angiographic suite with the 
sheath sutured in place in case there is a need for a 
second embolization session. 



9.6.2.2 

Personal Technique 

As previously mentioned, medical management of 
obstetric bleeding after delivery is conducted by 
using drugs such as uterotonic drugs (oxytocin) 
and prostaglandin E 2 agonist. The latter has a vaso- 
constrictor effect and thus causes arterial spasm 
(Fig. 9.6). 

For this reason, when an embolotherapy is 
planned we recommend immediate cessation of 
prostaglandin E 2 agonist infusion. In case of arte- 
rial spasm at the ostium of the uterine artery, the 
use of a coaxial system with a microcatheter is then 
required. It is possible to successfully catheterize 
the distal part of the uterine artery in most cases. 
In these circumstances, the preferred embolic agent 
is the one that can be easily delivered through a 
microcatheter, such as PVA (Polyvinyl alcohol} or 
Embospheres. We prefer to use particles with larger 
diameters, such as Embospheres 700-900 mu.. Even 
if these particles are used for the above-mentioned 
reasons, additional Gelfoam embolization of inter- 
nal iliac arteries is performed because of the exten- 
sive collateral pathways of the female pelvis. 

In the absence of arterial spasm, embolization 
with Gelfoam pledge of both uterine and internal 
iliac arteries is always performed in order to obtain 
a bilateral proximal and distal embolization to 
prevent rebleeding. Even with Geltoam pledge, we 
always use large-cut sizes to prevent embolization 
that is too distal. Embolization with coils is not per- 




e artery involving p: 
n(c) (arrow) 



(a), and disi.il segments !b,cl. Sp.'.sm induced .! complete 



Interventional Man;', gem em of Postpartum Hemorrhage 



formed for two reasons: first, it attempts the proxi- 
mal occlusion that might be less effective; secondly, 
it could "burn the bridge" for a subsequent emboli- 
zation in cases of rebleeding. However, 
have the potential to stop a bleed from a small 
as shown in Fig. 9.7. 



not treat the 

Finally, the infertility 

tomy is an important it 
s tion group. Although th 
1 only treatment available to control a PPH 

conditions, it should, however, be only ust 

last resort. 



nal laceration (Fig. 9.8). 
sociated with hysterec- 
ie in this young popula- 
surgical procedure is the 



9.6.2.3 

Surgical Treatments 



tin- 



lateral internal iliac ligation and hysterectomy a: 
surgical treatments that unfortunately a: 



Results 



still very commonly used to control PPH. The 
ol hypogastric ligation is to reduce the blood flow, 
allowing normal coagulation to control the bleed- 
ing. However, ligation is associated with a high fail- 
ure rate since it is proximal, and the bleeding may 
continue through collateral vessels. Moreover, liga- 
tion will make the embolization procedure much 
more challenging. Hysterectomy is the other sur- 
gical treatment that is widely used. This surgery 
is a high-risk procedure in patients with DIC and 
hemodynamic impairment, and hysterectomy will 



Since the first embolization of PPH performed by 
Brown in 1979, the reported success rate in 138 
patients over a 20-year period was as high as 94.4% 
[35-43]. To date, 160 patients have been treated at 
our institution (the first author's institution) by 
selective uterine and/or internal iliac arteries embo- 
lization for intractable bleeding following delivery. 
Despite the variety of the etiologies and risk factors 
in our series, no maternal deaths were observed. The 
main cause of hemorrhage was related to uterine 
atony, with an incidence of 75%. Cesarean delivery 




Fig.9.7a-d. Angiogram of :ig:'.: iiiterii.il iliac artery demonstrates ci 
n using mi croc. it holer and emoo^izalion with n 



n (double arrow): super selective 
rsi. (Courtesy of Patrice Garance) 




■illation. LaLi results 

e of the transfer, 

i the angiographic 

in hemoglobin was 

emoglobin level ot 



'ed acute 
on of 4 . 



was performed in 30% of our popul 
and clinical data recorded at the til 
or at the arrival of the patient i 
suite, showed that a mean drop 
4.5 g/dl (+/- 9) with a median h 
7.14 (ranging from 3 to 10.2). 

A total of 20% of patients rece 
transfusion, defined as transfut 
units of packed red blood cells. Hemodynamic status 
and blood parameters showed that 30% of patients 
developed shock, and 50% developed DIC. Hysterec- 
tomy was performed in six patients, despite the fact 
that embolization was initially successful to stop 
bleeding and improved blood parameters. However, 
rebleeding occurring at .in average of 6 h after embo- 
lotherapy justified hysterectomy. No second session 
of embolization was performed. If we consider that 
a subsequent hysterectomy represents a failure of 
the procedure, our success rate was also 94.4%. In 
our experience, embolization was always effective in 
the correction of blood parameters and made it pos- 
sible for gynecologists to perform the hysterectomy, 
when needed, in a better coagulation and hemody- 
namic status. On the other hand, shock, DIC, and 
acute massive transfusion were not the indicators 
that were able to predict the effectiveness of selec- 
tive arterial embolization. Indeed, these indicators 
considered individually or together were not statis- 
tically significant in predicting the success of the 



procedure. However, despite the latter statement, 
hysterectomies were all performed in the group of 
patients with shock, DIC, or acute massive trans- 
fusion. We did not find any relationship between 
contrast media extravasations observed during the 
procedure and patients' clinical and hemodynamic 
statuses (Figs. 9.9, 9.10). In all, 71 patients were 
referred from other hospitals where embolization 
was not available due to the absence of an interven- 
tional radiology unit. The median transfer time was 
5.48 h, and this concurred with the time reported in 
the literature [44]. The transfer itself did not repre- 
sent a major risk factor [44]. What was critical was 
to offer the optimal medical managements prior to 
and during the transfer. 

In our experiences, abnormal placentation did 
not affect the effectiveness of the procedure, con- 
curring with the findings of Desc argues et al. [43]. 
However, Vandelet et al. observed in a series of 29 
patients that when an emergency postpartum embo- 
lotherapy is attempted, obstetrical history constitute 
a major risk factor and, furthermore, that transfer 
increases the morbidity rate [45]. 

Embolization can also be successful however 
more challenging after failure of bilateral IIA liga- 
tion for primary PPH [46]. The failure was related to 
the extensive development of pelvic collateral path- 
ways following internal iliac ligation. The bleeding 
artery was a branch from the epigastric artery. The 
cases described above may imply that the transcath- 
eter embolization should be the first line of thera- 
peutic approach when patients are hemodynami- 
cally stable. It also emphasizes the importance of 
thorough knowledge of possible collateral pathways 
post-surgical ligation of internal iliac arteries, and 
the physiological condition of pregnant w 



Fertility and Pregnancy 

Even though the first goal o( embolization following 
PPH is to achieve hemostasis and overcome a life- 
threatening condition, this technique clearly helps 
the patient to avoid hysterectomy, thus preserving 
fertility. 

Evaluation of the fertility in these patients is 
somewhat difficult because of the lack of informa- 
tion on patient desire for future pregnancy. This 
information is difficult to obtain if it was not previ- 
ously indicated in the record during the period of 
clinical monitoring of the pregnancy. Stancato et 



i. Momigirmi'iii of Poitpiir 




ri Healed 



ame fertil- 
5 observed 



al. reported three pregi 

by embolization lor PPH. Moreover, thn 
pregnancies resulted from the three wc 
series who desired to conceive [47]. The 
ity rate following PPH embolization w; 
by Ornan et al., with six pregnancies occurring 
after a long-term follow-up of 11.7 years (+/- 6.9) 
[48]. Salomon et al. followed 17 women between 12 
and 80 months after pelvic embolization for PPH. 
Tliev observed six pregnanues in live women [4'i]. 
In the these series, four women with history of PPH 
developed a new PPH in their following pregnancy. 



Causes of PPH, in this study, were related to the 
placenta in all cases. Nevertheless, in two patients 
who underwent hysterectomy to stop bleeding, no 
pathological evidence indicated precisely the causes 
of these recurrences of bleeding. 

Finally, fetal growth retardation (FGR) is reported 
to occur in patients after uterine artery emboliza- 
tion; this was reported in one case by Cordonnier 
etal. [50]. 

While the technique, embolic agents and clinical 
conditions of patients with PPH and fibroid embo- 
lization (UFE) are different; UFE ii 



i of 139 patients 

[51]. The incidence 

by Goldberg [52]. 

tudy following 



with term pregnancy. In i 
treated for fibroids, 17 pregn; 
14 women who desired ti 
ofFGR seems higher in 
However, in a recent 1; 
671 patients who had UAE for symptomatic fibroids, 
Carpenter etal. found 26 completed pregnancies in 
which only one case of FGR was recorded, support- 
ing the evidence of normal placentation [53] also 
documented in the Ravina series [54]. Carpenter 
etal. also found that first- and second-term bleeding 
occurred in 40% and 33%, respectively, miscarriage 
was found in 27% and primary PPH was observed 
in 20% [53]. 



Prophylactic Approach 



PPH in patients with a diagnosis of abnormal pla- 
(placenta accreta, increta and percreta) is 




Fig. 9.10a,b. Late ph 



higher than in other patients. This supported the 
idea of temporarily limiting the blood flow to the 
uterus in this high-risk patient population. The so- 
called prophylactic approach is achieved by selective 
catheterization of internal iliac arteries using femo- 
ral puncture, which is followed by the introduction 
of balloon catheters in each internal iliac artery. The 
balloon is inflated prior to the delivery. Kidney etal. 
performed this technique in five patients who were 
gravida 4 to 5 and para 1 to 4 before hysterectomies 
for sterilization [55]. The clear goal of such a proce- 
dure is to decrease blood loss and potentially prevent 
blood transfusion and surgical mortality. In case 
of concern for bleeding in patients with abnormal 
placentation, some authors use balloon occlusion as 
a first step to reduce flow in internal iliac arteries 
followed by internal artery embolization [31]. 

Our approach to patients with abnormal placen- 
tation in re. selectively emboli/e bilateral uterine dnd 
internal iliac arteries as soon as possible after delivery. 
Using the embolization technique, we obtained results 
similar to that of the prophylactic in controlling PPH, 
but without the risk of radiation to the fetus. 



9.10 

Complications 

A complication rate of 8.7% was reported in the 
literature [56-59]. This includes contrast-induced, 
puncture and embolization related complications. 
The reported complications related to the emboliza- 
tion include foot ischemia, bladder necrosis, rectal 
wall necrosis, nerve injury and uterine necrosis. 
These complications are caused by non-targeted 
vessel embolization. 

Uterine necrosis after arterial embolization was 
reported in one patient where the PVA particles of 
150 p-250 u were used. It seems clear that this com- 
plication occurred due to the small size of the par- 
ticles, causing distal embolization that led to myo- 
metrium ischemia [59]. We have been using PVA or 
Embosphere particles with a size range of 500-700 p. 
and 700-900 p. No complications have occurred in 
our latest 21 patients. Recently, a case of both uterus 
and bladder necrosis was reported when using Gel- 
foam. The complicat ion became evident 3 weeks after 
embolization [60]. The embolic agent was obtained by 
scraping the Gelfoam with a surgical blade, and the 
resulting product was then injected into the vessel. 
Deep embolization with smaller particles obtained in 
this way is the cause of this adverse event. 



the 



9.11 

Conclusion 

The selective transcatheter technique for emboliza- 
tion of uterine and/or internal iliac arteries 
management of intractable bleeding after delivery ii 
safe and effective. In order to create the best hemo- 
dynamic and clinical conditions for this therapy, ; 
strong multidisciplinary collaborator 
to optimize clinical outcomes. 



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10 Fibroids 



Gary P. Siskin, Jei 
Arnaud Fauconn 



rey [. Wong, Anne C. Roberts, Jei 
r, Pascal Lacombe, Alexandre L, 



;rre Pelage, 

t, and Jafar Gol; 



10.1 Uterine Fibroid Embolization: Practice Development 



Gary Siskin 



The practice model for interventional radiology is 
changing and nowhere is that more evident than in 
the care surrounding patients undergoing the uter- 
ine artery embolization procedure for symptomatic 
uterine fibroids. For many years, interventional 
radiologists have had it good. The techniques that 
we have worked to develop given our skill set and 
expertise have often been some of the most interest- 
ing and cutting-edge procedures performed within 
all of medicine. Given the minimally invasive nature 
of our specially, physicians referred patients to us 
and relied on our expertise to deliver this state- 
of-the-art care to their patients. Problems arose 
when it became evident that we accepted very little 
responsibility towards delivering the pre-procedure 
and post-procedure care associated with these pro- 
cedures and the disease processes bringing these 
patients to our attention. Physicians from a vari- 
ety of specialties have learned that it is within their 
skill set to perform these procedures, and are doing 
so for obvious economic reasons but also because 
they have the infrastructure, training, and desire to 
follow these patients throughout an entire episode 
of care. 

Interventional radiologists now understand that 
this practice model can no longer continue. Instead, 
interventiona lists must accept a number of respon- 
sibilities, including generating referrals, provid- 
ing the expertise to evaluate and prepare patients 
for our procedures, and caring tor patients as they 
recover from our procedures. 

Uterine fibroid embolization (UFE) represents 
one of the best examples of a procedure that can 
only become a successful part of an interventional 
practice if that practice is willing to take on the 
responsibilities inherent to this new model. In fact, 
generating referrals and providing pre- and post- 



G. Siskin, MD 

Associate Profess;:'!' of Radiology ai'.d Ol"s;elncs and Gynecol- 
ogy, Alba nv Mroical Cellar. -.7 New Scot km;: Avenue, MC-113, 
Abany NT 12208-3479, USA 



procedure care are mandatory components of a UFE 
practice. While most interventional radiologists 
would quickly state that this is not a radical depar- 
ture for them and their style of practice, it is not 
until one becomes immersed in the nuances of this 
procedure and this patient population that the enor- 
mous nature of this commitment and the demands 
on one's time that are required for it to succeed can 
be understood. 

The patients potentially served by UFE are dif- 
ferent to those often seen within an interventional 
radiology practice because they are healthy people 
with a lifestyle-altering problem. Because these 
patients are electively choosing to seek medical 
care, they make demands on health-care provid- 
ers that patients with greater morbidity often do 
not. In addition, this often represents the first time 
that these patients are seeking treatment for a medi- 
cal problem. In today's world, with so much medi- 
cal information available to patients on television, 
in newspapers, and on the internet, it is no wonder 
that these patients tend to present for their consulta- 
tions already armed with a large amount of informa- 
tion regarding UFE and other treatment options for 
fibroids. In addition, women in general are known 
to be active participants in the decision-making 
process surrounding their health care and these 
patients are certainly no exception. 

Interventionalists also have to become prepared 
to work with gynecologists since they are often the 
primary care providers for this patient population. 
Typically, gynecology patients do not require the 
services offered by interventional radiology. There- 
fore, gynecologists are not accustomed to referring 
patients to us. More importantly, they are not accus- 
tomed to having another specialty offer an effective 
treatment for a classic "female problem" that only 
they have treated in the past. It is clear that their 
first impression, as a specialty, has been to view UFE 
with skepticism and even as a threat to their prac- 
tice. Therefore, gynecologists have not often been 
immediately forthcoming with referrals although 
recent acknowledgment by the American College 



of Obstetrics and Gynecology of the effectiveness 
or potential for effectiveness of this procedure has 
been indicative of the growing level of acceptance 
of this treatment option within the OB-GYN com- 
munity. 

Taking these characteristics into account, one 
can see that a potential conflict exists between well- 
informed patients desiring ;in active role in their 
own health-care, and gynecologists perceiving LIFE 
as a threat to their practice and therefore not provid- 
ing their patients with information about this proce- 
dure. This conflict forms the basis for the require- 
ment that interventional radiologists participate in 
generating referrals for LIFE because gynecologists 
are not, in general, going to help start a LIFE service. 
However, it has been our experience that in time, 
once many LIFE procedures have been performed at 
an institution with outcomes consistent with those 
reported nationally and internationally, gynecolo- 
gists begin referring patients and contributing to 
the continued success of this service. This does 
take time and in our case, several years have passed 
between our first cases, when all patients were self- 
referred, and now, when the majority of cases are 
referred from our local and regional gynecologists. 
This trust was earned and grew largely from our 
ability to understand the above-stated conflict and 
to find ways to reach out directly to patients while at 
the same time educating gynecologists and assuring 
them that UFE will not lead to the demise of their 

The cornerstone of our practice development 
effort was the belief that the long-term success of a 
UFE service relies on cooperation from gynecolo- 
gists. We do believe that patients are more informed 
than they have ever been about matters concerning 
health care and that they are indeed directing health 
care decisions. However, it must be acknowledged 
that most patients still receive their health-care 
information from their physicians. The relationship 
between a patient and her gynecologist is often one 
of trust and, therefore, patients still rely heavily on 
their advice. It is probably reasonable to assume that 
direct and aggressive patient advertising will almost 
certainly lead to a short-term increase in the number 
of UFE procedures performed by an interventional 
radiologist. Ultimately, however, it is our belief that 
gynecologists will not appreciate attempts at work- 
ing around them and they will likely hurt your UFE 
practice by simply not supporting it. 

With this in mind, we utilized several strategies 
for generating referrals to our UFE program: (1) 
i directed at gynecologists and patients 



regarding UFE; (2) education directed at our- 
selves regarding fibroids and treatment options for 
fibroids; (3) consistent support of the relationship 
between patients and their gynecologists; (4) care 
which meets the expectations of our patients and 
their gynecologists; and (5) accessibility for patients 
and gynecologists to the providers of this service. 
With this approach, we have earned referrals from 
local and regional gynecologists that are strongly 
supported by patient interest and positive word- 
of-mouth from patients going through UFE at our 
institution. 

Our first task was to educate gynecologists about 
UFE. Interventional radiologists working within an 
academic institution may have an advantage here 
since they are more regularly exposed to educational 
activities. Offering lectures to medical students and 
residents concerning interventional radiology and its 
role in the care of OB-GYN patients is a first step that 
will likely lead to participation in journal clubs and 
departmental grand rounds. Our focus on educating 
students and residents was done with a clear under- 
standing that educating students and residents will 
lead to future gynecologists that have a good under- 
standing of the role of our services. This has a good 
chance of translating into long-term success since it 
is well known that after graduation, residents often 
remain in the region near where they have trained. 
Education efforts, however, were not just directed at 
trainees. Staff and community gynecologists often 
attend these meetings, providing us with an oppor- 
tunity to make these physicians aware of what we 
can do for their patients. We also extended offers to 
provide lectures to physician groups in surround- 
ing community hospitals in order to increase their 
awareness of this procedure as well and found that 
monthly staff meetings or grand rounds at commu- 
nity hospitals make an excellent forum for this type 
of presentation or discussion. 

Once physicians became more informed about 
UFE, we recognized the importance of informing 
patients about this treatment option. Keeping the 
cornerstone of our practice development philoso- 
phy in mind, we recognized the challenge to increase 
patient knowledge without directly advertising and 
therefore inviting the perception that we do not need 
gynecology. We utilized the public relations depart- 
ment in our own hospital to help us with this. Once we 
had just a few patients who had a successful outcome 
after UFE, our hospital PR department brought these 
patients to the attention of our local news media. 
Every local newspaper and local television station 
has health reporters looking for stories of new and 



Uterine Fibroid Erritnr-iiziiiion: ^ fact ice Development 



exciting breakthroughs hi medical care and our com- 
munity was no exception. Once we had patients with 
good stories to tell, these success stories were printed 
in newspapers and were made the subject of televi- 
sion news reports. It was our belief that these infor- 
mative reports regarding this new procedure were 
not "direct advertising" yet had the same desired 
effect in reaching out to potential patients, making 
them aware of this option. Our efforts to educate our 
local gynecologists also enabled us to participate in 
patient- directed programs at community hospitals. 
Ultimately, we were able to meet our early goal to pro- 
vide patients with the information necessary to ask 
their gynecologists questions regarding UFE, and to 
provide the information to gynecologists enabling 
them to answer those questions. 

Efforts to educate both gynecologists and 
patients, however, are not enough. The final step in 
the education process involved the need to educate 
ourselves about uterine fibroids and the treatment 
options available to patients with fibroids. As rela- 
tionships are established with gynecologists and 
patients suffering from symptomatic fibroids, itwill 
become clear that knowledge about embolization is 
not enough. It is impossible to become an expert on 
UFE without knowing and understanding uterine 
fibroids and where UFE potentially fits into the man- 
agement of these patients. Patients will undoubt- 
edly ask you questions about the "other" options 
and they expect you to know the answers. There- 
fore, attending conferences and reading books and 
articles about fibroids will be an important part of 
a practice development strategy. Reading should not 
be limited to medical journals and textbooks. Books 
written for the lay population should also represent 
mandatory reading because these are the books that 
your patients are reading. Similarly, familiarity with 
commonly visited web-sites and chat groups is nec- 
essary because this is where patients today are often 
receiving their medical information. 

While education has always been an important 
component of our efforts to develop this part of 
our practice, providing care that meets and exceeds 
the expectations of our patients and our referring 
physicians is arguably more important for the long- 
term success of a UFE service. Acceptable outcomes 
and future referrals are dependent on our ability to 
provide excellent patient care and we strive to reach 
that goal at every step of the process. That is because 
good outcomes speak for themselves. 

Meeting the expectations of referring gynecolo- 
gists is fairly straightforward. Gynecologists expect 
that UFE will be offered to patients with the high- 



est probability of success and that we will achieve 
the success that we claim can be expected with this 
procedure. Therefore, familiarity with expected 
outcomes is mandatory for interventional radiolo- 
gists as is a fair assessment of a patient's probabil- 
ity of success with this procedure. Gynecologists 
also expect that their patients will be comfortable 
during the procedure and that these procedures are 
performed with an appropriate level of expertise. 
We have therefore encouraged all gynecologists to 
observe procedures performed on their patients. 
Every gynecologist who has taken us up on that offer 
has consistently referred patients to us. Gynecolo- 
gists also expect reliable communication with our 
office so that they are aware when a patient is con- 
sidering this procedure, has undergone the proce- 
dure, and has demonstrated clinical improvement. 

When gynecologists refer patients to interven- 
tional radiology for UFE, they are doing so with 
the understanding that everything surrounding the 
UFE procedure will be managed by the intervention- 
alists, including insurance pre-approval, hospital 
admission, pain management, and initial assessment 
in the event of a complication. There is no reason 
why any interventional radiologist cannot observe 
a patient overnight (it necessary) and provide pain 
management services during a patient's recovery 
from UFE. It is perfectly' acceptable to consult anes- 
thesia as pain management protocols are developed 
but it is not acceptable to perform this procedure and 
then rely on gynecologists to manage the pain expe- 
rienced during recovery. No, we cannot perform a 
hysterectomy in the event of a complication requir- 
ing that procedure. We can, however, assess that 
patient, communicate with their gynecologist if we 
suspect a complication, and maintain an appropri- 
ate level of involvement in that patient's care during 
the management of that complication (facilitating 
imaging and researching questions that arise during 
these episodes). By taking on these responsibilities, 
we will earn our place as legitimate providers of this 
service. If an interventional radiologist is not willing 
to take on these responsibilities, then it is unreason- 
able to expect referrals since most of the hard work 
still rests on the shoulders of the gynecologist. 

In our experience, meeting the expectations of 
the patients has been more challenging. As a result, 
we have changed a lot about the way we practice 
and have carried these changes over to virtually 
all aspects of our interventional radiology practice. 
Patients expect to be seen by a physician in consulta- 
tion before any management decisions are made and 
any procedures are performed. For decades, inter- 



vi-nuoaiil i-.idKik'aisrs were peitonmng pocedu]e<. 
that are essentially equivalent to surgery without 
ever meeting their patient outside of a brief pre- 
procedure visit immediately before the procedure 
started. Today, this cannot be tolerated and patients 
being considered for UFE must be seen in consulta- 
tion first and we believe that this is best performed 
in a true outpatient clinic setting in order to meet 
the expectations of our patients. 

In order to effectively pa nicipaieind in ieal patient 
management, interventionalists require an infra- 
structure within their practice to manage patients 
in both the inpatient and outpatient setting. One 
would be hard-pressed to find a clinical specialty 
that does not consider space designed exclusively 
for establishing, maintaining, and fostering the 
physician-patient relationship a priority for their 
clinical practice. Most radiologists, however, work 
within hospital departments or outpatient imaging 
centers that are not optimized for "non-imaging" 
outpatient consultations. Therefore, interventional 
radiologists seeking to develop this type of outpa- 
tient practice will need to overcome this obstacle by 
finding appropriate space either within or outside 
the hospital setting in order to evaluate patients in a 
true outpatient office. 

An equally important expectation held by patient', 
is the need for both expertise and compassion from 
their physician and the team making up an interven- 
tional practice. Attention must be paid to establish- 
ing rapport and communicating honestly and effec- 
tively with patients since this will form the basis of 
a successful doc tor- patient relationship. Creating a 
good rapport with patients in an outpatient clinic 
setting will increase their comfort, enhancing the 
discussions about their medical history and treat- 
ment options. As technology has improved, most 
physicians often focus on diagnosing and treating 
the disease causing the patient to seek treatment. 
While this is of course a necessary component of 
any medical treatment, time should be set aside to 
understand how best to treat both the disease and 
the way that the disease has affected the patient's 
quality of life. As medical knowledge and technology 
have improved, most physicians, and perhaps inter- 
ventionalists in particular, have become focused on 
diagnosing and treating disease. An interventional- 
ist skilled at diagnosing and treating complex medi- 
cal problems but understanding that disease and the 
procedures used to diagnose and treat disease have 
implications on a patient's quality of life, will have 
the insight necessary to successfully contribute to 
the overall care of their patients. 



We have found it to be very helpful for our patients 
to make sure they have the opportunity to speak 
with a female nurse who is familiar with all aspects 
of this procedure and we have devoted the resources 
necessary to support nurse practitioners and a nurse 
clinician who are themselves experts in UFE and in 
the care of UFE patients. Nursing support is critical 
to success with UFE because it enables more patients 
to confide in our team regarding the true nature of 
their symptoms and as a result, the true nature of 
their expectations. Once these non-physician pro- 
viders are integrated into a practice, the physicians 
must respect their role as the patient advocate within 
the practice and support them in the eyes of the 
patient so the patient is comfortable in their deal- 
ings with them and has confidence in utilizing all of 
the personnel resources within a cohesive practice. 

It is also important to be accessible to patients to 
be willing to address their concerns before and after 
their UFE procedure. This requires a commitment 
on the part of an interventional radiology service 
because these patients do ask questions and do make 
demands on staff. There is no doubt that nursing 
staff dedicated to providing this type of care to these 
patients is critical for success. We have always tried 
to anticipate the needs and concerns of our patients 
and make it a rule to proactively call patients indi- 
vidually at defined times during the recovery period 
in order that they know we are there for them. In 
addition, a willingness on our part to address con- 
cerns via e-mail added a level of convenience not 
experienced by most patients and, in truth, is easier 
for us since focused answers to questions canbe pro- 
vided in very little time. When this part of our ser- 
vice runs smoothly, patients are almost uniformly 
impressed and very satisfied, which often leads to 
positive feedback to their gynecologist, family, and 
friends (all potential sources of future referrals). 

By taking the "education" and "service" approach 
to practice development, we have been successfully 
moving towards our initial goal or having local and 
regional gynecologists mention UFE in the list of pos- 
sible treatment options for uterine fibroids. It was and 
still has never been our expectation that every patient 
with fibroids gets referred for UFE. Including UFE in 
that list is a big step for most gynecologists but by 
no means assures you of referrals. It does, however, 
assure that patients will ask questions and gynecolo- 
gists will need to provide answers. Even if a gynecolo- 
gist still recommends hysterectomy for most patients, 
the mere fact that UFE is listed as an alternative to 
surgery will provide an option for patients looking for 
a nonsurgical ti 



uterine Fibroid Ensboii virion: ^lactice Develop m 



It has also never been our expectation Co "take 
these patients away" from the gynecologist. We 
understand that nobody controls a patient. In fact, 
it is our belief that any group claiming to have "con- 
trol" over a patient or group of patients is doing so 
because they have established the outpatient based 
practice that enables them to do so. Being confident 
in our ability to provide that service, we divert the 
focus away from "control", support the relationship 
between a patient and their gynecologist, and do not 
undermine that relationship in any way. Therefore, 
we communicate frequently with referring gynecol- 
ogists and require that every patient be under the 
care of a gynecologist (preferably their own) before 
undergoing the UFE procedure. When patients tell 
us that they are angry with their gynecologist for not 
discussing UFE, we defend that gynecologist and 
explain that it takes time for any physician to feel 
comfortable recommending a new procedure. We 
would rather not have patients sever their relation- 
ship with a gynecologist because of UFE because, 
again, that does not bode well for the long-term suc- 
cess of our program and, more importantly, is not 
necessarily in the best interest of our patients. Yes, 
we are not happy when we hear that, but we look at it 
as an opportunity to communicate with this gyne- 
cologist, educate him or her about UFE, and add to 
the number of patients from that practice treated 
successfully with UFE. 

We are pleased to report that the referral pattern 
for UFE has changed with time. As mentioned, most 
of our referrals now come from gynecologists instead 
of from the patients themselves. In addition, several 
practices in our area send almost all patients with 
fibroids to our oil ice before treatment decisions are 
made, simply to educate them regarding all avail- 
able treatment options. This has clearly exceeded 
our expectations. Most other practices may not be 
as forthcoming, but they are still willing to refer 
patients who are interested in nonsurgical alterna- 
tives and I believe that represents an achievable goal 
for any interventional radiologist interested in pro- 
viding this service. Yes, there are still gynecologists 
in this area who deny all knowledge of this proce- 
dure (even with success! u I patients in their practice) 



but the number of physicians discouraging patients 
from UFE has dropped significantly. 

Now, our task is to sustain this level of interest. 
We continue to provide the above-described level of 
care to our patients and continue to communicate 
frequently with referring gynecologists (with copies 
of letters always sent to primary care practitioners). 
We regularly participate in local health fairs in order 
to interact directly with referring physicians and 
potential patients. In our region, there is a women's 
health fair sponsored by ACOG and we are regular 
participants in that event. We believe this demon- 
strates our commitment to this service to the large 
number ot gynecologists participating m I'll is event 
and we also like to take advantage ol events that will 
provide us with opportunities to interact with gyne- 
cologists face to face. We have also put together a 
summary of our own experience, which we sent out 
to all gynecologists in this region, both to continue 
with our education efforts and to establish ourselves 
as the experts in this region. We also continue to 
provide educational lectures to house-staff in gyne- 
cology and continue inviting students and residents 
to our lab to observe procedures. We have clearly not 
stopped with our efforts to develop this service. 

Inconclusion, a UFE service requires a levelof com- 
mitment not typically required for other interven- 
tional radiology services. Without that commitment, 
success is not likely and you will quickly find that 
all parties participating in the care of these patients, 
including the patients themselves, expect this level 
of commitment. This effort, however, is not without 
its reward. UFE works and has a tremendous impact 
on both the disease process and the patient's overall 
quality of life. When you successfully treat a healthy 
patient with their first significant health problem, 
you have a high probability or making that patient 
very happy. This is what makes the effort worth it, 
especiallywhen you begin noticing that most patients 
undergoing UFE are satisfied with their results. Gyne- 
cologists have already recognized the outcomes that 
are associated with UFE and making the effort that 
is described throughout this chapter will cause them 
to take notice and contribute to the development of a 
successful UFE practice. 



10.2 Pre-op Work-Up and Post-op Care of 
Uterine Fibroid Embolization 



J. Wong and Anne C. Roberts 



Introduction 125 

Epidemiology 125 

Traditional Therapies 125 

■ J ;"it:'.i.--j.i::ysi.:i[ogv of H Li raids 126 

Svmptoms Mil,: S : s j i s :■ ■:■( ribiY'L":^ i iiickiJing 

What Symptoms Should Prompt Treatment) 128 

Differential Diagnosis of Fibroids 129 

Pre-procedure Evaluation I3J 

What is the Place of En'.boiizaiiorj in 

rsticiits Desiimg !-'iegnancy? 132 

Consent 134 

Post-procedure Care of Patient 134 

Unusual Coiiiplicaticns in 

Individual Case Reports 136 

Post-procedure Imaging 136 

Conclusion 137 

References 137 



10.2.1 
Introduction 

10.2.1.1 
Epidemiology 

Uterine leiomyomata, also known as uterine fibroids, 
are the most commonly occurring pelvic tumor in 
women, occurring in 20%-40% of women aged 
35 or older [51]. The size and prevalence increase 
with age until menopause, when they often regress 
in response to the decreasing hormone levels that 
occur. Women of African heritage not only have a 
30% higher prevalence than white women [58], but 
also experience faster fibroid growth and onset at 
a younger age. Uterine leiomyomatas' high preva- 
lence and significant sympti was ranging from pelvic 
bleeding to infertility represent a significant health 
issue in relatively young women. 

i.;.WosG,MBChB, BMedSc 

Senior House Officer, Royal National Orthopaedic Hospital, 

London, UK 

A. C.Roberts, MD 

University of California, 5 a:'. I 'lego Mec.jca! Center, Division of 

Vascular and Inteiven:iona! Radiology, !■■'■ West Arbor Drive, 

San Diego, California, 92103-8756, USA 



10.2.1.2 

Traditional Therapies 

Traditionally symptomatic fibroid shave been treated 
either surgically or medically. Surgical treatments 
include hysterectomy, myomectomy (either by open 
procedure, laparoscopic;! I iy or hysleroscopically), 
myolysis or endometrial ablation. 

Hysterectomy is a definitive and curative treat- 
ment. In the US, more than 600,000 hysterecto- 
mies are performed per year, while in Europe the 
number varies from 73,000 in the UK to 200,000 
in Germany. Over a third of those performed in 
the US are performed for symptomatic uterine 
fibroids [34, 56, 74, 107]. Most patients are pleased 
with the results of this procedure [51, 88] which not 
only removes the fibroids but also eliminates the 
potential risk of other uterine malignancies such 
as endometrial carcinoma. However, hysterectomy 
exposes the patient to standard anesthetic and sur- 
gical risks, a prolonged post-operative inpatient 
stay (2.3 days vs. 0.83 days for UAE [87]), and an 
prolonged time to return to work (33 days vs. 11 
days [87]) and leaves the patient infertile. The mor- 
bidity ranges from 17%-23% [41, 59] dependent 
upon the approach and mortality of 10-20/1000 
[33]. Common long-term complications include 
abdominal adhesions, sexual dysfunction, vagi- 
nal prolapse and urinary incontinence associated 
with laxity of pelvic musculature. Myomectomy 
involves surgically resecting the leiomyomata 
from the uterus, retaining potential for fertility. 
Myomectomy can be performed laparoscopically 
or hysteroscopically if the offending fibroid is on 
either the serosal or mucosal surfaces. It is, how- 
ever, associated with excessive blood loss [53], a 
significant complication rate (25% vs. 11% for UAE 
[72]), a prolonged hospital stay (2.9 days vs. days 
following UAE [72]} and a longer time to return to 
normal activities (36 days vs. 8 days following UAE 
[72]). It can be technically challenging and conver- 

of patients [93]. Myomectomy carries additional 



;.Wo:ig;iiid A.C.Roberts 



risks of rupture of the pregnant uterus and recur- 
rence of the fibroids [28] (43% [30]). 

Myolysis involves coagulating the serosal or sub- 
mucosal fibroid through the use of hysteroscopi- 
cally or laparoscopic;! lly placed probes that apply 
an electric current or laser directly to the fibroid, 
inducing shrinkage. This procedure does not carry 
the risks of an open laparotomy and can be done as a 
same-day surgery. Cryomyolysis is based on a simi- 
lar concept only the fibroid is instead frozen with 
liquid nitrogen. Both procedures result in a loss of 
fertility. 

Themedicalalternative involves hormonal manip- 
ulations with a variety ol pharmaceuticals. Types of 
medications include oral contraceptives, NSAIDs 
and gonadotrophin releasing hormone (GnRH) ana- 
logues. The most common of these is Lupron, which 
is a GnRH analogue and blocks estrogen production 
artificially, creating a state of menopause. A woman 
initiated on a GnRH agonist has shrinkage of the 
fibroids, and a decrease in symptoms; however, after 
stopping the GnRH agonist the fibroids re-grow and 
the symptoms tend to recur. Therefore, GnRH ago- 
nists are usually reserved for those women nearing 
menopause or with planned surgery to aid intraop- 
eratively. However, it has been shown that pre-treat- 
ment with a GnRH agonist has no significant effect 
on intraoperative blood loss [102]. 

.MRI-guided focused ultrasound tibi'oid ablation 
is the newest of the non-invasive techniques and 
is still in the experimental stages. The ultrasound 
waves are directed from a transducer into a small 
focal volume. The tissue at the focal point receives 
condensed energy and increases in temperature, 
causing protein denaturation, cell death and coagu- 
lative necrosis. While a commercial device is avail- 
able, long term data on this procedure does not yet 
exist [45]. 

The first report of uterine artery embolization 
(UAE) was in 1979 when embolization was used to 
stop postpartum bleeding [44, 63]. Since then, embo- 
lization in the setting of pelvic trauma, post-obstet- 
ric bleeding, ectopic pregnancy and AV malforma- 
tions has been well documented. In 1994, Ravina 
et al. [69] described pre-operative UAE prior to 
scheduled myomectomy for symptomatic fibroids 
with the intention of reducing intraoperative blood 
loss. However, reduction in patients' fibroid -related 
symptoms led to a number of patients deciding to 
forego surgery and the group then began to evaluate 
UAE as a definitive therapy. UAE is now a recognized 
alternative to traditional therapies and with the con- 
tinued publication of high quality research demon- 



strating successful outcomes, UAE has become a 
alternative to the more traditional the uterus-spa: 
ing therapies for treating uterine fibroids. 



10.2.2 

Pathophysiology of Fibroids 

Leiomyomata are benign neoplasms consisting of 
smooth muscle cells. Although the pathogenesis of 
fibroids is not well understood, several predispos- 
ing factors have been identified, including age (late 
reproductive years), African-American ethnicity, 
nulliparity, and obesity. The genetic basis for the 
strong predisposition to African-American women 
has yet to be mapped, but non-random tumor-spe- 
cific cytogenetic abnormalities have been found in 
25%-40% of pathological specimens [75]. Estrogen 
receptors are found on leiomyomata in a higher 
concentration than normal myometrial tissue [108] 
causing the fibroids to be responsive to the female 
sex hormones. Thus, with pregnancy, fibroids may 
enlarge [14, 57, 89] by up to 25% [2] and in the post- 
menopausal state, when estrogen levels fall, leiomy- 
omata will decrease in size due to the reduced hor- 
monal stimulation. Progesterone receptors have also 
been found in elevated levels in leiomyomata com- 
pared with myometrium [12, 81, 95, 108] and stud- 
ies suggest a growth promoting effect [15, 32, 49]. 
Androgens may have a role in leiomyomata growth; 
5-a androgens have been found in myoma biopsies, 
suggesting sensitivity to the hormone [73]. Clinical 
improvement is frequently seen when androgenic 
therapies such as danazol and gestrinone are used 
[22, 25], further supporting this theory. 

Leiomyomata are vascular tumors and angiogen- 
esis is vital to their growth. They have been shown 
to have more veins and arteries and greater vessel 
caliber than normal myometrium [29, 31]. One of 
these angiogenic growth factors, basic fibroblastic 
growth factor (bFGF), has been found in increased 
concentrations in the extracellular matrix of leio- 
myomatous tissues when compared with normal 
myometrium [60]. bFGF has been shown to stimu- 
late mitogenic activity on both myometrial and 
leiomyomatous smooth muscle cells [54], while the 
receptor for bFGF has been found to be dysregulated 
in the leiomyomatous uterus [7]. 

Leiomyomas originate within the uterine wall, 
but can extend into the uterine cavity from the 
submucosal surface (see Fig. 10.2.1) and into the 
abdominal cavity from the subserosal surface. Like 



p Work-Up and Post-op Ore of uterine Fibroid Embolizatio 




Fig.l0.2.1a,b. Sonographic appearance 
of a submucosal fibroid, a A well circum- 
scribed hypoechoic round mass with 
some internal heterogeneity is charac- 
teristic of a leiomyoma, b Doppler can 
be used to show the hypervasculnrily of 



polyps, these tumors can be flat or pedunculated 
(Fig. 10.2.2). Vascular supply comes primarily from 
the uterine arteries, a branch of the anterior division 
of the internal iliac artery, but collateral supply can 
arise from the ovarian arteries and the vesicovagi- 
nalarteries[61]. 

The mechanism by which fibroids cause abnor- 
mal uterine bleeding is not known. However, there 
have been several theories proposed. One theory 
claims that the increase in size of the endometrial 
surface area causes the bleeding and is therefore 
most pertinent to submucosal fibroids [91]. The 
scularity and vascular How to the uterus 
ult of fibroids hits also been held responsible 



[91]. Jha et al. chose to measure vascularity as an 
indicator of success. They found that hypervascular 
tumors were more susceptible to UAE than hypo- 
vascular tumors [4?]. Fibroid eel hilarity was studied 
by deSouza et al. who found that leiomyomas that 
were high in signal intensity on T2-weighted images 
prior to embolization showed a significantly greater 
reduction in volume at 4 months, compared with the 
leiomyomas thai were low in siaiul intensify [2~]. 

Another theory describes the ulceration of a 
submucosal fibroid into the endometrial surface 
[91]. The fibroids may compress the venous plexus 
within the myometrium which may lead to uterine 
engorgement and greater bleeding [91]. The latest 



I. Wong and A. C. Roberts 




Fig. 10.2.23-c. An 18-year-old female who is 17 weeks preg- 
nant. Patient present with right lower ouadrant abdominal 
pain. a Ultrasound aemonstiaies a .aige heterogeneous i 
b,c Sagittal and axial views osi MK demonstrate a 
lated subserosal fibroid iijsri'J'.'s.vi. Regions of high at 
withal the fibroid indicate a degree o: necrotic oege iteration 
of the fibroid siala was sa speeded. The patient was 
the operating :oo:i'. at winch time, a puipie, :o:sed, 
lated fibroid was founo.Tne fibroid was torsed 360° 



theory proposes that the dysregulation of several 
angiogenic growth factors or their receptors may be 
responsible for vascular abnormalities that lead to 



dysregulation of the va 
and cause menorrhagt 
evaluated premenopausal < 
abnormal bleeding, wome 
ing were significantly mor 
intramural (58% vs. 13%) o 
(21% vs. 1%) when comp; 
women [19]. 



ular structures in the uterus 
[90]. In a recent study that 
tl women with and without 
nen with abnormal bleed- 
ore likely to have either an 
submucosal leiomyoma 
■ed with asymptomatic 



10.2.3 

Symptoms (and Signs) of Fibroids 
(Including What Symptoms Should 
Prompt Treatment) 



The most common symptom of uterine fibroids 
is abnormal uterine bleeding occurring in 30% of 
women with fibroids [16], which commonly causes 
I is associated with fibroids located in 



the submucosa. The two abnormal bleeding patterns 
that are most commonly associated with uterine leio- 
myomas are an increase in the amount of blood loss 
per month, menorrhagia, and prolonged (>7days) 
vaginal bleeding, otherwise known as metrorrha- 
gia. Many women will experience both heavy and 
prolonged vaginal bleeding, commonly referred to 
as meno metrorrhagia. Exceptionally heavy flow 
and the passage of clots is colloquially known as 
'Hooding'. Clinically, il is defined as total blood loss 
exceeding 80 ml per cycle or menses lasting longer 
than 7 days. 

When large in volume, fibroids exert a mass effect 
on other pelvic structures such as the bladder, bowel 
and the lumbosacral plexus giving rise to symptoms 
of urinary frequency, abdominal distension, con- 
stipation, bloating, and back and leg pain. Gyneco- 
logical symptoms include pelvic pain, miscarriages, 
menstrual cramps (subserosal and/or intramural 
tumors predominantly disturb uterine contractil- 
ity), infertility, and dyspareunia. Unlike menorrha- 
gia, fibroids must be large to cause this class/subset 
of symptoms. Therefore, patients who do not present 



Pre-op Work-Up and Post-op Ore of uterine Fibroid Embolization 



with bleeding tend to have subserosal < 
ral fibroids instead of submucosal fibroids. Studies 
have shown no difference in complication rate post- 
UAE in patients with large uteri (>780 cm') or large 
fibroids (>10 cm diameter) compared with smaller 
uteri or fibroids [48, 68]. Control of menorrhagia 
post-UAE has also shown to be independent of ini- 
tial uterine size or fibroid size [37, 48, 85]. There are 
a few studies that contradict this trend. Jha et al. 
observed that larger pre-treatment uterine volumes 
showed worse outcome. For every 100 cm' increment 
in volume, they noticed volume reduction after UAE 
decreased by 20% [11]. Conversely, Bradley et al. 
noted good volume reductions in patients with par- 
ticularly large fibroids [83]. 

Initial studies have shown that UAE can improve 
menorrhagia in 90°ri ot patients at 1 year after ther- 
apy and pelvic pressure symptoms by 91% at 1 year 
after therapy [S3]. On average, the volume of the 
fibroids decrease by 30%-60% and the associated 
symptoms (of mass effect) are successfully treated 
in 71% of patients [72]. A study comparing myomec- 
tomy to UAE suggests myomectomy is superior in 
treating symptoms relating to the pelvic mass effect 
while UAE is superior for treating menorrhagia 
[38]. 

Although fibroids ar 
female population ove 
mately 20%-40% of wo 
symptomatic [16]. If the woman is asymptomatic 
no therapy would be warranted. If the woman is 
symptomatic, the options for treatment should be 
explained and the decision left to her. 



e extremely c 

r 30 years of age, approxi- 

women with fibroids are 



be more specific at distinguishing between these 
[wo diagnoses [39]. 

Adenomyosis causes similar symptomatology 
as fibroids with menorrhagia, enlargement of the 
uterus and pelvic pain. Characterized by the ectopic 
growth of endometrial tissue in the myometrium, 
adenomyosis causes diffuse enlargement of the 
uterus [64] and has been suggested to predispose the 
patient to clinical failure after UAE [55, 65]. However, 
Siskin etal. [80] showed symptomatic improvement 
in 12 of 13 patients (92.3%) who underwent UAE for 
adenomyosis. They also noticed significant reduc- 
tions in the median uterine volume (42%), median 
fibroid volume (71%), and mean junctional zone 
thickness (33%) [80]. In our practice, we have seen 
clinical improvement in a patient with concurrent 
adenomyosis (Fig. 10.2.5) and leiomyomas. Endo- 
vaginal ultrasound can be used to detect thicken- 
ing of the endometrial stripe and the ill-defined 
hypoechoic areas characteristic of adenomyosis, 
unless performed meticulously, can be inaccurate 
and MRI is the imaging modality of choice to make 
this diagnosis. 

The symptoms of mass effect may be caused by 
other processes that should be excluded. The first 
symptoms of ovarian carcinoma, another contrain- 
dication to UAE, are usually a result of its significant 
mass effect. As such a large ti 
before symptoms are evident, i 
tend to be in the advanced stages on presentation. 

Leiomyosarcomas are malignant tumors of the 
uterus with an incidence of less than 0.3% in fibroid 
uteri [42], and present with similar symptoms and 
radiologic presentations to that of benign disease 






10.2.4 

Differential Diagnosis of Fibroids 

It is imperative that other causes for presenting 
symptoms are excluded prior to decision to proceed 
with UAE. For menorrhagia, the differential diagno- 
sis includes adenomvosis dig. 10.2.3) and a range 
ol endometrial disorders. Endometrial carcinoma 
is an absolute contraindication to UAE (Fig. 10.2.4) 
and all women with endometrial bleeding should 
be investigated with endometrial biopsy to try and 
exclude endometrial cancer. Endometrial polyps are 
benign nodular protrusions of the endometrial sur- 
face that are a common cause of dysfunctional uter- 
ine bleeding and abnormal endometrial thickening, 
a sonographic feature shared with endometrial car- 
. MRI or hysteroscopy have been shown to 




;. Wong and A.C.Roberts 




Fig. 10.>.4a,b. A 70 -year-old female wilh endome- rial ciircincrno and fiLToids. a 1 'elayeo post-goi;o.inium Tl -weighted sog.nol 
image of -he oelris. i'r.e a<r,:i'.ski indic.te Iwc- siibniiiti'-:;.!! iibroids. Note i he difference in signal imens;".y heiween them. The 
Inghei qan.;. nidicoies gieoief vasculoiiiy. while the :eo : .:ceo signal intensity necrosis. An e:idome;ria' carcinoma is seen at 
the fundus of die uterus (rifrpir!. b T r-weigraed so git -a I to si -spin echo non-oreadi hold imogr .:■[" [lie pelvis. Two s-iruuucosol 
fibroids are seen odiacen: 10 die uterine ■."only. The junior imirgins of die endometrial care in:: 1 mo i aii'mr; ore more cleorly seen 
with the distinct increase .n sigmil intensity a; die uterine cavity 




i-'ig. !i).:. "o,h.T::ese sogir.al T_-\ve;ghicC ,:r.rges demo us title diffusa arienciiiycsh 
characteristic punctate markings seen in. diffuse adenomyosis i u/jifr arrow) can 
UAE, the adenomyosis " 



[43]. Unfortunately, it is currently impossible to nant disease [77]. As current literature suggests that 
i'li sti mulish these tumors from benign leiomyomata leiomyosarcomas do not respond to embolotherapy 
witlKnit]Xif]iologicex; : mi!ii;Ttioii. Onepriper has sug- [■!!)] and metastasize early with .1 poor pro^no.-ds 
gested that Doppler US shows higher peak systolic (20% 5-year survival with any extra-uterine spread) 
velocity within leiomyosarcoma as compared to [109], this undetectable malignant diagnosis is an 
leiomyomata [5, 21] while there are several reports of understandable concern. However, one must con- 
using MR] to distinguish between benign and malig- sider the low prevalence in comparison to the mor- 



Pre-op Work-Up and Post-op Care of uterine Fibroid Embolization 



Cality of hysterectomy for benign disease excluding 
pregnancy (1:1600) [78]. Continued fibroid growth 
after the cessation of estrogen stimulation (e.g. 
menopause) should raise suspicion of leiomyosar- 
coma and should be investigated with needle biopsy 
[13, 47]. Likewise, if rapid interval growth is seen 
following UAE, the suspicion ot malignancy should 
be raised. 

The differential diagnosis of pelvic pain is wide 
and includes ovarian vein varices, pelvic infection 
and endometriosis. Untreated pelvic infections are 
an absolute contraindication to UAE. They are a 
known cause of a hydrosalpinx a collection of fluid 
in the fallopian tube and a recognized cause of infer- 
tility. This diagnosis is best established on hystero- 
salpingography. 

Evaluating patients with symptoms ot fibroids 
can be challenging and is best approached by work- 
ing in conjunction with the patient's gynecologist. 
A good working relationship with gynecologists is 
important for the work-up of patients and ensures 
UAE is an appropriate choice of treatment. 



10.2.6 

Pre-procedure Evaluation 

The first step in the interventional ist's evaluation of 
a woman with fibroids is a detailed patient history. 
The patient should have a gynecologic examina- 
tion, either prior to seeing the interventionalist or 
should be referred to a healthcare professional with 



expertise in gynecologic care. Patients should have 
had a recent Papanicolaou smear of the cervix and 
if menorrhagia is a presenting symptom, then an 
endometrial biopsy should be performed to rule out 
neoplasm. Baseline laboratory tests should include 
CBC and renal function. The pre-procedure assay 
of follicle stimulating hormone (FSH) levels maybe 
pertinent, but is not currently routine practice. 

The role of imaging in uterine fibroids is not only 
to characterize the number, type and size of the 
tumors, but also to screen for other causes of the pre- 
senting symptoms. Ultrasound is typically the ini- 
tial imagm;; modality used in the work- up ot uterine 
fibroids, but it is subject to operator variability and 
therefore lacks reproducibility (Fig. 10.2.2). Ultra- 
sound is best suited as a screening test for fibroids 
and to exclude any obvious pelvic pathology. MRI 
not only provides the consistency required for post- 
procedure comparisons [13, 26], but also reliably 
excludes adenomyosis and all but stage I carcinomas 
of the endometrium [13]. At our institution the same 
MR sequences are used pre and post UAE and are 
described in Table 10.2.1. 

Some investigators have assessed the arterial 
supply to the uterus with dynamic gadolinium- 
enhanced three-dimensional fast imaging with 
steady-state precession MR angiography [47]. It is 
clear that imaging aids not only with diagnosis, but 
also provides information that can be used to pre- 
dict outcome of UAE. 

One of the first details noted is the location of 
the fibroid. A 31-patient study showed that submu- 
cosal fibroids displayed 30%-40% greater reduc- 



Table 10.2.1. MR ii 



g sequences 






le artery emboli; 



i.oroiul lusie f:c:v. ti'.e mid kidneys r .a the symphysis penis 

Sagittal T2 turbo spin echo (TSE) BH - 6 mm skip zero 

Sagittal T2 TSE non-BH - 6 mm skip zero 

Axial oblique Tl 2D FLASH. BH DE IP and OP (perpendicular to the endometrial : 

Axial oblique Tl BH is,'. me slice thickness jinc .ingle .is oblique Tl ) - 6 mm skip z. 

Straight axial T2 BH - 8 mm skip zero 

Following hand inieciioii of !>'■ ml gadolinium via butterfly needle 

Sagittal Tl 2D FLASH BH IP FS as above. 

Axial oblique Tl 2D FLASH BH IP FS (perpendicular to the endometrial stripe) 

Straight axial Tl 2D FLASH BH FS (for easier communication) 

For those who do nor respond to uterine ar:< : ■■■ :■::,■• is ■.;., :: 

Same sequences as above, except with MRA> V :-tV tT.s_T:n^ ninadal arterit 

Coronal 3D FLASH BH 2 ram skip zero. Arterial, portal ver.ujs. delayed phi 

yost-p:ccessi:ig us.ng subliacuons ..in..: Ml Pa 

BH, breath hold; DE, double echo; IP, in phase; OP, out of phase; FS, fat 



i eluded usii'.g 40 mis of g.ido.iijium 



]. Wong and A. C. Roberts 




Fig. 10.2.6a,b. A 35-ye.ir-old ferrule with a sijbiVjUccs.il fihio.d. ,1 Tl -weighted sagittal in 
fibroid (asterisk) enlarging the endometrial cavity. Note the low signal intensity on T2- 
base on the endometrial wall. This was laken uist prior to UAE. b T-> -weighted sagittal 
later post UAE. Note ihe fibroid previously seen h.is v inn. illy disappeared 



;e of the pelvis shows a submucosal 
rehire images .is weil as the broad 
aage of ihe pelvis performed 1 year 



tion in volume when compared with intramural or 
subserosal fibroids [47] (Fig. 10.2.6). This could be 
explained by the vascular anatomy of the fibroid 
which favors distribution of the embolization par- 
ticles to the inner aspect of the uterus, i.e. the sub- 
mucosal surface [8]. However, their close proximity 
to pathogens in the uterine cavity has been hypoth- 
esized to account for their increased incidence of 
infective complications [97]. 

Burn et al. [13] studied the relationship between 
signal intensity characteristics on MR and total per- 
centage volume reduction in 17 post-UAE patients. 
They noted that, on T!-weighted images, tumors 
showing signal intensity brighter than that of myo- 
metrium compared with those of lower intensity 
than myometrium showed poor response to UAE 
(p=0.008), also reported by Jha et al. [47]. This MR 
characteristic is thought to result from hemorrhagic 
necrosis and the presence of blood breakdown prod- 
ucts. Therefore, if seen in a fibroid pre-UAE, it likely 
has already undergone degeneration and loss of vas- 
cular supply and will not respond well to emboliza- 

Meanwhile, onT2-weighted images, tumor inten- 
sity brighter than that of skeletal muscle compared 
to those equal to or lower than that of skeletal 
muscle was predictive of good response (p=0.007), 
echoed also by deSouza and Williams [27]. High 



signal on T2-weighted images was presumi 
due to increased fibroid cellularity and/or v; 
ity [13]. 

The indications and contraindications i 
[Table 10.2.2. 



Table 10.2.2. A si 

Absolute contrai 



Asy:"i;p;c:'.:.itic fibroids 


Coagulopathy 




.-letn.ii'.cv 


Immunocomprom 


ised 


Pelvic active infection 


Contrast allergy 
Renal impaiimem 





10.2.7 

What is the Place of Embolization in 

Patients Desiring Pregnancy? 

Currently, UAE is not recommended as the first line 
of therapy in patients with infertility presumed to be 
caused by fibroids. Patients in whom fibroids are not 
symptomatic but who are infertile, should be evalu- 
ated for other causes of infertility and, if fibroids are 
the cause, the potential for myomectomy. Inpatients 
who are symptomatic from the fibroids (menorrha- 
gia, bulk symptoms) and whom myomectomy is not 



Pre-op Work-Up and Post-op Ore of uterine Fibroid Embolizatio 



an option, UAE should be attempted before proceed- 
ing with a hysterectomy as UAE may adversely affect 
fertility. 

Vascular anastomotic communications between 
the uterine and ovarian arteries provide a route 
by which embolization materials can affect the 
ovarian blood supply and ovarian function, either 
permanently or temporarily [71]. One case report 
describes embolic microspheres found within the 
ovarian arterial vasculature of a pathological speci- 
men following uneventful UAE [66]. Unintentional 
embolization of the ovarian arteries is theorized 
to cause ovarian failure. However, the incidence of 
ovarian failure post UAE is no different to hysterec- 
tomy [100]. In fact, it is not clear whether UAE has 
any effect on ovarian function at all. There are stud- 
ies that support its lack of effect [3, 17, 99, 100] and a 
few case reports that document transient or perma- 
nent amenorrhea [92, 98]. 

It is thought that the ovarian arteries shrink with 
age leading to increased ovarian dependence upon 
uterine-tubal anastomoses [9]. This may explain an 
increased chance (from0% incidence compared with 
21%) of ovarian failure post UAE in patients aged 45 
years or older [18]. A similar study looking at basal 
FSH after UAE showed a significantly increased risk 
of perimenopausal FSH levels in patients older than 
45 years [84]. Thus, older women appear to be more 
at risk of losing their ovarian (unction than younger 



Uterine devascularization is another proposed 
mechanism. Devascularization has been reported in 
one case [98] to cause endometrial atrophy resulting 
in persistent amenorrhea. Endometritis secondary 
to a perivascular necrotizing arteritis has been seen 
following UAE with gold-colored gelatin micro- 
spheres, however, as an eosinophilic component was 



seen in this patient, a hypersensitivity reaction to 
the gold could have been the cause [76]. It has been 
theorized that a devascularized endometrial lining 
may not be able to support a term pregnancy [23], 
however, there are two reports of twins pregnancies 
delivered at term [35,70] where the endometrial vas- 
cular reserve would have been tested. 

A paper published in 2004 quoted 53 published 
pregnancies worldwide following UAE [36] and 
concluded that compared with those with prior 
laparoscopic myomectomy, pregnancies following 
UAE were at increased risk for preterm delivery and 
malpresentation (Table 10.2.3). However, an earlier 
paper by the same authors comparing pregnancies 
following UAE to those of the normal obstetric pop- 
ulation concluded the miscarriage and complica- 
tion rate was higher following UAE [35], but noted 
that the UAE population is not directly comparable, 
not least due to the older average age, a similar dif- 
ference also seen in the laparoscopic myomectomy 
group. In fact, one study showed no difference at all 
[79]. Other smaller studies have not del 
difference in obstetric complications. 

If left untreated, pregnancies in 
known leiomyoma have higher caesarian section 
rates (39%) and antepartum hemorrhage (>500 ml) 
rates (48%) [52]. One study has shown the inci- 
dences of preterm delivery (less than 37 weeks), 
preterm premature rupture of membranes, in 
utero growth retardation (less than 5th percen- 
tile), placental abruptio, placenta previa, postpar- 
tum hemorrhage (more than 500 cc), and retained 
placenta are not significantly increased in women 
with myomas compared with the general popula- 
tion [103]. However, in this study cesarean sections 
were significantly more common in women with 
myomas (23% vs. 12%). 



Table 10.2.3. Prevalence of obsti 
laparoscopic myomectomy 



I'jlalion, those fofowjig "JA!-_ and lhose following 



Spontaneous abortion 

Postpaitun; rieniujiiiagea 
Preterm delivery a 
Cesarean deliverya 
?mall :-i[ gestational agea 
\!a.pi esentationa 



/51 


24%) 


/35 


6%) 


/32b 


16%) 


/3S 


63%) 


/22c 


5%) 


1/35 


11%) 



20/133 (15%; 

1/104 ( i%; 

3/104 ( 3%; 

61/104 (59%) 
B/95C ( 8%; 

3/104 ( 3%; 



]. Wong and A. C. Roberts 



is the remembered that thepresence of normal 
1 assays and normal menstruation are not 
the only factors that assure a successful pregnancy. 
Further studies must be performed before UAE can 
be regarded as a safe procedure for women desiring 
future fertility. 



10.2.8 
Consent 



When obtaining consent for UAE, we 
potential sequelae listed in Table 10.2.4. 



is d is ill ssed when obtaining cc 



I. Complicat 

BlrT.Jli 
Hri!"j;':t-.'![1'.,1 

[nlvclion of c.ttheter sl 
J. Compli cations jssoii.it 
Contrast reaction 
Exaceibauon of renal i 



d witli placing ciili'.elei 5 



d with angiographic procedur 



efficiency 



3. Complications associated with emboli?.; I ion 
Damage vessels requiring surgery (dissectior 
disruption, extravasation) 
Embolization of structures other than uterus 
bowel ischemia, bladder ischemia, nerve or n 
ischemia, skin 
Ovarian failure 
■i. Iiileclion of uterus reciuii j::g iiysleieciomv 
5. Failure of procedure to correct symptoms 



Crampy pelvic pain commonly occurs within the 
first 24 h of UAE and is usually controlled with a 
patient control led analgesia il-'i'A) pump using mor- 
phine or another narcotic. Patients should be placed 
on an anti-inflammatory prior to the embolization 
and while in the hospital. Toradol intravenously 
prior to the embolization and during the hospital 
ization appears to be very effective. It is reasonable 
to develop a set of standard orders that the patient 



will r 



r the most 



eventual! 



Patients should be 
son for r 



charge, analgesi 
consisting of : 



i is the most 
[105]. On dis- 
s switched to oral medications, 
i-steroidal anti-inflammatories 
(NSAIDs) and narcotics. The NSAIDs should be 
taken around the clock for approximately 10 days 
with narcotics used as needed. The peak of the pain 
usually occurs during the first 8-12 h although once 
they are discharged from the hospital, their pain 
maybe more troublesome for the first day home and 
will gradually resolve within the next week. If, after 
improvement of the initial post-procedure pain, 
the patient develops recurrence of pain, she should 
immediately report back to the interventionalist 
since this can represent infection or possibly fibroid 

Nausea is also a common side effect of UAE and 
can be accentuated by the narcotic analgesia. Anti- 
emetic medication should therefore be routinely pre- 
scribed. Transdermal scopolamine placed behind 
the ear prior to beginning the procedure may be 
helpful in decreasing the amount of nausea. 

Post-embolization syndrome should be expected 
in all patients post UAE and consists of low-grade 
fever, malaise, nausea and leukocytosis.lt can occur 



Table 10.2 .5. Complici 



10.2.9 

Post-procedure Care of Patient 

The post-procedure period consists of hospitaliza- 
tion and the outpatient follow-up. Inpatient stays 
typically are less than 24 h, so the majority of the 
patient care will be on an outpatient basis. There 
have been some reports of patients being success- 
fully treated on an outpatient basis [86]; however, 
in most practices a short hospitalization seems 
to be preferred by most patients. Using a study of 
400 patients Spies et al. reported a comprehensive 
list of complications, some of which are shown in 
Table 10.2.5 [20]. 



LompJk" 



Leiomyoma passage 
jiecurreiii/pfolonged p.ii 
L"iina:y tiac.l infection 
Endometritis 
Femoral nerve injury 
Arterial injury 
Urinary retention 
Vaginal discharge 
!-!emjiioiii.i 

Deep vein thrombosis 
Pulmonary embolism 



!- : ei"cenr;'.ge i%; pievalei: 



Pre-op Work-Up and Post-op Care of uterine Fibroid Embolization 



anytime aftertheprocedure from a fewhours to a few 
days and requires only symptomatic treatment. This 
can lead to a diagnostic dilemma as uterine infec- 
tion, a complication that may lead to hysterectomy, 
also presents with a fever. If a sudden rise in tem- 
perature to greater than 38.5° occurs with increas- 
ing pain, one should suspect infectious etiology 
and admit the patient for further investigations and 
possible antibiotic therapy and appropriate inter- 
ventions [24, 101]. Two patients have died from fatal 
pelvic sepsis post UAE [104]. The common findings 
between these cases were a symptom-free period 
after UAE and presentation with a 24 h history of 
gastrointestinal symptoms. Antibiotic therapy was 
too late to prevent overwhelming sepsis. The source 
of the infection in these cases was a necrotic uterus. 

Like hormonal treatments for fibroids, UAE has 
also been known to cause amenorrhea. Two studies 
totaling 650 patients showed that at 12-16 months 
post UAE, between 94% [86] and 98% [6, 82] had 
normal menses, respectively. There has also been 
reported transient episodes of amenorrhea and 
menopausal symptoms [86]. 

Thromboembolic complications including pul- 
monary embolism, deep vein thrombosis and arte- 
rial thrombosis [67] have been reported. There have 
been two deaths from pulmonary embolism [62]. 
One study chronicled blood coagulation markers 
post-UAE [1, 10]. This showed that prothrombin 
tnigmenl 1.2, plasniin-i'._-antiplasmin complex and 
thrombin-antithrombin complex increased as a 
result of UAE, suggesting that a prothrombotic state 
may result after the procedure. Prophylactic treat- 
ment with anticoagulation or venous compression 
devices may be appropriate for patients thought to 
be at higher risk for thromboembolic complications, 
such as exogenous sources of oestrogen or a history 
of thromboembolic events. In most patients early 
ambulation and NSAIPs ore pobablv sulhcient to 
prevent thromboembolic complications. 

In some patients a chronic vaginal discharge last- 
ing longer than 2 months and described as a "major 
irritant" occurs following UAE. This has been 
reported by Walker and Pelage [104] to occur in 
4% of patients. In another report Walker etal. [106] 
describes this vaginal discharge to be caused by a 
persisting sinus that connected a superficial necrotic 
excavation within the fibroid to the endometrial 
cavity through a perforation in the endometrium. 
This results in a slow persistent drainage of necrotic 
material into the uterus and subsequently the vagina 
[106]. There were 16 patients with a chronic vagi- 
nal discharge that were treated with hysteroscopic 



opening of the sinus and resection of the necrotic 
tissue. Following the procedure 94% of the women 
were either completely cured or had a very mild dis- 
charge [106]. 

The passage of leiomyoma tissue commonly 
occurs with those fibroids in contact with the endo- 
metrial surface. This phenomenon has been seen up 
to 12 months after the UAE procedure. This symp- 
tom is associated with signif ic;int pain, bleeding and 
most importantly, infection [86]. In cases of sus- 
pected fibroid expulsion, MR] should be performed 
as many fibroids do not pass through the cervix 
spontaneously or remain attached to the uterine 
wall and therefore require dilatation and curettage. 

Once discharged, between 3.5% [20] and 10% [86] 
of patients return to the emergency department, 
with between 4% [20] and 6% [72] requiring re- 
admission. If a patient is re-admitted, it is essential 
that someone from the interventional team be avail- 
able by telephone or pager during their stay. Current 
literature quotes between 8 days [20, 83, 104] and 
17 days [87] time required from work/time to recov- 
ery [20] (see Table 10.2.6). 



Table 10.2.6. Hospitr- 
embolization [27] 



w b 


rfpitienl 


12(2) 




438 (80) 




70(13) 




28(5) 




1.3 night 


5(0-11) 



Hospital stay (nights) 1 



Mean hospital stay ■: range! 

Inadequate length o: hospital stay 66 (12) 

Indications for LOS >1 night 98 (18) 

Pain/nat.sea/vomiting 75 (14) 

Pain/fever 16 (3) 

Hypertension 3 (0.6) 

Respiratory depression 1 (0.1) 

Aspiration pneumonia 1 (0.1) 

Pulmonary edema 1 (0.1) 

Seizure 1 (0.1) 
Dissatisfaction with inter vent ion a I care 17 (3) 

Dissatisfaction with ward care 70 (13) 

' Those staying a n.ghts or longer: 1 7 for a nigh Is, four tor 
4 nights, three for ."■ nights, two for 6 nights, one for 
7 nights and one for 1 1 nights. 

Values in parentheses are percentages unless otherwise 
indicated. 



;.Wo:ig;iiid A.C.Roberts 



As a routine, patients should be followed-up either 
by phone or in clinic at 24-48 h and 1-3 weeks after 
discharge to monitor symptom control and screen 
for early complications. 



10.2.10 

Unusual Complications in Individual Case 

Reports 

There are a few unique complications reported fol- 
lowing UAE. One case describes a 27-year- 
who, 3.5 years post UAE presents with : 
dysmenorrhea and menorrhagia which was thought 
to be due to retained fragments of calcified fibroids 
seen on ultrasound [96], Passage of these fragments 
resulted in resolution of her recurrent symptoms. 

Another case features a transient necrotic- 
appearing area on the right labium minus 5 days 
post UAE in a 38-year-old woman [1101- This was 
thought to be due to non-target labial emboliza- 
tion during UAE, perhaps of the internal pudendal 
artery. Spontaneous resolution occurred during the 
ensuing 4 weeks. 

Generalized oedema of the face, body and 
extremities was a complication seen in one 41-year- 
old patient 24 h following UAE [94]. In this case, a 
transient spike in vascular endothelial growth factor 
(VEGF} level was seen to coincide with the oedema. 
VEGF has permeability-increasing activity for vas- 
cular endothelial cells [46] and was hypothesized to 
have been released by the hypoxic fibroids. 

One 48-year-old patient required an emergency 
hysterectomy following massive vaginal hemorrhage 
1 month following UAE [50]. Histological examina- 
tion of the bleeding uterus did not provide defini- 
tive answers, but it was hypothesized that the bleed- 
ing originated from partially infracted myometrial 
tissue, adjacent to the treated fibroid, in which sev- 
eral large blood vessels were noted. 



10.2.11 
Post-procedure Imaging 

The best imaging to evaluate the perfusion and size/ 
volume of the fibroids following the procedure is 
MR. The timing of the imaging is not standard- 
ized. In our practice we typically image at 6 months 
which gives a chance for the fibroids to have changed 
in volume and offers the patient an opportunity to 



visualize the decrease in size of the fibroids. How- 
ever, perfusion changes (as measured by immediate 
reduction in maximal leiomyoma enhancement as 
seen on MR) immediately after the procedure have 
been shown to be predictors of clinical response at 
12 months (as measured by length, blood loss, and 
associated pain of menses) [27]. 

The MR characteristics post embolization have 
been well documented. One should expect an 
increase in signal intensity on Tl-weighted images 
[27, 47] immediately following UAE and a reduction 
in signal intensity on T2-weighted images after the 
first month [4]. deSouza et al. [27] demonstrated 
that reduction in leiomyoma perfusion (as mea- 
sured by maxiin.i I gadolinium enhancement on Tl- 
weighted images) immediately after UAE correlated 
with a clinical response after 12 months. Unlike the 
fibroids themselves, the myometrium tends to reper- 
fuse to normal levels during that time and thus once 
again appear bright on contrast-enhanced images. 

Long-term follow-up is indicated 3-6 months 
after the procedure. Pelage et al. [67] have empha- 
sized the use of Tl-weighted contrast-enhanced MR 
to evaluate fibroid perfusion and in turn predict 
long-term outcome. Areas of complete infarctionand 
partial infarction can co-exist within a given fibroid 
tumor and are clearly demarcated as areas of dark or 
bright signal, respectively. This study showed that 
fibroids that had homogenously complete infarction 
at 3-months post procedure had 100% infarction at 
3 years. If the fibroid was incompletely infarcted at 
3 months, then only 40% of the fibroids were com- 
pletely infarcted at 3 years. However, the volume 
reduction was similar between these two groups. 
They observed that areas of incomplete infarction 
(viable fibroid tissue) were more likely to re-grow 
and to potentially am^e re lapse ol symptoms. Their 
conclusion was that the success of the procedure may 
be better measured by the achievement of complete 
infarction, as opposed to absolute volume reduction 
[38]. 

It is important to evaluate the uterine and fibroid 
volumes as patients that show poor reductions in 
uterine volume post embolization may be more 
likely to require hysterectomy [4]. MR not only pro- 
vides easily understood images that can be shown 
to patients, but also information that can be used 
to predict future fibroid shrinkage or to predict 
regrowth and possible further therapy. 

Post- operative knowledge of the fibroid vascu- 
lature is of particular interest when UAE results in 
negligible shrinkage and persistent symptoms as 
it may suggest possible sources of alternate blood 



p Work-Up and Post-op Ore of Uterine Fibroid Embolizatio 



supply, such as ovarian or vesicovaginal arteries. In 
this scenario, MR angiography is indicated to evalu- 
ate the status of the ovarian vasculature. 

Using transvaginal ultrasonography, one can 
visualize the thrombosed uterine arteries repre- 
sented by tortuous, brightly echogenic tubular 
structures in the adnexal region. This radiographic 
sign has been named the 'white snake' sign and its 
persistence 6 months after UAE has been shown to 
correlate with more favorable symptomatic out- 



10.2.12 
Conclusion 

Uterine artery embolization has become a recog- 
nized alternative to traditional surgical therapies 
for uterine fibroids. It has also become the pro- 
cedure that has forced interventional radiologists 
out of the role of simply performing a procedure 
and into the role of a true clinical consultant and 
physician directly caring for patients. The actual 
procedure of UAE is by and large straightforward. 
It is the consultation with the patient prior to the 
procedure, educating her about the options for treat- 
ing her fibroids, and the possible complications and 
alternatives that has become important. The care 
of the patient following the procedure is the most 
challenging part of the i nte r vent iona list's job. There 
always seems to be a new situation or problem that 
arises no matter how experienced the intervention- 
alist is. This field continues to undergo tremendous 
knowledge growth, and there will be many more 
clinical aspects of UAE that will be elucidated in 
the months and years ahead. It is critically impor- 
tant to try and stay abreast ol the mtoimnlie'ii being 
reported on the clinical aspects of UAE in order to 
provide appropriate counsel and care for patients 
with uterine fibroids. 



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J. Wong and A. C. Roberts 



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Gynecol 100:881-882 



10.3 Fibroid Embolization: 

Anatomy and Technical Considerations 



Anne C. Roberts 



Introduction 141 

Anatomy 141 

Fibroids 141 

Vascular Anatomy and Variants 

Uterine Arteries 141 

ribioid Vascularity 143 

Oviuian Ajteiies 144 

Tubo-ovarian Anastomoses 144 

Equipment 145 

Catheters and Microcatheters 1 

Embolization Materials 145 

Medications 1 47 

Technique 148 

Endpoints 15 i 

References 155 



10.3.1 
Introduction 

The anatomy of uterine fibroids and uterine artery 
embolization (UAE) consists of the fibroids, their 
position in the uterus, and the vasculature associ- 
ated with the uterus. The vasculature of the ovarian 
arteries is also important because of the potential 
for collateral blood flow from the ovarian arteries 
supplying the fibroids. Communication between the 
uterine arteries and the ovarian arteries are also 
important because of the risk of embolization of the 
ovaries through uterine- 



10.3.2 
Anatomy 



10.3.2.1 
Fibroids 



Fibroids are classified by their position in the uterus. 
Serosal fibroids are found in the outer layer of the 
uterus and expand outward. They usually do not 
affect bleeding during the menstrual period, but 
may cause symptoms due to their size and pres- 
sure on other pelvic organs such as the bladder and 
bowel. Intramural fibroids develop within the sub- 
stance of the uterus. They enlarge the uterus and 
can cause both bleeding and pressure symptoms. 
Submucosal fibroids involve the inner layer of the 
uterus, and cause the most problems with heavy and 
prolonged periods and sometimes gushing bleeding 
also described as flooding. Submucosal and serosal 
fibroids maybe pedunculated, protruding from the 
uterine wall, sometimes with long stalks. 

The size, position, and number of fibroids in the 
uterus have a bearing on the success of the emboli- 
zation procedure. The vascular anatomy also has a 
major impact on the success and complications of 
the embolization procedure. 



10.3.3 

Vascular Anatomy and Variants 



10.3.3.1 
Uterine Arteries 



A. C. Roberts, MD 

University of California, 5s:i ! 'ieac Medical Center, Divi 
Vascular and Interveiv.ioi'.a! kiidiology, 200 West Arbor 
San Diego, California 92103-8756, USA 



The uterine blood supply is prinmnlv from the uter- 
ine arteries. The uterine arteries arise as branches 
of the internal iliac (hypogastric) arteries. In most 
cases, the internal iliac artery divides into a poste- 
rior division that gives off the iliolumbar, the lat- 
eral sacral and the superior gluteal arteries and an 
anterior division that gives rise to parietal branches 
(the obturator, inferior gluteal and internal puden- 



A.CRooerrs 



dal arteries) and visceral branches (the superior 
vesical, middle hemorrhoidal, uterine and vaginal 
arteries) [1], However, the anatomy is variable and 
variant vascular patterns occur in about 10%— 15% 
of the population [2]. When the arterial anatomy is 
studied angiographically, the divisions can be into 
three branches in 14%, four or more in 3% and one 
main branch in 4% [3]. The anterior division is par- 
ticularly variable in terms of its branching pattern. 
The uterine artery arises from the anterior divi- 
sion of the internal iliac artery usually close to, or 
in common with the middle hemorrhoidal or vagi- 
nal artery. There are several configurations for 
the origin of the uterine artery. It can be the first 



branch of the inferior gluteal artery (Fig. 10.3.1a); a 
second or third branch of the inferior gluteal artery 
(Fig. 10.3.1b); a trifurcation of the uterine artery, 
inferior gluteal artery, and superior gluteal artery 
(Fig. 10.3.1c); or the first branch of the hypogastric 
artery (Fig. 10.3. Id) [4]. The most common variants 
are for the uterine artery to be the first branch of the 
inferior gluteal, or for it to arise from the trifurca- 
tion of the uterine artery, inferior gluteal artery and 
superior gluteal artery [4]. In some cases no uterine 
artery is identified. 

The uterine artery has a very characteristic 
U-shaped configuration, with a parietal or descend- 
ing segment running downward and medially, then 




ig. 10.3.1. a Most common configuration ;45 : 'o :. The uterine a: tery is the firsi hraritL-j of the i:ilv: ior gluteal, b An u 
variant (6%) the uterine artery is ,i second or third branch ■ 'I" ihe mle: ioi gluteal ai Let v. c The second most common configure 
tion (43%). There is a irifu read on of the superior gluteal, inferior gluteal and ir.erine ai i^ry. il A:'.o".hci aiicommon configuratioi 
(n%i. The a;erine artery is the first branch of the inieri'.al iliac, [•■ivxuv.al :t: snuv: ior gluteal and inferior gluteal 



Fibroid Emboliz 



ii'.il Tedin. ■;.-. ■.■liiiilr: 



there is a transverse segment coursing medially, and 
then an ascending segment, which runs along the 
side of the uterus. The uterine artery crosses above 
the urethra, to which it supplies a small branch [5]; 
it enters the broad ligament and reaches the side of 
the uterus about 2 cm above the cervix. As it reaches 
the uterus, it gives off a descending cervical branch, 
which surrounds the cervix and anastomoses with 
branches of the vaginal artery [1, 5]. The anastomo- 
sis of the uterine artery with the vaginal artery leads 
to formation of the "azygos arteries", two median 
parallel arteries located on the anterior and pos- 
terior position of the vagina [2, 5]. The main uter- 
ine artery courses upward along the lateral side of 
the uterus, giving rise to intramural branches to 
the anterior and posterior surfaces of the uterus. 
These intramural arteries in the uterine muscle are 
extremely tortuous and are termed "arcuate arter- 
ies" [3] or "helicine arteries" [2]. There are anasto- 
moses between the arcuate arteries on either side [3, 
4]. The uterine artery terminates in a tubal branch 
and an ovarian ramus that anastomoses with the 
ovarian artery [1], 

The vaginal artery may arise as a branch from 
the hypogastric artery directly, from the uterine 
artery or from the superior vesical artery. In one 
angiographic study it arose from the anterior divi- 
sion of the internal iliac artery just below the uter- 
ine artery in 50% of patients [3]. In a small per- 
centage (9%) it arose from a common trunk formed 
with the uterine artery. It anastomoses with the 
descending branches of the uterine artery and 
forms a network of vessels around the vagina [1]. 
Only the superior third of the vagina is function- 
ally connected to the uterus via arterial collaterals. 
The lower third of the vagina receives more blood 
from the urethral arterial collaterals. The vesicular 
artery, arises from the anterior division of the inter- 
nal iliac artery usually above the uterine artery, 
but in 1% of patients was found to be a common 
trunk with the uterine artery [3], Very occasionally 
the round ligament artery can supply the uterus. 
This artery arises directly from the external iliac 
artery or from the proximal epigastric artery and 
can supply the uterus, which may be important in 
fibroid embolization [6] or as a cause of recurrent 
vaginal bleeding after embolization for postpar- 
tum hemorrhage [7]. It may be a cause of failure of 
UAE to infarct the fibroid [8] . 

The uterine veins parallel the arteries forming the 
plexuses that end into the internal iliac vein; uter- 
ine veins merge with vaginal plexus downward and 
with the ovarian veins upwards. Venous blood from 



the upper part of the uterus drains into the 
veins, while most of the venous uterine blood is col- 
lected into the iliac vein [5]. 

The anatomy of the uterine artery has relevance 
to the procedure of UAE. When the uterine artery 
arises from the anterior division of the internal iliac 
artery, the contralateral oblique projection gives the 
best visualization of its origin, allowing for easier 
catheterization [4, 9]. When the uterine artery is 
arising from several stems, then the ipsilateral pro- 
jection is the best for visualization [4, 9]. 

The most common complications which have 
been reported with uterine artery embolization are 
amenorrhea, either permanent or transient pre- 
sumably secondary to ovarian failure [10-13], or 
are related to the fibroid, including infection of the 
fibroid, or fibroid expulsion [12]. However, rarely 
non-target embolization occurs. This non-target 
embolization may be due to some of the variant 
anatomy described above, or may be due to reflux 
out of the uterine artery into arteries that originate 
close to the uterine artery. Case reports of labial 
necrosis [14], vesicouterine fistula [15, 16], i 
of the cervix and vaginal [16, 17], bladder 
[18], buttock necrosis [19, 20], have been reported. 
Sexual dysfunction after uterine artery emboliza- 
tion has also been reported. It is unclear what is the 
cause of this dysfunction; however, it is possible that 
the uterovaginal nerve plexus may have been dam- 
aged by the embolization, resulting in an adverse 
effect on sexual arousal and orgasm [21, 22]. Embo- 
lization of the cervicovagmal branch may have an 
impact on both vaginal and clitoral sensation [21, 
22]. Although, these complications appear to be 
extremely rare, they should raise the awareness of 
the importance of careful evaluation of the vascula- 
ture to look for aberrant vessels, and to avoid reflux 
of particles into neighboring arteries. 



10.3.3.2 

Fibroid Vascularity 

Intramural fibroids are the most common type of 
fibroids. Their blood supply monies bom one or 
more nutrient arteries. As the fibroid increases in 
size, the nutrient artery, and the arcuate artery 
enlarge [4]. Submucosal fibroids also obtain their 
blood supply from the nutrient arteries. However, 
with subserosal fibroids, the fibroid may adhere 
to other structures, and derive blood supply from 
those adjacent structures [4], including the ovar- 



A.C.RoLicrrs 



10.3.3.3 
Ovarian Arteries 



The ovarian arteries arise from the ventral surface 
of the aorta just below the origin of the renal arter- 
ies. In 80% of individuals there is a single ovarian 
artery on each side [2]. In more than 70% of patients, 
Hie ovarian arteries originate lrom the ventral sur- 
face of the abdominal aorta a few centimeters below 
the origin of the renal arteries. The arteries are small 
normally less than 1 mm [2]. The ovarian arter- 
ies course downward and laterally over the psoas 
muscles and the ureter. They tend to be very tortu- 
ous distally, with a characteristic sinuous course. 
The arteries enter the pelvis, crossing the common 
iliac artery. They enter the broad ligament at the 
junction of the superior and lateral border of the 
broad ligament. The arteries continue beneath the 
fallopian tube, entering the mesovarium to supply 
the ovary [1]. Anastomoses occur with the ovarian 
rami of the uterine arteries, branches also extend 
to the ampullar)' and isthmica portions of the tube, 
the ureter and the round ligament [1], There is also 
a branch to the skin of the labia and inguinal area. 
Proximally there are branches to the ureter, perire- 
nal and periureteric fat. 

Variant anatomy of the ovarian arteries includes 
the gonadal artery originating from the renal artery 
in about 20% of individuals [2]. Very rarely the 
artery arises from the adrenal, lumbar, or iliac arter- 
ies [2]. In some cases, the right ovarian artery passes 
behind the cava and over the right renal vein. The 
left ovarian artery will occasionally also pass over 
the left renal vein [2]. There is very rarely ; 
trunk of left and right gonadal arteries, and 
sionally there are multiple gonadal arteries. 



10.3.3.4 

Tubo-ovarian Anastomoses 



Communications between the ovarian artery and 
the uterine artery has two potential adverse out- 
comes, it may allow continued blood supply to the 
fibroid, leading to failure of the procedure, and 
alternatively it can lead to permanent ovarian fail- 
ure following embolization. Because of these poten- 
tial problems, there has been considerable interest 
in how best to evaluate the ovarian arteries. Flush 
arteriography has been an approach to evaluating 
the ovarian arteries to determine if there is enlarge- 
ment of the ovarian artery and supply to the fibroid 
[23]. In one study [23] of 294 aortograms, 75 ovarian 



arteries were identified (25%) in 59 women (20%). 
Bilateral ovarian artery identification was seen in 16 
women, and unilateral identification in 43 women. 
In the bilateral group, there were six enlarged ovar- 
ian artery and 11 moderately enlarged 
arteries were considered small. When the 
artery was enlarged it was supplying fibroids, in 
most cases these were large fundal fibroids although 
in some cases there had been previous pelvic or 
tubo-ovarian surgery [23]. 

In the majority of patients undergoing UAE, tubo- 
ovarian anastomoses are not identified. However, 
when they are seen prior to embolization, meno- 
pausal symptoms (amenorrhea, hot flashes) are 
common although usually transient [4]. Razavi et 
al. [24] have described three main angiographic pat- 
terns of anastomoses between uterine and ovarian 
arteries. Type I anastomoses are divided into type la 
and type lb. In both types the ovarian arteries are a 
major source of blood supply to thefibroid, with anas- 
tomosis between the ovarian artery and the intramu- 
ral uterine artery. In type la (13%), the flow in the 
tubal artery is towards the uterus, without evidence 
of retrograde reflux in the direction of the ovary on 
selective uterine angiograms. In type lb (9%), flow 
in the tubal artery was towards the uterus, but reflux 
into the ovarian artery is seen on the preemboliza- 
tion selective uterine angiogram. Type II (4%) has 
direct fibroid supply from the ovarian arteries, with 
the flow to the fibroids being anatomic independent 
of the uterine artery. Type III (6%) has flow in the 
tubal artery towards the ovary on selective uterine 
angiograms, with an ovarian blush being present. 
In 8% there were bilateral anastomoses of the lb or 
III type, and in 68% there were no anastomoses pres- 
ent [24]. In evaluating for menopausal symptom 
the incidence of menopause following the procedure 
was 6% overall, 16% in patients over the age of 45, 
and in patients with bilateral type lb and/or type III, 
50°(i became menopausal. 

Cicinelli et al. [5] described an interesting 
tern of collateral flow between the uterine and o 
ian arterial supply to the uterus. In doing 
ments of blood flow in premenopausal women, this 
group found there is more blood flow to the uterus 
from the ovarian artery during the follicular phase, 
whereas in the luteal phase most of the uterus is sup- 
plied from the uterine artery. Whether this change 
in blood flow patterns is changed in patients with 
fibroids is not clear. No studies of the effect of the 
phase of the menstrual cycle on the effectiveness of 
uterine artery embolization have been performed at 
this point. 



Fibroid Emboliz 



i: Anatomy and Technical Car 



10.3.3.5 
Equipment 

10.3.3.5.1 

Catheters and Micro catheters 

10.3.3.5.1.1 
Catheters 

There are a number of catheters that can be used 
for uterine artery embolization. If an aortogram is 
being performed, a standard aortic flush catheter 
such as a pigtail catheter, or a catheter such as an 
Omni Flush (Angiodynamics, Inc., Queensbury, 
NY), or Varrel Contralateral Flush (VCF) (Cook, 
Inc., Bloomington, IN), is appropriate. For selec- 
tive catheterization of the internal iliac artery and 
uterine artery a 4-F or 5-F Cobra 2 (C2) catheter is 
a standard catheter. The C2 catheter is positioned 
into the contralateral iliac artery over a standard 
guidewire; however, an angled Glidewire (Terumo 
Medical Corporation, Elkton, MD) can be very help- 
ful in performing the subselective catheterization. 
The uterine artery tends to be prone to spasm and 
minimizing wire use will help to avoid spasm, which 
will help to decrease complications such as arterial 
dissection. To access the ipsilateral internal iliac and 
uterine artery, the C2 catheter can be formed into 
a looped configuration, a Waltman loop [25]. This 
configuration allows for subselective catheteriza- 
tion. The Waltman loop technique was originally 
described with a larger catheter than is now usually 
used, and with smaller catheter sizes the looped con- 
figuration is more likely to be lost as the catheter is 
being manipulated. It is very important that a soft 




Fig. 10.3.2. A long- reverse curve ail liefer. V'erv useful for c nth - 
eterizations in the pelvis an J for uterine artery embokzal ion. 
Tip is tapered to 4 F. Radiopaque marker at genu of catheter 
marks the point where the cnlheler should be positioned over 
the aortic bifurcation 



wire be used in a catheter that has been formed into 
a Waltman loop, otherwise the shape will be lost. 
An alternative catheter is essentially a preformed 
Waltman loop; this is a long reversed curve catheter 
(RUC, Roberts Uterine Catheter, Cook, Inc, Bloom- 
ington, IN) (Fig. 10.3.2). The catheter is 5 F taper- 
ing to 4 F at the distal end, with a soft, atraumatic, 
radiopaque tip, there is a small radiopaque marker 
where the catheter makes a sharp loop or genu and 
the catheter has excellent torque control. This cathe- 
ter allows the benefits of the Waltman loop, with less 
chance of losing the looped configuration during 
manipulations. 

10.3.3.5.1.2 
Microcatheters 

Initial descriptions of UAE included the routine use 
of microcatheters; however, many operators reserve 
these catheters for times when standard catheters 
are not appropriate. If the artery is small, there is 
marked spasm, or there are branches such as the 
cervicovaginal artery that the standard catheter has 
difficulty getting past, then microcatheters may be 
very helpful. The small size and the flexibility of 
these catheters helps to avoid spasm and allows for 
distal placement of the catheter [26]. A number of 
microcatheters also have a hydrophilic coating that 
gives improved trackability. allowing tor improved 
catheterization of tortuous arteries. Use of a high- 
flow microcatheter is usually the best for emboliza- 
tion since the larger lumen of these catheters helps 
avoid clogging of the catheter with the embolic 
material, and allows for a more rapid embolization 
procedure. Such high-flow catheters include the 
Renegade Hi-Flo catheter (Boston Scientific, Natick, 
MA}, the MassTransit catheter (Cordis, Miami, FL), 
and EmboCath (Biosphere, Rockland, MA). 

Disadvantages ot the in icrcRtat Meters include the 
additional, high cost of the catheters. They are also 
more difficult to see, may require a leading wire 
which can induce spasm in front of the catheter, and 
since they are prone to clog, a more dilute suspension 
of embolic material should be used which increases 
the time of the procedure, and more importantly 
tends to increase the fluoroscopy time. 



10.3.3.5.2 
Embolizatioi 



A variety of embolic materials have been used for 
treating uterine fibroids. Although there are at least 



theoretical benefits of using one material compared 
to others, it is not clear at this time if there are any 
clinical differences [27]. It is probably most impor- 
tant for the operator to feel comfortable with the 
material used, and to use it appropriately. 

70.3.3.5.2.1 

Polyvinyl Alcohol Particles (PVA) 



1'VA [.'articles probably remain tlir most . 
embolic used for uterine fibroids. These particles 
have been used for many years in a variety of vascu- 
lar beds and are considered to be safe and effective. 
PVA is available from a number of manufacturers. 
It is important to recognize that different manufac- 
turers produce different versions of PVA. Some of 
the PVA is quite jagged and tends to clump together 
such as PVA Foam particles (Cook Inc., Blooming- 
ton, IN) or Contour PVA particles (Boston Scien- 
tific, Natick, MA) (Fig. 10.3.3). It is very important 
with all types of embolic material to use a solution 
that allows for the best possible suspension of the 
particles. Clumping of PVA may be a function of 
the contrast dilution, and enough contrast should 
be used to allow the particles to be free floating 
and not aggregated. With PVA Foam particles, an 
iodine concentration of 240 mg/mL contrast tends 
to give the best suspension (Charles Kerber, M.D., 
personal communication) (Fig. 10.3.4). The irregu- 
larly shaped PVA particles were those used in the 
original description of uterine artery embolization, 
and a size of 300-500 um seemed to be the best size 
for this application. This PVA works well with the 
4- to 5-F catheters, but is more likely to jam in the 
microcatheters [27]. Although the jagged nature of 
the PVA has been considered by some to be a nega- 



interlockit 

embolizati 

Spheric; 

Microspht 



mid consider that these particles allow 
; which may make for a more efficient 



PVA is now available (Contour SE 
:s; Boston Scientific, Natick, MA), PVA 
Plus (Angiodynamics, Inc., Queensbury, NY), Bead 
Block (Terumo) which has a smooth surface and a 
more uniform size distribution (Fig. 10.3.5}. These 
particles should minimize catheter clogging, and 
may provide a better matching of the embolic to the 
vessel size. Because these particles are more homo- 
geneous, it is recommended that the size of the 
particles should be larger than the irregular PVA 
particles, so a size of 500-700 pm or 700-900 pm 
is usually used. There are increasing reports sug- 
gesting a higher clinical and imaging failure with 
spherical PVA. 




Fig. 10.3.4. Different dilution of coniriist chonges i Li e scsr 
sic-:: of ihe PVA, when 140 nig/iii! is use,: [here is S'lspcj^jo 
the PVA in solution. In other dilutions it floats or sinks 



10.3.3.5.2.2 
Embospheres 

A newer embolic which is a tris-acryl collagen- 
coated microsphere (Embospheres, Biosphere Medi- 
cal, Rockland, MA) was the first embolic approved 
by the FDA specifically for fibroid embolization. 
These particles are hydrophilic and nonabsorbable. 
They have a very smooth surface, and are softer and 
more deformable than PVA. They are easily admin- 
istered through a microcatheter since they have a 
reduced tendency for clumping and aggregation. 

The embolic comes inpre-filled syringes to which 
the same volume of undiluted contrast is added. It is 
recommended that several minutes be allowed after 
adding the contrast so that the microspheres achieve 

Another microsphere also made by Biosphere 
Medical isEmboGold, the microspheres are manufac- 
tured with the addition of gold, which is used to pro- 
vide coloring. This product is specifically not cleared 
by the FDA for use in uterine fibroid embolization 
and has been associated with delayed pain and/or 



Fibroid Emboliz 



ii'.il Tedin. ■;.-. ■.■liiiilr: 






e uniform and with sinooih.ci' e;".ee?. ii E rub osp he< 



loth and very u 



rash when used in these procedures (Biosphere Medi- 
cal Instruction for Use for EmboGold Microspheres). 
There has been the report of endometritis in seven 
patients after uterine artery embolization when the 
Hmlx'Goki microspheres were used [28]. 

10.3.3.5.2.3 
Gel foam 



Absorbable gelatin sponge (Gelfoam, Ph; 
Upjohn Co. Kalamnzoo, MI) has been widely used 
for intraarterial embolization. It is considered a 
"temporary" agent that may allow recanalization 
of the embolized artery. Because of the perception 
that it is a temporary agent its use is suggested for 
patients who may want to preserve their fertility [29]. 
Gelfoam causes an acute arteritis of the arterial wall 
that induces thrombosis [30]. There is resorption of 
Gelfoam in 6 weeks after embolization with mini- 
mal tissue reaction [30]. Whether the artery always 
recanalizes is not clear [29, 31]. Gelfoam has been 
used for uterine artery embolization with pathologic 
verification of coagulation necrosis of the fibroid 
[32] and essentially the same success rates published 
toy oilier particle embolizations [33]. 

Gelfoam can be placed through a microcatheter 
[33], but it does tend to clog the microcatheter. Very 
small pieces and careful flushing between pieces 
can help in avoiding occlusion of the catheter. 

10.3.3.5.2.4 

General Considerations 

The embolic particles are usually delivered using a 
three-way stopcock to which a syringe containing 
the particle -contra st mixture is attached. A 1-ml or 



3-ml injection syringe is attached to the second port 
and then the stopcock is attached to the catheter. 
The particles can be re-suspended by transferring 
the contents of syringes from one to another, allow- 
ing mixing. The injection of the particles should be 
done using a slow, pulsatile injection, and watching 
the progress of the contrast into the uterine artery. 
If there is rapid flow of the particles away from the 
catheter then fluoroscopic monitoring is not required 
for the entire 1-ml injection. When the flow begins to 
slow, then more rigorous monitoring with fluoros- 
copy is required to avoid over embolization. 

Gelfoam can be delivered by cutting the gelatin 
sponge into small fragments that are placed in a 
solution of saline and contrast. These are injected 
through the catheter. The Gelfoam pieces can also 
be place in a syringe with a saline and contrast solu- 
tion with a three-way stopcock and macerated by 
the to-and-fro motion of between the two syringes, 
making a slurry of the Gelfoam. There is a tendency 
for Gelfoam to clog microcatheters so very careful 
technique is required if a microcatheter is being 
used, and the use of one of the larger lumen micro- 
catheters is recommended. 

Since the communications between the uterine 
artery and the ovarian arteries have been measured 
at 500 microns, particle sizes larger than 500 u.m 
should help avoid having particles cross the anasto- 
moses to enter the ovaries [9, 30, 34]. 



10.3.3.5.3 




Medications 




Most of the r 


medications 


embolization e 


re focused 



management. However, these medications are most 
effective if they are given prior to the development 

Most patients will benefit from a pre -procedure 
anxiolytic medication. Lorazepam (Ativan) 1 mg 
given sublingually is an excellent pre-medica- 
tion. It is preferable to give a medication that can 
be administered sublingually since this allows the 
medication to be absorbed much more quickly, and 
to bypass the first pass through the liver that occurs 
if the drug is given as a swallowed, oral, medica- 
tion. A pre-medication that helps control anxiety 
makes other anti-anxiety and pain medications 
more effective. During the procedure an anxio- 
lytic such as midazolam (Versed) 0.5-1 mg titrated 
to patient comfort, and a pain medication such as 
fentanyl (Sublimaze) 25-50 mg titrated to patient 
comfort should be given. The patient will ideally be 
on a PCA pump following the procedure, so start- 
ing the PCA (particularly if a low-dose continuous 
infusion is being prescribed) during the procedure 
can provide another way of giving pain medication. 
The pain medication can provoke nausea in some 
patients. Although intravenous anti-nausea agents 
can be administered, the prophylactic placement 
of a scopolamine patch containing 1.5 mg scopol- 
amine (Transderm Scop, Novartis) behind the ear 
is very effective at decreasing the severity of nausea. 
It is contraindicated in patients with narrow angle 



Anti-inflammatory agents are very important to 
help in the control of pain. An intravenous nonste- 
roidal anii-int la minatory should Lv administrated. 
Ketorolac (Toradol) is an excellent agent. It has 
potent analgesic and anti-inflammatory activity; it 
also inhibits platelet aggregation, which is revers- 
ible within 24-48 h following discontinuation of the 
drug. The first dose should be given prior to begin- 
ning the procedure and then it should be continued 
while the patient is hospitalized. In most young, 
healthy women, Toradol is given in an intravenous 
dose of 30 mg every 6 h. The total length of treat- 
ment with Toradol cannot be more than 5 days. 

The use of prophylactic .intibiotics is controver- 
sial and there are no studies to determine whether 
antibiotic prophylaxis reduces the risk of infectious 
complications [35]. Most practitioners will give a 
single dose prior to beginning the procedure. Cefazo- 
lin (Ancef) 1 gm is a popular agent tor prophylaxis 
but there is no consensus as to which agents should 
be used [35]. Some practitioners give an antibiotic 
following the procedure for 5-7 days [36]. Others 
believe that any potent ia I infectious episodes can be 



more properly identified and cultured and treated if 
peri- or postprocedural antibiotics have not masked 
or disguised the organism responsible [22]. In addi- 
tion, there is always the concern for selecting out 
more resistant organisms that may prove more diffi- 
cult to treat. It is possible that prophylactic antibiot- 
ics destroy normal G rant -positive organisms allow- 
ing Gram-negative bacteria to proliferate [37]. 

Spasm is a concern during catheterization, and is 
relatively easy to induce with a guidewire or cath- 
eter. The development of spasm can reduce the 
efficacy of embolization by limiting the delivery of 
embolic particles. This can lead to premature clo- 
sure of the larger uterine artery possibly leaving the 
distal branches patent [30]. The first strategy should 
be careful techniques to minimize the development 
of spasm, use of non-ionic contrast, careful use of 
guidewires and catheters, and possibly the use of 
micro catheters. The most common pharmaco- 
logic treatment of spasm is the use of intraarterial 
nitroglycerin (100-200 meg) via the catheter. Some 
operators will give this as a routine medication in 
all patients. Others will give it only in patients when 
spasm develops. It is not known whether the fibroid 
vasculature responds to nitroglycerin or if only the 
normal uterus vasculature responds. If the latter, 
then the routine use of nitroglycerin may be coun- 
ter productive since it would only cause vasodila- 
tation of the normal vascularity potentially allow- 
ing increased embolization of the normal uterus. 
Although other vasodilators such as nifedipine 
have been given for peripheral vascular disease pro- 
cedures, they are not commonly administered to 
patients undergoing uterine artery embolization. 



10.3.3.5.4 
Technique 



10.3.3.5.4.1 
Arterial acces 



ight common femoral artery is the most 
i site for arterial access. It is the most famil- 
iar and tends to be the most comfortable for the 
operator. Usually the entire procedure can be easily 
performed from a single arterial puncture. The con- 
tralateral artery is certainly very easy to approach 
with a C2 catheter as described above. The ipsilateral 
artery can be more difficult, partial lurry if a long, 
reversed curve catheter is not used. Occasionally 
the patient's anatomy will require the other femoral 
artery to be accessed. 



Fibroid Emboliz 



ii'.il Tedin. ■;.-. ■.■liiiilr: 



Because of the potential ditliculty of accessing 
the ipsilateral artery, some authors have advocated 
a bilateral common femoral artery approach [38]. 

The rational for this approach is that the more 
difficult ipsilateral catheterization is avoided, and 
injections of contrast can be performed simultane- 
ously decreasing the amount of imaging sequences. 
There is at least a potential for decreasing the 
patient's radiation exposure. The concern regard- 
ing bilateral femoral artery punctures is that the 
risk of a puncture site complication is doubled. In 
addition, the use of bilateral femoral artery sheaths 
and placement of overlapping catheters in the distal 
aorta potentially increases the risk of thromboem- 
bolic complications [30]. 

Although an upper extremity approach using a 
brachial, axillary or radial artery puncture could 
be used, in actual practice this is almost never per- 
formed. It does have the advantage of not requir- 
ing the ipsilateral catheterization of the femoral 
approach, but there are significant disadvantages. 
The brachial and radial arteries have a very small 
caliber raising the concern for direct catheter trauma 
or thrombosis of these arteries. In addition, this 
approach requires the manipulation of the catheter 
in the region of the great vessels placing the patient 
at risk of a cerebral vascular event. 

10.3.3.5.4.2 
Catheterization Techniques 

Whichever access is chosen, a 4- or 5-F sheath 
depending on the catheter.which is going to be used, 
is placed into the artery. A sheath is a good idea when 
embolization is going to be performed, in case there 
is clogging or damage to the catheter that would pre- 
vent a wire from being placed through the catheter 
to allow an exchange. If there is embolic material 
in the catheter that would be unsafe to deliver, the 
catheter can be removed and replaced with a fresh 
catheter if a sheath is in place. The sheath also facili- 
tates the exchange of catheters and the manipulation 
of the catheters at the groin, which otherwise might 
enlarge the puncture site leading to a hematoma. 

My technique tor embolization of uterine fibroids 
starts with placing a flush catheter that allows a con- 
tralateral approach (VCF or Omni Flush catheter) 
into the aorta and positioning it just below the level 
of the renal arteries. The image intensifier is centered 
over the pelvis and a angiogram is performed which 
allows for visualization of ovarian artery collater- 
als, and provides visualization of the iliac anatomy 
(Fig. 10.3.6a). The flush catheter is then positioned 



at the aortic bifurcation with the tip in the contra- 
lateral common iliac artery and a wire (most com- 
monly a Glidewire) is advanced into the contralat- 
eral common femoral or superficial femoral artery 
(Fig. 10.3.6b). The flush catheter is removed and the 
RUC catheter is advance over the wire until the genu 
of the catheter, with the radiopaque marker, is lying 
directly on the aortic bifurcation (Fig. 10.3.6c). The 
wire is then pulled back into the catheter until it is in 
the ipsilateral portion of the catheter. The catheter is 
pushed up at the groin, which causes the catheter to 
form a loop in the aorta (Fig. 10.3.6d). As the cath- 
eter is pushed in at the groin, the tip of the catheter 
moves up in the contralateral artery. Once the tip of 
the catheter is above the internal iliac artery, the wire 
is taken out, the catheter is flushed, and a contrast 
syringe is placed on the catheter. The catheter can 
then be rotated so that the tip points medially (rota- 
tion of the catheter usually will not rotate the tip of 
the catheter without the catheter being moved either 
forward or back). With the catheter directed medi- 
ally it could be pulled down at the groin, advancing 
the tip into the internal iliac artery (Fig. 10.3.6e,f). 
Using a small amount of contrast to help visual- 
ize the arterial anatomy the catheter can be gently 
advanced and twisted to select the uterine artery 
(Fig. 10.3.6g,h). When the uterine artery is catheter- 
ized, the catheter can be gently pulled into the artery 
to approximately the level of the transverse section 
of the artery. If the artery is very small, then a micro- 
catheter can be used to access the uterine artery. In 
this event, the RUC catheter is pushed up so that the 
tip is just at the origin of the uterine artery allow- 
ing good blood flow through the artery. Following 
embolization of the contralateral artery, the catheter 
is advanced at the groin to allow the tip to disengage 
from the uterine artery. An injection of contrast can 
then be performed to verify appropriate emboliza- 

The catheter is then advanced at the groin until 
the tip is back in the aorta (Fig. 10.3.6i) and then the 
catheter is pulled back at the groin and manipulated 
until the tip of the catheter engages the internal iliac 
artery (Fig. 10.3.6j,k) the tip is then maneuvered 
into the uterine artery using small injections of con- 
trast for guidance (Fig 10.3.61). Once the artery is 
catheterized, and embolized, the catheter is again 
advanced at the groin disengaging the tip and the 
catheter is advanced up into the aorta until the tip 
of the catheter is above the bifurcation. The cath- 
eter is then pulled back using the tip to engage the 
contralateral iliac artery, and continuous pulling 
back allows the tip to slide down the contralateral 



!- .l~i ■ v.; ;-. i li !"■■ ■li/.-l.on: Aiiao'-m.v and Techn.ca. 




Fie. 10. .1.6. a A. r"i gi .m -a- in ■.■:".';".! a:ii".g pelv..: anaiomy, n :■ u>ri;:e a: onies idem idea, b Hush c .'■. I he le? used io position .i Glide- 
wire over the him re a ti on. c The KUC catheter has been posnion.eo over the Pifuicanoii. The radiopaque marke: designates Ih.e 
spot where the loop will ibii'i ;.irJoii , l. this must lie on the bifurcation, d The catheter is being pushed : ap ;it [he giom and 
;'. loop is heginmng to tor in in die noma. The tip or" die catheter !,<nou) has moved fiom the region of ti'.e common ftmorii' 
;:: rery towards die internal kiac artery. e,f The catheter l.p is Lvin.g .uiraiued above the Hirer mil iliac and then with some con- 
trast an injection is pulled down with gentle manipulation until it enters die internal iliac artery. g,h Tlie caliieler dp is the;: 
manipulated and gently mdlecl down, giving injections •:■< contrast to visa adze I lie ate: ine arterv. it is gciniv on Leo down until 
appropriately portioned, or it spasm results, dien slec.sioi: made whedier io use a miciocaiheie:. i Following die rmooliziitioi 1 . 
of die contralateral uterine a: rery the catheter is again advanced a: die groin until die tip of die catheter I .rr> t i il- : is above the 
aortic bifurcation. Then ii is pu.led down, advanc.ng the catheter lip into- liie common iliac artery. i,k T.ie caiiietri i ,; a. iked 
..".own pointed media..v L i n I j . it engages to inlernal .Lac artery, Ihe ha may Lien or tamed s.ightk :■.■ t:v ami oaiheieiize ih.e 
uterine artery. 1 The catheter is positioned .n the uterine artery a no if in gooo position then emoojz.adon can proceed 



external iliac and into the common femoral artery 
until the catheter is again settled agninst the aortic 
bifurcation. Continued withdrawal of the catheter 
will allow the catheter to be taken out of the sheath. 

The benefit of this type of catheter is that essen- 
tially the entire catheterization can be performed 
without having a guidewire in the internal iliac or 
uterine artery thus helping to prevent spasm. In 
addition since the catheter is being maneuvered 
without a wire in place, injection of the contrast 
allows for visualization of the vessels and conse- 
quently a much faster catheterization with minimal 
fluoroscopy time. 

An alternative way of catheterizing the uter- 
ine artery using selective catheters is described by 
Andrews [30]. Following an aortogram, the flush 
catheter is used to direct a wire over the iliac bifur- 
cation. A 4-F Berenstein catheter (or another selec- 
tive catheter such as a C2) is then placed into the 
contralateral common iliac artery. Repeat imaging 



of the internal iliac maybe necessary to better visu- 
alize the origin of the uterine artery. A guidewire is 
then placed, and the catheter is advanced in to the 
internal iliac artery. The wire is used to gently probe 
for the uterine artery. Road mapping is probably 
very helpful at this point, although it can increase 
dose rates relative to conventional fluoroscopy in 
some angiographic suites [39]. The course of the 
wire when it is in the uterine artery will be medi- 
ally directed initially and then will turn cephalad. 
If the wire does not engage the uterine artery, then 
the catheter can be advanced distully, beyond the 
expected point of origin and contrast injected as 
the catheter is slowly withdrawn. When the uterine 
artery origin is reached, contrast will be seen, the 
catheter is held in position and the guidewire rein- 
troduced and again gentle probing is used to try and 
access the uterine artery. Once the wire is in place, 
then the catheter is advanced gently into the first 
1-2 cm of the artery and a uterine artery angiogram 



is performed. If there is little or no flow, then it may 
be necessary to place a microcatheter and withdraw 
the primary catheter into the internal iliac artery. In 
any case after the initial uterine artery angiogram 
some type of catheter needs to be advanced more dis- 
tally into the uterine artery, ideally into the medial 
aspect of the horizontal segment, past the cervico- 
vaginal branch, if it is identified. After embolization 
of the contralateral uterine artery, a Waltman loop is 
formed using the selective catheter, and the catheter 
is directed into the ipsilateral uterine artery using 
the soft end of the Glidewire. Again angiography fol- 
lowed by more selective catheterization and emboli- 
zation is performed on the ipsilateral side. 

This dependence on the guidewire for location of 
the uterine artery, and advancement of the catheter 
is much more likely to lead to spasm than used of 
the long reversed curve catheter, if spasm occurs, 
then nitroglycerin (100-200 meg) can be given to 
help relieve the spasm. Alternatively, slow injection 
of saline may break the spasm and allow resumption 
of flow [30]. 

Very occasionally it is not possible to embolize 
one of the uterine arteries, despite multiple cath- 
eters, guidewires, microcatheters and even alterna- 
tive access sites. If an artery is difficult to catheter- 
ize, the first approach should be to access the other 
uterine artery and embolize it, prior to spending a 
great deal of time on the difficult artery. After suc- 
cessful embolization of one artery, a reattempt of the 
difficult artery should then be tried. In some cases 
there is flow redistribution which can facilitate the 
catheterization [40]. After occluding the flow in one 
uterine artery, there is vasodilatation of the contra- 
lateral uterine artery that may make embolization 
easier [30]. If, despite considerable effort, one is not 
able to embolize the artery, rather than sending the 
patient to surgery, it is reasonable to have the patient 
come back for another attempt in a few weeks or a few 
months [41]. The fibroids that have been successfully 
embolized decrease in size, changing the positioning 
of the uterus, which in turn may change the angula- 
tion of the artery allowing for easier catheterization. 

10.3. 3.5.4.3 

Use of Closure Devices 



There has been increased use of percutaneous clo- 
sure devices for closing the femoral artery punc- 
ture site. These devices are particularly helpful in 
patients that are being anticoagulated. There are a 
number of types of hemostatic devices: hemostatic 
patches, collagen-mediated devices, and suture 



closure devices. There has been a debate regard- 
ing the use of these devices in women undergoing 
uterine artery embolization. The concern is that 
in young women with essentially normal arteries, 
manual compression is usually effective in obtain- 
ing hemostasis in 15-20 min, and after 4-6 h of bed 
rest there is a very low incidence of bleeding or other 
puncture site complication. However, because of the 
post-embolization pain patients may have more dif- 
ficulty holding their leg still, particularly if they are 
getting substantial doses of narcotics. Also, if one 
wanted to perform the embolization procedure as 
an outpatient procedure, having an effective arterial 
closure would be beneficial. Two studies evaluating 
closure devices inpatients undergoing angiographic 
procedures came to different conclusions. In one 
evaluation of a percutaneous suture- mediated clo- 
sure device in 100 patients undergoing angiographic 
procedures, primarily uterine artery embolization 
procedures (65 patients), were retrospectively com- 
pared with patients not having the closure device 
[42]. This report described a 5% major complication 
rate (all in women undergoing UAE). One patient 
required thromboendarterectomy and patch angio- 
plasty to repair the common femoral occlusion, as 
well as amputation of a gangrenous toe. There were 
also two cases of external iliac artery dissection, one 
with distal embolization. 

A second study [43] was a prospective, although 
not randomized study, evaluating only patients 
undergoing UAE. This study had 342 patients 
enrolled, 328 of them received a suture-mediated 
closure device. There were no major complications. 
Approximately 21% of the patients complained of 
anteromedial thigh pain that responded to non- 
steroidal anti-inflammatory medications. This 
pain was postulated to result from irritation of the 
anterior femoral cutaneous nerve and presumably 
results from the nerve fibers being trapped by the 
sutures during deployment. 

If closure devices are going to be used, then com- 
plications can be minimized by adherence to meticu- 
lous sterile technique and confirmation of the appro- 
priate indication and anatomy. Whether the potential 
risk of the closure device is outweighed by patient sat- 
isfaction and convenience is not clear at this point. 



1 0.3. 3. 5. 4.4 
Radiation Exposure 

Since uterine artery embolization is performed i 
relatively young patients, some of whom are desirin 
future fertility, it is critical that radiation exposur 



Fibroid Embolization: Ana:o:r.y :i:id Technical Consider 



be minimized. The gonads are among the most radi- 
ation-sensitive organs, and the potential for malig- 
nant degeneration increases directly with cumula- 
tive radiation dose [39]. In order to have the best 
success rate and the least complications, the angio- 
graphic equipment should be of high quality. There 
must be adjustable collimators, and the capability 
of serial radiography and digital subtraction [35]. 
Ideally the unit will be equipped with reduced-dose 
pulsed fluoroscopy and last image hold. The unit 
should be able to perform oblique and compound 
angulation to facilitate selective catheterization. 
There should be a mechanism for recording patient 
radiation dose, such as dose-area product or cumu- 
lative dose at the interventional reference point or 
skin entrance dose [35]. Although roadmapping can 
be useful in subselective catheterizations, the acti- 
vation of roadmapping can disable the low-dose or 
pulsed fluoroscopic modes and may cause marked 
increase in dose rates [30]. 

There are angiographic techniques that can 
reduce a patient's radiation exposure. Such variables 
include minimizing the number of images acquired 
during the procedure, perhaps electing to record a 
image from the last fluoroscopic image from each 
injection of contrast which avoids dedicated DSA 
runs and increase the number of images acquired 
during the procedure [39]. Minimizing the amount 
of image magnification and the degree of imaging 
obliquity will decrease radiation exposure. Full 
magnification can increase the dose by 30%-155% 
[30, 38, 39, 44]. The obliquity of the image intensi- 
fier can be changed frequently but with only a slight 
degree of angulation to avoid one area of the patient 
getting most ofthe radiation beam. If an oblique view 
is required for catheterization, the imaging configu- 
ration should be restored to a frontal projection as 
soon as the catheterization has been achieved [30]. 
Raising the patient as far from the beam source as 
practical while simultaneously minimizing the dis- 
tance between the patient and the image intensifier 
can decrease the dose for fluoroscopy and imaging 
by up to 50% [30, 39]. Tight collimation is critical to 
decrease exposure. 



10.3.3.5.5 
Endpoints 

The angiographic endpoint ol uterine artery embo- 
lization with non-spherical PVA or Gelfoam is usu- 
ally until there is stasis or near stasis in the artery 
[35, 45-49]. 



There have been studies looking at microspheres 
in animal models that demonstrate these particles 
are more effective than PVA particles in achieving 
target vascular occlusion and tissue necrosis, with a 
more segmental arterial occlusion [50]. A small study 
of patients undergoing uterine artery embolization 
followed by myomectomy demonstrated aggregation 
of the PVA in vessels in the perifibroid myometrium, 
and microspheres within the fibroid arteries [51]. 
These findings seem to confirm the animal studies 
that microspheres are more likely to penetrate the 
fibroid vasculature than PVA. Because of this more 
complete arterial occlusion, the end point of emboli- 
zation is felt to be different with spherical emboliza- 
tion particle [52]. The particle size should be larger for 
spherical embolization particles than for non-spheri- 
cal PVA particles [52]. Non-spherical PVA is usually 
300-500 um in size while spherical particles should 
be 500-700 or 700-900 urn. The degree of penetration 
into the vascular system is actually greater with PVA 
spheres, and they may occlude on an even more distal 
level than tri-acryl spheres, perhaps because of dif- 
ferent compressibility properties [50]. Since a more 
targeted embolization is possible with calibrated 
microspheres a limited embolization is preferred. 
Instead of embolizing until there is complete stasis 
in the uterine artery, the embolization is stopped 
when: (1) no residual hypervascularization related to 
the fibroids is visible, (2) there is flow redistribution 
with identification of normal myometrial branches, 
(3) easy reflux into the ovarian artery that was not 
present earlier, (4) filling of cross-uterine branches, 

(5) stasis in the distal part ofthe uterine artery, or 

(6) reduced flow in the proximal part of the uterine 
artery [34, 50, 53]. This results in a "pruned tree" 
appearance ofthe uterine artery [50, 51]. 

Although there are theoretical advantages to the 
use of Embospheres, clinical studies have not shown 
an advantage over PVA particles [27]. The volume 
decrease ofthe fibroids, and the uterine volume reduc- 
tion is similar between Embospheres and PVA [54]. 
The volume of microspheres required for an embo- 
lization is larger than the volume of PVA required to 
complete an embolization [27], In both retrospective 
and prospective study there does not seem to be a dif- 
ference in post procedure pain or the use of narcotic 
use between PVA and microspheres [27, 55]. 

J 0.3. 3. 5. 5.1 

Ovarian Artery Supply 



There is no current consensus regarding the appro- 
priateness and timing of searching for and treat- 



A.C.RoLicrrs 



ing collateral blood supply [35]. Some practitioners 
obtain an initial aortograms with the catheter at 
the level of the renal arteries prior to the uterine 
artery embolization (Fig. 10.3.7) [23, 56]. Others do 
not evaluate the ovarian supply or perform an angio- 
gram after the embolization [30, 31]. Those who do 
not evaluate the ovarian supply may wait and evalu- 
ate the patient's clinical symptoms. If the symptoms 
do not respond appropriately, patients can either get 
an magnetic resonance angiographic (MRA) study 
to evaluate for ovarian collaterals (Fig. 10.3.8) or 
undergo another angiogram [30]. If there are large 
n collaterals found on the initial study, there 



is debate about how to handle these arterial collater- 
als. Some operators will wait to see how the patient 
responds to the initial uterine artery embolization 
and if there are continued symptoms will bring the 
patient back for a repeat angiogram and emboliza- 
tion. Some routinely get consent for embolization 
of the ovarian arteries prior to the procedure, and 
if they are large, will embolize the ovarian arteries 
during the initial procedure [30]. 

If large ovarian arteries are found, they maybe 
embolized with relatively large embolic particles, 
PVA 500-700 p.m or spherical embolic particles 
700-900 urn (Fig. 10.3.9a,b). Alternatively many 




Fig. 10.35. 


a Right ova 


nan artery supplying fibroid, b Post 


rmlX'!iz::l.i 


a, stasis ir. 


ovarian artery and no supply to 


fibroid 







Fibroid Emboliz 



ii'.il Teclin. ■;.-. -.'lisiilrr 



operators will use Gelfoam for embolization of the 
ovarian arteries [30, 31]. 

In conclusion, the success of uterine artery embo- 
lization for uterine fibroids is dependent on an 
understanding of the anatomy, and particularly an 
appreciation ol the v.iri.nu rmntomy rii.u am be the 
source of some unusual complications. There are a 
number of technical considerations that can influ- 
ence the ease of the procedure, and the safety of the 
procedure. The operator should be well versed in the 
variety of catheters that can be used for this proce- 
dure, as well as the characteristics of the embolic 
materials. Attention needs to be paid to radiation 
safety; there are a number of factors that the opera- 
tor controls and which can markedly decrease the 
radiation exposure for both the patient and the 
operator. 



Cookbook: 

5-F sheath 

• Bents en 

• 15-J standard wire 
. Glidewire 

4- to 5-F catheters 

• Flush catheter (if planning aortogram) 

• Selective catheters 

- C2 catheter 

- Bernstein or Kumpe catheters 

- RUC catheter 
Micro catheters 

• Hydrophilic, high-flow catheters 
Microwires - if using micro catheters 

• Hydrophilic 
Embolic materials 

• Non-spherical PVA (300-500 u.m) 

• Biospheres 500-700 urn, 700-900 urn 
Medications 

• Ativan 1 mg sublingual as preop 

• Fentanyl 

• Versad 

• Scopolamine 1.5-mg patch behind ear 

• Ancef 1 gm (or other prophylactic antibiotic) 

• Nitroglycerin (100-200 meg aliquots) as 
needed for spasm, or may be given 

"p rop hylac t ically" 

• Toradol 30 mg 



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10.4 Results and Complications 



Jean-Pierre Pelage, Arnaud Fau 



, and Pascal Laco: 



Introduction 157 

Technical Success 157 

Clinical Success 158 

Patient Satisfaction 159 

Quality of Life After Embolization 159 

imaging Evaluation 159 

Volume Reduction 159 

Residual Fibroid Perfusion 160 

Treatment Failures 161 

Cost Analysis 152 

Complications 165 

Fen -procedural Complications 163 

Aug. g: .ipinc CompJCJtions Ic3 

Noma r gee Embolization 163 

Radiation Exposure 164 

Post- Procedural Complications 164 

Post-Embohzation Pain 164 

Ovarian Failure 164 

Uterine Necrosis and Infection 165 

Vaginal Discharge and Expulsion 

of Uterine Fibroids 166 

Pulmonary Embolism 167 

Uterine Sarcoma 168 

Death 163 

Compilative :i".udics He;vcee:i Uterine Fibroid 

Embolization tr.d Surgery 1^8 

Uterine Fib: .<i.1 :■■ mk-.A-.ttt .-.n Versus 

Hysterectomy 168 

Uterine Fib- id :■■ mh .1 /.>i : i, Versus 

Myomectomy 169 

Fertility After Hmbolization 170 

Conclusior 1 71 

References 171 



10.4.1 
Introduction 

Since the first reports of its use as a therapeu- 
tic option for women with symptomatic uterine 
fibroids, uterine artery embolization has become 
increasingly accepted as therapy for this patient 
population. With the increasing frequency of its 
use in this setting, a greater understanding of both 
the advantages and the potential risks of this pro- 
cedure has occurred. 

With the growing popularity of uterine fibroid 
embolization (UFE), the scientific evidence has 
also greatly improved. Evaluation of results asso- 
ciated with UFE has included clinical success rate 
and uterine/fibroid volume reduction. Cost, recov- 
ery time, change in quality-of-life and patient 
acceptance are other important considerations. 
The associated risks of complications associated 
with UFE are of paramount importance before 
offering this procedure to young women interested 
in future fertility. 

There is, however, enough scientific data from 
the literature to suggest that UFE is a highly effec- 
tive, minimally invasive alternative to surgery 
and is now widely accepted for the management of 
fibroid -re la ted symptoms. This chapter summarizes 
the published results of UFE with respect to clini- 
cal benefits and potential complications, change in 
health-related quality-of-life measurements, fibroid 
devascularization and uterine volume reduction, 
and patient satisfaction. The initial studies compar- 
ing embolization to surgical procedures will also be 
presented and their results discussed. 



J.-P. Pelage, MD, PhD; P. Lacombe, MD 

Department of Radiology H6pil.il Aiv.oroise Pare, 9, Avenu 
Charles De Gaulle, 92104 Boulogne Cedex, France 

A.FAUCONNIEH,MD,PhD 

repartmen: o: Obstetrics and Gynecol' igy. Centre Hospital.; 
de Poissy, 10, rue du Champ Gaillard, 78300 Poissy Cede; 



10.4.2 

Technical Success 



Technical success has been described as successful 
embolization of both uterine arteries [1, 2]. The 
reason is that, except in rare cases, the procedure 



is unlikely to be successful unless both arteries 
are treated [2, 3]. In early series, complete occlu- 
sion of both uterine arteries to stasis with poly- 
vinyl alcohol (PVA) particles, often supplemented 
with either gelatin sponge pledgets or coils, was 
the standard end-point of embolization [4-7]. With 
the introduction of tris-ncryl gelatin microspheres, 
the appropriate end-point has become a subject of 
discussion [8]. Limited embolization of the uter- 
ine arteries leaving patent the main arterial trunk 
has been reported [9, 10]. The reported technical 
success rates range from 84% to 100% with most 
series reporting more than 95% technically suc- 
cessful procedures [1,4, 7,9]. 

Increasing operator experience will likely 
improve the technical success and efficiency of the 
procedure, with concomitant reduction of proce- 
dure duration and fluoroscopy time [1, 7], 



10.4.3 

Clinical Success 



Clin 



s has bee 



red by the de 



of improvement or the freque 
symptoms [11]. In most studies, these symptoms 
include heavy menstrual bleeding, pelvic pain and 
bulk-related symptoms (pressure, bloating and uri- 
nary frequency). In most of the published stud- 
ies, PVA particles were used as the embolization 
agent [5-7, 11-15]. Success rates for treating men- 
orrhagia, pelvic pain and bulk-related symptoms 
ranged from 81% to 96%, 70% to 100% and 46% 
to 100%, respectively [4-6, 16-19]. In a series of 
305 women, Hutchins reported control of men- 
orrhagia and bulk-related symptoms in 92% of 



cases at 12 months [4]. Three prospective studies 
with more than 200 patients enrolled have been 
recently published in the gynecological literature 
[7, 9, 11]. From a cohort of 508 patients undergo- 
ing UFE using PVA particles in Canada, signifi- 
cant improvements were reported for menorrhagia 
(83%), dysmenorrhea (77%) and urinary frequency 
(86%) at 3 months [11]. Menorrhagia was signifi- 
cantly improved with a reduction in the mean men- 
strual duration from 7.6 to 5.4 days [11]. Walker 
and Pelage [7] reported on their experience with 
UFE in 400 women with symptoms tk" fibroids with 
a mean clinical follow-up of 16.7 months. Men- 
strual bleeding improved in 84% of women and 
pelvic pain was improved in 79%. In a series of 
200 women, Spies reported similar results with 
improvement of menorrhagia and bulk symptoms 
in 90% and 91% of cases, respectively at 12 months 
[9]. Recently, Marret reported 83.5% overall clini- 
cal improvement of symptoms at a mean follow-up 
of 30 months in 85 patients [20]. With objective 
measurements of menstrual blood Ioss.Khaund et 
al. [21] reported significant reduction from 162 ml 
pretreatment to 41 ml at 36-48 months. The results 
of the largest prospective studies are summarized 
in Table 10.4.1. 

In the short-term, UFE using gelatin sponge 
pledgets alone seems to show comparable results as 
those obtained with PVA p;ir tides [22]. Katsi'uofu 
reported improvement in menorrhagia and in bulk- 
related symptoms in 98% and 97% of cases respec- 
tively at 4 months after embolization [22]. 

The initial experience with the use of tris-acryl 
microspheres mirrors the results obtained with 
PVA particles [10, 14]. Spies reported significant 
reduction of menstrual bleeding and pelvic pain 
in 92% of treated patients at 3 months [14]. Pelage 



Table 10.4.1. Results of iij ree prospective studies ; in chiding more :han J 00 paueiii; : : evahiaiing meriiv fibroid embolization 

Study Number Mean Efficacy Efficacy Efficacy Efficacy on Uterine Fibroid Hysterec- Permanent 

of follow- on men- on pain on pelvic urinary volume volume tomy for amenorrhea 

patients up in orrhagia pressure frequency redution reduction complies- (mean age in 

months (%) (%) tion (%) years) 



:taL 



200 



90% 



(2001a) 

Walker and 400 16.7 84% 

Pelage (2002) 

Pron etal. 538 8.2 83% 

(2003b) 

NA, data not mentioned in the cited paper. 

"Mean reduction at 12 months; b Median redu 



NA 
79% 
77% 



NA 



38%a 


58%a 


0% 


2=5 (NA) 


57%b 


77%b 


1% 


7% (48.4) 


35%c 


42%c 


NA 


NA 



it 9.7 months; 'Median reduc 



Results and Complies 



reported complete resolution of menorrhagia in 85% 
of patients with a mean follow-up of 30 months [10]. 
In a multicenter study reporting the use of tris-acryl 
microspheres larger than 500 urn, complete resolu- 
tion of menorrhagia was observed in 84% of treated 
women at 24 months [23]. In a recent randomized 
study comparing tris-acryl microspheres and PVA 
particles forUFE, Spies demonstrated no significant 
difference between the two types of embolization 
particles in any of the outcome variables [24], 

The recurrence rate after UFE has been reported 
to be lower than 10%, most cases beeing related to 
regrowth of fibroids not infarcted after the initial 
procedure [20]. The long-term rate of recurrence 
due to the growth of new fibroids instill to be deter- 
mined [25]. 



10.4.4 

Patient Satisfaction 

Patient satisfaction with the clinical outcome of UFE 
has usually been measured with follow-up ques- 
tionnaires and correlates well with symptomatic 
improvement [7, 26]. 

Worthington-Kirsch et al. [26] surveyed their 
cohort of 53 patients for satisfaction with the pro- 
cedure and reported that 79% of the patients inter- 
viewed would choose the procedure again. Walker 
and Pelage [7] reported that 97% of patients were 
pleased with the outcome and would recommend 
UFE to others. In their treatment of 200 consecu- 
tive patients, Spies et al. [9] reported that patient 
satisfaction paralleled the symptom results and that 
these results remained stable during the course of 
follow-up. 



10.4.5 

Quality of Life After Embolization 



A broader measure of outcome is the change in 
quality-of-life after UFE. Health-related quality- 
of-life questionnaires usually measure param- 
eters such as energy, vitality, mood, pain, physical 
energy, social functioning, and sexual function 
[26, 27]. There has been relatively little written 
about the impact of UFE on quality-of-life, in 
part because until recently there have been few 
validated fibroid-specitk" quality-of-life question- 
naires. Standardized quality-of-life questionnaires 



such as the SF-36 and the SF-12 have been used 
to a limited extent in UFE [27]. Spies et al. [27] 
found that there were significant improvements in 
health-related quality of life and fibroid-specific 
symptoms in 50 patients undergoing UFE. A dis- 
ease-specific quality-of-life instrument for fibroids 
has been developed [28]. It has been used as one 
measure of outcome in a recent study comparing 
the outcome of UFE using PVA particles and tris- 
acryl microspheres [24]. Smith et al. [29] confirmed 
significant improvement in health-related quality 
of life scores after UFE. High levels of satisfac- 
tion were observed even when subsequent therapies 
were necessary after UFE. 

These published studies confirm the usefulness 
of measures of quality-of-life in assessing outcome 
and have particular utility when comparing relative 
outcome of UFE with other fibroid therapies. 



10.4.6 

Imaging Evaluation 

10.4.6.1 

Volume Reduction 

Uterine volume reduction and fibroid shrinkage 
are evaluated after embolization as part of imaging 
outcome (Fig 10.4.1). Within 3-6 months after UFE, 
a 25%-60% reduction of uterine volume has been 
reported [4-7, 11, 19]. The reduction in volume of 
the dominant fibroid ranges between 33% to 68% 
at 3-12 months [5-7, 9, 11, 18, 19]. From the Cana- 
dian Trial with a cohort of 508 patients, published 
median uterine and dominant fibroid volume 
reduction were 35% and 42%, respectively [11]. In 
a cohort of 454 patients, Ravina et al. [30] reported 
a marked 55% reduction in the size of the domi- 
nant fibroid at 6 months. Walker and Pelage [7] 
evaluated follow-up ultrasound imaging of fibroids 
in 400 patients who underwent UFE demonstrat- 
ing 58% and 83% median reduction of uterine 
and dominant fibroid volumes, respectively, with 
a mean clinical follow-up of 16.7 months. Similar 
fibroid volume reductions have been reported with 
the use of gelatin sponge or tris-acryl microspheres 
[22, 31]. 

Fibroid location within the uterus may correlate 
with outcome. Spies et al. [32] reported that smaller 
baseline leiomyoma size and submucosal location 
were more likely to result in a positive imaging 
(Fig 10.4.2). Jha et al. [33] confirmed that 




Fig. 10.4. la, b. A Ji9-yei;r-.:ild woman wit:: fi broj i"! - ivla :-fd Menorrhagia aad pelv\- pressiiiv. a Piv- embolization sag;t:al Tl- 
ivei glued !vik! iiemoiirUiaies a muhilihioid uiei ns. b r'osi-emoii-lizatioi"! sagina! 7.: -weighs: Miv; ■ ■bl-.i ijieJ 'a monllis afier enino- 
lization demonstrates a marked v.i-hune red u-.: lion of io-'i. The patient's :ondi;ioii a as a Is:' gready improved 



submucosal location was a strong positive predictor 
of fibroid volume reduction. MRI is also useful for 
quantitative assessment of signal intensity and mor- 
phological changes before and after UFE. Burn etal. 
[34] noted that the mean reduction in fibroid volume 
was 43% at 2 months and 59% at 6 months. In addi- 
tion, pretreatment MRi findings may help predict 
the success of the procedure. They reported that high 
signal intensity on Tl-weighted images before UFE 
was predictive of a poor response and high signal 
intensity on T2-weighted images was predictive or 
a good response in terms of volume reduction [34]. 
deSouza and Williams [35] demonstrated that 
fibroid with high signal T2-weighted images before 
UFE showed significantly greater volume reduction 
than those low signal intensity. 

Using three-dimensional color Doppler sonogra- 
phy, Fleischer et al. [36] found that hypervascular 
fibroids tend to decrease in size after UFE more than 
their isovascular or hypovasailar fibroids. McLu- 
cas et al. [15] showed that the initial peak systolic 
velocity was positively correlated with the shrinkage 
of fibroids and uterine volume reduction. 

In addition to volume reduction, the detection 
of new fibroids should be a priority since it is very 
common with other uterus-sparing therapies [20]. 
The remaining question is the duration between 
UFE and clinical recurrence due to new fibroids and 
whether this interval is different from that seen after 
myomectomy. 



10.4.6.2 

Residual Fibroid Perfusion 



The MRI appi 
embolizati 



fibroids after 
well described [33]. The 
signal intensity increases on Tl-weighted images 
indicating the presence of proteinaceous material 
related to hemorrhagic intaivtion [33]. In these 
fibroids, there is no enhancement after contrast 
injection (Fig. 10.4.2) [35]. In some cases however, 
some fibroids may not be completely infarcted 
after embolization and there may be some areas 
of residual perfusion [31, 37]. Arterial spasm lead- 
ing to insufficient devascularization, unilateral 
embolization or additional fibroid supply from the 
ovarian artery have been shown to result in persis- 
tent fibroid perfusion (Fig. 10.4.3) [2, 37]. Because 
the technical goal of UFE is to cause complete 
infarction of all identified fibroids, it is important 
to assess after embolization the frequency with 
which the infarction occurs [37]. Complete devas- 
cularization of all the fibroids, is the necessary 
precursor of symptom improvement in the long 
term (Fig 10.4.2) [25, 37]. This has been demon- 
strated when viewing the long-term imaging out- 
come of embolization, because complete fibroid 
infarction does result in long-term improvement 
of symptoms, whereas incomplete infarction may 
predispose to regrowth and clinical recurrence 
(Fig. 10.4.3} [37]. 



Results and Complies 




Fig. 10.4.2n,b. A 4 f; -yea i- old woman wili" fibroid -relate J mniorrh.igiLi. a Pre-rir.hojzjLion sagiUa! ■."ontrasi-enhjiiced MRI 
shows a single iiyp^iv.- sauar inlraiuura. fibroid (F). b Posl-embolizaiion oonlias.'-er.ban./ed MR! obtained j mo:r;hs a fir:' 
ei)ib"'l:/.jli.:'ii oemonsiiaies :■. ■."omrleie J ev.i ^ j n 1 .; :■ Lz-.i I :oji of the c-nii.ioiizc-i'i nbroid widi a normai myomeiiiLil perfusion The 
parent's addition has also grea.ly improved 



In addition, the degree of gadolinium enhance- 
ment is not correlated with fibroid volume reduction 
[35, 37]. Therefore, these data suggest that ultra- 
sound may not be useful for the imaging follow-up 
particularly in patients who have recurrent symp- 
toms [37]. This observation may change if a more 
accurate means than color Doppler is developed to 
assess residual fibroid perfusion with ultrasound 
[38, 39]. 



10.4.7 

Treatment Failures 

Another measure of outcome is the effectiveness 
of UFE in avoiding other treatments for fibroids, 
as measured by subsequent medical therapies or 
additional surgery. For example, hysterectomy or 
additional hysteroscopic resection or myomectomy 
for clinical failure or recurrence after UFE is an 
important measure of safety and a key outcome 
measure of UFE [2]. Spies et al. [9] reported nine 
(4.5%) hysterectomies out of 200 patients within 
12 months of therapy. Seven of the patients under- 
went hysterectomy for clinical failure after UFE. 
The other two patients underwent incidental hys- 
terectomy for treatment of a tubo-ovarian abscess 
and an adnexal mass. In a series of 400 
Walker and Pelage [7] reported 23 (6%) 



failures or recurrence. Of these, nine (2%) required 
hysterectomy. In their ongoing clinical experience 
in 80 patients Marret et al. [20] reported a 10% 
recurrence rate at a mean time of 27 months. In 
this study, hysteroscopic resection of submucosal 
fibroids was the most common intervention for 
recurrent fibroids and the number of hysterecto- 
mies was not mentioned [20]. Among the reported 
causes of failures, adenomyosis has been fre- 
quently involved [7, 40]. There are only four case 
series reporting the use of arterial embolization in 
patients with adenomyosis with or without uter- 
ine fibroids [41-44]. Uterine artery embolization 
is an effective procedure in the short-term but is 
associated with a high rate of clinical recurrence 
with up to 30% of embolized women ultimately 
requiring hysterectomy [43, 33]. Embolization may 
however be an option in young women with diffuse 
adenomyosis interested in future fertility since no 
uterus-sparing treatment is effective [44]. Even 
in the presence of two apparently normal uterine 
arteries, additional supply to the fibroids may come 
from other arterial sources, more commonly from 
the ovarian arteries [45-47]. The degree of ovarian 
supply varies but a potential predictor of clinical 
failure is the presence of ovarian artery supply not 
only to the uterus but also to port ions of fibroids not 
supplied by the uterine arteries [2]. If the patient's 
condition does not improve after embolization and 
fibroids in the distribution of the ovarian supply do 





Fig. 10.4.3a-c.A 40-ye.ir-::i[J ivkjii ivi:h linrcid -related mon- 
orrhagia, a Immedi.'.te post-embolizaiion sagittal contr.ist- 
enhanced MSI :. obtained 14 h after embeli7.alion! shows two 
viable fibroids [Fl and FJ; with persis-ent enhancement of 
the peripheral portion ; iirtvirj). Ii At o moo.: lis post- emboli- 
zation contra st- enhanced MRI shows that Fl and F2 are still 
viable. The paiieo.t, howeve:, :eponed T.aiked iT.provemenl 
in symptoms, c At 12 months post-embolization contrast- 
enhanced MR! shows ih.it H ;'.nd rl growing. The patient 
reported worsening symptoms an;: may consider another 
embolization procedure 












m. Fl ^^^^^B 



not infarct, then additional ( 
zation may be considered [2, 47]. 



artery emboli- 



10.4.8 

Cost Analysis 

Admittedly, measuring medical costs is very diffi- 
cult. Nevertheless, in the current health care envi- 
ronment, in which cost considerations are impor- 
tant, careful study of the costs of UFE should be a 
priority. The cost information can be used to ana- 
lyze the cost effectiveness of UFE compared to other 



therapies for fibroids. The cost should include the 
overall hospital cost as well as the length of recovery 
after UFE. An initial analysis by Subr am ani an and 
Spies [48] evaluated the cost associated with UFE. 
They found that the facility cost of UEE compared 
favorably with that of hysterectomy. A subsequent 
comparative study conducted at the same institution 
concluded that procedure-related costs were lower 
with UFE than with abdominal myomectomy [49]. 
Using a decision model comparing the costs and 
effectiveness of UFE and hysterectomy, Beinfeld et 
al. [50] deduced that UFE was more effective and less 
expensive than hysterectomy. In Canada, Al-Fozan 
et al. [51] reported that UFE v 



Results and Complies 



lower hospital tost and a shorter hospital stay com- 
pared with abdominal myomectomy, abdominal 
hysterectomy and vaginal hysterectomy. In France, 
it has been demonstrated that UFE was more cost- 
effective than vaginal hysterectomy [52]. 



10.4.9 
Complications 

Complications associated with UFE can be classified 
as minor or major based on their severity evalu- 
ated by the level of care required, the interventions 
necessary and the final outcome [53]. Two different 
systems (from the Society of Cardiovascular and 
Interventional Radiology, SCVIR, and the Ameri- 
can College of Obstetrics and Gynecology, ACOG) 
developed to allow standardized reporting of com- 
plication severity have been used to precisely assess 
complications following UFE [53]. From a cohort of 
400 women, the peri-procedural morbidity was 8.5% 
according to the SCVIR classification system and 5% 
according to the ACOG system. Most complications 
were minor and occurred during the first 3 months 
after UFE. Five major complications (1.25%) were 
reported in this group of patients. There was only one 
hysterectomy (0.25%) for complication in this study 
[53]. From the Canadian trial, the overall complica- 
tion rate after UFE was 8% [54]. In another study, 
the rate of readmissionfor complications from UFE 
was 17% [55] . All readmissions were due to infection, 
of which all but one were treated conservatively and 
median time to readmission was 3 weeks [55]. 



10.4.9.1 

Peri-procedural Complications 



10.4.9.1.1 

Angiographic Complication: 



Complications that can occur at the common femo- 
ral artery puncture site include formation of a hema- 
toma, pseudoaneurysm, or arteriovenous fistula, 
dissection or thrombosis of the common femoral 
artery, and infection [53, 56]. Vessel perforation is 
even more unusual than arterial dissection but may 
be problematic in that it could either cause occlusion 
of the uterine artery prior to embolization or can 
cause bleeding from the perforated vessel which may 
itself require embolization as treatment (Fig. 10.4.4) 
[56]. 



Arterial vasospasm is the most common compli- 
cation associated with passage of the guidewire and 
catheter into the uterine artery. Because of its diam- 
eter and tortuosity, the uterine artery is prone to 
spasm. In theory, embolization of an artery in spasm 
may not result in a lasting occlusion since relaxation 
of the vessel can increase luminal diameter enough 
to allow flow around the embolization particles [2]. 
This may lead to a false angiographic end-point 
with secondary redistribution of the embolization 
particles [2, 10]. The systematic use of microcath- 
eters and microguidewires has been shown to mini- 
mize the occurrence of spasm and medications such 
nitroglycerin or papaverine may be effective to treat 
spasm p]. 



10.4.9.1.2 

Nontarget Embolization 

The potential effects of non-target embolization 
warrant this type of monitor ins and concern during 
uterine artery embolization procedures. An aware- 
ness of non-target embolization was established 
more than two decades ago in association with pelvic 
arterial embolization procedures performed for a 
variety of different indications [57]. This risk was 
highlighted by the report of a patient experiencing 
labial necrosis after uterine artery embolization [58], 
The pat lent presented 5 days after embolization with 
vulvar pain and a tender, hypopigmented, necrotic 
appearing area on the labium. Ultimately, the labial 
lesion was self-limited, resolving completely within 
4 weeks. This finding was attributed to non-target 
embolization into the internal pudendal artery, pos- 
sibly due to retrograde reflux of embolic particles 
[58]. 

In 2000, Lai et al. [59] reported on a patient who 
experienced sexual dysfunction after uterine artery 
embolization. In this report, the patient experienced 
a loss of orgasm response to sexual stimulation after 
uterine artery embolization. These findings have 
been potentially attributed to embolization of the 
cervicovaginal branch of the uterine artery, again 
highlighting the potential risk of non-target embo- 
lization during UFE. The cervicovaginal branch 
can often be visualized angiographically arising 
from the distal descending segment or proximal 
transverse segment of the uterine artery [60]. It is 
believed that this vessel is responsible for supply- 
ing the uterovaginal plexus, which are the nerves 
surrounding and innervating the cervix and upper 
vagina [59], This case has led many interventional- 




Fig. 10.4.4. A 46-ycji--j]; woman i v l t :: fibroid -related nienor- 
it.sgia. Selective ca:lic;eriz.uion of a thin right uterine artery 
was performed but vessel yerfoialion occurred (arrow) with- 
out clinical consequence. However, supers elective catheteriza- 
tion and embolization was s'accrssftkly performed using a 
microcatheter 



ists to adopt the practice of positioning their angio- 
graphic catheter or microcatheter beyond the origin 
of the cervico vaginal branch during uterine artery 
embolization procedures. 



pulsed fluoroscopy, bilateral catheter technique with 
simultaneous embolization and focus on magnified 
fluoroscopy [7, 63]. 



10.4.9.2 

Post-Procedural Complications 



10.4.9.2.1 
Post-Embolizatioi 



After embolization, almost all patients exp> 
a self-limited post-emboliz.it ion pniri lasting 6-24 h 
[5, 6, 12, 16, 64]. Some patients will even present 
with a post-embolization syndrome consisting ol 
pelvic pain, nausea, vomiting, mild fever and gen- 
eral malaise [65]. Several strategies involving 
intravenous, epidural and patient- controlled 
gesia have been utilized to manage the pain as 
ated with UFE [5, 6, 12, 16, 18, 26]. Most of the centers 
have been admitting their patients for 1-2 days to 
provide aggressive management of pain [5, 6, 12. 
Walker and Pelage [7] reported that post-embo- 
lization pain was stronger than period-type pain 
in 68% of women and worse than expected in 40% 
of cases. Recent approaches of the pain issue have 
included outpatient uterine artery embolization or 
less aggressive embolization of the uterine arteries 
[10, 65, 66]. When UFE is performed as an outpa- 
tient procedure, up to 10% of embolized women will 
ultimately require readmission for pain [66]. When 
a more limited embolization of the uterine arter- 
ies is performed, post-embolization pain seems to 
be less even if recent reports comparing aggressive 
and limited embolization have not demonstrated 
any difference in terms of pain [10, 67]. 



10.4.9.1.3 
Radiation Exposure 

Radiation doses during uterine artery embolization 
are higher than with common radiological proce- 
dures but within acceptable limits [34, 61, 62]. The 
mean estimated absorbed ovarian dose has been 
reported to be 22 cGy with a mean fluoroscopy time 
of 22 min and a mean number of 44 angiographic 
exposures [62]. These figures were compared to the 
published radiation dose for tubal recanalisation 
(3 cGy} and pelvic irradiation for Hodgkin's dis- 
ease (up to 3,500 cGy). It is obvious that meticulous 
attention should be paid to cutting the screening 
times by coning and streamlining technique [63]. 
Radiation can also be limited by using low frequency 



10.4.9.2.2 
Ovarian Failure 

The onset of amenorrhea and other symptoms of 
menopause is a well-documented complication fol- 
lowing uterine artery embolization, with a reported 
incidence as high as 14% [68, 69]. Symptoms com- 
monly associated with menopause including amen- 
orrhea, vaginal dryness, hot flashes, mood swings, 
and night sweats have all been reported after uterine 
artery embolization [6, 7, 68, 70]. While the incidence 
of this complication can still be considered low (less 
than 4%), the impact of this complication can be 
quite significant, especially in patients wishing to 
preserve fertility options after embolization [53]. 



Results and Complies 



Several theories, however, have been proposed to 
serve as possible explanations for this complication. 
Small embolization particles administered within 
the uterine arteries can potentially make their way 
into the ovarian arterial circulation through patent 
uterine-to-ovarian anastomoses, increasing the 
risk of reduced ovarian perfusion and subsequent 
ischemia [6, 71]. This theory is supported by the 
demonstration of angiographically visible anasto- 
moses between these two arterial beds in up to 10% 
of cases [71]. In addition, several reports described 
the presence of embolization particles in the ovar- 
ian arterial vasculature, within an oophorectomy 
specimen obtained utter Uf-'H [7, 72], Microspheres 
smaller than 500 um in diameter can pass within 
the ovarian arterial circulation after uterine artery 
embolization performed in sheep, which may offer 
some guidance as to particle size selection for this 
procedure [47]. 

Ovarian ischemia may also happen alter aggres- 
sive embolization of both uterine arteries when 
to ovaries are supplied by the uterine arteries [47, 
73]. Using ovarian Doppler flow measurements, 
Ryu et al. [74] demonstrated that more than 50% of 
patients have decreased ovarian arterial flow after 
embolization of both uterine arteries to stasis. Nev- 
ertheless, the rate of amenorrhea mainly depends 
on the age of the patient at the time of treatment [68, 
75]. Chrisman et al. [68] reported a 14% incidence 
of ovarian failure mainly in women over the age of 
45. Spies et al. [76] reported that patients older than 
45 years of age are at an increased risk of experi- 
encing significant increases in follicle-stimulating 
hormone (FSH) levels when compared to baseline. 
Based on this study, Spies et al. [76] concluded 
that there is approximately a 15% chance of a sig- 
nificant change in FSH levels after uterine artery 
embolization in patients older than 45 years of age. 
Conversely, Ahmad et al. [77] reported no signifi- 
cant changes in menstruation or follicle-stimulat- 
ing hormone (FSH) levels in patients younger than 
45 years of age. 



10.4.9.2.3 
Uterine Necrosi 



One of the potentially more serious compli 

of uterine artery embolization is the 

an infection after embolization. Several studies have 

reported cases of pelvic sepsis after uterine artery 

embolization [6, 78, 79]. However, when several of 

the largest published series are considered in aggre- 



gate, the overall rate of significant infection after 
embolization remains low and can be estimated at 
<1% [6, 7]. It has been suggested that submucosal 
fibroids, pedunculated subserosal fibroids or large 
uterine fibroids may be at increased risk for infec- 
tion after embolization i hss. 10.1.5 and 10. 4.(0 [61, 
79]. The severity of this particular complication 
was made clear by the publication of the first death 
due to infection reported in a 51-year-old patient 
who underwent uterine artery embolization to 
treat abnormal bleeding attributed to submucosal 
fibroids [80]. After an immediate post-procedure 
period highlighted by a urinary tract infection the 
patient returned to the hospital 1 week later with 
abdominal pain, diarrhea, vomiting, and fever. 
Despite antibiotics, the infection required a total 
abdominal hysterectomy and bilateral salpingo- 
oophorectomy. Blood cultures ultimately were posi- 
tive for Escherichia coii. Two weeks later, the patient 
died due to a multiorgan failure [80]. Most interven- 
tional radiologists consider that large pedunculated 
subserosal fibroids should not reasonably be embo- 
lized. Conversely, it has been reported that the rate 
of necrosis or infection of large uterine fibroids is 
not as high as generally considered [120]. 

It is often difficult to know exactly how to manage 
patients presenting with signs that might indicate 
the presence of a uterine infection after emboliza- 
tion [5, 82]. The diagnosis is made even more dif- 
ficult by the fact that mild fever is often seen during 
the normal post-procedure recovery period [7]. 
Anyway, a patient presenting with increasing pelvic 
pain, high fever, vaginal discharge and leukocytosis 
a few weeks after uterine artery embolization should 
be immediately admitted for appropriate testing 
with imaging evaluation and treatment (Fig. 10.4.7) 
[5, 82, 83]. 

Bilateral occlusion of the uterine arteries during 
uterine artery embolization clearly increases the 
risk of global uterine ischemia and subsequent 
infarction in patients undergoing this procedure 
[10]. In fact, it is not unreasonable to assume that 
uterine ischemia occurs in all patients undergoing 
this procedure and that this ischemia likely contrib- 
utes to the post-procedure pain that is commonly 
;d by most patients after embolization. 
:ly this transient ischemia wors- 
ens to the point where the uterus becomes glob- 
ally infarcted. There have been reports of diffuse 
uterine ischemia and necrosis after uterine artery 
embolization [84, 85]. The typical presentation of 
uterine ischemia consists of long-standing pelvic 
pain which persists for several weeks associated 



with fever and elevated white blood cell count [7]. A 
contrast enhanced pelvic MRI may be useful in this 
setting to confirm the presence of uterine devas- 
cularization [121]. Ultimately, these patients may 
require a hysterectomy for pain relief [54]. In most 
cases however, imaging studies have been helpful in 
confirming myometrial perfusion nod absence of 
myometrial ischemia in most patients after uterine 
artery embolization [81]. While the reported risk 
of uterine necrosis is far less than 1%, steps such 
as avoiding complete stasis during embolization or 
using large embolization particles may reduce this 
risk even more (Pelage et al. 2003). 



10.4.9.2.4 

Vaginal Discharge and Expulsion of 

Uterine Fibroids 

A reported complication alter uterine artery embo- 
lization has been a persistent vaginal discharge 
[86]. This discharge, which is often characterized 
as brown or red-brown in color, can begin within 
Fig. 10.4.5.Gross specimen of hysterectomy obtained 3 months d a y S ofthe embolization procedure and can poten- 
after embolization to a M-tmmU woman with a large fundal t|al] ^ for sgveral months [?] y ina , dischar g e 
1 1 _"■ i"-. ■ i i.i ... ,"i:i ii": .".:.:ii'.r".c-: i .: v- ■.: ia\-..i v,-.:a n~ - n .:• 1 1 .-. .-<i\:.. ' "r , , 

Ht., uziu,-, v,„s P e, formed Jf m< .mail non-s P laical PVA ™Y be more Sequent in patients with submucosal 
particles. A large infarcted fibroid (F) is seen in the uterine fibroids or when embolization of the uterine arter- 
cavity and associated fund a J pei roration is seen {arrow) ies to stasis has been performed (Fig. 10.4.8) [7, 53]. 





Fill. !0.-!.6a,ti. .-,.■: '-.. i - .■ I ■ ■:■■■■ in .Hi v.:::: .niU :r'.:i:c-. : -■•■ 1 1 1 l~ : ■ ■::■:■■. a !•' re -t:'.: ;.•■■: !ii;i:i. 
ped^nc.ilalcd SLibseio : ial libioid : Fl. b Ai i> mentis posi-= , jj]bi:--lii:-.it:oji MRI shov 
red li i." : L o :i . The p.-tienl ul:iina:elv reguued iiivoiiic-clomy 



Results and Complies 




Fig.10.4.7. A 47-ye.ir-::ild wonuii with high fever and pain 
after embolization. Computed :omogiap:'.y scan obtained 
1 weeks after eT.^onziiiion because of pelvic pain and fever. A 
I:n rge infected fibroid f.i.'tc. 1 .si ) comaining air bubbles I aiic irj 
is seen. The patient ivas irea:eci by iivsterectomy 



Fig. 10.4.8a,b. A -13-year-old woman with vaginal discharge 
after embolization. Bilateral embolization of the uterine 
arrui :(.'!< wjs perform ci using small non-spherical PVA par- 

ddilional coils, a Pos-t-eiy.oojzado:'. sagittal T2- 
wtijihled Mil obtained <■ months after embolization shows a 
hiii,!- v^ri;" between .he surface of the fioroid and the uterine 
L^vily (an ■«■■}. b Hysterosalpingogiam shows endometrial 

:<: (.j. ..-,■. ,i r. o ■:"":: stent u'.::"i eocome".: il:s.T:'.ir ."■.:ls 
iniectecl in me uterine arteries are seen isliiis) 




Chronic vaginal discharge may be considered very 
troublesome by the patient and may also interfere 
with sexual life [86]. When hysteroscopic evalua- 
tion or hysterosalpingo^rrim is performed, chronic 
endometritis or endometrial atrophy may be found 
[86,87]. 

The presence of a brown or red-brown vaginal 
discharge, however, is potentially a sign of impend- 
ing transcervical passage of an embolized fibroid 
(Fig. 10.4.9) [7]. This event has be 
described and frequently reported 
has been reported to occur both a few weeks after 
the embolization procedure and after a period of 
time as long as 4 years [88-91]. Typically, patients 
experiencing passage of a fibroid, report symp- 
toms including vagiiuil discharge, hemorrhage and 
crampy pelvic pain [53]. Patients at an increased 
risk for expulsion include those with submucosal 
fibroids and those with intramural fibroids that 
have significant contact with the endometrial 
cavity [90]. Transcervical fibroid passage often 
occurs without incident (Fig. 10.4.10) [7], In rare 



i both well 
8-90]. This 



cases, retention of fibroid fragments within the 
endometrial cavity can potentially increase the 
risk of infection after embolization. If retention of 
a fibroid fragment is confirmed by imaging evalu- 
ation, the fibroid can be resected hysteroscopically 
(Fig. 10.4.9} [7]. 



10.4.9.2.5 
Pulmonary Embolis 



As is the case with most invasive procedures, deep 
venous thrombosis and pulmonary embolus repre- 
sent rare but potential complications of the uterine 
artery embolization procedure [53]. Patients taking 
oral contraception are known to be at increased risk 
for venous thromboembolic disease and there may 
be a transient hypercoagulability after embolization 
[92-94]. 

There have been at least two deaths reported in 
association with massive pulmonary embolism dis- 
ease after uterine artery embolization [95]. While 




Fig. 10.4.9a,b. A 40-year-.:' Id wcr.ur. will; v.;gi;- ; ;il i.1iy;:i;-,; s- ..in..: h e: :i '."■-:" i ha ye .1 :"[ - 1 r::'.b::liza:io::. a Pre era bo 
we it hied X!K! shows a l'.:>ie iiyuaeariiarv fibroid if".:, b A 2 -m out hi ;" , :: , s[-enib-. 'kz;:l ion MKI shows that mos 
has bee;: expelled die residua! pail Ii;:to:\ ) is s;ili attached and recalled hys:eroscopi<: resection 



.zation sagittal T2- 
part of the fibroid 



the exact source of the thrombus was not deter- 
mined in this case, it was likely from either deep 
venous thrombosis within the lower extremities or 
from pelvic vein thrombosis [96]. 



10.4.9.2.6 
Uterine Sarcoma 

It is inevitable that interventionalists will at some 
point perform the uterine artery embolization pro- 
cedure on a patient with a leiomyosarcoma instead 
of the more common benign uterine fibroid [97]. 
Leiomyosarcomas of the uterus are very uncom- 
mon tumors, with an incidence of less than 0.2% of 
uterine fibroids [98-100]. The difficulty in distin- 
guishing between a fibroid and a leiomyosarcoma 
is that there are no clinical or imaging features 
that clearly allow differentiation between these two 
entities [101, 102]. So far three patients with uterine 
sarcomas have been embolized [100, 103]. Common 
et al. [104] reported another case where uterine 
artery embolization was successfully performed, 
but continued growth of the fibroid prompted 
hysterectomy 6 months after embolization. These 
cases support the use of follow-up imaging, partic- 
ularly contrast-enhanced MR1, after embolization 
because failure to respond to embolization would 
warrant consideration of a malignant diagnosis 
and a subsequent recommendation for hysterec- 
tomy [105]. 



10.4.9.2.7 
Death 

Four deaths have occurred following UFE, two 
from pulmonary emboli and two due to infection 
in approximately 50,000 cases [80, 85, 95]. A careful 
analysis of the two cases of infection suggests that 
early diagnosis and appropriate management would 
have probably avoided such a fatal consequence [106]. 
It should be remembered that the mortality rate for 
hysterectomy for benign disease excluding compli- 
cations of pregnancy is 1:1,600 [107]. A recent review 
from Japan of 923 women having hysterectomy for 
fibroids found a 6% serious complication rate and 
one death due to pulmonary embolus [100], 



10.4.10 

Comparative Studies Between Uterine 

Fibroid Embolization and Surgery 

10.4.10.1 

Uterine Fibroid Embolization Versus 

Hysterectomy 

Pinto et al. [108] reported the results of a random- 
ized clinical trial inpatients assigned to two groups: 
those given the option of UFE or hysterectomy and 
those not informed of alternative treatment. The 
of UFE was 86%. The hos- 



Results and Complies 




Fig. 10.4. 1 On, b. A 4? -ye.; i-old wouun wit:: cc:y.p!e : .e i" e s ■. ■ ' [ 1 1 l ■:■ j"j of S"y:r'.p:c:v.s aftei embokzLition. a Pit-eiiibi.-liz.tiion SL"igiit:'.l T2- 
wejeliic: YR[ allows a ■s::u'.\ pedunculated sub-niti joslU iibroki i F). She underwent j tailed a: tempi of lrys:eri:isoopu resection 
prior to embolization, b Ai .i-nio:i:hs posl-eiiiboiiz.ilion MR! shows that the whole fibroid has been spontaneously expels.". 
The uterus is virtually normal 



pital stay for patients treated with UFE was 4.1 days 
shorter than for those who underwent hysterectomy 
(Table 10.4.2). Of women who underwent UFE, 25% 
had minor complications, in contrast to 20% of 
those who underwent hysterectomy having major 
complications [108]. 

A recent multicenter cohort study comparing 
UFE to hysterectomy has been completed by Spies 
et al. [109]. For UFE patients, there were signifi- 
cant reductions in blood loss scores and menor- 
rhagia questionnaire scores compared to baseline 
(Table 10.4.3}. At 12 months, a larger proportion of 
hysterectomy patients had improved pelvic pain. 
There was no difference between the two groups 
in the proportion of patients with improvement in 
urinary symptoms or pelvic pressure. Similarly, no 
difference between both groups was found in terms 
of quality-of-life scores [109]. 



10.4.10.2 

Uterine Fibroid Embolization Versus 

Myomectomy 

At the time this chapterwas written, only retrospective 
studies had been published [110-112]. In their retro- 



spective re view of 16 myomectomies and 32 emboliza- 
tions, McLucas and Adler [17] found that myomec- 
tomy patients experienced longer hospital stays and 
more complications than UFE patients. In their ret- 
rospective review of subgroups of patients undergo- 
ing UFE and myomectomy, Broder et al. [Ill] found 
that overall symptoms impi'oved in 92% UFE patients 
and 90% myomectomy pntients, respectively, and that 
94% of UFE patients were satisfied with the choice of 
their procedure compared to 79% of myomectomy 
patients (Table 10.4.4). However, re intervention rates 
among myomectomy patients were lower than in UFE 
patients (3% vs. 29%, p < 0.001). In their analysis of 
111 consecutive patients who underwent abdominal 
myomectomy or UFE, Razavi et al. [112] reported 
clinical success rates ol 64% vs. 92% lor menorrhagia 
(p< 0.05), 54% vs. 74% forpelvic pain (not significant) 
and 91% vs. 76% for bulk-related symptoms (p < 0.05) 
(Table 10.4.5). They found shorter hospitalization and 
recovery for patients treated with UFE, vs. 2.9 days 
and 8 vs. 36 days respectively [112]. They concluded 
that efficacy appears to be greater with UFE in treat- 
ment of menorrhagia, and surgery may be a better 
choice for symptoms related to mass effect of fibroids. 
Several randomized studies are ongoing and should 
confirm these encouraging preliminary results. 



Table 10.4.2. Resuhs •:■< n .-.indonuzed iiiiil comparing embo- 
lization to abdominal hysterectomy i Pinto et al. 2003) 



Table 10.4.4. Results of .i study comparing embolizatio 
abdominal T.voT.ecioiv.v ( [1 1 1 ] ! 





Embolization 
(n=40) 


Hvsleie 
(n=20) 


:»„„ 




Embolization 
(n=51) 


Mvomectomv 
(n=30) 


Statistics 


Hospitalization (days) 


1.71 ± 1.59 


5.85 ± 2.52 


Mean age (years) 


44 


38 




p=0.001 


Recovery (days) 
Per-oper.itive 
complications (%) 


9.50 ± 7.21 
25 


36.18 ± 
20 


20.47 


Mean follow-up 

(months) 

Clinical efficacy (%) 


92 


49 
90 




p=0.03 

NS 


Minor post-operative 
complications (%) 


50" 


20 b 




Secondary treatment 
for failure or com- 


29 


3 




p=0.004 


Major post-operative 2.5 C 
complications (%) 

3 Hematoma at the puncture site, vaginal d 
b Parietal hematoma, urinary tract infectio 


13* 




plication (tt) 

5e:ond:uy 
hysterectomy (%) 

!- : atienl': : 
satisfaction (») 


12 
94 


3 
79 




p< 0.05 

NS 



'' Phlebitis of the lower limbs, paiiel-.il hematoma, bleeding 
requiring transfusion. 



Table 10.4.3. Results of .i prospective cohort study comparing Table 10.4.5. Res u lis of a retiospeclive study comparing etv.oo- 
embolization to hysieieclomy (Spies et a I. 2004b) lization to abdominal myomectomy ([112]) 



Impiovement of 83% 88% 

pe.vic pain 

(at 6 months! 

Improvement in 75% 73% 

urinary frequency 

(at 6 months! 

Post-operative com- 14.7% 34% 

plications (ACOG 

classification! 

Post -operative com- 3.9% 12% 

plications (SCVIR 

classification) ,, ,. ,. ... 

• Hospitalization 0< 

ACOG, American College of Obstetrics and Gynecology; (days) 

SCWfi, Society of Cardiovascular and jitetveml 'iial Radiology. Recovery (days) 8 



Mean age (years) 4 
Mean follow-up 1 
(months) 

Efficacy on < 

menorrhagia (%) 
Efficacy on I 

pelvic pain (%) 
Efficacy on 3 

pelvic pressure (%) 
Complication 1 



a Endometritis, prolonged post-embolization 
b Abscess, transfusion, occlusion. 

'■' Embolization performed as an outpatient procedui 



NS 

p< 0.05 
p< 0.05 
p< 0.05 

p< 0.05 

., amenorrhea. 



10.4.11 

Fertility After Embolization 



Fibroids can affect fertility and the incidence of 
miscarriage. The efficacy of LIFE on pregnancy and 
fertility has yet to be fully established [113]. Patients 
who have had UFE have become pregnant and had 
successful deliveries [6, 7]. The ability of women 
treated with uterine artery embolization for differ- 
ent types of obstetrical or gynecological hemorrhage 
to conceive and deliver successfully is well-known 
and long-term follow-up is already available [114, 



115]. However, in these cases the embolization agent 
has usually been resorbable gelatine sponge which 
does not produce as distal a block as non- resorbable 
particles and therefore may affect the uterus differ- 
ently [13, 115], Encouragingly, ultrasound and MRI 
observation of the uterus following embolization 
demonstrates rapid revascularization of the normal 
myometrium and an essentially normal 
of the endometrium on 3- to 6-month MRI e 



Results and Compile 



nations [81]. The rapid revascularization may be 
due to the rich collateral supply in the pelvis which 
compensates for the complete occlusion of the uter- 
ine vessels produced by embolization [82]. The pub- 
lished evidence on fertility after embolization is still 
scanty whereas the literature on pregnancy follow- 
ing myomectomy is extensive. Until recently, most 
authors reserve LIFE for women who no longer desire 
fertility [113]. Other groups like ours, have taken a 
more open approach and now offer embolization to 
patients who desire future fertility particularly if 
hysterectomy, repei.it of multiple myomectomy 1 is She 
only surgical alternative [10]. Even if at the moment, 
reports of pregnane viol lowing uterine artery embo- 
lization remain anecdotal, questions of numerator 
(number of live births) and denominator (number 
of women attempting to conceive after emboliza- 
tion) will be determined soon by the results of large 
prospective registries. From available prospective 
studies, fecundity and delivery rates are encourag- 
ing and similar to those reported after myomectomy 
[30, 110, 116-119]. When pregnancy occurs, the rate 
of intrauterine growth retardation does not seem to 
be increased by potential alterations in uterine blood 
flow after embolization. Nevertheless, in interpret- 
ing fertility rates and pregnancy outcome follow- 
ing LIFE, it should be taken into consideration that 
women undergoing UFE are not similar to the gen- 
eral obstetric population. Large prospective studies, 
uidudnu randomized truik comparing emlxil na- 
tion and myomectomy in women interested in future 
pregnancy may answer the remaining questions. 

It appears that after pluridisciplinary evaluation 
with gynecologists and interventional radiologists 
involved, UFE can be offered to women who plan 
future pregnancy if the only surgical options are 
repeated myomectomy or hysterectomy. 



10.4.12 
Conclusion 

In conclusion, uterine artery embolization is both 
a safe and effective procedure to offer patients 
with symptomatic uterine fibroids. UFE has been 
described as a valuable alternative to hysterectomy 
and recurrent multiple myomectomy. Clinical suc- 
cess rates for control of heavy menstrual bleeding, 
pelvic pain and bulk-related symptoms have been 
reported to be 80%-95% of patients treated with 
a low rate of recurrence. The risk of major com- 
plications, including pulmonary embolism, uterine 



infection and/or infarction and ovarian failure is 
low, with many of these complications potentially 
treatable without additional surgery. However, addi- 
tional studies are needed to compare UFE to other 
uterine-sparing therapies such as single myomec- 
tomy and to provide pregnancy outcome after treat- 
ment. By gaining an understanding of results and 
complications described in this chapter, the prac- 
ticing interventionalists can seek information from 
patients regarding their risk for certain complica- 
tions and maybe more comfortable when discussing 
indication for UFE with gynecologists. 



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10.5 How to Minimize Failure after UFE 



* Golzarian and Jean Pierre Pel. 



CONTENTS 


10.5.1 


Introduction 177 


10.5.2 


Definition 177 


10.5.2.1 


Clinical Success or Failure 177 


10.5.2.2 


!iu,ig!:~.g Success 177 


10.5.3 


Failures Associated with UFE 1 


10.5,3,1 


Catheterization Failure 178 


10.5.3,1.1 


Vessel Damage 17S 


10.5.3.1.2 


Vascular Anatomy and Variants 


10.5.3.1.3 


Ovarian Artery 178 


10.5,3.2 


Spasm 179 


10.5,3,3 


Embolic Agents 180 


10.5.3.4 


Patient Selection 183 


10.5.3.4.1 


!-:bi'Oi; Location I8. ! 


10.5.3.4.2 


Adenomyosis 184 


10.5.3.4.3 


Undiagnosed Leiomyosarcomas 


10.5.4 


Conclusion 184 




References 1 85 


10.5.1 




Introduction 



Ten years after Ravina et al. first introduced the 
concept of embolization as a definitive therapy for 
symptomatic fibroids, uterine fibroid embolization 
(UFE) is accepted as a safe alternative to surgical 
treatment of fibroid tumors. Technique and mate- 
rials have been greatly refined. Much progress has 
been made in our understanding of fibroid vascula- 
ture, management of postoperative pain and compli- 
cations, and causes of treatment failure. According 
to the literature, the failure rates vary between 6% 
and 14% [1, 2]; however, there is still some confusion 
as to how to define success, failure or recurrence. In 
this chapter, we discuss the causes of failure after 
UFE and the different options available to 



J. Golzarian, MD 

Professor of Radiology, Pirec 

Radiology, University of Io' 

200 Hawkins Drive, 3957 IPP, 

J.-P. Pelage, MD, PhD 

Department of Radiology !-!6piul Ambroise Pare, 9, 

Charles De Gaulle, 92104 Boulogne Cedex, France 



r. Vascular and Interventional 
., Department of Radiology, 
wa City, IA 52242, USA 



10.5.2 
Definition 

10.5.2.1 

Clinical Success or Failure 

Clinical success is measu red by the resolution or the 
degree of improvement ot symptoms [2], The goal 
of UFE is to resolve or sign it ion nth' improve symp- 
toms. However, UFE is associated with no clini- 
cal benefit in some patients. This is one definition 
of failure. Another definition of failure is when a 
patient experiences clinical improvements in symp- 
toms initially, but the improvements are not sus- 
tained long-term. This "recurrence" of symptoms 
may not necessarily be caused by new fibroid recur- 
rence, however. The exact fibroid recurrence rate 
has not yet been established. One report indicated 
that the recurrence rate after UFE was lower than 
10% in a patient population followed by ultrasound 
[3]. In early reports on uterine artery embolization 
(UAE), most imaging follow-ups were obtained by 
ultrasound, and the reduction of the volume was 
considered an important factor for success. The 
:erine and fibroid volumes, although 
: not determinant factors of success, 
ularization of fibroids is associated 
of the tumors, resulting in 
i most patients. With our better 
understanding of UFE, it is generally accepted that 
there is a high rate of regrowth of noninfarcted 
fibroids after the initial procedure. This is associ- 
ated with a higher recurrence of symptoms. There 
is a shift to a new definition of success or failure 
based on the infarction of fibroids as demonstrated 
by imaging. 



reduction of u 
important, art 
Partial devasc 
with partial 



10.5.2.2 
Imaging Success 



Most authors agree that to obtai 
clinical outcome, complete deva: 



the best durable 
ularization of all 



J. Golzarian and J.-P. P 



fibroids is necessary [3, 4]. Although partial devas- 
cularization of fibroids can be associated with clini- 
cal improvement, failure to obtain complete devas- 
cularization may affect long-term clinical response 
and may lead to high recurrence rates [4]. Enhanced 
MR1 best demonstrates fibroid perfusion after UFE. 
In cases of persistent perfusion of fibroid(s), patients 
need to be informed of the higher risk of recurrence 
of symptoms and require close follow-up. Thus, per- 
sistence of contrast enhancement of fibroid(s) after 
UFE should be considered no better than a partial 



10.5.3 

Failures Associated with UFE 

Several causes of failure associated with UFE have 
been identified. These include the inability to can- 
nulate uterine arteries, arterial spasm, flow restric- 
tion, variation of vascular anatomy, and/or misdi- 
agnosis of fibroids as a cause of symptoms. Another 
important cause of failure is insufficient emboliza- 
tion, with recanalization of the fibroid vasculature 
occurring minutes to hours after the procedure's 
completion [5]. 



10.5.3.1 
Catheterization Failure 

To obtain technical success, both uterine arteries 
need to be embolized. Cannulation failure of one or 
both arteries can occur due to technical or anatomic 
conditions. Most technical failures of catheteriza- 
tionare related to anatomic variation. Vessel damage 
during the procedure is a rare cause of failure. 



10.5.3.1.1 
Vessel Damage 

Perforation and dissection of the uterine artery 
are less common causes of failure [6]. These com- 
plications can occur with the use of hydrophilic 
guidewires associated to the arterial tortuosity 
(Fig. 10.5.1). Vasospasm occurring primarily in 
patients undergoing hormone therapy is an impor- 
tant cause of vessel damage. Careful catheterization, 
use of a microcatheter and experience of operator 
performing the procedure are all important fac- 
tors in reducing this type of failure. In cases where 



the perforation or dissection of the vessels prevent 
appropriate embolization, a second procedure is 
needed in order to obtain successful devasculariza- 
tion of all fibroids (Fig. 10.5.2). 



10.5.3.1.2 

Vascular Anatomy and Variants 

There are some important anatomic variations asso- 
ciated with failure. These include tortuous artery, 
small uterine artery in one or both sides, absence 
of uterine arteries, ovarian artery supply of the 
fibroids and other less common variants such as a 
round ligament artery supply [7]. 

In the Ontario study, 5.!! fJ o of patients {'•! patients! 
experienced failure ol bilateral uterine artery embo- 
lization. In 18 out of 32 patients, uterine arteries 
were either too small or too tortuous to catheterize, 
or the vessel origin angles were too tortuous or steep 
for access [6]. In these situations, a second delayed 
procedure, usually with a contralateral approach, 
was successful most of the time [6]. 

Segmental arterial tortuosity may provoke flow 
limitation to the fibroids. Positioning the catheter 
past the tortuosity may increase the flow by correct- 
ing the curve of the artery; however, catheteriza- 
tion of the tortuous segment can increase the risk 
of spasm. The angulation of the origin of the uterine 
artery can be very acute, making distal catheteriza- 
tion more difficult, even with a microcatheter. If the 
microcatheter can be placed securely in the proxi- 
mal uterine artery, embolization can be performed 
with a highly diluted embolic materials solution and 
a very slow injection. 



10.5.3.1.3 
Ovarian Artery 



The role of ovarian arteries as a cause of failure is 
well known. Ovarian arteries may feed the fibroids 
through different pathways. The visualization of 
an ovarian artery is not systematically associated 
with failure. In one study, 25% of patients had large 
ovarian arteries before embolization [8]. Only arter- 
ies that directly participate in feeding the uterus 
cause failure. In cases of a small uterine artery or 
absence of one or both arteries, the ovarian artery 
supply should be suspected (Fig. 10.5.3). However, 
additional supply to the fibroids may come from the 

l arteries, even if large sized bilateral uterine 

i are present [9, 10]. 



r.cw [.:■ M:m;v..;e F.'ili::> :ift;r 'i-r 




Fig. 10.5.1 a-c. L'FE in a jxit.enl wjiii lic^vy Meeding. a Ton u.:i us origin or" ihc ; ighl uterii'.e .-I'.esy. b ;-vi i"o:Li:io:r oi" uie Li:;ery by 
(he guidewire. c Disuil uterine Linery whs s'.'.civsskkly i.-theteiiztd alio enioojzjiion coiiki be performed 



There are fewcase reports on ovarian artery embo- 
lization with good clinic.) I outcomes [11], Emboliza- 
tion of ovarian arteries can be proximal with the 
use of Gelfoam torpedo, or they can be distal after 
selective catheterization of the ovarian artery distal 
to the tubo-ovarian artery using a microcatheter 
(Fig. 10.5.3). Although we always discuss the pos- 
sibility of this variant pathway with patients, our 
policy is not to embolize the ovarian artery before 
discussing the problem with the patient in a second 
clinical visit. 



10.5.3.2 
Spasm 

Embolization of uterine arteries for fibroids is based 
on preferential flow to the tumors, also called flow- 
directed embolization. The occurrence of spasm 
results in reduced flow to the perifibroid plexus, 
which is the target of embolization (Fig. 10.5.4). 
Thus, spasm may lead to insufficient delivery of 
embolic material to the fibroid tumors [5]. 

Spasm may be related to hormone therapy. 
For those patients undergoing hormone therapy 
(Lupron), the treatment should be discontinued 
prior to embolization. Embolization can only be 
performed once menstrual periods are resumed. 



The most common cause for spasm is related 
to the catheterization. Careful catheterization is 
essential, although spasm can occur even in expe- 
rienced hands. Use of a smaller catheter size (4 F) 
with hydrophilic coating and smaller hydrophilic 
guidewires (0.021" instead of 0.035") may reduce the 
occurrence or spasm. Systematic usage of the micro- 
catheter is now recommended. The guiding catheter 
is placed at the origin of the uterine artery or even in 
the internal iliac artery. However, even with the sys- 
tematic use of a microcatheter, spasm was present in 
31% of cases in a recent study by Spies et al [1]. 

The use of the Roberts Uterine Catheter (Cook, 
Inc., Bloomington, IN) can be helpful to reduce the 
spasm. The benefit of this type of catheter is that the 
entire catheterization can be performed without a 
guidewire in the uterine artery, thus helping to pre- 
vent spasm (please see Chap. 10.3). 

In our experience, use of vasodilators in the pres- 
ence of spasm was not very helpful. When spasm 
occurs, the guiding catheter needs to be pulled out 
of uterine artery until the spasm is resolved. Some- 
times the microcatheter should be pulled out of 
uterine artery as well. In cases of persistent spasm of 
the left uterine artery, one can remove the catheter 
and proceed to the embolization of the right uterine 
artery before re-catheterization of the left side. If a 
flow-limiting spasm persists, the use of smaller sized 



I.Golzananand J.-P. Pi 




Fig. 1 0.1. 2 a -g. He.:vv bleeding in a 42-yeni -eld patient. a Pelvic angiogram demonstrates both uterine arteries, b Left hypogas- 
l: :c angiogram -hoiv; ".he left uterine .11 teiv Willi a proximal angulation, c Uterine- a: tery angiogram demonstrates a dissection 
at the horizontal segment of the artery, it Palieni '.mdei weni sn-;%: e^sniJ catheterization and embolizali' 'ii of the right uterine 
artery, e Pelvic angiogram at the end of the procedure shows no more fibroid blush ana uterine artery, f Pane:'/ complained 
of symptoms recurrence after b months. A nr\v proce-ritire is performed. The right internal iliac angiogram demonstrates the 
persistence of uterine artery occlusion, g Let": internal mac angiogram shows ihe recanahzation C'i the uterine arteiy with 
revascalat izaiion of ".he uterus. After successful entnodzatio:;, patient is symptom free after 2 years 



r.cw [.:■ M:ni:v..:'.e H:;ilu:'c after 'i-r 




Fig. 10.5 .3a- e. A 37 - ye.; i- old patient wi:h symptomatic fibroids. She 
was offered a hysterectomy as the only alternative. a,b Left uterine 
artery catheterization and embolization. The final angiogram at the 
termination of the embolization ;tii!oiii l:\r.es the left ovarian artery 
(b). c Right internal iliac angi' 'gj.nn shows die absence of right uter- 
ine artery. dCathete: izjiLon ot' the right ovarian artery demonstrates 
the supply to the uterus by this artery, e r ist.il catheterization and 
embolization of the ovai i-.iu ,11 teiv with successful clinical outcome 



embolic materials associated with complete stasis of 
the uterine artery can reduce failure (Fig. 10.5.4). 



10.5.3.3 

Embolic Agents 

The first embolic materials used for UFE were non- 
spherical polyvinyl alcohol (11PVA) particles, which 
were familiar to most interventional radiologists, 
readily available, inexpensive, and had a long his- 
tory of being well tolerated. Variation in the size of 
the particles and the tendency for them to aggregate 
is thought to provoke a proximal vessel occlusion or 
unpredictable level of occlusion [12]. The aggrega- 
tion of the particles may also cause microcatheter 



occlusion. However, dilution and slow infusion of 
nPVA particles during the embolization procedure 
can reduce the tendency for particulate aggregation, 
which may subsequently lead to a more distal embo- 
lization [5, 13]. Diluted PVA solution is also associ- 
ated with much less clumping and microcatheter 
occlusion [1, 14]. The accepted endpoint with nPVA 
has been complete stasis in the uterine artery as 
evidenced by a standing column of contrast. 

Other newer agents have been introduced for 
use in UFE. Gelatin-coated trisacryl microspheres 
(Embospheres, Biosphere Medical Inc., Rockland, 
MA} were the first spherical agents and offered the 
theoretical advantage of a more uniform and tar- 
geted embolization of the perifibroid plexus [15]. 
Their compressibility, llso made microcatheter clog- 



J. Golzarian and J. -P. P 




Fig. I0.7.!a-f. A .i 7-year-old poiiein k:i:. Ke.ivy bleeding related [.:■ ;i 7-a-i in:rani'.;r<il fibroid. n,h k:g!u i.r.eriiie nrleiy n::a..: gr.m 
demonstrates sposm :,::ton\ due to lathetenzation. c Left serine .i::ery <ingi.:-gr.;iu i:ivK< ::ir [Vc..:.ii£ ,i::ery to the fibroid 
(,jn L i!i). d Embodzoiion of I lie main feeding artery .in..: potency of die myome;rial arteries, e V.R\ obtained prior to die embo- 
lization shows a large :ntra:r.u;al mass, f MR! oo tamed I mom lis after die em bo I. zati on shows on almost normal uterus 



ging less likely. A new endpoint was proposed with 
Emtio spheres, with a limited embolization of uter- 
ine arteries resulting in a "pruned-tree" appearance 
of the vasculature [15]. 

In a prospective, randomized study, Spies et 
al. [1] compared nPVA with Embospheres. There 
was a significantly higher rate of microcatheter 
clogging in the nPVA group, but no difference 
in success rates, either by imaging criteria (non- 
enhancement ot all fibroids) or clinical outcome. 
Moreover, the intensity of pain and the compli- 
cation rates were similar. In choosing between 



embolic agents with identical clini 
one needs to weigh the ease of handling, the total 
volume of particles required, the time for reach- 
ing the expected endpoint (with longer times being 
associated with higher radiation doses), and the 
cost of the agents. 

In response to the rapid adoption of Embospheres 
for UFE, many companies have introduced the 
spherical PVA (sPVA) [16, 17]. Preliminary animal 
studies demonstrate that sPVA is safe, and the FDA 
has approved its clinical usage in UFE patients. An 
animal study has recently demonstrated a different 



e Failure after UFE 



penetration of sPVA particles compared to trisacryl 
microspheres. The authors have demonstrated 
that the sPVA particles have a more distal penetra- 
tion than the trisacryl microspheres [18]. Interest- 
ingly, in clinical usage, the embolization endpoint 
is unpredictable and achieves much faster and with 
less embolic volume than with other embolic agents, 
witnessing a proximal occlusion. The number of 
vials needed to achieve the same endpoint with 
nPVAwasat least twice as less. There are an increas- 
ing number of reports on failure after UFE with 
Contour SE (SPVA from Boston Scientific Corpora- 
tion). At our institution, we have ceased using sPVA 
for UFE due to a high rate of imaging and clinical 
failure (Fig. 10.5.5). The reason for the higher fail- 
ure rate associated '.villi sPVA particles is not under- 
stood. One explanation for insufficient emboliza- 
tion could be a proximal occlusion of the uterine 
artery. Laurent et al. have demonstrated that Con- 
tour SE particles are highly compressible (please see 
Chap. 10.6). This compressibility may be associated 
with the deformation of the spherical shape of the 
particles becoming more oval. The deformation of 
particles, as well as higher clamping, might explain 
the early proximal occlusion. However this proxi- 
mal plug will move distally reopening the uterine 
artery. In fact, re-catheterization of the embolized 



left uterine artery at the end of the procedure showed 
early reopening in some of our patients. Pelage et 
al. suggested changing the embolization endpoint 
with the sPVA to a complete occlusion of the uter- 
ine artery [19]. With this new protocol, they have 
obtained a good fibroid infarction rate after UFE. 
Although this new technique might be effective, it 
has not yet been tested in a comparative study with 
any other accepted embolic agents. We believe that 
sPVA must be used with great caution, and patients 
should be carefully followed to ensure an acceptable 



10.5.3.4 
Patient Selection 

10.5.3.4.1 
Fibroid Location 

Fibroid location within the uterus may influence 
the outcome of embolization. Submucosal fibroids 
were more likely to respond to UFE [20]. Submu- 
cosal location was a positive predictor of fibroid 
volume reduction after UFE [21]. The subserosal 
fibroids are also believed to be associated with less 
volume reduction after embolization (Fig. 10.5.6). 




Fig. 10.5.5a,b. MRI obtained before and after rT.ixazation with sPVA. s 
embolization, b tiihanced MR obtained _ ; months p'st-embohzation shi 
fibroid (arrow) 



jiov demonstrates small fun J a! myomas before 
s the persistent uptake in the partially necrosed 



J. Golzarian and J. -P. P 




MRI before embolization shows a large sub- 
no volume change with persistent uptake 



Some authors suggest that in the presence of a large 
subserosal fibroid, the laparoscopic removal needs 
to be offered as the first option. In patients with 
multiple fibroids and a large subserosal fibroid, a 
combined laparoscopic resection of the subserosal 
fibroid and UFE is a good alternative to hysterec- 
tomy. Systematic use of MRI will help with appro- 
priate patient selection, reducing the possibility of 
failure after UFE. 



10.5.3.4.2 
Adenomyosis 



Early recurrence of symptoms can occur when uter- 
ine artery embolization is performed on patients 
with adenomyosis (please see Chap. 10.4}. Uterine 
artery embolization for adenomyosis is reported to 
be effective to control the bleeding initially [22, 23]; 
however, this clinical success is short-term. There is 
a high rate of clinical recurrence after embolization 
of the uterine artery for adenomyosis. In a recent 
study by Pelage et al., 44% of the patients required 
an additional treatment, including hysterectomies 
in 28% of the cases [24]. 

Undiagnosed adenomyosis [25, 26] can be a 
cause of failure after uterine artery embolization 
when MRI is not used as the imaging modality. 
Enhanced MRI is an excellent technique for diag- 
nosing adenomyosis. To reduce the risk of failure 
related to improper patient selection, most centers 
use enhanced MRI as the screening technique of 



10.5.3.4.3 

Undiagnosed Leiomyosai 



Unrecognized malignancy can be responsible for fail- 
ure after UFE. This was a cause for treatment failure 
in two patients (2/538) in the Ontario trial [2]. How- 
ever, the incidence of uterine leiomyosarcomas in UFE 
patients is less than 1% and would not be a 
cause of failure [27]. Identifying a leiomyosai 
is still difficult with imaging. The pre-embolization 
MRI aspect of sarcoma can be completely identical 
to ,i huge leiomyoma with high cellularity. MRI find- 
ings of leiomyosarcoma include large heterogeneous 
masses and hemorrhage or cystic necrosis. However, 
even a histopathological diagnosis of uterine leio- 
myosarcoma is difficult to achieve. 

Leiomyosarcoma should be considered in cases 
where uterine size increases and symptoms persist 
after a technically successful UFE. Close clinical 
and imaging follow-up is necessary to detect and 
treat potential malignancy after UFE. 



10.5.4 
Conclusion 

Appropriate patient selection, careful catheteriza- 
tion and knowledge of different anatomic variants 
are important factors to minimize the failure after 
UFE. Systematic use of contrast-enhanced MRI is 
therefore essential, not only prior to the procedure, 
but also to monitor the perfusion of fibroids after 



e Failure after UFE 



embolization. The selection of embolic materials is 
also important. The newer materials need moreclin- 
ic.il evaluations before being generally accepted. 



1. Spies IB. AllisonS, Flick P et al. (2004 i Polyvinyl p.lcohol 
particles and tris-aoryl gelatin microspheres for uterine 
artery em be I i /Mi. ■.:■!; far k- 1 ■ ■ ■nyi eiias: resulls ot ,i j ,i n ,". :":"_ - 
ized comparative study. J Vase Interv Radiol 15:793-800 

2.Pron G, Bennett J, Common A et al. (2003) The Ontario 
Uterine Fibroid Embolization Trial: uterine fibroid reduc- 
tion and symptom relief .'Tie: uterine .'.rtery embol.zutioii 
for fibroids. Fertil Steril 79:120-127 

3. Marret H, Le Brun Keris ¥, Acker O, Cottier JP, Herbreteau 
D (2004) Late leiemvoma expulsion after uterine artery 
embolization. I Vase Interv Radiol 15:1483-1485 

4. Pelage IP, Guaou-Guaou N, Jha RC, Ascher SM, Spies JB 
(J004) Uler.ne fibroid tumors: long-ierm MR imaging 
outcome after emoo.izatiom kadiology 2.10:803-80'' 

."■.Spies IB (2303; Uterine artery embolization for fibroids: 
understanding the technical causes of failure. 1 Vase Interv 
Radioll4:ll-14 
6.Pron G, Bennett J, Common A et al (2003) Technical 
results and effects of operator experience on uterine artery 
embolization for fibroids: the Ontario Uterine ribioi.t. 
Embolization Trial, j Vase Interv Radiol 14:545-554 
7. Saraiya PV, Chang TC, Pelage JP, Spies JB (2002) Uterine 
artery rep.acem.eiit tfv die reunJ .igumein artery: an ana- 
tomic variant discoverer. J i intra uterine artery emboliza- 
tion for leiomyomas. 1 Vase interv Radiol 13:939-941 
S.Binkert CA, Andrews RT, Kaufman JA (2001) Utility of 
nonselective abdominal aortography in cemonsiratiiig 
ovarian artery collaterals in patients undergoing uter- 
ine artery embolizalion for fibroids. I Vase Interv Radiol 
12:841-845 
9. Nikolic B, Spies JB, Abbara S, Goodwin SC (1999) Ovarian 
artery supply of uterine fibroids as. a cause o: ireaimenl 
failure after uterine artery embolization: a case report. J 
Vase Interv Radiol 10:1167-1170 

10. Pelage JP, Walker WJ.le Dref O, Rymer R (2003) Ovarian 
artery: angiographic appearance, embolization, and rel- 
evance to uterine fibroid embolizanoii. Cardiovasc Imer- 
vent Radiol 26:227-233 

ll.Barth MM and Spies BJ (2003) Ovarian artery emboli- 
zation supplementing uterine embolization for leiomyo- 
mata. J Vase Interv Radiol 14:1177-1182 

12. DerdeynC, MoranC, Cross D, Dietrich H.DaceyR (1995) 
Polyvinyl alcohol panicle size and suspension character- 
istics. AJNR Am J Neuroradiol 16:1335-1343 



13. Choe DH, Moon HH, Gyeong HK et al. (1997) An experi- 
ment)! study of embolic eftect according to i illusion rate 
and concentration of suspension in transarterial particu- 
late embolization. Invest Radiol 32:260-267 

14. Golzarian J, Torres C, Sun S.Valenti D (2004) Compari- 
son of two different angiographic end-points for uter- 
ine fibroic. embolization with PVA. A multicentre study 
(abstract). J Vase Interv Radiol 15:S173 

15. Pelage JP.LeDref O.Beregi JP et al. (2003) Limited uterine 
arlerv embolization wilh Iris-acryl gelatin microspheres 
for uterine fibroids. J Vase Interv Radiol 14:15-20 

16. Redd D, Chaouk H, Shengelaia G et al. (2002) Comparative 
sluoy ^ PVA particles, Embo spheres and Gelspheres in a 
rabbit renal artery embolization model (abstract), i Vase 
Interv Radiol 13:S57 

17. Siskin GP, Bowling K.Virmani R.Jones R.Todd D (2003) 
Palho.ogic evaluation of a spher.ea. polyvinyl aleoi'.ol 
emit o.ie agent in porcine renal model. I Vase liueiv Radiol 

18. Laurent A, WassefM, Pelage JP et al.(2005) In vitro and in 
vivo deformation of TGMS and PVA microsphere in rela- 
tion with their arterial location (abstract). J Vase Interv 
Radiol 16:S77 

19. Pelage :P : 23051 Late breaking absiracts. 30 lh Annual 
Meeting or the Soneh" oi Interveiti.onal kau.okgv. New 
Orleans, LA. April 2 

20. Spies J, Roth AR, Jha R et al. (2002) Uterine artery embo- 
lization for leiomyomata: factors associated with suc- 
cessful svmpiomatie and imaging outcome. kadiologv 
222:45-52 

21. Jha RC, Ascher SM.Imaoka I, Spies JB (2003) Symptomatic 
fibioleiomyomr-t.:: \!k imaging ■.:■:' the uterus bej-re anil 
after uterine arterial embolization. Raeliology 217:223- 
235 

22. Siskin GP, Tublin ME, Stainken BF, Dowling K, Dolen EG 
(2001) Uterine artery embolization for the treatment of 
udenomyosis: eliitieal response and evaluation with MR 
imaging. Am I Roentgenol 177:297-302 

23. Pelage JP, Jacob D, Fazel A, Narnur J et al. (2005) Midterm 
results of uterine artery embolization for svmpiomatie 
adenomyosis: initial experience. Radiology 234:948-953 

24. Goodwin SC, McLucas B, Lee M et al (1 999) Uterine artery 
embolization tor tire treatment of uterine leiomyomala: 
mid-term results. J Vase Interv Radiol 10:1 1 59-1 1 65 

25. Smith SJ, Sewall LE, Handelsman A (1999) A clinical fail- 
ure of uterine fibroid embolization due to adenomyosis. J 
Vase Interv Radiol 10:171-1174 

26. Common AA, Mocarski EM, Kolin A et al. (2001 ) Thera- 
peutic fa:. tire oi uterine fibroid embolization caused by 
uitdei being .e. e' m vo sarcoma. I Vase Inlerv Radiol 12:1 449- 
1452 

27. Pattani SJ, Kier R, Deal R, Luehansky E (1 995) MRI of ute- 
rine leiomyosarcoma. Vagn kesen imaging 13:331-333 



10.6 Perspectives 



e Laurent, Jean-Pie 



e Pelage, and Jafar Golzaria 



Introduction 187 

How to Predict and Improve 

Long-T^ini CliiiLi.il Success 187 

Technical Opiimizaiion tor 

Uter in e F ibro i d E mboliza ti on IBS 

Reported Success Rates 188 

Calibrated Microspheres for 

Uter in e Ar te ry E mb o li zat ion 189 

Microsphere Penetration in 

Vasculature and Vascular Topology 190 

Size, Number, and 1 ''ilutio:; o'i Microspheres IS 

New Generations of 

Spherical Embolization Particles 191 

Detectability of Embolization Materials 191 

Drug-Eluting Microspheres 191 

Resorbable Embolic; ion Materials for 

"Jtennr HI":clJ Eiv.oolization 19.' 

How Can We Improve Uterine Functionality 

after Embolization! 194 

Conclusion 194 

References 195 



10.6.1 
Introduction 

With severalyears of experience with uterine fibroid 
embolization, sufficient data are now available to 
allow some perspectives on the outcome of this pro- 
cedure and discuss future directions for research. 
We have already learned that approximately 90% of 
patients will have symptomatic improvement while 
10% will not improve [20, 30, 40]. As previously 
discussed in the chapter on how to minimize failure, 
there are different reasons for the procedure to fail. 



A. Lai-rekt, MD, PhD 

Associate Professor, Center for Research in Interventional 

Imaging (Cr2i APHP-INRA) Jouy en Josas, 78352 France 

J.-P. Pelage, MD PhD 

Department of Radiology Hopital Aaibroise Pare, 9, Avenue 

Charles De Gaulle, 92104 Boulogne Cedex, France 

J. GOLZARIAN, MD 

Professor of Radiology. I )i rector, Vascular and Interventional 
Radiology, University of Iowa, Department of Radiology. 
200 Hawkins Drive, 3957 JPP, Iowa City, IA 52242, USA 



Potential causes of failure are of technical origin 
(i.e. failed catheterization of the uterine artery, false 
angiographic end-point, uterine artery spasm or 
flow restriction), maybe related to anatomical varia- 
tions (ovarian artery supply to the (ibroids in partic- 
ular), or due to the presence of associated conditions 
(mainly adenomyosis) [42], Beyond the short-term 
improvement in symptoms, the future acceptance 
of this procedure also depends on the durability of 
symptom control. Clinical failure or recurrence may 
be the outcome when some of the fibroids do not 
infarct following embolization [25, 26]. Optimiza- 
tion of the outcome from uterine fibroid emboliza- 
tion should be a priority for future clinical research. 
One of ihe primary clinical challenges in managing 
patients undergoing uterine fibroid embolization is 
the control of post-embolizat ion pain [34, 47]. Post- 
procedural pain is the justification for performing 
uterine fibroid embolization as an inpatient proce- 
dure at most centers as opposed to an outpatient 
procedure which may be more easily accepted by 
both the patients and the referring gynecologists. As 
for liver chemoembolization, preclinical research is 
ongoing with drug elu ting beads loaded with differ- 



sofr 



a greater de; 
growth of nt 



dications. The same platforms may 
) load hormones in order to achieve 
e of fibroid infarction or prevent the 
fibroids. The objectives of this chap- 
perspectives and future 
d with uterine fibroid emboli- 



10.6.2 

How to Predict and Improve Long-Term 

Clinical Success 

Given that short and mid-term outcomes indicate a 
safe procedure with a few major complications and 
symptomatic improvement in nearly all patients, 
one of the most important question is the durabil- 
ity of the procedure in the longer term. Three dis- 



tinct types of treatment failure have already been 
reported after embolization. 

• Early failure corresponds to temporary improve- 
ment or absence of clinical relief after emboliza- 
tion [42, 26]. Most of these failures are of techni- 
cal or anatomical origin: unilateral uterine artery 
embolization, severe arterial spasm leading to a 
false angiographic end-point of embolization, 
additional arterial supply to the uterus from 
other sources such as the ovarian arteries [23, 
42]. Prevention and identification of these causes 
of failures is mandatory in order to reduce the 
rate of early failures. As recently stated by Spies 
[42] and our group [24], the systematic use of 
mitrocatheters may reduce the occurrence of 
spasm or flow-restriction and may allow better 
distribution of embolization particles and more 
targeted devascularization of all the fibroids. 
Ovarian artery supply to the fibroids should also 
be investigated and informed consent to perform 
additional embolization should be obtained from 
the patient [23]. Early failures are also related to 
associated conditions mimicking fibroid symp- 
toms [16]. in our experience, long-term results 
observed in women with adenomyosis are not as 
good as in those with uterine fibroids (Pelage et 
al. 2005). Finally, endometrial evaluation should 
always be performed in patients with irregular 
cycles, intermenstrual or continuous bleeding 
or periods lasting more than 14 days to exclude 
endometrial abnormalities accounting for bleed- 
ing symptoms [26]. 

• Clinical recurrence has been reported after an 
initial improvement and usually occurs within 
2-3 years. This population of patients is of para- 
mount importance for the future acceptance of 
embolization as a valuable alternative to myo- 
mectomy and other emerging uterus-sparing 
therapies. Most of these recurrences are related 
to progression of viable fibroids or regrowth 
of fibroids with partial devascularization after 
embolization [16]. As for the surgeons, small 
fibroids left in place during myomectomy or 
still perfused after embolization account for 
these secondary treatment failures [27]. We have 
already demonstrated that post-procedure imag- 
ing is crucial to predict such clinical recurrence. 
The use of contrast-enhanced MRI allows early 
detection of residual perfusion of the fibroids 
after embolization [27]. In our practice, we have 
found that a 24-h post-embolization contrast- 
enhanced MRI Is strongly predictive of the 6- to 
12-month post-embolization appearance [28]. In 



addition, there is a strong statistical correlation 
between residual fibroid perfusion and clinical 
recurrence, with virtually all patients with viable 
fibroids presenting with symptom recurrence at 
some time during the follow-up [28]. Future clin- 
ical studies comparing embolization to myomec- 
tomy should take the imaging appearance into 
consideration. 

Late recurrence is observed when new fibroids 
occur usually 5 years or later after embolization 
[2b]. MRI may be useful to detect new fibroids 
actually even before the patient's symptoms 
worsen [27]. 



Recently, two minimally invasive therapies have 
been introduced to treat uterine fibroids. High fre- 
quency focused ultrasound and transvaginal para- 
cervical clamping of the uterine arteries have been 
reported in the management of symptomatic uterine 
fibroids [10]. From our own experience with the use 
of uterine fibroid embolization, we know that unless 
complete devascularization of all identified fibroids 
is obtained after these therapies, the results in terms 
of recurrence will not be better than after myomec- 
tomy and may be higher than after embolization. 



10.6.3 

Technical Optimization for Uterine Fibroid 

Embolization 

1D.6.3.1 

Reported Success Rates 

The reported clinical success rates as high as S5% 
90% in all studies maybe considered disappointing 
to some skeptical observers. Similarly, the published 
reduction in uterine and dominant fibroid volumes 
is around 25%-60% and 33%-68% at 3-12 months 
[20, 30, 40, 47]. Even if it has been suggested that 
residual fibroid perfusion is more important than 
shrinkage after treatment, one may notice that these 
figures remain too low to compete with those of 
surgery where all the fibroids are actually resected. 
Thus, in one retrospective comparison between 
myomectomy and embolization, bulk-related 
symptoms were more quickly and more frequently 
resolved after surgery [32]. Is thereaway to increase 
the percentage of fibroid and uterine volume reduc- 
tion and can we get more consistent results from one 
patient to another? The technique of embolization 
has changed dramatically in recent years and the 



objectives were mainly to improve safety because 
efficacy was already well demonstrated in the first 
reports. 



10.6.3.2 

Calibrated Microspheres for Uterine Artery 

Embolization 

Trisacryl-gelatin microspheres (TGMS) were devel- 
oped to address some of the perceived shortcomings 
of non-spherical embolization pail ides of polyvinyl 
alcohol foam [14]. TGMS are compressible, which 
allows easy passage through a microcatheter with 
a luminal diameter smaller than that of the micro- 
spheres. The hydrophilic interaction of TGMS with 
fluids and a positive surface charge reduce the for- 
mation of aggregates. It has been demonstrated that 
calibrated TGMS are easy to deliver and unlikely 
to clump in vessels and lead to a rapid and reliable 
decrease in local blood flow [1, 6, 21, 24]. 

Theoretically, the calibration of microspheres 
should allow better control of the level of occlusion, 
which depends on the number of injected particles 
and the penetration of the embolic agent into the 
tissue [21]. Many interrogations were formulated 
about the advantages, risks, and effects of spheri- 
cal agent by opposition to non-spherical PVA that 
were commonly used in uterine fibroid emboliza- 
tion [43]. The risk resulting from the use of small 
microspheres has been clearly understood and the 
rationale for choosing the proper size for uterine 
fibroid embolization is now defined [24, 25, 41]. 
New embolization techniques including the use of 
large microspheres and a more limited embolization 
of the uterine artery have been successfully used in 
several studies [11, 24, 25, 41]. The utility of cali- 
brated microspheres is now accepted by a majority of 
operators. The introduction of the limited technique 
of uterine artery embolization with the use of large 
calibrated microspheres has opened a new era in 
the field of peripheral embolization [24. 25]. Widely 
used in neuroradiology, these more sophisticated 
techniques applied to uterine fibroid embolization 
have raised the issue of reduced efficacy compared 
to a more aggressive embolization [2]. 

Several ".pheriatl embolization materials are no 1 .-.' 
available on the market. After the introduction of 
TGMS (Embosphere, Biosphere Medical), which 
was approved in Europe (CE approval) in 1997, in 
the USA (FDA approval) for general embolization in 
2000 and specifically for uterine fibroid emboliza- 
tion in 2002, two PVA -based microspheres have been 



developed [33, 39]. Contour SE (Boston Scientific) 
and Bead Block (Biocompatibles) were approved 
recently in Europe and in the US. The three types 
of microspheres available have calibers within the 
same size ranges (100-300, 300-500, 500-700; 700- 
900; and 900-1200 jim). 

Although calibrated and spherical in shape, the 
different types of microspheres are clearly differ- 
ent when considering their hydrophilic properties, 
superficial tension, ionic charge which therefore 
give different mechanical properties including 
rigidity and elasticity. For example, the rigidity 
at 70% compression is about 12 g for TGMS, a few 
grams for Bead Block and is quite absent for Con- 
tour SE (Fig. 10.6.1). In addition. Contour SE has a 
lower and incomplete elastic recovery than Bead 
Block and TGMS. PVA-based miaospheres which 
are much less rigid and less elastic than TGMS may 
be deformed in microcatheters and arteries and may 
lead to a more distal occlusion [36]. 

Inanexperimentalanimal model, it has beenfound 
that after embolization of the kidney, the uterus, or 
the liver in the sheep with 500-700, 700-900 and 
900-1200 u.m microspheres that, for each caliber, the 
level of occlusion was more distal with Contour SE 
compared to TGMS of the same size [36]. These dif- 
ferences could be explained by a higher intravascular 
deformation of CSE compared to TGMS (Fig. 10.6.2). 
There were fewer differences in terms of location 
between TGMS and Bead Block (Fig. 10.6.2). 

Clearly the differences between embolization 
microspheres available on the market have made the 
situation very complex for the users. Specific techni- 
cal recommendations are necessary for each type of 
embolization materials and the use of such products 




Fig. 10.6.1. In vitro compression of three types of calibrated 
microspheres available on the market 



requires a learning curve for the operator. However, 
calibrated microspheres are so easy to handle and 
provide at least the same results as compared to 
non-calibrated particles, that the innovation will 
stay. Moreover, these microspheres also have the 
unique property of having the potential to be loaded 
with virtually any type of medication or drug. The 
clinical use of microspheres loaded with doxorubi- 
cin in patients with hepatocellular carcinoma has 
already started.lt is too early to analyze the prelimi- 
nary results bin lite revolution ol emholotherapy is 
in motion. In order to enhance the effects of embo- 
lization to devascularization or shrink fibroids, the 
adjunct of hormones maybe beneficial. In vitro and 
in vivo preclinical evaluation of such technologies 
have already started. 



10.6.3.3 

Microsphere Penetration in Vasculature and 

Vascular Topology 

Vascularization of uterine fibroids comprises sche- 
matically dilated and tortuous peripheral vessels and 
smaller intra-tumoral vessels [37, 46, 50]. It has been 
recently demonstrated that a logical target for embo- 
lization is the peri-fibroid arterial plexus [24]. 

However, the sizes of these vessels have not been 
studied by means of plastic molding. One proposal 
could be to measure the microspheres and vessels 
sizes in histological specimens of patients operated 
after embolization, as was done for other tumors, 
and to confirm that there is a threshold for the pen- 



ilibrated microsph 
[15]. 

It could be of great interest t 
of these peripheral arteries i 
and 900 u.m regardless of the s. 
fibroid. Since drug-loaded mil 
become available, for 



i inside the ti 



■it Id i 



clinical interest to s 
moral component. 



lectii 



/erify that the size 
lges between 500 
: or location of the 
[spheres will soon 
to prevent tumor 
;ine that it could be of 
ly occlude the intratu- 



10.6.3.4 

Size, Number, and Dilution of Microspheres 

Theoretically, small microspheres should distribute 
distally in small arterioles, and one could imagine 
completely filling a tumoral process with radioac- 
tive microspheres or drug-eluting beads. The path- 
ological studies did not confirm this hypothesis: 
tissular distribution of beta-emitting microspheres 
smaller than 40 urn has been studied experimen- 
tally in rabbit liver and clinically [3, 29]. Pillai 
[29] observed an inhomogeneous distribution of 
microspheres and a formation of clusters, while 
Campbell [3] found that the median cluster size 
was ten times the size of the microsphere and the 
distance between the clusters. 

In practical terms, this means that even small 
microspheres are not homogeneously distributed, 
contrary to what could be expected from their small 
size alone. Therefore, radiation or drug concentra- 
tion could potentially be higher than expected in 




Fig. 10.6.2. In vivo defor- 
mation of three types 
of calibrated micro- 
spheres. The leiigih ;u.d 
width o: Iluee ;ypes of 
i]iii"K':if-h=?!'es ha* bee:', 
measured o:i histobgijjl 
slides Lifter r:i;L'i.:iliZLi:ii:--:''. 
of sheep kidneys. The 
microsphere deforma- 
tion was calculated by 
the formula: deformation 
{%} = 100 x (length- 
width]/width. The graph 

r boxplots. A 
view of the jefoi minion 
of each microsphere type- 
is given oef >w lite gray.': 






cluster areas, and low or null between the clusters. 
Several reasons may account for the formation of 
clusters of microspheres such as insufficient dilu- 
tion, specific vascular topology or specific Theologi- 
cal conditions in small vessels. 

The dilution is the unique factor which can be 
taken in consideration by the operator. Since the 
number of microspheres per millimeter of sediment 
is very high (about one million for small calibers), 
an adapted dilution has to be used. Without appro- 
priate dilution, each 0.1 ml of sediment contains 
thousands of microspheres. The usual dilution rec- 
ommended for clinical practice for microspheres is 
xlO, for instance 2 ml of microspheres in a 20-ml 
solution (contrast material and saline). One may 
suggest different optimal dilutions for larger sizes, 
i.e. over 600 u.mand for smaller microspheres. Given 
the number of microspheres in a vial/syringe of 
100 u.m, higher dilutions (xlOO or even X1000) may 
be appropriate (Fig. 10.6.3). This has to be balanced 
with the acceptable amount of iodinated contrast 
medium injected. 



10.6.4 

New Generations of Spherical Embolization 

Particles 

10.6.4.1 

Detectability of Embolization Materials 

The detectability of embolization particles has long 
been a matter of debate among interventional radi- 
ologists. Since calibrated microspheres have a high 
content in water, they are not detectable by fluoros- 
copy, CT, or MR scan, and operators cannot localize 
them during and after embolization. 

Some favor radio-opaque particles in order to 
perform embolization without adding iodinated 
contrast material. Other potential advantages of 
being able to identify the location of microspheres 
include detection of non-target embolization, con- 
trol of the homogeneity of distribution of the par- 
ticles, evaluation of the intra- or extra-tu moral loca- 
tion of the microspheres, follow-up of the migration 
of the microspheres during time. The information 
regarding the distribution of the particles obtained 
at the time of embolization may have a significant 
impact on clinical practice with optimization of 
embolization protocols. 

To obtain a radio-opaque microsphere, it is neces- 
sary to add a spec i lie component that often radically 




Fig. 10.6.3. Number of microspheres contained in 0.1 ml of 
microsphere sediment. This number is very high for small 
microsphere sizes (below 500 urn ;. A Sutlicienl dilution i x] 
or XlOO) of these riiicrospi'.eres is ris.'-ndaiory io ensure a 
homogeneous distribution of the microspheres in the vascular 
network and Io itvoid ti'.e for million of clusters 



changes the mechanical properties of the micro- 
spheres (compressibility and iniectalulity) so that no 
product is available at the moment. We have chosen 
a completely different research approach. Since the 
goal of embolization is to produce targeted occlu- 
sion of the peri-fibroid arterial plexus and since the 
imaging tool used before and after embolization 
is MRI, it seemed logical to develop a microsphere 
detectable during MRI. Similarly to unenhanced 
computed tomographic studies obtained after arte- 
rial chemoembolization of the liver just by detect- 
ing the areas of trapped lipiodol, MRI detectable 
microspheres maybe localized around the fibroids. 
Precise detection of the microspheres after embo- 
lization without using any contrast material could 
be helpful to optimize technique. Again, it could be 
of interest to confirm the diagnosis of non-target 
embolization in patients with unusual clinical man- 
ifestations after treatment [7, 18, 35, 49]. In vitro and 
in vivo preclinical results are encouraging since we 
have been able to successfully mark and detect with 
MRI the microspheres in different organs such as 
the kidneys, the uterus, and the liver (Figs. 10.6.4, 
10.6.5). 



10.6.4.2 

Drug-Eluting Microspheres 

Another potential application is to use the micro- 
spheres as a platform to load medications. Different 
manufacturing processes, which are coming from 
the drug industry for pharmaceutical purposes are 




Fig. l0.6Aa,b. In vilro deteciabdiiy of MR marked microspher 
■.■:■:■;. ii :.i:.i! ge.ose i A) ;-.:'. cl : L'.ej" evaluated using N ' K I : b : 




Fig. 10.6.5. In vivo deteciabilr.y of 700-900 p.m MR 
marked microspheres after ren.il artery emboliza- 
tion in the sheep. The lei": kidney ''.as bee:" 1 , emboli- 
zed with trisacryl-gelaii:'. mien ■ splices contain ing 
an MR marker iL), and the right kidney with con- 
trol tnsacryl-gelati:'. microspheres (R). MRI study 
of the explanted kidneys was performed 24 h after 
embolization (3D SPGR Tl, slice thickness). MR 
marked microspheres are delectable in the corti- 
cal area. No control microsphere is detected in the 
opposite side 



being transposed to drug delivery embolic devices. 
The first products already available in the field of 
interventional radiology have been developed to 
treat liver disease. Two types of microspheres are 
available: those which behave like sponges able to 
absorb large amounts of drug in solution or those 
produced from specific polymers able to adsorb 
a given drug which reaches high concentration 
inside the biomaterial (Geschwind [F, unpub- 
lished data). In the first case the release system 
can be considered as a ready-to-load platform for 
water-soluble drugs, but a release can occur in the 
medium before and during injection. In the second, 
the product is more susceptible to release on long 



Similarly, drug-loaded microspheres for fibroid 
embolization can be developed in different direc- 
tions. Vasoactive drugs, prothrombotic agents, and 
antiangiogenic factors can enhance or prolong the 
duration of arterial occlusion. Hormones, growth 
factor inhibitors, and antimitotics may prevent 
local tumor regrowth. Antalgic or anti-inflamma- 
tory drugs may reduce post-embolization pain after 
fibroid embolization. Post-embolization pain is the 
reason for keeping patients in hospital after emboli- 
zation at most centers. Following initial experietkv 
with the use of embolization, there have been several 
attempts to reduce pain at the time of embolization 
by, for example, mixing I id oca ine with the particles. 
Post-embolization pain is usually considered as a 






local effect of embolization on the fibroids and on 
the myometrium [34]. Reduction in the intensity of 
ischemia or inflammation observed in the uterus 
may help to reduce post-embolizat ion pain [47]. Dif- 
ferent research projects are ongoing to evaluate the 
feasibility and the effects of loading of analgesics or 
anti-inflammatory drugs in calibrated microspheres 
(Fig. 10.6.6). 

The theoretical advantages of drug-loaded 
implants are numerous: a higher local concentra- 
tion and a lower total dose of drug compared to a 
svstemic administration mid tuially the possibility 
of using drugs that are potentially toxic via the sys- 
temic route (Fig. 10.6.6). Preliminary tests should be 
conducted in order to evaluate the diffusion of the 
drug. The diffusion area is composed of the vessel 
wall and the perivascular space, which comprises 
veins, lymphatic ducts and interstitial tissue. Within 
the few hours following embolization, a foreign 
body reaction develops around the microsphere. 
This inflammatory response may modify the drug 
release in two ways: either by creating a barrier 
which reduces the diffusion of the drug, or by elimi- 
nating the drug in the process. 

For these reasons the drug release is a very prom- 
ising strategy but its efficiency needs to be demon- 
strated experimentally first in animals and then in 
patients. In animals it has to be proven that: first, 
the systemic level of the drug is null or much lower 
than after a systemic administration, second that 
the microsphere can release the loaded drug in sig- 
nificant amounts, third that there are evident signs 
of the biological action of the drug, fourth that no 
adverse local or general event or side effect occurs, 
and finally that the primary effect of the micro- 



spheres is not changed by the loaded drug. There- 
fore, it remains to be proven in patients that drug- 
loaded microspheres are safe and effective in terms 
of symptoms or tumor recurrence. 



10.6.4.3 

Resorbable Embolization Materials for Uterine 

Fibroid Embolization 

It maybe hypothesized that, compared to materials 
which are slowly degradable, resorbable embolics 
would be more able to restore uterine artery integ- 
rity. A gelatin sponge is mainly used to perform 
hemostatic embolization [19]. This biodegradable 
intravascular embolization agent has also been suc- 
cessfully used for fibroid embolization. Mid-term 
results seem to be comparable to those obtained 
with non-spherical PVA particles or calibrated 
microspheres [12]. 

However, the ma in advantage of resorbable embol- 
ics for uterine fibroid embolization is still not proven. 
The gelatin sponge can be supplied in three forms: 
as a powder containing small fragments, as a sheet 
from which different sized sections can be cut or as 
thicker blocks or cubes making ii possible to obtain 
large pledgets [12, 19, 38]. The major limitations asso- 
ciated with its use for uterine fibroid embolization are 
the absence of calibration and the great variability in 
the resorption speed, which is influenced by many 
factors such as nature, homogeneity, size, enzymatic 
potential, and local inflammatory response [39]. 
Recanalization after arterial embolization using gela- 
tin sponge ranges from 3 weeks to 4 months and even 
long-term occlusion has been reported [39]. 



Plasmatic Concentration of Ibuprofenaccordng to time 





[ 










Brebis 30072 MS 
— .— Brebis 11284 MS 
■ Brebis 3122 MS 
Brebis 30305 MS 
—•—Brebis 30B1 MS 
-•—Brebis 30023 MS 

„ Brebis 3158 Sol 
— Brebis 301 13 Sol 






\ 








,/T 








u\ 
















/£^£ 


"-*""V"_, 




| 






1/ 










" I 





Fig.lO£A. r.oi 
leyels ol ibuprofen 



, ,< plnnulU 
: after injection in 
a (twu sheep labeled 
sol) or after embolic l:on ::f the uterine 
arteries with — icrii'pheri'K loaded with 
the same ?m::uni of iliupMlen (sheep 
MS). The peak is r:)ta:ned immediately 
after int-a arterial i:t|t'Ct:on whereas a 
more progressive plasmatic distrflju 
tion is observed wi|- rhe "oade.. muri: 



Resorbable calibrated microspheres with con- 
trolled resorption time could be advantageously 
proposed for uterine fibroid embolization. Theo- 
retically, such a product could better guarantee 
that uterine artery and branches recover a complete 
functionality after embolization than non-resorb- 
able particles. 



10.6.5 

How Can We Improve Uterine Functionality 

after Embolization? 

Fertility is still a controversial issue among inter- 
ventional radiologists and gynecologists. 

Once hemorrhage is stopped or necrosis of the 
tumor is obtained, occlusion of uterine arteries and 
vessels is no longer necessary. A long-lasting arte- 
rial occlusion may alter the uterine artery func- 
tionality. The stakes include the preservation of the 
uterine artery to maintain the functionality of the 
uterus (fertility, sexuality) but also possibilities of 
re-embolization in case of recurrence. 

Since embolization may become a first-line treat- 
ment in women still wishing to conceive, it becomes 
of paramount importance that embolization not only 
preserve the uterus but also its functionality. Sur- 
prisingly, uterine artery functionality after embo- 
lization is unknown and no angiographic, MRI, or 
Doppler study has ever addressed this issue. 

Embolization may lead to a reduced uterine blood 
flow during gestation and it is well known that uter- 
ine blood flow is crucial for fetal growth and sur- 
vival [8, 48]. A bilateral uterine artery emboliza- 
tion blocks the main arterial supply to the embryo 
and it has been demonstrated that the reduction in 
uteroplacental blood flow using ligation [5], clamp 
[4], occlusion [13] or embolization [■■!?] significantly 
affects fetal and placental weight. 

An experimental study has demonstrated that 
PVA and TGMS had a varying impact on fertility in 
the sheep [22]. When PVA particles used for uterine 
artery embolization were compared to TGMS, a sig- 
nificant decrease in subsequent fertility and lower 
birth weight of the newborns were observed sug- 
gesting intra-uterine growth retardation [22]. These 
functional results strongly suggest that emboliza- 
tion with these two embolic agents lead to vascular 
occlusions at different sites and with different long- 
term consequences. The histopathological analysis 
of resected sheep uteri confirmed this hypothesis. 
PVA particles tend to form large-sized aggregates, 



which obstruct the trunk and first branches of the 
uterine artery [25], In contrast, because of its block- 
ade of more distal vessels, TGMS may exert a weaker 
impact on resistance of uterine and/or fetal umbili- 
cal arteries. 

Even if the rate of recanalization lor PVA and 
TGMS was not significantly different in our long- 
term implantation study, the transvascular migra- 
tion was very different between the two prod- 
ucts (Fig. 10.6.7) [25]. Transvascular migration 
of embolization particles was first described by 
Tomashefski et al. [44]. PVA aggregates were found 
almost exclusively in the intima, and no PVA par- 
ticle was observed outside of the vessel (Figs. 10.6.7, 
10.6.8) (Pelage et al. 2003c). Conversely, TGMS 
were found in intima (about 50%) in media adventi- 
tia (25%) and outside the vessel (25%) (Figs. 10.6.7, 
10.6.8). Thus, a more proximal locution associated 
with the absence of transvascular migration of PVA 
aggregates could create a permanent blockade of 
the uterine artery accounting for the intra-uterine 
growth retardation. Cases of intra-uterine growth 
retardation have already been reported after uter- 
ine artery embolization in human [17]. In his retro- 
spective analysis ot 50 published cases of pregnancy 
after uterine artery embolization, Goldberg et al. 
[9] found that women who become pregnant after 
UAE are at risk of conceiving newborns with small- 
ness for gestational age. However, in agreement with 
our experimental results, hypotrophy of newborns 
after UAE is not systematically related to a prema- 
ture delivery. Thus, among the four cases of new- 
borns (22% of live births) small for gestational age 
(< 5th percentile) reported recently by Pron et al. 
[31] three were delivered at term. 



10.6.6 
Conclusion 

It is our goal to perfect our technique in order to 
get more consistent results, reduce complications, 
and establish uterine fibroid embolization for a 
durable time period. Large calibrated microspheres 
are equally effective to smaller non-calibrated par- 
ticles to target the peri-fibroid arterial plexus. Cali- 
brated microspheres are so easy to deliver through 
microcatheters that one may predict the progres- 
sive replacement of non-spherical particles in the 
near future. MRI has become the reference imag- 
ing tool before and after embolization. The use of 
contrast-enhanced studies allows early detection 




Fig. !0.ri.?ii,b. T:-;tjtsv:i.sluLhj- migrat :oi'. 01" non-spherical PV'A particles and tris-acryl microspheres: bil.iieral u.erine artery 
embolization in :Jjc- sheep was pe'iormed 3C momhs earlier loiwiii slaining;. a A:: at.g:vgatc of PVA particles (in bi.iik) is 
located in the media. No PVA particle is seen in the media or outside of the vessrh The imet na! elastic limiljns is rupt-ired. 
A recanalizatioii o: ;he embolized artery is visible, b One tris-acryl microsphere I in ir/uri') is visible oi;:s;de the vessel. Ho".h 
intern. 1 1 and c.v.erna: clasnc iintit-.ins are i upitned and indicate tile ".rakctorv ■.:■! the nucivsphciT ey.cltisio:'.. A lvc.i:::i.i;-.i ::■ <n 
of the embolized artery is also visible 




Fig.WAS. Distribution oi :;o:;-spherical PVA particles and 
tris-acryl microspheres: bilateral uterine artery embolization 
in tiie sheep was pel formed 30 months ear her 

of viable portions of fibroids which are associated 
with clinical recurrence in the long-term in a more 
sensitive way than Doppler ultrasound. Given the 
experience of liver chemoembolization where the 
effects of embolization particles and drugs are com- 
bined, the future of uterine fibroid embolization will 
probably consist in the use of X-rays or MRI detect- 
able microspheres loaded with hormones, analgesics 
or anti-inflammatory drugs. As stated recently, "in 
ten years from now, who will remember that the 
revolution of embolotherapy started with uterine 
fibroids...". 



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26. Pelage JP, Jacob D, Le Dref O, Laurent A (2004a) Leiomy- 
oma recurrence after uterine artery embolization. I Vase 
Interv Radiol 15:774-775 

27. Pelage )P, Guaou-Guaou N, Jha RC, Aseher SM, Spies JB 
(2004b) "Jterine fibroid tumors: long-term MK imaging 
outcome after embolization. Radiology 230:503-809 

28. Pelage )P, Brouard R, Jacob D, Boudiaf M, Abitbol M, 
Le Dref O (2004) Perfusion of uterine fibroids evaluated 
using contra st-ehanceol magentic resonance imaging per- 
formed 24 hours after embolizal ion is a predictor of clini- 
cal outcome [abstract]. Radiology (P): 613 

29.Pillai KM, McKeever PE, Knutsen CA, Terrio PA, 
Prieskorn DM, Ensminger WD ( 1 ''"''I ! Microscopic analy- 
sis of arterial microsphere distribution in rafbit live: and 
hepatic VX2 tumor. Sel Cancer Ther 7:39-48 

30. Pron G, Bennett J, Common A, et al. (2003b) The Ontario 
uieiine fibroid embolization trial: Uteiine fibroid redtic- 
lion and symptom relief after uterine artery embol.zation 
for fibroids. Fertil Steril 79: 120-127 

31. Pron G, Mocarski E, Bennett J, Vilos G, Common A, 
V.:nde:burgh '. :2 '■'■':■:■ Pregnancy after uterine artery 
embol.zation tor leiomyoma ta: die Ontario mulucenler 
trial. Obstet Gynecol 105:67-76 

32.Razavi MK.HwangG, Jahed A.Modanloo S, Chen B (2003) 
Afdommal myomeciomy versus uler.ne fibroic, emboli- 
: of symptomatic uterine leiomyo- 
571-1575 

33. Redd D, Chaouk H, Shengelaia G, et al. (2002) Compara- 
live study of PV'A particles, Embosoaeies and Girl spheres 
in a rabbi: renal artery embolization model [abstract], 
J Vase Interv Radiol 13:S57 

34. Roth AR, Spies JB, Walsh SM, Wood BJ, Gomez-Jorge J, 
Lew ER (2300) Pain af:e: uteinir artery emO'-.i;o","i'.'ii 
for leiomyomata: .:iin its severity be predicted and does 
seveniy predict outcome. ■ \\v.-l interv Radiol 11:1047- 
1052 

35. Ryu RK, Chrisman HB, Omary RA, et al. (2001) The vas- 
cular impacl of uterine aioery embolization: prospeciive 
sonographic assessment of ovarian arterial circulalion. 
J Vase Interv Radiol 12:1071-1074 

36. Saint-Maurice JP, Wassef M, Namur J, Merland J), 
Laurent A (2003) Vascula: distribution of two types o\ 
microspheres (Fmbospitere and Contour SEj: a oompara- 
live studv [abstract^. Presented al tar annual meeting of 
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ety of Europe. Antalya. T.i; .-.ev, September 2 a -24 

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Surg Gynecol Obstet 14:215-234 

38. Siskin GP, Englander M, Stainken BF, et al. (2000) Embolic 
a gen i used io: a In one fibio.d emoo.izaiion. Am j Koenl- 
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39. Siskin GP, Dowling K, Virmani R, Jones R, Todd D (2003) 
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40. Spies JB, Aseher SA, Roth Arm, Kim J, Levy EB, 
o-omez-lorge I i^Oioaj i.-ter;ne anery embo.izaiioij for 
leiomyomata. Obstet Gynecol 9S:29-34 

41 . Spies JB, Benenati JE, Worth in gton-Kirsch RL, Pelage JP 
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42. Spies JB (2003) Uterine artery embolization for fibroids: 



understanding the I 



;s of fai-are. 1 V.ist Interv 



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artery embojzatio;; i"i: : leiomyomas. ■ Vase Interv K:i-.i .-.:■! 
15:793-800 

44. Tomashefski JF, Jr., Cohen AM, Doershuk CF (1988] Long- 
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1272 

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col. 1970 )an;35(l):21-30 



11 Pelvic Congestion Syndrome 



Introduction 199 

Pathophysiology 199 

Gonadal Vein Reflux 199 

Pelvic Varicosities 200 

Clinical Considerations 20 1 

Pre-procedure Workup 201 

Cross-Sectional Imaging 202 

Alternative Therapies 204 

Anatomy 204 

Tedjiiiqiir ■ if OviiiiLUi V'e:"!vg:o;'hv 

and Embolization 204 

T[';ii;s:ug'.:lar Route 204 

Tibiofemoral Route 206 

Post-procedural Care 206 

Follow-up 207 

Sclerosis of Labial or Buttock Varicositie: 

Other Techniques 208 

Tips and Tricks 208 

Technical Difficulties in Right Ovarian 

Vein Cannulation 208 

Venous Spasm 209 

Results 209 

Complications 210 

How to Prevent or 

Troubleshoot Complications 210 

Conclusion 210 

References 211 



varicocele; however, the clinical syndrome of pelvic 
pain in women resulting from gonadal vein reflux 
is less appreciated than the corresponding entity 
of symptomatic varicocele in men. In addition it is 
being increasingly recognized that visible varicose 
veins of the bullocks, bbki, or lower extremities may 
be secondary to ovarian vein reflux. 



11.2 
Pathophysiology 

Pelvic congestion is a complex subject. When con- 
sidering the pathophysiology, two components must 
be considered (Fig. 11.1); gonadal vein reflux, which 
is the commonest cause of pelvic varicosities, and 
the pelvic varicosities themselves, which are felt to 
be the principle cause of pain in pelvic congestion 
syndrome. Each may be seen without the other, and 
both can be present in asymptomatic patients. 



11.2.1 

Gonadal Vein Reflux 



11.1 

Introduction 



The association between varicose veins in the pelvis 
and pelvic pain in women has been known since the 
description of tubo-ovarian varicocele by Richet 
in 1857 [1]. However, it was not until 1976 that the 
phrase "pelvic congestion syndrome" was coined by 
Hobbs [2] to describe a syndrome of chronic pelvic 
pain and heaviness due to pelvic varicosities. The 
pelvic varicosities are almost always secondary to 
reversed flow in the ovn nan vein, in essence a female 



,2211 Wesbrook Mall, 



L. Machas, MD 

Deportment of Radiology, UBC Hosp it- 
Vancouver BC.V6T 2B5, Canada 



Reversed flow in 
of absent or incompetent valves, or because of struc- 
tural or functional obstruction. Anatomical studies 
show that 13%-15% of women lack valves in the left 
ovarian vein and approximately 6% on the right and 
that when valves are present, 43% on the left and 
35%-41% on the right are incompetent [3, 4]. When 
the valves are incompetent, m 
diameter increases from the r. 
7.5 mm [5]. 

Some authors suggest that re 
is a common etiology of o 
does not reflect the author's experi 
study of 48p.it ients with pelvic conges t ion syndn 
found that 83% had extrinsic compression of the left 
renal vein between the aorta and the superior mes- 
enteric artery resulting in the "nutcracker phenom- 



ial of 3.8 mm to 

vein obstruction 

r ein reflux. This 

:e. A Belgian 




enon" [6] (Fig. 11.2). The ovarian and internal iliac 
veins can serve as important collateral pathways 
when there is obstruction of the iliocaval venous 
system. The significant interconnections and rela- 
tive paucity of valves can result i 
blood flow in either direction [7]. 



11.2.2 

Pelvic Varicosities 



The evidence that pelvic 

is indirect. Pelvic varicosities are more frequently 
seen in women with pelvic pain than in asymptom- 
atic patients. In one study of transuterine venogra- 
phy, 91% of patients with chronic pelvic pain had 
evidence of pelvic varicosities compared with 11% 
of control patients [8]. When intravenous dihydro- 
ergotamine (a vasoconstrictor), is administered to 
women during an acute attack of pelvic pain there 
is both a decrease of pelvic venous diameter and a 
significant reduction in pain [9]. 

Ovarian varicosities are more frequent after preg- 
nancy [10] due to hemodynamic and physiologic 
factors which result in pelvic venous hypertension S MA. Contrast d 
during pregnancy. The capacity of the 



may increase 60 times 

contributing to both ve 

incompetence. As the veins dilate during pregnancy, 

the valve cusps separate and become incompetent 

[in. 

Pelvic veins are uniquely predisposed to become 
dilated, even without pregnancy. Many pelvic veins 
are devoid of valves and have weak attachments 
between the adventitia and supporting connective 
tissue [12]. Although this is different from veins 
elsewhere in the body the histology of pelvic vari- 
cosities is similar to that of varicose veins elsewhere, 
including fibrosis of the tunica intima and media, 
muscular hypertrophy and proliferation of capillary 
endothelium. 

There are many possible reasons to explain why 
some patients with ovarian vein reflux have no pain 
while others are in agony. Most importantly, there 
are marked individual differences in how pain of 
any kind is perceived and significant variations 
between women in the density of nerves in the ovar- 
ian vein [13]. There may also be physical changes 
in the pelvic organs of women with pelvic conges- 
tion. Compared with normal women of similar age 
and parity, women with chronic pain due to pelvic 
congestion have a larger uterus and thicker endome- 
trium and as many as 56% have cystic changes in 
their ovaries [14]. In addition menstrual disorders 
such as menorrhagia and polymenorrhea are more 
frequent in women with pelvic congestion syndrome 
[15]. 




'Nutcracker phenomenon". Axial CT image demon- 

ntrast in the distal left renal vein does not extend 

narrowed central win compressed between aorta and 

d preferentially through retrograde flow 



Pelvi,: Congestion Syndrome 



11.3 

Clinical Considerations 

The symptom complex of pelvic congestion syn- 
drome includes pelvic heaviness or pain of vary- 
ing severity typically exacerbated by long periods 
of standing, with exercise, or at the end of the day. 
These symptoms may be worst in the premenstrual 
period. Associated dyspareitnia is trequent, mani- 
festing as pain at the time of sexual intercourse or 
intense pelvic cramping immediately after. Some 
women note that intercourse is paintul at the end of 
the day but not in the morning, presumably because 
venous engorgement of the pelvic tissues which had 
occurred after a day ot standing is relieved by hours 

In addition to paraovarian varicosities many 
patients have labial varicosities and varicose veins 
in their legs secondary to, or exacerbated by, ovar- 
ian vein reflux. Clues to the presence of ovarian vein 
reflux include varicosities on the buttocks and pos- 
terior aspect of the thigh, or varicose veins of the 
leg which recur immediately after surgical repair. 
Treatment of these visible varicosities can occur as a 
part of the therapy in women presenting with pelvic 
congestion syndrome who are also troubled by cos- 
metically or physically symptomatic superficial 
veins. With the resurgent interest in the treatment of 
lower extremity varicosities, patients are more fre- 
quently presenting solely for treatment of vulvar or 
lower extremity varicose veins. When questioned, 
these patients often report minor levels of pelvic dis- 
comfort. In a recent study of 160 women presenting 
primarily for treatment of lower limb varicose veins, 
26 (16%) were found to incidentally have symptoms 
of pelvic congestion syndrome [16]. Twenty four of 
the 26 women underwent ovarian venography, and 
ovarian vein reflux was demonstrated and treated 
by embolization in 24 (92%). 

The diagnostic criteria for pelvic congestion syn- 
drome are not universally agreed upon [17]. Some 
physicians make the diagnosis on clinical grounds 
without the aid of imaging. Others use transuterine 
venography and base the diagnosis on the diameter 
of the ovarian veins, distribution of vessels, and 
delay in clearance of contrast medium, viewing the 
presence or absence of ovarian vein reflux as irrel- 
evant. However, the majority of modern literature 
bases the diagnosis on the presence of pelvic vari- 
cose veins filled by ovarian vein reflux, this is the 
model preferred by the author. In our experience, 
true pelvic varicosities without ovarian vein reflux 



Pelvic congestion syndrome is controversial and is 
not accepted as an entity by many practitioners. Like 
retrograde flow in the gonadal vein in men, critical 
analysis of both the disorder and its treatment are 
difficult because of the lack of standardized diag- 
nostic criteria, the fact that pelvic varicosities are 
seen in many asymptomatic women, and because 
there are numerous causes of chronic pelvic pain. 
Experienced gynecologists will frequently comment 
that they see dilated pelvic veins at laparoscopy in 
parous women who do not have symptoms of pelvic 
congestion. As described earlier, physiologic venous 
ectasia can be a normal consequence of pregnancy 
but flow should be antegrade in dilated but other- 
wise normal veins whereas in pelvic congestion syn- 
drome the patients have retrograde flow in tortuous 
varicosities. 

Chronic pelvic pain is defined as pelvic pain 
present for at least 6 months. It is common, affect- 
ing approximately one in seven women [18] and 
accounting for 10% of all referrals to gynecolo- 
gists [19]. Potential causes of chronic pelvic pain 
are listed in Table 11.1. In laparoscopic studies of 
women with chronic pelvic pain, approximately 
one third of patients will have endometriosis, one 
third other visible pathology such as PID, pelvic 
adhesions or ovarian cysts, and one third will 
have no obvious findings [20]. Whether utilizing 
the resources of a multidisciplinary pain clinic or 
applying surgical interventions, at least 20% of 
women with chronic pelvic pain can not be effec- 
tively treated [21, 22]. Due at least in part to the dif- 
ficulties in accurate diagnosis and lack of effective 
therapy, there is often significant psychological 
overlay [23]. Any physician investigating or treat- 
ing a patient with chronic pelvic pain may be faced 
with a frustrated complex patient whose symptoms 
are difficult to elucidate, diagnosis is elusive, and 
in chronic pain that has been refractory even to 
aggressive therapy. 



11.3.1 

Pre-procedure Workup 

All patients with chronic pelvic pain should have the 
benefit of clinical evaluation and shared care by a 
physician with expertise in chronic pelvic pain. A 
laparoscopy and pelvic ultrasound should be per- 
formed prior to radiologic interventions. Their role 
is to exclude other diagnoses, not to make the diag- 
nosis of pelvic congestion. If the clinical presenta- 
tion is recurrent lower extremity v 



J s of l" lire- nic pelvic r;i: 



Phvtiohgii- 
Ovui;iiio:'i 
Menstruation 

Pl'/tu" infhitmihitcn diseasi.' 

GL'tiiWurirtnrr 

;!'v.i:i;]ii/p: 
Endometriosis 

ribioics 

V,i!ig:~:n!V;y 

Prolapse 



Ga stro i n lest: n a! 

Ulcerative colitis 
Crohn's disease 
i >iveiticu litis 
Irritable bowel syndrc 
Malignancy 

Musiiilijskcktal 

Lumbar disc 
Sacral canal stenosis 
Spondylolisthesis 



I. .01 



d varicosities, these investigatior 
ry prior to venography in most c; 



Laparoscopy. Laparoscopy is the most effective 
means of diagnosing other causes of chronic pelvic 
pain and virtually all women with chronic pelvic 
pain should undergo this procedure. In particular, 
minimal lesion endometriosis, the most common 
cause of chronic pelvic pain, will not be detected by 
ultrasound and may only be detected by an expert 
laparoscopist. Dilated veins, however, often cannot 
be seen because of their retroperitoneal position 
and the increased intra-abdominal pressure and 
increased venous drainage with Trendelenburg 
positioning that are part of laparoscopic examina- 
tion. It should be noted that a negative laparoscopy 
in a woman with chronic pelvic does not exclude 
pelvic congestion. 



11.3.1.1 
Cross-Sectional Imaging 



Although imaging car 
cose veins [24], direct v 



dilated ovarian veins with venography is still felt 
to be the gold standard for accurate diagnosis of 
pelvic congestion. The author reserves cross-sec- 
tional imaging as a means to exclude other causes 
of pelvic pain, and does not view a normal noninva- 
sive imaging study as a contraindication to ovarian 
venography when there are symptoms which might 
be due to pelvic congestion. 

Ultrasoun d. Ovarian and pelvic varices are seen 
as multiple dilated tubular structures with venous 
Doppler signal around the uterus and ovary on 
both transabdominal or transvaginal US with 
color Doppler. Sonographic diagnostic criteria 
for pelvic congestion have been published. These 
include: (a) a tortuous pelvic vein with a diameter 
greater than 4 mm, (b) slow blood flow (about 
3 cm/s), and (c) a dilated arcuate vein in the myo- 
metrium that communicates between bilateral 
pelvic varicose veins [25]. The author prefers to 
rely on abnormal accentuation of blood flow with 
Valsalva maneuver (Fig. 11.3) rather than utiliz- 
ing strict size criteria. Venous diameter can vary 
considerably with body position, nervousness 
or hydration, or there may be physiologic ecta- 
sia from prior pregnancies, but without valvular 
incompetetence. 

Ovarian cysts may be seen in women with pelvic 
congestion syndrome ranging from a few cysts to 
polycystic ovary syndrome produced by estrogen 
overstimulation. 

CT and MM. On CT and MRI pelvic varices are 
seen as dilated tortuous paraovarian or parauter- 
ine tubular structures, frequently extending to the 
broad ligament and pelvic sidewall or paravaginal 
venous plexus [26,27] (Fig. 11.4a,b). 

Dilated ovarian veins are frequently seen on CT 
scans in asymptomatic women, highlighting the 
importance of correlating the imaging and clinical 
findings. Rozenblit et al. (2001) reported seeing 
dilated ovarian veins in 63% of parous women with- 
out symptoms of pelvic congestion and in 10% of 
nonparous women [28]. 

On Tl-weighted MR images, pelvic varices have 
no signal intensity because of flow-void artifact; 
on gradient-echo MR images the varices have high 
signal intensity. After the intravenous administra- 
tion of gadolinium, Tl gradient-echo sequences 
demonstrate blood flow in pelvic varices with high 
signal intensity. On T2-weighted MR images they 
usually appear as an area of low signal intensity; 
however, possibly because of the relatively slow flow 
through the vessels, hyper intensity or mixed signal 
intensity may also be noted (Fig. 11.4c). 




Fig. 11. 3a,b. Ultrasound imaging of pel 

varicosities, b Wiili Valsalva maneuver there is strong 
differentiate physiologic venoms ectasia from ovarian 



i T:';ii]::v.;gi :'.;;] grey scale tifiaS' 'ini; demons; ra:ing j ■!=.". JLjylc- let: adr.rxal 
.iccemuaiion of flow Within die varicosities. This can be a usef.il sign 10 




Cross sectional imaging of pelvic congestion 

Transverse C~ image clemonsiradng contrast 

posterior to the bladder, b 3D 

tec; image from a CT angiogram', showing a J if: ted 

cluster of varicosities in the left side 

:.':' the pelvis, c Sagittal T. weigir.ed fa: :ai poivs sed Ma image 

demonstrating dilated pelvic veins posterior to the bladder 



11.4 

Alternative Therapies 

Therapeutic modalities which have been applied 
to pelvic congestion syndrome include psycho- 
therapy, physiotherapy, analgesia alone, pharma- 
cologic ovarian suppression, surgery, and emboli- 
zation. Critical comparison of treatment outcomes 
between different therapies is difficult, if not 
impossible. Not only are a wide variety of thera- 
peutic endpoints described, but diagnostic criteria 
are different (or not described at all) in virtually 
every study. 

Multiple surgical treatments have been per- 
formed for pelvic congestion syndrome. Bilateral 
oophorectomy and hysterectomy with subsequent 
hormone replacement has been reported with symp- 
tom improvement in 66% of women [29]. Surgical 
ligation of the left ovarian vein has been described 
resulting in improvement in 73% of women [30], and 
left nephrectomy (at time of renal donation) with 
an 77.9% symptom improvement [31]. In the latter 
study of 273 female renal donors, 27 had evidence of 
left ovarian venous reflux, of whom 22 completed a 
questionnaire about symptoms. Of these, 13 reported 
pelvic pain and ten had reduced or absent symptoms 
after left nephrectomy. 

Isolated cases of laparoscopic ovarian vein liga- 
tion have been reported [32]; however, there are no 
large series published to date. Non-embolic inter- 
ventional treatments such as venous stenting and 
surgical bypass have been reported in small num- 
bers of patients when the varicosities are secondary 
to venous obstruction [33]. 



11.5 
Anatomy 

The entire venous network of the female pelvis is 
interconnected by an extensive anastomotic network 
that is virtually devoid ol valves. The ovarian plexus 
drains superiorly via (he ovarian veins: the left ovar- 
ian vein almost always drains into the left renal vein 
and the right usually directly into the vena cava , 
although in 8.8% there is drainage into the right 
renal vein [4]. The visceral system is composed of 
venous plexuses that surround the rectum, bladder, 
vagina, uterus and ovaries. The large uterine and 
vaginal plexuses drain mainly through two or three 
veins at the uterine pedicle. Although the latter two 
systems drain predominately into the internal iliac 



11.6 

Technique of Ovarian Venography and 

Embolization 

Ovarian venography is performed in the same 
manner as venography of the spermatic veins. The 
author favors performing ovarian venography on 
a tilting table with the patient at least 45° upright, 
however the majority of interventionists perform 
the procedure with the patient flat. There is no tiara 
ascribing an advantage to either method. It cannot 
be overstressed that the diagnosis of pelvic conges- 
tion syndrome cannot be made on venographic cri- 
teria alone, correlation with the clinical presenta- 
tion is mandatory! 



11.6.1 
Transjugular Route 

Under ultrasound guidance a sheath is introduced 
into the left internal jugular vein. The sheath is used 
for patient comfort during the procedure. A catheter, 
usually multipurpose shape, is positioned into the 
peripheral portion of the left renal vein. A left renal 
venogram is performed with the patient performing 
a Valsalva maneuver. In the authors' opinion, only 
retrograde flow within the ovarian vein with the 
visualization of paraovarian varicosities constitutes 
a positive study (Fig. 11.1). Reflux of contrast down 
to the ovary without opacification of varicosities 
constitutes a negative venogram regardless of the 
diameter of the ovarian vein (Fig. 11.5a,b). 

If there is ovarian vein reflux and varicosities, the 
catheter is then advanced into the distal left ovarian 
vein and forceful injection is performed to identify 
all collateral channels. The catheter is then directed 
into each of the major brandies and embolization of 
the main ovarian vein and all visible collateral chan- 
nels with glue, tetradecyl sulfate, or Gianturco coils 
is performed, extending cranially to within 2 cm of 
the ovarian vein origin (Fig. 11.6). The author's pre- 
ferred method is place the catheter selectively into 
the origin of each of the two or three caudal branches 
of the main ovarian vein and inject tetradecyl sul- 
phate 3% (2 cc mixed with 0.5 cc of contrast) with 
the patient performing a Valsalva maneuver as the 
liquid is being injected (have the patient do this 



Pelvic. Longesiion Syndrc 




Fig.ll.5a,b. Normal ovaria:'. vei'ograNiy. a Selective icu ovarian venogram uei 
ian plexus and nor ma J collaterals communicating wim the left internal iliac 
ovarian subtraction venogram. The paraovarian plexus is opacified but -- J: 



venogram demonstrating rell 
'.liac vein. No vi 

dilated irreguli 



..._ theparaovar- 
b Selective right 

typical of pelvic 



only during injection or they will faint!). I continue 
this until static sclerosant is seen at the catheter tip. 
Depending on the anatomy, I will occasionally "cap 
off" these the distal ovarian vein branches with a 
Gianturco coil (Cook, Inc, Bloomington, IN). These 
most distal coils (usually 38-5-5) are extruded hold- 
ing the catheter firmly in place, while advancing 
the guidewire, resulting in a tightly coiled, compact 
configuration. Once all major branches of the ovar- 
ian vein have been injected with sclerosant (this 
may take up to 15 cc, but typically is less) there will 
typically be hazy, static opacification of the pelvic 
varicosities. I will then withdraw the catheter leav- 
ing a trail of the same contrast opacified tetradecyl 
sulphate 3% mixture by injecting as the catheter 
is withdrawn to immediately above the iliac crest. 
After the sclerosant is injected, it is critical not to 
flush the catheter vigorously, or the sclerosant will at 
best be diluted, and at worst distributed elsewhere. 
A coil is laid immediately above this (usually 30-8- 
10) in an elongated configuration to within 2 cm of 
the ovarian vein origin. This is achieved by holding 
the guidewire in place and withdrawing the catheter 
as the coil is deployed. The elongated configuration 
is favored to decrease the likelihood of recanaliza- 
tion. A gentle venogram is then performed to con- 
firm occlusion, appropriate position of the upper 




1.6. Post-emboli 

opacified sclerosant i: 
occluding the proximal ovarian > 



first i 



coils, and that there is not a parallel channel which 
lly will opacity only after the main ovar- 
is occluded. If there is still rapid retrograde 
the ovarian vein after elongated coil deploy- 
■e overlap a second elongated coil with the 
the configuration of a double helix. At the 
il end of the ovarian vein it is critical that 
the coil does not protrude into the renal vein or infe- 
rior vena cava. If the coil does project it should be 
removed with a nitinol snare and replaced. 

The same multipurpose shape catheter is then 
directed into the right ovarian vein. A right ovar- 
ian venogram and, if needed, embolization are per- 
formed in the same fashion as described for the left. 
If the ovarian venograms are negative, then bilateral 
internal iliac venograms are performed as rarely 
isolated pudendal vein reflux will cause sympto- 
matic pelvic varicosities (Figs. 11.7a,b). We do not 
routinely study the internal iliac veins if ovarian 
vein reflux is found; however, other interventionists 
do this routinely [34], 



11.6.2 

Trail stem oral Route 

A catheter, usually a Cobra catheter is introduced 
into the right femoral vein and directed into the 
peripheral left renal vein. Selective ovarian venog- 



raphy and embolization are performed using the 
same diagnostic criteria and methods as described 
for the transjugular route (Fig. 11.8). The catheter is 
then exchanged tor ;i Simmons II catheter or equiva- 
lent and right ovarian venogram performed. This 
approach has the disadvantage that a 180° bend is 
required for selective catheterization. This can be 
particularly troubling for cannulation of the right 
ovarian vein as pushing the catheter may result in 
advancement of the entire catheter up the IVC rather 
than advancement of the catheter tip. 



11.6.3 
Post-procedural Care 

Patients are kept inbed fori h postprocedure. Unless 
sedation was used, no special recording of vital signs 
is necessary. Mild pelvic cramping is common for 
which over the counter anti-inflammatory agents 
are taken as needed and instructions are given to 
avoid any activity involving Valsalva maneuver such 
as lifting, vigorous, or "hitting type" sports (includ- 
ing golf) for 3 full days beginning the day after the 
procedure. The patient should be advised that if she 
has persistent discomfort at the end of 3 days she 
should continue these instructions until resolution. 
There are no restrictions on resumption of sexual 
activity. For reasons not clear to the author, the first 




Fig. 11.7a,b. Intent I ikac w/.o g:aphv. a Nor ma] slue' v. Selecliw :n:eciion c( contias: in right ir 
prominent pelvic a:ras:o:"i: otic connections, bc.i no varicosities -.n e seen, b ! J elv:c varicosity ir: 
is bulbous dilation of the left pudendal vein. On cleaved . ir. .-ges- sAigsiish drainage of contr 



Pelvic Congestion Syndrome 



period after embolization is often unusually heavy 
and patients should be warned of this and the fact 
that this is almost invariably transient. 



11.6.4 
Follow-up 

The patient should be seen approximately 3 months 
post-procedure tor clinical examination and ultra- 
sound. Post-treatment ultrasound will normally 
reveal persistent dilated veins in the pelvis, but 
normal or no accentuation of flow with Valsalva 
n duplex exam (Fig. 11.9). 



11.6.5 

Sclerosis of Labial c 



1 Buttock Varicosities 



The varices are directly cannulated using a 25 gauge 
butterfly needle (or standard needle with extension 
tube) under direct vision or (rarely) ultrasound 
guidance (Figs. 11.10a,b). I prefer to have the patient 
on a tilt table at approximately 45 degrees upright 
to allow distension of the veins as they often col- 
lapse with the patient supine. Contrast is then gently 
injected, not to evaluate drainage, but to allow esti- 
mation of the amount of sclerosant needed. I prefer 
I- 1 ., tetradecyl sullate, although some practitioners 
use other agents such as polydoconal or sclerosant 
foam. The same amount of sclerosant is injected 
as contrast was needed to opacify the veins. The 
patient is instructed to wear tight underwear for 
the rest of the day, otherwise there are no specific 
instructions. 

The most important aspect of treating labial, but- 
tock or lower limb varicosities that might be related 
to ovarian vein reflux is to treat the highest point of 
reflux first. This implies doing ovarian venography 
and embolization and then waiting at least 3 months 
before treating more distal veins. The author's expe- 
rience is that approximately 25% of veins will sub- 
side adequately just with ovarian vein embolization 
although this has not been confirmed by data. 



Fig.11.9. Expected ultrasound findings posl ■ 
embohzLili on. I'aated adiiexa. veins remain bu 
■nous blood flow with Valsalva 




Fig. 11.8. Left ovarian venogram via femoral r 
skating dilated ovarian vein and par 
which drain into the left internal iliac vi 





often required, b left Libiiil ven .:■£;' inn using bulteiriy ;ieedie 



Cookbook: (Materials) 



10) 



First choke: 

• 7-F 11-cm long sheath (Cordis or Terur 

• 7-F Multipurpose catheter (Cordis) (we 
instead of 5-F because puncture hole size is not 
important in venous procedures as it is in arte- 
rial studies. The stiffness of the 7-F catheter is 
a considerable advantage when catheterizing 
the right ovarian vein) 

• 0.035 TSCF guidewire (Cook) 

• 0.035 Angle-tipped Glidewire (Terumo) 

• Gianturco coils (Cook) 

• 3% Tetradecyl sulphate (Omega, Montreal) 



Inc 



se of severe spasm, 
. F Microcatheter (Bi 
> Microcoils (Cook) 



r aberrant anatomy: 
ston Scientific) 



noacrylate 

femoral approach: 5-F Cobra catheter for 

Simmons type II catheter for right 



11.7 

Other Techniques 



dilated l 



■ methods for directly opacifying 
eins besides selective catheteriza- 



ns. These include transuterine 
injection of contrast material and direct injection 
of contrast material into vulval varices [8]. Except 
as a precursor to sclerosis of vulvar varicosities, 
these techniques are rarely used now because most 
radiologists are less comfortable both with the tech- 
niques and interpretation of the findings, and they 
do not allow direct progression to therapy. Noninva- 
sive imaging modalities have nearly replaced these 
forms of venography for purely diagnostic investiga- 



11.8 

Tips and Tricks 

11.8.1 

Technical Difficulties in Right Ovarian Vein 

Cannulation 



Inability to locate or cannulate the right c 
vein is the most common reason for technical fail- 
ure. The right ovarian vein origin is more variable 
in location than the left. It is usually located imme- 
diately anterior and inferior to the right renal vein 
orifice. The author's approach is to perform a right 
renal venogram to insure that the ovarian vein does 
not arise from the renal vein, and assess for acces- 
sory renal veins. I then withdraw the catheter to the 



Pelvi,: Congestion Syndrome 



renal vein orifice, rotate 2° anteriorly and advance 
the catheter 1-2 cm, rotating anteriorly another 2° 
with each pass if unsuccessful. If the ovarian vein 
orifice is not found, gentle probing along the IVC 
wall in an up and down motion extending from the 
right renal vein orifice to the iliac confluence is 
performed, beginning laterally, and rotating ante- 
riorly slightly between each sweep. It may arise to 
the left of the midline. The right ovarian vein arises 
from the inferior vena cava at an acute angle, which 
can make catheterisation from the femoral route 
especially difficult. Use of a multipurpose shaped 
catheter from the jugular route greatly facilitates 
this. 



11.8.2 
Venous Spasm 

If spasm of the ovarian vein occurs during selec- 
tive catheterization then forceful injection of 5 cc 
of normal saline followed by a wait of 4-5 min is 
usually sufficient to allow resolution. The use of 
injectable vasodilators such as nitroglycerin has 
not been successful in the author's hands. If resolu- 
tion of spasm is not possible, the procedure can be 
attempted on another occasion and at that instance 
the patient provided with sublingual nifedipine and 
intravenous sedation prior to the procedure. 



11.9 
Results 

Edwards et al. (1993) reported the first published 
case of ovarian vein embolization for pelvic con- 
gestion syndrome [35]. Since then, the treatment of 
pelvic congestion syndrome by embolization has 
been reported using coils alone [36], glue alone 
[37], or by coils with glue [38], gelatin sponge [39], 
alcohol [40], sodium morulate [34], or tetradecyl 
sulfate [41]. Most authors embolize one or both of 
the ovarian veins, although orhers routinely occlude 
the internal iliac veins in addition [34, 36]. As previ- 
ously noted when discussing alternative therapies, 
critical comparison between embolic techniques 
is difficult due to lack of common diagnostic and 
therapeutic criteria. The variability of the literature 
is illustrated by the sampling of reported series that 
follows. It is also apparent, however, that regardless 
of the technique or embolic agent used there is a 
striking similarity in patient outcomes. 



After embolization of 40 patients with enbucr- 
ylate and lipidized oil and 1 with enbucrylate and 
coils, Maleux et al. (2000) found that 58.5% of their 
patients had complete symptom relief and 9.7% par- 
tial symptom resolution at 19.9 months [36]. Tech- 
nical success rate was 98%. The authors found no 
difference in rate of symptomatic response whether 
ovarian venous reflux was bilateral (nine patients) 
or unilateral (32 patients}. 

Using enbucrylate and coils Carpasso et al. (1997) 
reported the results of embolization in 19 women with 
pelvic congestion syndrome [36]. A total of 13 patients 
required unilateral embolizat ion a ad six bilateral. Five 
patients developed recurrence treated successfully by 
embolization. Initial technical success rate was 96.7%, 
and there were no complications. At mean follow-up 
of 15.4 months, 73.7% of patients reported improved 
symptoms with pain relief rated as complete in 57.9%. 
The authors noted that the eight patients who had only 
partial or no relief suffered from dyspareunia and felt 
this was a negative prognostic factor. (By comparison, 
most studies report that dyspareunia is a symptom 
that does respond to treatment). 

Cordts et al. (1998) described ovarian vein 
embolization in nine women with symptoms of 
pelvic congestion syndrome using coils and absorb- 
able gelatin sponge [37]. Embolization of both ovar- 
ian veins was performed in four women, of the left 
ovarian vein alone in four patients, and of a left obtu- 
rator vein that communicated with vulvar varices in 
one patient. The authors reported that eight of the 
nine women (88.9%) had more than 80% immedi- 
ate relief but that two women had a mild to mod- 
erate return of the symptoms at 6 and 22 months. 
Improvement in symptom relief varied from 40% to 
100% at a mean time of 13.4 months. 

Clinical outcomes appear similar when the inter- 
nal iliac veins are routinely occluded. Venbrux et al. 
(1999) followed 56 women for a mean of 22.1 months 
after embolization with coils and sodium morulate 
[36]. The internal iliac veins were also occluded in43 
of 56 patients at a separate procedure 3 to 10 weeks 
after ovarian vein embolization. The technical suc- 
cess rate was 100%. Three patients developed recur- 
rent varices, two of whom were treated with repeat 
embolization. Using visual analogue scales to meas- 
ure pain, a mean 65% decrease in VAS score was 
recorded. Two patients (4%) reported no change in 
their symptoms, no patients had worsening of their 
pain after embolization. 

In the aforementioned studies embolization was 
performed in patients with ovarian vein reflux due 
to absent or incompetent valves. In a Belgian study in 



which 83% of 48 patients had pelvic congestion syn- 
drome due to extrinsic compression of the left renal 
vein between the aorta and the superior mesenteric 
artery (nutcracker syndrome), the technical success 
rate of ovarian vein embolization '.vas %% [(>]. The 
initial clinical success rale was 86% with long-term 
pain reduction in 75% of the patients. No difference 
in outcome was described between patients who had 
renal vein compression and those who did not. 

In one of the most intriguing studies of the treat- 
ment of pelvic congestion syndrome to date, Chung 
and Huh (2003) reported on 106 women with pelvic 
congestion syndrome confirmed by laparoscopy 
and venography who did not respond to medica- 
tion after 4-6 months treatment [42]. The patients 
were prospectively randomized into three groups: 
embolization with Gianturco coils; hysterectomy 
with bilateral oophorectomy and hormone replace- 
ment therapy; and hysterectomy with unilateral 
oophorectomy. At 12-month evaluation by visual 
analog scale pain scores was carried out: embolo- 
therapy was significantly more effective at reducing 
pelvic pain, compared to the two surgical therapies. 



cedure has not successfully relieved the symptoms. 
The two most important aspects to minimize the 
impact of this are excluding other causes of chronic 
pelvic pain before embolization, and managing 
patient expectations. The first is accomplished by 
working with clinicians with expertise in pelvic pain 
or pelvic congestion syndrome, the second by com- 
munication with the patient and the referring clini- 
cians. Most series report symptom improvement in 
70%-80% of patients. This implies that it will not be 
effective in 20%- 30% ot women undergoing the pro- 
cedure. The reasons for this include the following: 
the pain may not have been related to pelvic conges- 
tion (and the pelvic varicosities were an incidental 
finding), inadequate embolization or recanalization 
of the pelvic vessels (uncommon), or adequate time 
maynothavepassedsincetheprocedure.lt may take 
up to 6 months for a chronic pain syndrome of any 
type to respond to therapy, even after removal of the 
stimulus, and in pelvic congestion this is certainly 
true. It is critical to tell the patient, the referring 
doctor, and the patient's primary care physician this 
fact before and at the time of the procedure or the 
radiologist will be the recipient of innumerable com- 



11.10 

Complications 

Ovarian vein embolization is generally remarkably 
benign; most authors report no complications of the 
procedure and no worsening of symptoms. In our 
first review of our own patients, 9% developed a 
transient worsening of their pelvic pain immedi- 
ately after embolization, felt most likely to be related 
to post-embolization ovarian phlebitis [39]. Both 
patients returned to their baseline symptoms within 
weeks, with only anti- inflammatory and analgesic 
therapy. An analogous condition is seen in men after 
varicocele embolization. Venbrux et al. (1999) [35] 
and Chung and Huh (2003) [42] each reported two 
patients in whom coils embolized to the pulmonary 
circulation; the coils were snared without clinical 
sequelae in all four cases. 



11.11 

How to Prevent or Troubleshoot 

Complications 

From a physicians' perspective, the principle "com- 
plication" is dealing with patients in whom the pro- 



11.12 

Conclusion 

There are two distinct patient groups to whom 
ovarian embolization can be applied. The more fre- 
quent and traditional indication is chronic pelvic 
pain. Pelvic congestion syndrome remains a poorly 
understood entity whose existence, let alone appro- 
priate criteria for diagnosis and methods of inves- 
tigation and treatment are still under question. The 
similarity of outcomes between a wide variety of 
surgical procedures and varied methods of radio- 
logic embolization do suggest that it is a real entity 
but we are lacking a robust method of identifying 
those patients in whom intervention is likely to 
result in symptom relief. Until the unlikely arrival 
of such a tool, it bears repeating that there are few 
areas of interventional radiology where the correla- 
tion of clinical presentation and radiologic findings 
is of more importance than pelvic congestion. It is 
essential that any radiologist treating women with 
chronic pelvic pain work closely with a gynecologist 
or pain specialist. 

A second patient group presents with varicose 
veins of the perineum or legs. This indication has 



Pelvic Congestion Syndic 



become more important as endovascular treatments 
for lower limb varicosities have increased. Although 
these patients require less complicated clinical man- 
agement, specific knowledge or shared clinical care 
with an expert in lower extremity venous disease is 
essential to eood clinical results. 



Richer NA (1857) Traite practique d'ai 
chururv.iale. '-■ Chnmeioi, Librnire Lditeur, Paris 
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Ahlberg NE, Bartley O, et al. (1965) Circumference of the 
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Ahlberg NE, Bartley O, et al (1 966) Right and let. gonad o I 
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Kennedy A, !-!em;iigway A . ! ■■■■'■ ; Radiology of ova nun 
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36.Venbrux AC, Lambert DL (1999) Embolization of the 
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864 



sso P, Simons C, et al. (1997) Treatment of sympto- 
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eter embolization. Acta Radiol 38:1023-1025 133 



Genitourinary 



12 Varicocele Embolization 



David Hunter and Galia T. Rosi 



Introduction 215 
Anatomy 215 
Pathophysiology 216 
Diagnosis 216 
Clinical Considerations 217 
Alternative Therapy 217 
Percutaneous Embolization 217 
Catheterization Technique 218 
Hot (Boiling) Contrast Sclerotherapy 220 
■Coil Embolization 221 
Tissue Adhesives 222 
Detachable Balloons 222 
Complications 222 

Efficacy of Treatment and Comparison to 
Surgery 22.3 
Conclusion 221 
224 



12.1 

Introduction 

Varicocele is defined as an abnormal distention of 
veins in the pampiniform plexus. 

The association between testicular atrophy and 
dilated scrotal veins was noticed as early as in the 
first century AD [1]. Ivanissevich in a 1960 article 
[2] remarked that the clinical association of varico- 
cele with pain symptoms had been noted as early as 
1541 by Ambrois Pare who described the varicocele 
as "a compact pack of vessels filled with melancholic 
blood". In the same article Ivanissevich described 
one of the earliest extensive experiences with supra- 
inguinal ligation of the internal spermatic vein as a 
curative measure [2]. In the late nineteenth century 
it was first shown I 



D. Hl-nteh, MD; G. T. Rosen, MD 

I'ep.utment of Kodioiogy. ; J -447 r"LUiv:ev.-Urjiveisny Medi- 
cal Center, University o:' M:ii:'.e-sota, 500 Harvard Street >.£., 
Minneapolis, MN 55455, USA 



result in restoration of fertility [3]. Widespread 
acceptance of the relationship between varicocele 
and male factor infertility, however, came only in 
the 1950s based on work by Tuloch [4]. 

Surgical correction has always been the main 
therapeutic option for correction of varicocele. In 
1980 Iaccarino [5] was the first to describe a per- 
cutaneous method for treatment of varicocele. The 
steady advancement in embolization techniques and 
materials has led to the development of the modern 
percutaneous procedure that is considered to be a 
safe, simple and effective alternative to surgery. 



12,2 
Anatomy 

The veins of the spermatic cord form a loose, tortu- 
ous plexus after emerging from the mediastinum 
of the testis. These vessels are named the pampini- 
form plexus. The veins in the anterior portion of the 
plexus coalesce to form the internal spermatic vein 
(ISV). The ISV passes through the inguinal canal 
and then ascends through the retroperitoneum 
alongside the spermatic artery, until it drains into 
either the left renal vein on the left side, or the inf ra- 
renallVC on the right side. Additional venous drain- 
age of the testis, which becomes important following 
occlusion of the ISV, includes the external pudendal, 
vasal and cremasteric veins (Fig. 12.1}. Alternative 
drainage pathways of the ISV include the peri-renal, 
retroperitoneal and lumbar veins. 

Other anastomoses can exist between the ISV 
and other venous outflow channels in the retroperi- 
toneum and pelvis. These anastomoses can permit 
reflux and varicocele formation even in the pres- 
ence of a competent valve in the proximal ISV. The 
resulting condition is termed an aberrantly supplied 
varicocele. The reported rate of this phenomenon 
is 17%-19% of patients examined with spermatic 
venography. Percutaneous treatment of this type of 
varicocele is possible, but requires 



n of the 



'.'. Hunter and G.T. Rosen 




the renal vein, particularly in cases with renal vein 
outflow obstruction due the compression of the vein 
between the aorta and superior mesenteric artery, 
the so-called nutcracker effect. Proponents of either 
theory further postulate that a bilateral effect could 
occur by venous crossover to the right testis [8]. 

There are con t lie tins; opinions about the lateral- 
ity of varicocele. Some authors feel that the condi- 
tion is predominantly lei 1-sided, with at most 30% 
of patients having a bilateral problem [9]. In other 
studies [10, 11], including one in which venograms 
were performed bilaterally regardless of the physi- 
cal exam findings [II], bilateral ISV incompetence 
to an enlarged pampiniform plexus was found in 
70%-80% of patients. 



12.4 
Diagnosis 



Fig. 12.1. Accessory veins. Perivesical [thin iirraw), External 
pudendal [arron-itCiiiisj, Cremasteric {white arrow), Vasal 
[thick arrow) 

ISV at the very least above and below the segment of 
the vessel at the level of the venous collateral com- 
munication. Treatment of a varicocele with this type 
of complex anatomy has a success rate that is some- 
what lower than one with classical anatomy [6]. 



12.3 
Pathophysiology 

There is still debate about how, when, and to what 
extent varicocele affects fertility. A total of 10% of 
all men have a varicocele. Most are both asymp- 
tomatic and not associated with infertility. How- 
ever, among infertile couples the incidence of a 
varicocele increases to 30% [7]. Why should the 
dilatation of the veins of the pampiniform plexus 
impair spermatogenesis? A related question in 
patients with a unilateral varicocele, is how unilat- 
eral venous abnormality produces bilateral testicu- 
lar dysfunction? Several theories have been postu- 
lated to explain the pathophysiology of varicocele. 
The most popular among the theories involves the 
adverse effect of elevated testicular temperature on 
spermatogenesis [8]. Another theory is that reflux of 
adrenal or renal metabolites that could inhibit sper- 
matogenesis reach the left testicle by back flow from 



The clinical assessment of 
'eful physi 



ust start with 
. The patient should 
be examined in a warm room in the standing posi- 
tion, and preferably after standing for 5 min. The 
examination should include palpation and Doppler 
of the scrotum during a Valsalva maneuver. The 
grading system as developed byDusiN and Amelar 
[12] is the most commonly used to classify varico- 
celes, and includes the following categories: 

• Grade 1, varicocele palpable only during a Val- 

• Grade 2, varicocele palpable in the standing posi- 

• Grade 3, varicocele detectable by visual scrutiny 

However, the limitations ol physical examination 
are well documented [13], and the standard of care 
involves employment ot additional diagnostic meth- 
ods. These include thermography, color flow Doppler 
sonography, and venography [14-16]. Although each 
of these tests has reported standards that are used to 
make the diagnosis ol varicocele, the standards are 
not universally accepted and the accuracy of each test 
has frequently been called into doubt. A varicocele 
that is present on an imaging study but not on physi- 
cal examination is termed a subclinical varicocele. 
Embolization or surgical treatment of subclinical 
varicocele is a frequent practice in subfertile males 
with no other explanation tor infertility. 

Those who advocate treating subclinical varico- 
cele claim that even though the angiographically 



demonstrated degree of reflux is indeed lower in 
subclinical cases, the improvement in semen analy- 
sis and fertility rates that is seen after embolization, 
appears to be about equal for the clinical and sub- 
clinical varicocele patients [17]. 



12.5 

Clinical Considerations 



varicocele directly are becoming more common [19]. 
The techniques for surgical ligation have improved 
adequately so that percutaneous options are often 
not discussed with patients unless the patient has 
read about it, usually on the Internet, and requests 
the information directly. This approach clearly 
limits the number of percutaneous procedures per- 
formed . 



Varicocele can result in pain and infertility, and 
either or both may be present in any patient. One 
important additional group of patients that has been 
studied in several prospective studies in Europe is 
adolescent boys. In most cases of adolescent varico- 
cele, the diagnosis is made incidentally on routine 
physical examination. Pain and dysfunctional sper- 
matogenesis with or without testicular atrophy is an 
unfortunately frequent outcome for these patients 
and many advocate preemptive treatment for them 
as well [18]. 

The most common semen abnormality in patients 
with varicocele and infertility is poor sperm motil- 
ity, followed by abnormal morphology, and then 
depression of sperm count. The isolated finding of 
abnormal sperm motility has been referred to as a 
stress pattern. The normal World Health Organiza- 
tion (WHO) values [13] for the commonly evaluated 
parameters studied during semen analysis include 
the following: 

• Volume: 1.5-5.0 ml 

• Sperm count or density: greater than 20 million 
sperm/ml 

• Motility: greater than 60% normal motility 

• Morphology: greater than 60% normal forms 

• Forward Progression (scale 1-4): 2+ 

• Viscosity: no hyperviscosity 

• White blood cells: 0-5 per high power field 



12.6 

Alternative Therapy 

Until the development of the percutaneous approach, 
surgical ligation of the ISV was the only available 
therapy. Several surgical procedures can be used, 
which differ primarily based on the level of ligation 
of the spermatic vein. The common sites for sur- 
gical ligation are retroperitoneal, inguinal or sub- 
inguinal. Laparoscopic methods of performing the 
ligation, and microsurgical operations that treat the 



12.7 

Percutaneous Embolization 

The percutaneous treatment of varicocele is aimed 
at decreasing the engorgement of the pampiniform 
plexus by occluding the incompetent ISV and its 
collaterals. 

The use of percutaneous sclerotherapy as a treat- 
ment for varicocele was first described in 1980 [5]. 
The most commonly used embolization method in 
the USA, which is the use of metal coils (Fig. 12.2), 
was described in 1978 [20]. Ever since, additional 
materials and methods have been reported includ- 
ing modified coils such as the new Amplatz vas- 
cular plug, boiling contrast, detachable balloons, 




Fig. 12.2. After coils bad ::eeii Hiiced dually, these two coils 
were pkiced above ;hc c-nly l.-:ge c ■: ■ . IlM =■ j al. Notice how they 
are r.rsted iigh:ly inside e:;cb otb^r. It was not considered nec- 
essary (o place coils closer to the ISV origin 



D. Hunter and G.T. Rosen 



tissue adhesive?, and sclerosing agents such as con- 
centrated dextrose, sodium morrhuate, Sotradecol 
(sodium tetradecyl sulfate) [21], Varicocid [18], eth- 
anolomine [10], and alcohol [22], 



12.8 

Catheterization Technique 

Most studies have reported using a femoral vein 
approach. The left spermatic vein requires a double 
curve catheter to reach the ISV origin, and the right 
ISV is best entered with a sidewinder type cath- 
eter. Because of the double curve required to get 
into either spermatic vein, the femoral technique 
frequently requires coaxial catheters or a catheter 
exchange to reach an appropriate level in the ISV. 

In our experience, a right trans-jugular approach 
to both the right and the left spermatic veins is 
preferable as it facilitates deep catheterization and 
therefore accurate delivery of the sclerosing agent 
or occlusion device, obviates a femoral vein punc- 
ture and the small but important risk of femoral 
DVT, and allows a more rapid discharge post-pro- 
cedure with essentially no bleeding risk [11]. There 
is a small chance that manipulation through the 
right atrium may induce a dysrhythmia but such 
rhythm disturbances are almost always short-lived 
and resolve spontaneously. A heat re-shaped 5- or 
6-F Headhunter catheter with two to six sideholes in 
the distal2-3 cm (Fig. 12.3} can be used to select the 
left renal vein. The lordotic tertiary curve should be 
re-shaped into a kyphotic curve. While the catheter 
is being heated with a heat gun, a guidewire is kept 
in the lumen of the catheter to maintain catheter 
patency. The distal-most 3-4 mm of the tip of the 
catheter must be further modified to "point down- 
stream" for selection of the right spermatic vein. 
Alternative catheters such as angled tip catheters (JB 
1 or Vert shape), Cobra shape catheters, and varia- 
tions of these shapes have all been tried but with less 

Coming from the jugular or femoral approach, 
the most common first maneuver is to catheterize 
the left renal vein. The "C" shape of the reformed 
headhunter catheter makes this extremely easy from 
the jugular approach. Entry into the left renal vein 
from the If approach occasionally requires advanc- 
ing the wire far into the renal vein and then applying 
a counterclockwise twist or torque, thus pointing 
the catheter tip posteriorly. If the catheter tip passes 
either inferiorly or seems to be "caught" in the cen- 




Fig. 12.3. The lordotic 
;'. l-:y photic " ,: -" ilupe (. 
left ISV (arrowhead] 



has been reformed ir 
is slight reflux 



tral left renal vein territory, a gentle hand injection 
of contrast can be done to check position. If the hand 
injection reveals that the catheter is in a lumber 
vein, the catheter should be pulled back and rotated 
slightly clockwise or anteriorly, as the lumbar vein 
orifice is always posterior to the left renal vein ori- 
fice. Once the catheter tip is in the mid-portion of 
the left renal vein, a left renal venogram is done 
during a forceful Valsalva maneuver to document 
L ISV incompetence (Fig. 12.4) and also to estab- 
lish landmarks for selective L ISV catheterization. 
The left spermatic vein itself is also accessed using a 
counterclockwise rotation as the tip is pulled back, 
which rotates the tip of the catheter first posterior 
and then inferior since the curve is braced against 
the left renal vein origin. If the catheter tip enters 
the collateral from the proximal left renal vein to 
the adjacent par a lumbar, hemiazygous system, the 
tip is rotated gently clockwise to point it slightly to 
the left and anterior where the origin of the adjacent 
L ISV is always located. Once the L ISV origin has 
been engaged, and assuming that incompetence 
has already been documented by the renal veno- 
gram, the catheter is advanced only 2-3 cm into the 
vein and the first selective diagnostic venogram is 
done. A forceful hand injection is performed into 
theL ISV using 10 cc of diluted contrast media, with 
the catheter tip just past the origin of the vessel. The 
patient is instructed once again to perform a Val- 



V.iriu ■ceie r-! nil: -..-.iv .- [ .■ ii 





Fig. 12.4. During the left : e : "_ Li 1 venogram will: I he catl'.eter lip Fig. 12..". injection into the mid L [SV demonstrates a very 

nicely positioned in ilte mic.-left renal vent, a forceful Valsa.v.; aivpical finding . ■:" a single co:r.:na::: channel of the L LSV 

maneuver refluxes contrast not only clown the incompetent '.. passing clown through the inguinal eaual 
ISV but also down the IVC 

salva maneuver, while the operator looks carefully 
to both confirm reflux into the incompetent sper- 
matic vein and also to define the upper L ISV anat- 
omy. If free reflux is seen, confirming incompetence 
of the valve, the wire is advanced to the level of the 
mid to upper third of the SI joint and the catheter 
rotated down over the wire to the same position in 
approximately the mid L ISV. The catheter should be 
rotated and not "pushed" since that can cause buck- 
ling in the IVC or right atrium. Injections are done 
at approximately the mid-SI joint level to clearly 
define the remainder of the L ISV anatomy, confirm 
abnormal retrograde flow into a distended pampi- 
niform plexus (Figs. 12.5, 12.6), and delineate any 
connections to other veins that could act as sources 
for aberrant varicocele filling or as collaterals if the 
L ISV is eliminated. Only after all of the diagnostic 
studies have been completed, can a meaningful and 
accurate embolization or sclerotherapy be carried 

If no reflux is seen into the L ISV on either the left 
renal venogram or selective L ISV origin injection, 
but there is clear sonographic or physical examina- 
tion evidence of a varicocele, we routinely assume 
that the patient has retroperitoneal or pelvic bypass- 
ing collaterals mid believe I hat embolization of the 
ISV is still indicated. If, however, the only abnormal- 
ity is the semen analysis, and there is no physical 
exam or imaging evidence of reflux < 




Fig. 12.tia,b. Two patients who had recurrence of pain follow- 
ing surgical ligation of the L 15V. With the catheter tip in the 
mid L ISV just below the mid -portion of the L 5! joint, injec- 
tion in patient la; demonstrates one small channel through 
the inguinal canal, whereas patient (bi has no patent vessels 
that would suggest a recurrence. Patient (a) was treated, (b) 



D. Hunter and G.T.Kosen 



and a competent valve is clearly seen on the L ISV 
origin injection, the procedure on that side can be 
terminated. 

The procedure on the right side is similar 
although there is no way to do a preliminary veno- 
gram to confirm incompetence. This fact alone may 
have led to a substantial underestimation of right- 
sided incompetence reflected in much of the varico- 
cele literature. Coming from the femoral approach, 
the origin of the right ISV is easy to enter using a 
standard sidewinder catheter. From the IJ approach, 
the headhunter that was used for the L ISV needs to 
be modified so that the tip points more inferiorly 
(Fig. 12.7). The R ISV origin is usually located just 
anterior and inferior to the right renal vein. In order 
to find it, the catheter is placed into the right renal 
vein then pulled out, rotated slightly counterclock- 
wise, pushed down below the renal vein level and 
manipulated up and down on the vein wall until it 
"catches" on the R ISV orifice. Once the tip of the 
catheter just barely enters the origin, the first injec- 
tion is done with a gentle Valsalva to avoid dislodge- 
ment of the catheter. If the catheter tip is allowed 
to go too deep into the vein, the valve at the origin, 
which is frequently the only valve, can be bypassed, 
and an incorrect diagnosis of incompetence made. 
Once incompetence has been documented, the cath- 
eter is advanced over a floppy wire to the mid to 
upper third of the R ISV (Fig. 12.8), the anatomy of 
the remainder of the vein is clarified, and emboliza- 
tion or sclerotherapy performed. 





Fig. 12.7. Tertiary {thin arrow). Secondary {grey arrow). 
Primary {thick arrow) curves are all still kyphotic, but the 

disial tip is bent to point downward i.iirivwhcntl) 



Fig.l2.8a,b. Injection above ia) and at (b) the mid R ISV, dem- 
onstrates the typical parallel o 'liaierals and multiple channels 
at ihe level or" lire inguinal 'ipiiiie:'.: Ural nn;ke complete treat- 
n'.ent with coil placemen.! at surgical ligation .na.-Tnging 



Hot (Boiling) Contrast Sclerotherapy 

The use of heat to occlude veins is a well-documented 
and tested technique. Various heat sources have been 
used including boiling liquids, lasers, and radiofre- 
quency electrodes. One distinct advantage of heat 
is that it induces spasm and wall damage leading 
to occlusion with relatively minimal thrombosis. 
Embolization and non-heated liquid sclerotherapy 
techniques result in a large amount of thrombus, 
which, along with any mechanical blockade causes 
secondary venous obliteration. The same contrast 
that is used during the diagnostic part of the proce- 
dure can be heated in a metal container over a heat- 
ing plate for the sclerotherapy. This makes boiling 
contrast quick, inexpensive, universally available, 
non-toxic, and easily visible and therefore control- 
lable. The advantage of a boiling liquid over other 
heat sources and over all embolization techniques, 
is that it can flow into and obliterate any potential 
collaterals. While the patient is receiving extra seda- 
tion and the contrast is coming to a boil, the multi- 
sideholes catheter is allowed to drain so that the ISV 
is as empty as possible. When boiling temperature 
is reached, which is signified by the liquid dem- 



VjikViVle E:iiit , oiii.H,oii 



onstrating the bubbling action of a "rolling boil", 
the operator fills, as best as possible, a 10 cc plastic 
syringe with the boiling contrast, eliminates extra 
air, and injects the remaining 6-9 cc directly into 
the catheter under careful fluoroscopic control. No 
stopcocks or connectors are used to minimize any 
heat loss. A senior member of the team concurrently 
compresses the ISV where it crosses over the supe- 
rior pubic ramus (Fig. 12.9) to prevent any flow of 
boiling material into the pampiniform plexus. Any 
sclerosant or boiling liquid that is allowed to enter 
the veins of the pampiniform plexus will cause a 
very painful scrotal swelling and potentially testicu- 
lar atrophy. Injections are done without moving the 
catheter since the spread of the boiling contrast in 
volumes of 6-9 cc is usually adequate to cover the 
entire extent of the ISV as well as any collaterals. In 
most cases, three sequential injections of 6-9 cc of 
boiling contrast are sufficient to ensure a complete 
obliteration of the injected vein unless it is excep- 
tionally large. 

Overall, the angiographic or imaging success 
rate of the boiling contrast and other liquid scleros- 
ing agents is considered very high with a reported 
recurrence rate of 2%-19% [23]. 



12.10 

Coil Embolization 



i percutaneous technique in cur- 
rent use is that of coil embolization. Its primary 
and significant advantage over sclerotherapy tech- 
niques especially boiling contrast is that it is rela- 
tively painless requiring far less sedation. Gianturco 
coils (Cook), ranging in size from 5 mm to 8 mm 
are the most common sizes used [24], although 
some authors report using smaller or larger coils as 
needed based on the size of the vein. 

Coil sizing, stacking, and placement are clearly 
of paramount importance for technical success and 
avoiding complications particularly coil emboli- 
zation to the heart and lungs. The size of the coil 
should be 10%-20% larger than the diameter of the 
ISV at the level of deployment. Sizing the coil too 
small can result in pulmonary embolization, which 
is aesthetically and emotionally unpleasant, but due 
to the size of the coils is usually without any clini- 
cal consequences. Coil removal from the pulmonary 
artery can usually be done with minimal problems 
using :.i snare or 1 grasper [25], Usually more than one 
coil is deployed at any given site since a single coil 




Fig.l2.9a,b. Compression on the ramus (a) occludes retro- 
grade new where'i! ■;■ impressii.--" sliaJjily ■ 'IT die ramus (b) or 
tilted does not 

has a higher recanalization and failure rate than 
two or more "stacked" or "nested" coils. With the 
development of special tapered shape coils that are 
tapered in one or two directions, the need for mul- 
tiple coils is no longer clear although it has not been 
rigorously tested. The Amplatz Vascular Plug (AGA 
Medical, Minneapolis, MN) is a coil type device that 
is longer and more completely occlusive than stan- 
dard coils, is recapturable until a good "final posi- 
tion" has been confirmed, and will likely find an 
important role in the treatment of varicocele. Coils 
must be deployed proximal and distal to any major 
collaterals. If there are parallel veins, often both 
must be separately occluded. The minimal distance 
of the coils from the orifice of the ISV is somewhat 
debatable. Most European literature cites a distance 
of 6 cm from the origin as sate and effective, while 
others claim that embolization up to the level of the 
origin is preferable to avoid "dead space" in which 
clot could accumulate and potentially embolize. 

Some authors [26] favor the combination of coils 
and sodium tetradecyl sulfate (Thromboject 3%; 
Omega, Montreal, QC, Canada). The coils are deliv- 
ered relatively distally, at the level of the inguinal 
canal, not only to occlude the vein at that level but 
also to prevent reflux into the pampiniform plexus. 
The sclerosant is delivered proximal to the coils to 
occlude all the side branches that could become col- 
laterals. If necessary, coils can also be deposited in 
the proximal portion of the ISV to prevent pulmo- 
nary emboli. One coil that was never used in the 



D. Hunter and G.T.Kosen 



USA deserves special mention. This coil was made 
from tungsten, which obviously would markedly 
improve visibility. Unfortunately, one feature of the 
tungsten coil is that it was biodegradable leading 
to increased tungsten levels in the blood [27-29]. 
Though no adverse effects of tungsten in humans 
were ever described, the observation was concern- 
ing enough that their usage for this application has 
been discontinue!. 



i large balloon of 7-10 mm diameter was 7 or 8 F. In 
oducer catheter had to be plan 



to the level of the desired occlusii 
often technically very challenging e 
the femoral approach. 



12.13 

Complications 



feat that was 

illy from 



12.11 

Tissue Adhesives 

The most commonly used liquid tissue adhesives 
are cyanoacrylates. Their low viscosity makes their 
delivery easy through small coaxial microcatheters. 
However, their rapid polymerization when in con- 
tact with blood, can make precise and safe occlu- 
sion challenging. Usually they are mixed with an 
oil-based contrast media, such as Ethiodol (Savage 
Laboratories, Melville, NY). The contrast serves to 
both opacify the cyanoacrylate and slows the polym- 
erization time [30]. 

Another tissue adhesive that has been reported is 
enbucrylate (Histoacryl; B. Braun, Tuttlingen, Ger- 
many). It can be used when multiple collaterals are 
seen that are too small to be selectively catheterized 
[26]. 



12.12 

Detachable Balloons 

The use of detachable balloons to occlude the ISV 
was first described in 1981 [31]. Due to a lack of FDA 
approval for some of the devices and manufacturer 
related issues, the balloons have not always been 
readily available in the USA. From a technical stand- 
point, balloons were similar to coils in that they 
needed to be deployed above and below collateral 
connections. However, since the balloon occluded 
the vein completely, much like the Amplatz Vascu- 
lar Plug, only one was necessary at any given site. 
As with coils, it was common for users of balloons 
to perform some type of sclerotherapy on the vein 
segments between balloons to decrease the devel- 
opment of collaterals. Balloons suffered from two 
major drawbacks that severely limited their more 
widespread acceptance. The first was cost. The other 
was that the size of the catheter required to deliver 



A unique, and fortunately rare, but significant risk 
of the hot contrast or other liquid sclerotherapy, is 
distal reflux of the sclerosing agent. Inadvertent 
injection of a sclerosing agent into the pampini- 
form plexus can result in painful scrotal swelling, 
phlebitis, and testicular damage with depression 
of spermatogenesis and even irreversible testicular 
atrophy [11]. 

To prevent that a preliminary run with contrast is 
carried out to verify that the occlusion of the inflow 
into the pampiniform plexus is indeed complete 
and efficient. A specially designed device, which is 
essentially a gently curved piece of plastic with pad- 
ding on the edge that will press against the skin, 
was developed specifically to address this and was 
shown to be highly effective [32]. The device must be 
held exactly at a 90' angle to the bone. Fluoroscopy 
is used to verify its end-on position and to ensure 
that all contrast stays above the compressor during 
the injection. 

A different kind of complication is proximal 
reflux of the sclerosing agent, which can result in 
renal vein thrombosis. 

Other complications are extravasation.) nd dissec- 
tion. The ISV is a very thin-walled structure that can 
easily be torn by overly aggressive catliet 
lations or the use of glidewires. Gentle r 
and the use of a carefully controlled floppy w 
almost always prevent ISV damage. On c 
however, a small vein may go into spasm around the 
wire and catheter resulting in vein avulsion or dis- 
ruption during attempts to extract it. Hot contrast 
or sclerosants should definitely be prevented from 
reaching the retroperitoneum since they can cause 
ureteral or muscle injury and severe pain. Contrast 
extravasation at the time of catheter placement 
should prompt a change of the embolization method 
to one using coils or other mechanical devices. 

Another consideration with the use of sclerosing 
agents is the pain that is associated with their injec- 
tion. However it is usually of very short duration, 
nly 10-15 s, although rare instances 



]■ jii.-'impn- 



lasting up to several minutes in poorly sedated 
patients have been seen. The pain can be both alle- 
viated and "forgotten" with the use of agents such as 
Fentanyl and Versed. 



12.14 

Efficacy of Treatment and Comparison to 

Surgery 

Success of the embolization or sclerotherapy treat- 
ment can be defined as a technical success, which 
is the immediate angiographic closure of the ISV. It 
can also be defined as a long-term technical success 
based on the finding of persistent closure on the 
delayed or follow-up angiographic or other imag- 
ing study. Of particular note, the thermal damage 
caused by boiling contrast may result in some imme- 
diate spasm and stasis of contrast, but the vein gen- 
erally remains patent acutely. Success can also be 
defined as clinical success, that is, partial or com- 
plete resolution of the clinical signs and symptoms 
associated with varicocele. In particular, the most 
meaningful definition of success in couples with an 
infertility issue is the successful achievement of a 
pregnancy. 

The two parameters that are usually evaluated in 
the assessment oftheclinica let I k;kv of the treatment 
are semen analvsis change:; and the pregnancy rate. 

There is great controversy in the literature about 
the effectiveness of varicocele embolization. Accord- 
ing to one recent Cochrane analysis, the existing pro- 
spective randomized trials that satisfied their criteria 
for inclusion showed improvement in semen param- 
eters and symptoms, but no difference in pregnancy 
rate compared to no treatment [33]. However, some 
of the individual studies in that analysis did show a 
very significant improvement in pregnancy rate of 
the treated group [34]. When retrospective data or 
non-randomized control groups are included in the 
analysis, most an [hois do tiiul a significant difference 
in pregnancy rates between treatment and no treat- 
ment for varicocele. The historical rates that seem to 
have the most widespread acceptance suggest that the 
pregnancy rate for couples in whom there is docu- 
mented male infertility as the sole cause of infertil- 
ity is approximately 30% if the male receives either 
surgical or percutaneous treatment of the varicocele. 
This compares to a pregnancy rate of 16% for couples 
with the same history who undergo no therapy [35]. 
Thus, many clinicians and infertile couples are still 
interested in treatment for' 



When the percutaneous procedure is compared to 
surgical ligation, varicocele embolization has been 
shown to be an equally effective means of treatment 
and is associated with less post procedure discom- 
fort and more rapid return to normal activities [24, 
36-38]. 

The overall reported technical success rate as cited 
by the JVTR quality improvement guidelines are 83%- 
96% with a clinical or imaging detected recurrence 
rate at 6 weeks of 7%-16% [23]. All of the analyses of 
procedural and clinical etticacy are obviously influ- 
enced and potentially severely confounded by sev- 
eral poorly controlled variables. One problem is that 
the need for treatment of both sides has never been 
clarified and it is clear that di tferent authors have had 
markedly different opinions and angiographic find- 
ings on the subject. Another problem is that imaging 
follow-up is infrequent and impossible to quantify 
in a meaningful fashion. Therefore, the impact of 
aggressive and extensive treatment such as with coils 
plus sclerosants, boiling contrast or sclerosants is dif- 
ficult to compare with simple coil or ligation therapy. 
In addition, the inclusion criteria, particularly with 
respect to semen analysis variables are poorly con- 
trolled. As an example, patients who present with a 
very low sperm count, below 2 million/ml, seem to 
have a lower response rate to treatment and yet are 
usually lumped with more favorable patients in most 
analyses. 

One place where embolization or sclerotherapy 
appears to have established a definite niche is in the 
treatment of recurrence or failure following surgical 
ligation. In these cases, repeat surgery can be done 
with a different technique, but fearing another fail- 
ure, most surgeons will refer the patient for percuta- 
neous diagnosis and treatment. A total of 31 patients 
out of 40 with recurrence after surgery in one study 
[16], and 33 out of 39 patients in another [39] had 
successful diagnoses and treatment. The ISV veno- 
gram allows a precise anatomical definition of the 
cause and location of the veins responsible for the 
recurrent varicocele and the use of steel-coil embo- 
lization in both studies provided an effective means 
of treatment with improvement in semen quality 
and pregnancy rates [16, 39]. 



12.15 
Conclusion 



Even though some controversy exists about the justi- 
fication for any type of treatment of varicocele with 



::■. Hunter ami G.T.Rosen 



wide variation in results between different studies, 
we feel that current recommendations should advo- 
cate percutaneous embolization of varicocele as a 
safe, effective and potentially first-line treatment. 
Its overall efficacy is comparable to that of surgi- 
cal ligation with a shorter recovery period and less 
pain, permitting it to be conducted as an outpatient 
procedure. 

Our preferred embolization method is using boil- 
ing contrast. Other embolization techniques, such 
as coils, vascular plugs, other sclerosing agents, and 
detachable balloons are acceptable, and clearly less 
painful although more complex alternatives. The 
primary and important risk of any sclerosant type 
procedure is reflux into the pampiniform plexus, 
which might lead to orchitis and even testicular 
atrophy. The best way to avoid this complication is 
to use a compression device, rather than relying on 
manual compression. 



Catheter: 

• IJ approach #1: 

Heat reformed Headhunter 1 with extra side- 

• IJ approach #2: 

Heat reformed JB 1 with extra sideholes 
Femoral approach, renal double curve 
guider left and Sidewinder 1 right 

Micro catheter: 

None needed from the IJ approach 

Renegade from the femoral approach 

Embolic agent: 

Boiling contrast 

Amplatz vascular occluder, or coils, preferably 
with a tornado or other complex shape, and 
always at least two at each point of emboliza- 



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M i n :■ I-: u ■." ii i [\, et ill. :. 1 '■■''-I ' !-jiil"'0 1. ;:.:!..:■ 11 o:' varicocele will] 
etiianol. Nippon x.i:,.: Hosliasn] vlakl..]; Zassh. 54:570- 
375 (Japanese) 

23.Drooz AT, Lewis CA, Alien TE, Citron SJ, Cole PE, 
Freeman NJ, Husted JW, Malloy PC, Martin LG, 
Van Moore A, Neithamer CD, Roberts AC, Sacks D, San- 
chez O, Venbrux AC, Bakal CW (2003) Society of Inter- 
vention:]! Radiology standards of Practice Committee. 
Quality improvement guidelines :or percutaneous tran.s- 
caiheier emo-oli/ation. I Vase Inlerv Kadi.::. 14(9 Pi 2): 
5237-242 

24. 5 h Ian sky- Go id berg RD, VanArsdalen KN, Rutter CM, 
Soulen MC, Haskal ZJ, Baum RA, Redd DC, Cope C, 
Pentecosi m; (1997! 1-ercutaneou; varicocele embokza- 
tion versus surgical ligation tor die treatment of infertil- 
ity: changes in seminal parameters and pregnancy out- 
comes. J Vase Interv Radiol 8:759-767 

25.Chomyn JJ, Craven WM, Groves BM, Durham JD (1991) 
Percutaneous removal of a Gianiurco coil from the pul- 
monary artery with use of flexible intravascular forceps. 
] Vase Interv Radiol 2: 105-106 

26. Tay KH, Martin ML.Lisl Mayer A.Machan LS (2002) Selec- 
live spermalic venography jno varicocele embolization 
in men with circumaorlic left renal veins. 1 Vase Interv 
Radiol 13:739-742 

27. Barrett I, Wells I, Riordan R, Roobottom C (2000) Endo- 
vasctilar embolization of varicoceles: resorption o: fang- 
s:en coils in the spermatic vein. Cardiovasc Iniervenl 
Radiol 23:457-459. 

28.KampmannC, Brzezinska R, Abidini M et al (2002) Bio- 
1 -.— tr i .;■,: -i . .ii of iu:;g; : ien embolization coif; used in chil- 
dren. Pediatr Radiol 32:839-843 

29. Wells IP (2003) Biodegradation of tungsten emboli sat ion 
coils used in children. Pediatr Radiol 33:288 

30. Pollak )S, White RI (2001 ) The use of cyan o aery late adhe- 



sive? in peripheral embolization, i V.isc Interv Radiol 
12:907-913 

31. White RI Jr, Kaufman SL, Barth KH, Kadir S, Smyth JW, 
Walsh PC (1981 (Occlusion of varicoceles with detachable 
balloons. Radiology 139:327-334 

32. Hunter DW, Bildsoe MC.AmplatzK (1989) Aid for safer 
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33.Evers J, Collins ] (2004) Surgery or embolisation for vari- 
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CD 000479 

34.Madgar I, Weissenberg R, Lunenfeld B, Karasik A, 
Goldwasser B (1995) Controlled trial of high spermatic 
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63:120-124 

35. Skoog SJ, Roberts KP, Goldstein M, Pryor JL (1997) The 
adolesce: 1 .] varicocele: what's new with .:w\ old problem in 
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Lammert GK (1994) Clinical outcome and cost compari- 
son ■::' n ere tit a neons em I: oliz.U.' 'ii a no s.i: g:.:a: J i t;..i j ■ ■:' 
va-iiiocek. I A i drol 1 5[suppk:a8-- id 

37. N:csihlan H, Hi-hre HM, Schlingheider A, Nashan D.Pohl J, 

■ i : 1 99a ; iurg.ca. ligation vs. angiographic 

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dumi/.i'L rady for the treatment of varicocele related 

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38. 1'arich BM, S^hill WB, Erlinger C, Tauber R, Pfeifer KJ 
(1990) Semen parameters a no conception rates after sur- 
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Kelkar AK li 1 '" 1 ^; !- : osl-surgical recurrent varicocele: 
efficacv .;■■:' internal spermatic venography ^\■\ t } steel-coil 
embolization. Br ] Urol 77:124-128 



13 Embolization Therapy for High-Flow Priapism 



Jim A. Reekers 



Introduction 227 
Diagnosis 227 
Imaging 228 
Therapy 22a 
Embolization Therapy 228 
Technique of Embolization 22S 
Follow-up 230 
Conclusion 231 
References 231 



13.1 
Introduction 

Priapism is named after the Greek god, Priapus, son 
of Aphrodite and Dionysus. 

Priapism is a persistent erection of the corpora 
i of the penis, originating from distur- 
:o the mechanisms that control penile detu- 
:e. This affects only the corpora cavernosa. 
The corpora spongiosum of the glans penis and sur- 
rounding the urethra are not part of the process. 

The overall incidence ofpriapism is 1.5per 100000 
person-year [1], Priapism is broadly classified as 
high-flow and low-flow. Arterial high-flow pria- 
pism (HFP) is usually secondary to the laceration of 
a cavernous artery with unregulated flow into the 
lacunar spaces. This type ofpriapism is most of the 
times not painful because there is no ischemia. HFP 
is rare and onlv 200 cases have been reported in the 
literature. Nonetheless, because it is painless, it is 
possible that HFP is under reported. The other type 
is veno-occlusive priapism which is usually caused 
by corporeal veno-occlusion, and can be very pain- 
ful due to ischemia. 



J. A. Reekers, MD, PhD 

Department of Radiology, Gi -207, Academic Medical Center, 
University of Amsterdam, Meibergdreef 9, AZ 1 105 Amster- 
dam, The Netherlands 



The clinical presentation of these two types of 
priapism is different. HFP is often seen after an 
acute injury, and the onset can be delayed. This 
delayed onset may be due to initial vessel spasm, 
hemostasis with clot formation or a compressing 
hematoma. Reabsorption of this clot or hematoma 
is the mechanism for the late onset. The HFP is often 
less tumescent when compared with venous pria- 
pism. Priapism secondary to arterial causes may be, 
as mentioned before, significantly less painful than 
venous priapism and is not considered as an emer- 
gency. The major etiology of HFP is trauma, espe- 
cially in children or young adults; in older men, HFP 
is a rare event mainly caused by malignancy [2]. 
High-flow priapism in acute lymphatic leukaemia 
has also been reported [3]. 

Veno-occlusive priapism presents with a pain- 
ful erection, which can already have been there for 
days. Prolonged veno-occlusive priapism results 
in fibrosis of the penis and a loss of the ability to 
achieve an erection. Siami icam changes at the cel- 
lular level are noted within 24 h in veno-occlusive 
priapism, whereas arterial priapism is not associ- 
ated with fibrotic change. Veno-occlusive priapism 
most commonly is idiopathic, although there is a 
long list of other causes which include leukemia and 
multiple myeloma, sickle cell disease, thalassemia, 
spinal cord injury, spinal anesthesia and drugs. 



13.2 

Diagnosis 

Careful patient history and clinical signs and symp- 
toms are of paramount importance. As stated pre- 
viously, history of trauma with a painless priapism 
favors HFP. Cavernous blood coloration and gas 
measurement are very useful and easily available 
to distinguish between HFP and venous priapism. 
A bright red appearance of the cavernous blood is 
more in favor of HFP, which in turn is associated 
with a high po2 and low pco2. General diagnostic 



tests include complete blood count, platelets, differ- 
ential white blood cell count and reticulocyte 
and urine analysis for drugs. 



13.3 
Imaging 



Penile ultrasound and Doppler testing may bi 
sary to differentiate high-flow from low-flow pria- 
pism. In HFP, ultrasound reveals an hypoechoic, 
well-circumscribed region in the corpus caverno- 
sum. The Doppler will show an increased flow in 
the penile artery, uni-or bilateral, and an arterio- 
cavernosal fistula (Fig. 13.1). In patients with high- 
flow priapism, selective penile angiography may be 
required in order to identify the site of the fistula. 
Angiography should however not be done as a diag- 
nostic procedure, but always in combination with a 
planned therapeutic embolization. 



13.4 
Therapy 

The goal of all treatment is to treat the priapism 
while preserving future erectile function. This paper 
will only discuss the treatment options in HFP. 

There are some alternative treatment options 
for high-flow priapism, like ice packs where ice is 
applied to the penis and perineum to reduce swell- 
ing, corporal aspiration, massage, and pressure 
dressings. Pharmacological interventions are also 
used. This includes the use of alpha-agonists (e.g., 
metaraminol bitartrate) or methylene blue. Alpha- 
agonist agents counteract smooth muscle relax- 
ation. However, they may cause significant systemic 
hypertension. Methylene blue inhibits guanylate 
cyclase and has a second messenger inhibitory 
effect; thus, it inhibits smooth muscle relaxation. 
The effect of methylene blue is relatively short-lived, 
and priapism may recur. Any of these treatment 
options are often of little use in high-flow priapism, 
as a rupture of the artery does not subside spontane- 
ously. Surgical ligation of the fistula is an operation 
which is redundant now that embolization is widely 
used; however it is still performed. One of the main 
potential complications of this procedure includes 
long-term impotence. For HFP caused by inherited 
diseases, and malignancy conservative therapy is 
mandatory. 




Fig. 13.1. Ultrasound with Doppler in a patient after a bicycle 
irauma. Hopple:' shows high systolic velocity of 73 cra/s. Color 
Doppler demonstrates a fistula I black arrow) within a well-cir- 
cn m scr bed hypo echoic hematoma o: laceration in the corpus 



from the 



13.5 

Embolization Therapy 

The blood supply of the penis 
internal pudendal artery (IPA). The c 
artery is a distal branch of the IPA and g 
the bulbourethral artery at the base of the penis, 
subsequently dividing into the dorsal penile and 
cavernosal arteries. The anatomy of the internal 
pudendal artery has many variations, but usually 
comes from the anterior division. The most common 
presentation is shown in Fig. 13.2. One has to take in 
consideration that the inferior rectal artery derives 
from the IPA, which off course prevents selective 
embolization from the origin of the IPA with a flow 
guided embolic niieitt like particles ,is they will end 
also in the rectal mucosa. However, when a selective 
position cannot be achieved, proximal coil emboli- 
zation in the IPA might be performed (Fig. 13.3). In 
high-flow priapism one can see arteriovenous fistu- 
las or pseudoaneurysms, resulting in abnormal arte- 
rial inflow, which exceeds venous outflow capacity, 
resulting in tumescence. Fistulas can be uni-lateral 
or bilateral, and to achieve optimal results, all fis- 
tulas should be occluded (Fig. 13.4) [4, 5]. 



13.6 

Technique of Embolization 



.1 of movement for 



contra lateral access, over the 
the best stability and free- 



'-. mbokzation T;'.er;i;"-y tor H.gii-Hoiv Priaoisi 



Fig. 13.2. aThe most cc^nn;on;r:iaromy of the internal 
pudendal artery origin, b Selective catheterization of 
the internal pudcno.il .1 tt^jy with distal div 
the deep and dorsal branch 




fistulas are bilateral we start with a 5 F sheath in both 
common femoral arteries. The internal iliac artery 
is selectively catheterized with a multi-purpose tip 
catheter. A firmer catheter allows a more stable posi- 
tion where a glide-catheter might not have enough 
stability to act as a guiding for a micro-catheter. 

1 'msnostk' angiography is performed to establish 
the diagnosis and to guide the superselective embo- 
lization. A microcatheter 18" with a 14" floppy wire 
is used to position the tip of the microcatheter in/at 
the side of the fistula. The position has to be as selec- 
tive as possible to warrant erectile function after the 
procedure (Fig. 13.3). Spasm might be a problem, 
therefore local spasmolytics, like nitroglycerin, can 
be applied before selective catheterization. Systemic 
spasmolytic support, such as ca-blockers, can also 
be helpful. If the patient is using anticoagulant med- 
ication, this should be stopped, but only after con- 
sultation of the primary physician. 

Embolotherapy for high-flow priapism has been 
accomplished using a variety of agents including 
autologous clot, gelatin sponge pledgets, bucrylate 
and microcoils. It seems to be rational to advo- 
cate the use of temporary occlusive agents, such as 
autologous clot or gelatin sponge, to allow eventual 
recanalization and to preserve sexual function. 
However, in the literature it is shown that also more 
permanent agents show preservation of sexual func- 

When the microcatheter tip has a superselective 
position in/at the fistula we prefer to use a microcoil 
because this allows the most precise local occlu- 



sions without an inadvertent occlusion of nontarget 
branches. If we are not able to achieve this optimal 
position and stop in a more proximal position, we 
will use gelatin sponge but only with the catheter 
tip distally to the inferior rectal artery branch. We 
the del 



[■ op If. 



-ery 11 




Fig. 13.3. Emboliza:io:i 01" both uric r 11.1 1 pudendal arteries will 
coils in a pa i rem with pr i ay ism .-:id sickle cell disease. The nin 
of this treatment was to create p^rni. merit impotence and [■: 
prevent fibrosis 




5a- f. Posttraumatic HFP with bLliiter.il list'jlae. ii Left ; menial iliac artery angiography shows a fistula, b Selectiv- 
I PA. c After closure of the listu.a with gelatin sponge, d Selective right IPA shows 3 second fistula, e Micro catheter in sup 
lec:ive position, f t:'d res-Jt .itier embolization k:i:. gelaiin sp-.jnge. f'auem had a full :c,";:ive:y .i:'J regained normal en 
function 



never fully under control in this delicate area. Sec- 
ondly, after glue delivery the microcatheter has to be 
red and in case of a residual arteriovenous fis- 



tula selective catheterization has to be started again. 
However, successful glue embolization of HFP has 
already been reported [6]. 

After uni- or bilateral occlusion of all the list u la! s) 
has been achieved, the catheters and sheaths are 
removed. A color Doppler control after 24 h should 
be performed to document the local result. Although 
postembolization recurrence has been reported as 



high as 20%, it is lower in most publi 
not related to the embolic agent used [7]. 



13,7 
Follow-up 

Usually within hours after the embolization the pri- 
apism will be resolved. For normal erectile function 
to restore it might take up to 6-9 months [7]. As 



'-. mbokzation Tl'.era.'y tor H.gii-Hoiv Priaoisi 



"normal" can be an subject of discussion an objective 
test like the International Index of Erectile Function 
(IIEF) should be used in follow-up. According to this 
test 80% of all patients will regain normal erectile 
function, while 20% will have a slight change in the 
quality of erection [7]. 

One of the concerns of embolization treatment is 
the local radiation of the gonads. Reduction of radi- 
ation can be achieved with the combined approach 
of X-ray and ultrasound imaging to facilitate the 
supraselective embolization of the arteriocavern- 
ous fistula reducing the radiation exposure and the 
applied dose of contrast medium [8]. It seems ratio- 
nal to advise refrainment from reproductive activ- 



ity for a period of at least 3-6 months, although this 
recommendation is not supported in the literature. 



13.8 
Conclusion 

Embolization for HFP is currently the treatment of 
choice if conservative therapy fails. It is safe and 
effective with a very high success rate and also a 
high recurrence of erectile function. Super- selective 
catheterization is mandatory. Microcoils and gelatin 
sponge are the embolic agents of choice. 



Cookbook 


Introduction 


5-F sheaths 




Any 




Guiding 

Guide wire 

Selective cncJierizntLoii 

E :i j Li ::■ i i zation material 


Multipurpose 5-F 
(No glidecath) 
Terumo wire 35' 
Microcatheter 18" 
Gelatin sponge or 


coils 


Terumo 
Target (Bosl 
Cordis/Bost 


on Scientific) 

jn Scientific/ Cook 





1. Eland IA, van der Lei j, Strieker BH, et al. (2001) Inci- 
dence of priapism in the gei'rf.;. popiilauon. Urology 
57:970 

2. Kuefer R, Bartsch G Jr, Herkoraraer K, Kramer SC, Klein- 
sJimidi K. Vo.kmer ~jC [ J 00?; C.:.;:'£ing diagnosl :.: and 
;ke;\ip;ul :.: ..V:\"ep;S \:\ kigi".-flow .'::apis:v.. In: 1 Impol 
Res 17:109-113 

3. Mentzel HJ, Kentouche K, Doerfel C, Vogt S, Zintl F, Kaiser 
WA High-flow priapism in aa:;e lymphatic leukaemia. 
Pediatr Radiol 34:560-563 

4. Gorich J, Ermis C, Kramer SC, Fleiter T, Wisianowsky C, 
Basche S, Gottfried HW, Volkmer BG (2002) Interven- 
i.onal ;rea:nteni of iiir.im.iiii; priapism. I Endovaso Titer 
9:614-617 



?. i.:". L":ae:;h n i i-=ej: I!- rieisman V. i\re,;:: : [A. Je knike ".":. \! 
:2'i ; i] ; Hrghlv vclc-;uvc embolization oi biiatera. cavern- 
ous aneiies for pos:-lrauma:k" oenile arteria. priapism. 
Int ] Impot Res 13:354-356 

6. Gandini R, Spinelli A, Konda D et al. (2004) Superselective 
ei:ihoii;..ii;on in posttraumatic icioapi-::: with Glubrai; 1 
acrylic glue. Cardiovasc Intervent Radiol 27:544-548 

7. Savoca G, Pietropaolo F, Scieri F, Bertolotto M, Mucelli FP, 
Relgraiao '-. (J004) Sexua. itinaion .Life: highly selecuYe 
embolization o'i cavernous arteiy in palients with high 
flow priapism: long-ie:m fokownp. I Urol 172:644-647 

8. Bartsch G Jr. Kuefer R, Engel O, Volkmer BG (2004) Pria- 
pisms coioui-Doppler ■.litiasoaisJ-gLiide;". ,; i:o:.r : elec.ive 
embolization therapy. World J Urol 22:368-370 



Aortic-Iliac 



14 Endoleak: Definition, Diagnosis, and Management 



David Valenti and Jafar Golza 



Introduction 235 

Classification and Significance of Endoleaks 235 

Type I Endoleak 236 

Type II Endoleak 236 

Type III Endoleak 236 

Type IV Endoleak 237 

Type V Endoleak or Endotension 237 

Diagnosis of Endoleaks 237 

Computed Tomography 237 

Color Doppler Ultrasound 237 

Magnetic Resonance Imaging (MM] 245 

Angiography 245 

Treatment of Endoleak 245 

Type I Endoleak 246 
. Type IA Endoleak 246 
>. Type IB Endoleak 247 
) Type IC Endoleak 247 

Type II Endoleak 247 
. Transarteria! Approach 247 
> Translumbar Approach 24S 
1 Other Embolic Materials 248 

Type III Endoleak 249 

Type V Endoleak - Endot 

Conclusion 249 

References 249 



14.1 
Introduction 

Endoleak is defined as the persistent perfusion of 
the aneurysmal sac after endovascular aortic aneu- 
rysm repair (EVAR). A leak can appear during the 
first 30 days after implantation. This type of leak 
is called "primary endoleak". Secondary endoleak 
is one that occurs after 30 days. Leaks may also be 
classified as graft-related or non graft- related. The 
incidence of endoleak varies from 10% to 50% [1, 2]. 
In a report from EUROSTAR registry, the incidence 
of early endoleak was 18% [1]. A total of 69% of these 
leaks were graft related; 70% sealed spontaneously 
during the first o months without difference between 
graft-related and non graft- related endoleaks. There 
is not always a rational explanation of the cause 
of spontaneous resolution of some endoleaks and 
persistence or late occurrence of some others. The 
presence of outflow vessels (mainly lumbar arteries 
and inferior mesenteric artery) partially explains 
this phenomenon [3]. A leak communicating with 
these outflow vessels seldom disappears spontane- 
ously [4]. Thus, these vessels should be identified. 
Whatever the cause of a persistent leak, it should 
be identified, monitored and treated. The details of 
EVAR will not be discussed here, except in relation 
to endoleaks. 

This chapter will review classification and sig- 
nificance, diagnosis and treatment options for dif- 
ieivnt types of endoleak. 



D. Valenti, MD 

Royal Victoria Hospital, McGil! University Health Centre, 
McGill University, 667 Pine Avenue West, Suite A451, 
Montreal, H3A 1A1, Canada 

J. GOLZARIAN, MD 

Professor of Radiology, Direc 
Radiology, University of Io' 
200 Hawkins Drive, 3957 IPP, 



, Vascular and Intervention 
. Pe-pan merit of Radiolog; 
ns City, IA 52242, USA 



14.2 

Classification and Significance 

of Endoleaks 



A generally accepted anatomic classification for 
endoleak has been developed over the years [5]. In 
this system, leaks are defined by their inflow source, 
regardless of the number and type of other vessels 
involved in the outflow (Table 14.1). 



D.Valentiand J. 



I . }:'. 11 .".■■. e L- .-v cl:V : i.:':.:.;[k 



Types Mechanism 



Kow o: ig; nates from ineffective enjogrnfl ^e;i J at 

fixation zones 

kp ixiij];":! 

Distal 

Iliac occluder 

Branch vessel retrograde flow 

Single vessel (simple) 

Two or more vessel! cie.iuiig a drain i complex] 

J-j.vv res u l:s (:<::•:. si:ucl;i\iI endograf: :.iilu:e 

iunaional separation (modular devices] 

Endograft fracture or holes 



-Min 



i(<2d 



■ Major (>2 mm) 

Endoerafi fabric porosity 

!<30 days after endograft implantation) 



14.2.1 

Type I Endoleak 

Type I endoleak is caused by failure to achieve a 
circumferential seal at either the proximal (type 
IA) or distal end (type IB) of the stent graft. Type 
IC endoleak is due to non-occluded iliac artery in 
patients with aorto-mono-iliac stent and femoral- 
femoral bypass. With type I endoleak, the aneu- 
rysm is perfused directly from the aorta or the iliac 
arteries (inflows). The leak usually communicates 
through a channel (sometimes multiple channels) 
with the aneurysmal sac. There are several out- 
flow vessels, mainly lumbar arteries and inferior 
mesenteric artery (IMA) that communicate with the 
channel and or the sac (Figs. 14.1, 14.2). The pressure 
within a type I leak is systemic. The tension on the 
aortic wall remains high. 

Causes of primary type I endoleak include inap- 
propriate anatomy, with a significantly angulated 
neck, significant calcification/plaque at the proxi- 
mal or distal landing zone, a non-circular land- 
ing zone, malpositioning of the stent graft, type 
of endograft and under-dilation of the stent graft. 
Secondary type I endoleak can be due to aneurysm 
re-modeling, resulting in stentgraft migration, pro- 
gressive dilatation of the proximal neck, design and 
d imensions of stentg rafts or u nfavou rable infrarenal 
necks including the conically shaped neck and neck 
shorter than 15 mm. Grafts whose tixntion relies on 
radial force are more prone to caudal migration and 
type I endoleak than s. i alts with hooks [6].Endothe- 
lialization of bare stents at the landing zones may 



contribute to a certain fixation, but endothelializa- 
tion of the fabric itself does not occur. Proximal bare 
stent separation, as seen with the Vanguard device, 
and hook fractures, as seen with the EVT device, are 
also causes of delayed type I endoleak. Oversizing the 
graft by 20% is recommended to prevent a delayed 
endoleak. At the iliac level, type IB endoleak occurs 
when the limb of the graft is too short or migrates 
upward due to the sac's retraction pressure. 

Although a type I endoleak can seal spontane- 
ously, risk of rupture is high and intervention is 
indicated [4,7,8]. 



14.2.2 

Type II Endoleak 

A type II endoleak corresponds to the retrograde 
filling of the aneurysm mainly from lumbar arteries 
and/or IMA but also in rare situations from sacral, 
gonadal or accessory renal artery (Figs. 14.3, 14.4). 
Type II endoleaks can be associated with aneu- 
rysmal expansion and rupture; however, this risk is 
much less than with the type I and III endoleaks (0.5 
versus 3.4 %) [9, 10]. A leak in the setting of a shrink- 
ing aneurysm can generally be followed, without 
immed iate intervention. It is well established that up 
to 40 % of type II endoleaks will seal spontaneously. 
Some have advocated intervening in all endoleaks 
persisting beyond 3-6 months, while other groups 
recommended observing leaks in the absence of 
aneurysm expansion. We favor the last approach. In 
our experience with biphnsk" helical CT follow-up of 
more than 300 patients treated by EVAR from 1994 
to 1998, only three patients needed intervention for 
type II endoleak. 



14.2.3 

Type III Endoleak 

Type III endoleaks are caused by a structural failure 
of the implanted device, including junctional sepa- 
ration of modular components, due to migration 
or changes in vessel morphology with aneurysm 
shrinkage, holes in the fabric, and fabric tears due to 
graft strut fracture or erosion (Figs. 14.5, 14.6). Graft 
disconnections were not infrequent with the first 
stentgraft generation due to a short overlap between 
the main body and the limb [11]. 

Type III leaks allow direct communication 
between the aorta and aneurysm sac. They have sys- 
temic arterial pressure. Similar to type I leak, type 



Endc'leA: Pen nil ion, I > j5igjiosj-=, ;iiid Miin.iaemem 



III endoleak needs to be treated aggressively [10]. 
Type III endoleaks are considered to be the most 
dangerous, since there is an acute re-pn 
of the sac. 



14.2.4 

Type IV Endoleak 

Type IV leaks are caused by porosity of the graft 
fabric. They are seen at the time of device implanta- 
tion, as a faint blush on the post-implantation angi- 
ogram, when patients are fully anti-coagulated. It is 
important to rule out other types of endoleak before 
labeling a leak as type IV. They are rarely seen with 
current devices and will seal spontaneously. If a leak 
persists, other types should be excluded. 



14.2.5 

Type V Endoleak or Endotension 

Endotension (or type V endoleak) corresponds to 
continued aneurysm expansion in the absence of a 
confirmed endoleak [12, 13]. The expansion of the 
aneurysm in a type V endoleak may be due to an 
undiagnosed endoleak, presumably with very slow 
flow and suboptimal imaging (e.g. no delayed heli- 
cal CT acquisition). Endotension has been reported 
up to 18% in [14] a study evaluating the significance 
of endotension in 658 patients. The authors dem- 
onstrated that endotension is rare and concluded 
that it may represent missed endoleak rather than 
true aneurysm expansion in the absence of perigraft 
flow [15]. 

However, in most situations, endotension cor- 
responds to an accumulation of yellowish fluid 
(seroma) [16]. Endotension is more common with 
ePTFE grafts due to ultra-filtration through graft 



14.3 

Diagnosis of Endoleaks 

14.3.1 

Computed Tomography 

Contrast enhanced helical computed tomography or 
CT angiography (CTA) is considered the imaging 
technique of choice for the detection of endoleak. 
CTA is reported to be superior to aortography for 



the demonstration of small leak [17]. The technique 
is also able to demonstrate the patency of lumbar 
arteries and IMA. However, selective aneurysmal 
angiography is superior to CTA for the detection of 
outflow vessels [4, 18]. 

The value of biphasic or triphasic CT scanning 
has been established for follow up of EVAR [19, 20]. 
Some authors favor obtaining an unenhanced helical 
CT series. Rozenblit at al. have demonstrated that 
the unenhanced series were helpful to diagnose an 
indeterminate endoleak in one patient [20]. Impor- 
tant mimickers of endoleak include calcification, 
contrast within the folds of unsupported portions of 
the graft and residual endosac contrast from the ini- 
tial procedure when early CT follow-up is obtained 
at 1-3 days. This "pseudo-endoleak" was seen in up 
to 57% of patients [21]. 

It has been demonstrated that delayed acquisition 
uncovered up to 11% of endoleaks that were missed 
by arterial phase alone [19, 20]. An optimal CT pro- 
tocol for the monitoring of the aorta after endolu- 
minal therapy should include a delayed acquisition 
(Fig. 14.7). 



14.3.2 

Color Doppler Ultrasound 



Color Doppler ultrasound (CDUS) ii 
and cost-effective imaging modality. It is highly 
dependent on the operator and has limitations in 
obese patients and those with excessive bowel gas. 
Patients should be evaluated after 5-6 h fasting in 
supine and lateral position. The aorta is evaluated 
both transversally and longitudinally. Leak is sus- 
pected when a reproducible color and Doppler signal 
inside the aneurysm is visualized. 

Variable success is reported for the detection and 
localization of the source of endoleaks with ultra- 
sound, depending on technical factors, the imaging 
protocol, and the image quality. Reported sensitivi- 
ties for overall endoleak detection range between 
12% and 100%, with specificities of 74%-99% [22- 
26]. 

In a series of 55 patient with CDUS compared to 
biphasic CTA, CT was superior in detection of small 



leak. Discrepai 



onstrated by hel 
these leaks were 



es between helical CT and CDUS 
i eight patients (14.5%). In five 
■igraft leak that was clearly deni- 
al CT was not found on CDUS. All 
tmall and disappeared during the 
follow-up. For the diagnosis of endoleak, the sensi- 
tivity, the specificity, the positive and negative pre- 



["'. Valenti and 1. Golzarian 




Fig. 14.1 a-e. Type I en do leak, a CT Sian, a now shows Luge 
type 1A endoleak :'iom pioxima! end of an abdominal aortic 
■). b Aorta gram, lonlirms the type IA 
endoleak i iin-iurs). t Palm-.i; stent placement ji It.e proximal 
end to achieve a circumferemia! sea:. Pakv.az ?Q14, 47 ram 
<i I'epA'Vmen: of a ba Koon expand- 
able Palmaz stent, e Follow-up CT showing no leak 



Endoleak: Pelinilion, I >i;'. gnosis, and Mil ii.'-gejiiciji 




2a-f. A high-risk (ASA IV) 

rysm (AAA), a An aortogrom shows 

an AAA, a long irregular neck with 

occlusion of left renal artery (or 

b Follow-up angiogram 1 year after 

itgraft implantj- 

There is a type I endoleak (large 

ignificant angulation of 

neck (small a\ 

c Selective aneurysmal si 

tion from brachial approach shows the 

channel (black arrow), the sac (white 

] and lumbar arteries acting as 

low vessels (small Mack arrows). 

Embolization of the channel with 

:ak. f CT i 



:ndoleak.gCTsi 
mage ■: fl, obtained 1 year ;i 
vs no endoleak i 
hrinkage of the a 



eiuboli- 
.[.'. sig: , .i ! i- 



['. Viilenti and 1. Golz;i:uiii 




r, ii. ".':■ lea^.: 1 ■rr::'itio:\, I ■ !.igi:-.:iS;-=, and Man.: gem em 




Fig. [■!.. la-;. Type II endoleak. a Contrast enhanced CT shows an imp or in m peri -prosthetic leak i.,n roi; ). b Lei'; internal idac 
a: tery angiogram demonstrates a type [[ leak i btth'k iii ton) from iliolumbar artery i irfurc .iito'i i. c,it Translumbar appro a di 
has been used for the treamieni of this endoleak. CT and volume rendering reconsti uiticn shows die posidi.-n of ihe needle 
and the aneurysmal sac. The pressure in [he sac was din', measured showing a svstolic pressure of 160 mmHg. e Injection of 
(he sac shows die iiwolvemenl oi' the IMA : bi-.h'k , J i .■ i ■■ i : i . f t-: j ; j L" ■ dz.ii ion ■ if dir •:■; igiii oh die IMA. g Ar.er IM A e::::"-. -../o: !■ ::. 
"die origin o:' die lumbar artery is embolized. Anon 1 shows the lumbar aneiy as the outflow vessel, h The aneurysmal sac is 
dien rm.bo'izco with coils. Ai this poinl. ihe svsj.de press use in ".he sac drops to tOC imiiKg. A: the end ■ c" the picced-iiv. .he 
sac pressure was close to zero, i The tract (<iiTpir) was then embolized with tjelfoam. ; CT 'Obtained 8 months a tier emboliza- 
tion shows no more endoleak 



I' 1 . V;l!r:lii ;'.:lii 1. Oo]z;l:'iiill 




EndC'Jeak: Pefhihion, I > jsigjj0 5j-=, and Management 




Fig. 14.4a-h. Type II endoleak. a,b GT scan demonstrates an endoleak involving bo;h IMA and lumbar ii:;erie5. a Posterior 
endo'enk : ■■■, iiilc -.jnvwj.b Right lateral i cm ■;:<.! iir i-piri and a rum or position of I lie endoleak i black iinoiii. c Supr: ior me sent eric 
Lii'.gi' ■g:;uii c. em on si rates die op. ici ft cm ion of IMA (anted iiProit) through ;i:c o:' Ki ohin i laigc black iitioiri ,;nd die endoleak 
cuv'uy i.<ni.:iii black :T rrv> n ■ >. d i elective microcLdhele! placement :n the sac. Angiogram show; the aneurysm, oac lumbar artery 
i black iino i; s) Lind sperm ;i iic a:uery t nliirc <in'flir)i lic dug lis oiullow. s Coil embolizadon -.it the origin o:" die lumbar artery 
i ir/i.'K' hi iow) WLis initiated however, the catheter was pushro back and "die distal end o( the coil released Lit the on gi:i of die 
IMA (black arrow). The IMA was then einb- ikzed. t Angiogram shows ivo more endoleak with transient spasm of the arc of 
kiolan i iinoiLsi. g Left com men idac Lingiogram shews ::■:■ endoleak r'rom iliolumbar arterv. h Enhaiuvo CT obtained other, 
embolization demonstrates a small endoleak from lumbar artery (iirroH') 




Fig.l4.5a,b. Type III endoleak dui 
IMA 'small Mack arrow) and a lumb: 

in the aortic aneurysm (arrow] 



the endoleak i/ii'tv black arrow) with 
:!. b The wire is passed through the hole 



I' 1 . Vaiemi and 1. ijolzarian 




a-i. Ty:i I'.', endo!ea^ diic to :m"o:v.p!e:e sea! :U the iuiKLon 

i component?, a Angiogram from left groin demonstrates a type 

1 11 end o leak i white a><ow\ ,1 n: a lumbal' artery : bl.;<:k -.uiew). b Palnuz 
s ; e : : ". placement inflated :c 1 2 mm. c Control angiogram shows no more 
-.aK'KiL 




Eniik'JeA: 1 'etiiiiiioij, I > j;igjjOSj-=, and Man.; seiner 



dictive values CPUS as compared to helical CT were 
respectively 77%, 90%, 85%, and 85% [26]. 

Administration of an ultrasound contrast agent 
can increase the sensitivity for detecting endoleaks 
with color and power Doppler by 33%-300%; how- 
ever, the specificity may decrease by 17% to 30% 
[27-31]. Utilizing an ultrasound contrast agent may 
also enable detection of endoleaks that are not seen 
by CT angiography [30, 31]. 



14.3.3 

Magnetic Resonance Imaging (MRI) 

MRI and MR angiography can provide all the infor- 
mation during EVAR follow-up for Nitinol based 
stentgrafts. As to detection of endoleaks, results are 
comparable to CT angiography for detecting type I 
and type III endoleaks. Depending on the CT section 
thickness and imaging protocol, MR angiography 
may yield a greater sensitivity to detect slow flow 
type II endoleaks [32-35]. Blood pool magnetic reso- 
na nee angiographv has been i on ik! nsetn I in detecting 
small endoleaks. A study of six patients after EVAR 
using Ferumoxytol, a blood pool agent, showed four 
low flow endoleaks that were not detected by CT. 
Most importantly these patients also demonstrated 
no reduction in endograft size after EVAR [36]. Con- 
trast enhanced MRA (CEMRA) with time-resolved 
(TR) technique provides dynamic angiographic 
information - similar to conventional angiography. 
TR-CEMRA affords a more comprehensive evalua- 
tion than standard MR angiography. The source and 
flow direction of endoleaks can be depicted, improv- 
ing the characterization of the inflow and potential 
outflow of endoleaks. As this information impacts 
decision making for appropriate management, with 
advances in parallel imaging to reduce MR scan 
time, TR-CEMRA may become the routine method 
forpost-EVAR MR angiography [37]. Phase contrast 
imaging can be applied to demonstrate endoleak 
direction and quantify flow and velocity [38]. 

Although all these non-invasive techniques are 
reliable to demonstrate an endoleak, the characteri- 
zation and the type of endoleak can still be difficult. 



14.3.4 
Angiography 



Digital subtraction angiography (DSA) r< 

gold standard for characterization of the endoleaks 

and their endovascular treatment. 



Angiographic examination should include a 
global pigtail injection of the aorta at the level of 
renal arteries and inside the stentgraft. A flush cath- 
eter is placed just above the proximal attachment 
site. A power injector is used to achieve an adequate 
flow rate, (10-15 ml/s for 2 s). Next, the catheter is 
withdrawn within the graft (to a level just above the 
flow divider in a bifurcated device}. Frontal and/or 
bilateral oblique views are obtained, to search for 
distal type I and type III leaks. For these images the 
flow injection rate is decreased to 5-10 ml/s, to avoid 
reflux up to the level of the proximal attachment 
site, which could confuse the interpretation. Finally, 
selective arteriogram of the superior mesenteric 
artery (SMA) and both internal iliac arteries should 
be obtained, to hunt for type II leaks. On all the 
acquisitions it is important to carry the imaging 
out into the venous phase (i.e. 20-30 s) to search for 
slowly filling type II leaks. Images are acquired at 
2-3 frames/s for the first 10 s, after this the frame 
rate can be lowered to 1.0-1.5 frames/s. 

In case of type I endoleak, the origin of the sac 
is catheterized by placing the catheter between the 
stentgraft and aortic wall and intra-aneurysmal 
injection is performed for optimal evaluation of the 
outflow vessels. 



14.4 

Treatment of Endoleak 



There is a consensus that type I and III leaks should 
be treated on a relatively urgent basis. There is 
still debate regarding the treatment of stable type 
II leaks. Multiple algorithms are proposed for the 
treatment of the endoleaks (Table 14.2). In this chap- 
ter, we will discuss the treatment options for each 
type of endoleak separately. 



Table 14.2. Treatment algorithm 

Endoleak 



Type li ] ( Type III 
' 1 f Treat 



I' 1 . V';i>:m ;'.:1l1 1. GolziiiLill 



14.4.1 

Type I Endoleak 

Multiple modalities are available for the treatment 
of type I endoleak (Table 14.3). The choice of the 
optimal treatment is based on the source of the leak. 
Our policy in this matter is to use the least 
yet the most durable treatment. 



14.4.1.1 

Type IA Endoleak 

Placement of a proximal cuttor extension endograft 
is the most commonly used treatment in case of 
proximal endoleak associated with malpositioning, 
angulated neck or migration. This technique needs 
a new cut down and is not always feasible due to dif- 
ferent anatomical ami technical challenges. 

In case of proximal endoleak associated with an 
irregular neck with no migration, simple balloon 
angioplasty with large balloons (25-30 mm) or large 
Palmaz stent placement could be sufficient to apply 
the stentgraft to the aortic wall. This procedure can 
be performed under local anesthesia using along 12- 
F sheath that can allow the passage of a large Palmaz 
stent (Fig. 14.1). 

Embolization and coiling of the aneurysmal sac 
and the outflow vessels has been proposed as an 
alternative treatment for type I endoleak in selected 
patients [4, 39-42]. Historically, this technique was 
used when proximal extension cuffs were not avail- 
able. With current devices, proper size cuffs are 
generally always available. The majority of patients 
treated with this technique had extensive medical 
co-morbidities and short or highly angulated proxi- 
mal neck. Although there have been concerns about 
the long-term efficacy of this technique, the results 
seem to be encouraging. Gorich et al. [40] have suc- 
cessfully treated 13 patients with embolization (mean 
follow-up: 6.8 months). Sheehan et al. [41] have 
reported a high clinical success rate in nine patients 
with type I endoleak treated just by coil emboliza- 
tion with a mean follow-up of 24 months. We have 
treated 32 patients with type I endoleak from 1996 
to 2003. The majority of the patients received a Cor- 
vita stentgraft (ji, 28), two Talent endografts and two 
AneuRx. All patients were considered high risk for 
surgery. Embolization was successful in 29 patients 
with the occlusion of the outflow vessels and the 
aortic channel and/or sac. Three patients with large 
neck had persistent endoleak after several proce- 
dures. Six patients were lost to follow-up. Among 



Table H.3. Treatment of persistent type : 

Extension stentgraft or cuff 

Balloon angioplasty 

Bare stent 

Embohzittion 

S.itgicii] l"i 



the remaining 26 patients, four died of cardiac dis- 
ease between 7 to 90 days after the procedure. In all, 
22 patients could be followed with a mean follow- 
up of 38.6 months. The aneurysm shrank in 15 
patients and remained stable in five and increased 
in two patients with persistent endoleak. None of 
the patients with successful embolization has devel- 
oped a new endoleak or an aneurysmal expansion 
(Fig. 14.2). This study confirms that upon achieve- 
ment of thrombosis, embolization of the outflow 
vessels and the sac can be associated with long-term 
clinical success and freedom from endoleak. 

14.4.1.1.1 

Technique of Embolization 

The key to success for type I endoleak is to disrupt 
the communications between the inflow and out- 
flow vessels involved in the leak. Careful review of 
contrast enhanced CT scans will be helpful prior to 
the procedure, to select the best vascular access site 
(femoral or brachial). An aortogram is performed to 
more precisely define the entry site of the endoleak. 
Thereafter, the aneurysmal sac is selectively cath- 
eterised using either a 5-F multipurpose catheter or 
a 5-F cobra catheter by brachial or femoral access. 
In some situations a Side-winder II reverse curve 
catheter can be used. An intra-sac angiogram is then 
performed to better evaluate the outflow vessels. A 
selective occlusion of the outflow vessels is then per- 
formed (Fig. 14.2). If catheterization of the outflow 
vessels is difficult to achieve, coils can be placed in 
front of their origin. After outflow vessel emboliza- 
tion, the aneurysmal pouch and/or the leak channel 
are filled with additional segments of coil. Other 
embolic materials such as gelatin sponge fragments 
or thrombin can be used to induce the thrombosis, 
after extensive coil embolization of the channel or 
the sac and the collaterals. These agents may escape 
into the aorta more easily than coils during their 
injection and so should be infused with caution. 
The embolization endpoint Is stasis within the sac 
or non-visualization of the endoleak on final aor- 



r, ii ,■.'■■ :<?.;*: ] ■crr.iiiv::, I ■■.:.&::■:.'■.!■-, J MjiLiCjinei:; 



14.4.1.2 

Type IB Endoleak 

All treatment options for the type IA endoleaks are 
valid for distal endoleak. Incase of short landing or 
enlarged iliac artery, an extension endo-graft will be 
necessary. However most of type IB endoleaks can 
be treated with balloon angioplasty or bare stent 
implantation allowing the sealing of the stentgraft 
to the aortic wall. If the origin of internal iliac artery 
needs to be covered, it should be embolized to pre- 
vent from retrograde leak. 

Embolization of the sac or the channel, although 
feasible, is usually not indicated in type I-B 
endoleak. 



'nidus' of the lesion [43]. There are usually multiple 
inflow and outflow vessels. These vessels communi- 
cate most of the time through a channel. The chan- 
nel is different from the endoleak sac that is gener- 
ally seen during the angiogram and punctured in 
translumbar embolization. To achieve a successful 
embolization, the inflow vessels, the channel and/ 
or the sac need to be embolized (Fig. 14.3). Like in 
embolization of type I endoleak, the key is to disrupt 
the communications between the vessels involved 
in the leak. 



14.4.2.1 

Transarterial Approach 



14.4.1.3 

TypeIC Endoleak 

TypeIC leaks occur in cases where an aorto-uni-iliac 
stentgraft has been deployed, in conjunction with a 
femoral-femoral bypass graft. An occluder device 
is then placed in the contra- lateral common iliac 
artery. Its function is to prevent back filling of the 
aneurysm from the excluded common iliac artery. 
The treatment of these leaks requires completion of 
the intended thrombosis of the common iliac artery. 
Embolization is the simplest way to complete this, 
either by passing the occluder and embolizing cra- 
nial to it, or, by placing a second occluder device 
caudal to Nie original device. 

The occlusion of the iliac artery is usually sulti- 
cient to treat the leak. However, in cases of long-term 
type IC endoleak, many outflow vessels may have 
developed and the leak may communicate with mul- 
tiple lumbar arteries and the IMA. These enlarged 
vessels might be source of late type II endoleak. 
Thus, we usually embolize both the outflow vessels 
and the sac before occluding the iliac artery. Another 
attractive technique to achieve the occlusion of the 
common iliac artery is to perform an endovascular 
internal to external iliac artery bypass using stent- 
graft. This technique can allow the exclusion of the 
c preserving the internal iliac artery. 



14.4.2 

Type II Endoleak 

Persistent type II endoleaks usually have a complex 
architecture. They have been compared to the arte- 
i malformation with the sac forming the 



A 5-F Cobra 2 catheter (0.038") is placed in the SMA. 
Once the diagnostic catheter is stable in the proximal 
SMA, amicrocaiheter is advanced to the IMA via the 
Arc of Riolan. It is prudent to inject 5000 units of 
heparin prior to attempting the cannulation of the 
Arc of Riolan. Sim i la ily, vasodilators (Nitroglycerin, 
100-200 um) may be helpful to prevent spasm. 

In some situations, the sac can be accessed from 
internal iliac artery through iliolumbar and lumbar 
arteries. 

Regardless of the route chosen, the most impor- 
tant task is to access the channel or the sac. It is 
critical to disrupt the network between the involved 
vessels. This is more important than occluding 
any one vessel or even embolizing the endoleak 
sac (Figs. 14.3, 14.4). This explains the high rate of 
recurrence a tier I VI A emboli, '.alien alone (Fig. I4.tj 
compared to translumbar embolization for type II 
endoleak in one report [44]. 

There are many choices regarding eiiibolk agent. 
Permanent agents, such as coils are preferred. When 
using coils the origins of all involved vessels are 
cannulated and embolized. However, getting into 
lumbar artery origins may be very challenging. In 
practice coils are deposited as close as possible to 
the origins of the involved vessels (coils of 2-3 mm 
diameter, 2-3 cm long). Once branch vessels are iso- 
lated then large coils can be used to fill the channel 
and/or the aneurysmal sac. Inmost situations, if the 
channel between the inflow and outflow vessels is 
interrupted, the sac does not need to be embolized. 
Thus, in case of complex type II endoleak, the fill- 
ing of the endoleak cavity by translumbar approach, 
without treating the inflow or outflow channels. 
Some authors support the use of either a 5- to 10- 
ml solution of Gelfoam slurry, or a similar volume 
of saline mixed with 500-1000 units of thrombin. 



Alternatively the coils can be soaked in a solution 
with a high thrombin concentration (20,000 units of 
thrombin in 20 ml of saline). The origin of the IMA 
has to be embolized with several coils adapted to its 

diameter. 



14.4.2.2 

Translumbar Approach 

Previous experience with translumbar puncture of 
the aorta for diagnostic angiography showed that 
this puncture carries only minor risks, with a ret- 
roperitoneal hematoma rate of about 3% [45]. The 
aorta can be punctured under CT or fluoroscopic 

Careful correlation with prior CT images will 
help plan the puncture in relation to the markers on 
the stent graft. Ideally the left side access is used to 
avoid IVC. However, if necessary the puncture can 
be done through the IVC. When performed under 
fluoroscopic guidance it is useful to frequently rotate 
the X-ray tube from the AP to the lateral projection, 
and in between, to help in assessing the needle track, 
and to avoid puncturing the stentgraft. 

The translumbar puncture site is typically 8- 
10 cm from the midline. The access needle is angled 
at about 45°-60° anteromedially, aimed so as to pass 
just anterior to the vertebral body, avoiding the adja- 
cent transverse process. As described for traditional 
translumbar aortography, it may be useful to actu- 
ally aim for the vertebral body, then after bony con- 
tact, pull back 1 or 2 cm and aim more ventrally. 

(.■siiis; CI guidance the initial needle tip place- 
ment will be into the leak sac (Fig. 14.3). However, 
with fluoroscopic guidance and a relatively small 
leak, the initial puncture may end up in thrombus. 
In these cases, the leak sac can usually be found fairly 
easily using a hydrophilic guidewire and catheter. 

Onceintheangio-suite a proper angiogram of the 
sac is performed. Pressure measurements should be 
obtained within the sac. The measurement will show 
generally a systemic pressure. Coil embolization is 
then performed as for the arterial approach. 



14.4.2.3 

Other Embolic Materials 

The use of several other agents has been reported 
with translumbar treatment of type II endoleaks, 
including Onyx, Ethibloc, thrombin, and Cyanoacr- 
ylate [46-50]. 



There are multiple reports of the use of thrombin 
in the percutaneous, translumbar embolization of 
type II leaks. Most authors report the use of 500- 
1500 units of thrombin [49]. The only reported seri- 
ous complication occurred in a case where 8000 units 
were injected [50]. The complication was ischemic 
colitis in the recto-sigmoid region; the IMA was 
patent in this case. Despite the complication, the 
procedure was successful in sealing the endoleak. 

Onyx, (Micro Therapeutics, Irvine, Ca), is a bio- 
compatible liquid embolic agent. It is an ethylene 
vinylalcohol copolymer dissolved in various concen- 
trations of dimethyl sulfoxide (DMSO). Micronized 
tantalum powder is added to the solvent/polymer 
mixture at the time of production for radiopacity. 
When this mixture contacts aqueous media, such as 
blood, the DMSO rapidly diffuses away, with result- 
ing in situ precipitation and solidification of the pol- 
ymer. It forms a soft elastic embolus without adhe- 
sion to the vascular wall [51]. The polymerization 
process is time dependent and is mainly influenced 
by the amount of ethylene in the mixture; with less 
ethylene the polymer becomes softer. Onyx is avail- 
able in several different concentrations; the higher 
concentration is more viscous. Using a higher con- 
centration makes it easier to prevent the liquid from 
getting too far from the catheter tip. Since the poly- 
mer will solidity on contact with aqueous media the 
delivery catheter must be pre-flushed with DMSO. 
The embolization endpoint is stasis within the sac. 
A 'DMSO-compatible' catheter is required; DMSO 
will degrade most currently available catheters. 
Onyx is non-adhesive, allowing for easy removal of 
the delivery catheter, and of the polymer itself if the 
stentgraft is ever explanted.lt is quite expensive. The 
reported success rate is high [46], and the results are 
durable (personal communication}. 

Ethibloc (Ethnor Laboratories/Ethicon Inc., Nor- 
derstedt, Germany) is a cornstarch product which 
polymerizes on contact with ionic fluids; it develops 
a consistency similar to chewing gum, and subse- 
quently hardens further. It is an emulsion of zein (a 
water-insolubleprolamine derived from corn gluten), 
alcohol, poppy seed oil, propylene glycol and a con- 
trast medium. It can be mixed with Lipiodol (Labo- 
ratoireGuerbet, Paris, France) to allow for improved 
visualization. Pump flushing through a three-way 
stopcock can emulsify the mixture; 10ml of Ethi- 
bloc are mixed with 0.5 ml of Lipiodol. This mix- 
ture does not dissolve catheters. The system must be 
primed with a non-ionic fluid, such as 50% glucose 
to prevent solidification in the delivery device. The 
embolization endpoint is stasis of the injected sub- 



Endoleak: 1 'eh nil ion, I > j;igjjOSj-=, and Man.; gem er 



st be rapidly 
i prevent the 
. TL needles, 
ly, 



stance. It is important to slowly retract the delivery 
device while injecting the mixture. 

NBCA (Trufill n-BCA, Cordis Neurovascular) is 
liquid glue. The manufacturer provides three com- 
ponents in the kit; NBCA monomer, (a free-flow- 
ing clear liquid), ethiodol and tantalum powder (to 
increase the rad io-density of the glue). Polycarbonate 
syringes should not be used, only polyethylene or 
polypropylene are recommended by the manufac- 
turer. NBCA polymerizes rapidly on contact with 
ionic fluids. The injection catheter i 
removed from the embolization site 
catheter itself from being glued in pi; 
even if adherent to the glue, can be i 
The volume of NBCA to be injected is determined 
by test injections of contrast; the volume should be 
sufficient to completely fill the aneurysm sac and to 
initiate reflux into the involved lumbar arteries. The 
spinal artery must be avoided, if visualized it should 
be protected with a coil. The reported success rate is 
very high, with durable results [52]. 

Surgical ligation of all relevant branches is a pos- 
sible solution for type II leaks. However experience 
has shown that there are often more vessels involved 
in these lesion 1 ; than is imt Lilly suspected: and unless 
they are all clipped the surgical route approach risks 
failure or recurrence. Ligation can be accomplished 
by laparoscopic or open technique. 



14.4.3 

Type III Endoleak 

Angiography can confirm type III endoleak after 
placement of the pigtail catheter in the stent graft, 
just above the flow divider. If the cause is a sepa- 
ration of modular components there may be some 
difficulty in establishing guidewire access from one 
component to the next, but once this is accomplished 
deployment of a new extension is generally problem 
free. In some situations a new stentgraft needs to 
be implanted. When the leak is related to incom- 
plete circumferential seal of different components, 
angioplasty or bare stent implantation can seal the 
leak (Fig. 14.6). In case of fabric tear, re-implanta- 
tion of a new stentgraft or open conversion can be 
considered. 

Embolization is almost never indicated in type III 



14.4.4 

Type V Endoleak - Endotension 

There have been several reports of confirmed sys- 
temic pressurization within enlarging aneurysm 
sacs, despite the absence of visualized endoleak 
[12-16, 50]. Cases of sac enlargement and rupture 
have been recently reported even after treatment of 
AAA with open surgery. In one report, laparotomy 
demonstrated a seroma containing firm rubbery 
gelatinous materials [53]. Aortic puncture to ana- 
lyze and empty the accumulated fluid is one way to 
treat this type of endoleak. However, the fluid often 
re-accumulates during follow-up. If the endotension 
is related to serous fluid accumulation, there is no 
need for a surgical treatment even in case of rupture 
[53]. Other treatment options include retroperito- 
neal drainage of the fluid, explanation of the graft 
with open surgery or insertion of a new stentgraft 
to reduce the porosity. 



14.5 
Conclusion 

It seems certain that EVAR will continue to be a 
primary treatment for many years. Endoleak is an 
ongoing problem associated with EVAR. Imaging 
plays a critical role in detecting endoleak. CTA is 
the first line diagnostic modality. Optimal CTA pro- 
tocol needs to include a delayed acquisition. There 
are many endovascular options available for treat- 
ment of persistent endoleaks. The optimal treatment 
depends on the type of the endoleak. 



1. Cuypers P, Buth J, Harris PL, et al ( 1 99^ j Realistic expec.ta - 
tions for patients will; sie:'.:- graft treatment of abdominal 
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14. Gilling-Smith GL, Martin J, Sudhindran S, et al (2000) 
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19. Golzarian J.Dussaussois L, Abada HT, et al (1993) Helical 
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20. Rosenblit AM, Patlas M, Rosenbaum AT, et al (2003) Detec- 
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21. Sawhney R, Kerlen RK, Wall SD et al (2001) Analysis of 
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22. ElkouriS,Panneton|M, Andrews ICetal (2004) Computed 
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23. Wolf YG, Johnson BL, Hill BB, et al (2000) Duplex ultr 
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after endoluminal 



inal aortic aneurysm repai: 

24.Zannetti S, De Rango P, Parente 
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25. Pages, S, Favre JP, Cerisier A, et al (2001 ) Comparison of 
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26. Golzarian J, Murgo S, Dussaussois L, et al (2002) Evalu- 
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27.McWilliams RG, Martin J, White D, et al (2002) Detection 
of endrkeak with en Iran ecu ukra sound imaging: compari- 
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9:170-179 

23.McLafferty RB, McCrary BS, Mattos MA, et al (2002) 
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29. Raman KG, Missing-Carroll N, Richardson T, et al (2003) 
Co lor- flow duplex ultrasound scan versus comp tiled tom- 
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30.Bendick PJ, Bove PG, Long GW, et al (2003) Efficacy of 
ultrasound scan contrast agents in the noninvasive follow- 
up of aortic stent grafts. J Vase Surg 37:381-385 

31.Napoli V, Bargellim I, Sardella SG, et al (2004) Abdomi- 
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225 

32.Haulon S, Lions C, McFadden EP, Koussa M, etal(1998) 
Prospective evaluation of magnetic resonance imaging 
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33. Ayuso JR, de Caralt TM, Pages M, Riambau V, et al (2004) 
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repair of aortic aneurysms with ni thiol endoprostheses. J 
Magn Reson Imaging 20:803-810 

34.CejnaM, LoeweC, SchoderM, et al (2002) MR angiogra- 
phy vs CT angiography in die foliovv-up of Xiuno. stem 
gratis ;;'. ike endoitiminaliv i rented aortic aneurysms. Eur 
Radiology 12:2443-2450 

35.Lutz AM, Willmann JK, Pfammatter T, Lachat M (2003) 
Evaluation of aortoiliac aneurysm before endovascular 
repair: comparison of contrast-en'ianceo magnetic reso- 
nance angiography wit;; multidetector row computed 
lomegrapuic angiography uilh an automated analvsis 
software tool.] Vase Surg 37:619-627 

36. Ersoy H, Jacobs P, Kent KK, Prince MR (2004) Blood pool 
MR angiography of aortic stentgraft endoleak. AJR Am J 
Roentgenol 182:1181-1186 

37.Lookstein RA, Goldman J, Pukin L, Marin ML (2004) 
Time-resolved magnetic resonance angiography as a 
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38. Hellinger JC, Draney M.Markl M.Pelc N], et al (2003) Appli- 



!-_n; ; .ele.u-.: 1 'eliniiion, I iiagnosis, and KLi iu aejnejji 



cation of cine phase conlrasl magnelic resonance i ringing 
and SkA.YlM-'.agging for assessment of endo[eaks and 
aneurysm sac motion. Radiology 229:SS573, (Abstract) 
9.Amesur NB, Zajko AB, Orons PD, Makaroun MS (1999) 
Hmbokofinapy of pc-rs=:ste:ii endoleaks .i ]"tei enoO'Vascu- 
lar repair ofabdoniin.il aortic aneurysm with the ancure- 
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Hadiol 10:1175-82 

Gorich J, Rilinger N, Sokiranski R et al (2000) Treatment 
o: leaks after endovascula: repair o: aortic aneurysms. 
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Faries PL, Cadot H, Agarwal G et al (2003) Management of 
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47. Schmid R, Gurke L, Aschwa \\:,i:\\ M . et .'.! ! 2002) CT-guided 
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48. van den Berg JC, Nolthenius RP, Casparie JW et al (2001 ) 
CT-guideo thrombin injection into aneurysm sac in a 
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aortic aneurysm repair. AIR Am ■ Roen:genol 175:1 649- 
1651 

49. Ellis PK, Kennedy PT, Collins A], Blair PH (2003) The use 
of direct thrombin injection to tre.it a Type '.'. endoleak 
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SO.Gambaro E, Abou-Zamzam AM Jr, Teruya TH et al 
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injection for treatment of endoleak. Ann Vase Surg 
13:74-78 

51.Numan F, Omeroglu A, Kara B, Cantasdemir M, Adaletli 
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(Onyx). J Vase Interv Radiol 1 5:939-946 

52. Steinmetz E, Rubin BG, Sanchez LA, et al (2004) Type II 
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53.Thoo CHC, Bourke BM, May J (2004) Symptomatic sac 
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Endotension. J Vase Surg 40:1089-1094 



15 Internal Iliac Artery Embolization in the Stent-Craft 
Treatment of Aortoiliac Aneurysms 



i.l Introduction 253 

.1 H:"?o!ii;r.ii ■:'. ■'■[" ".hi; Liit^/na] I.kk" Ar.eiv J: 7 .' 

i.2.1 Technical Considerations 253 

: .2.1.1 Sequential vs Skr.uJMn^'.uis r!:'.".'."ii|i>\!:i:in of 1 1 As 255 

i.2.2 Complications 255 

i.2.2.1 Buttock Claudication 256 

•2.2.2 Sexual Dysfunction 256 

■2.2.3 Colon Ischemia 256 

■.2.2.4 Perinea! Ischemia/Necrosis 257 

■.2.2.5 Lumbosacral Plexus Ischemia 257 

i.2,3 Prevention 257 

■.2.4 Conclusion 25S 
References 25S 



embolization of previously patent vessel where no 
collateral supply has been established. Review of 
the surgical literature indicates that the claudica- 
tion of the buttocks and sexual dysfunction are the 
two most common symptoms. More serious but less 
commonly observed findings include bowel isch- 
emia/necrosis [5-8], lumbosacral plexopathy [8-11], 
bladder or rectal sphincter dysfunction [8], and but- 
tock or perineal necrosis in susceptible individuals 
[8, 11]. These complications have also been reported 
after IIA embolization associated with EVAR and 
will be further examined in this chapter. 



15.1 
Introduction 

Endoluminal placement of stent-grafts for the repair 
of aortoiliac aneurysmal disease is an accepted 
alternative to open surgical repair. According to 
various reports, approximately 25'-'b-50% of these 
patients will develop endoleak. The incidence of 
endoleak varies according to the patient's anatomy, 
device used, and method of post procedural surveil- 
lance. As described elsewhere in this book, the most 
common endoleak is type II. To reduce the risks of 
both type I and II endoleaks, occasionally it is nec- 
essary to embolize the internal iliac artery (IIA) to 
prevent retrograde flow into the aneurysm. Studies 
suggest that between 24 '',(> and 45 L1 o of patients under- 
going endovascular aortoiliac aneurysm repair of 
(EVAR) will need IIA embolization [1-4]. Although 
the utility of tin 1 , approach has been questioned [■■!], 
IIA embolization remains a common practice. 

Loss or reduction of flow in II As is not completely 
benign and can be associated with various clinical 
symptoms. These are more likely to occur in the 
setting of acute IIA occlusion such as intentional 

M.K. Razavi.MD 

Director, Center for Research and Clinical Trials, St. Joseph 

VviSiiilai' Institute, urjnge, CA ;, 2868, USA 



Embolization of the Internal Iliac Artery 

As mentioned above, statu sot the internal iliac arteries 
is an important anatomic consideration in the treat- 
ment of aortoiliac aneurysms. Indications for emboli- 
zation of IIA in association with EVAR include aneu- 
rysm of the IIA or ec tat ic or aneurysmal common iliac 
artery (CIA) involving the origin of IIA. Additionally, 
extension of stent- graft into the external iliac artery 
(EI A) may become necessary if the CIA is judged to be 
too short for adequate or safe anchoring of the device 
or if there is a distal type-I endoleak. This will lead to 
loss of antegrade flow in the IIA. 

Occasionally, communications between branches 
of an uninvolved IIA and distal lumbar arteries can 
create type-II endoleaks (Fig. 15.1). This can be a 
more technically challenging situation and embo- 
lization of the distal branches should be attempted 
only if growth of the aneurysm sac has been docu- 
mented (see Sect. 15.2.1). 



15.2.1 

Technical Considerations 



al rule, the most pro: 
nt(s) of IIA is emboliz 



V. K.R.;z;iv: 




Fig. I.'.l.a ■ \--:';fLiS!-ei]:'.i"i:'.ivd CT 'jf abdomen shoiv^ ;,;■>. abdominal ac:;k" .■:\^:-iy<m wj:ji pa trill Jumbai Li : '. J airenor 
lu irrsrs. Pa lien; developed ,1 iype '.'. ei'doleak ai'.e: encoer.-:! plL^'emejji. I> Non-o.nti ;'-i CI -lion- flue ^ ll l h ■.: ■ k z ^ ■ ■ 
lumbar arteries and the sli: through a b:an:li at die internal iliac ariery 



vent retrogr 
Attempts sh 



de flow into the aneurysm (Fig. 15.2). 
uld be made not to interrupt the corn- 
between the anterior and posterior 
trunks of the IIA when possible. This practice has 
been observed to reduce the complications associ- 
ated with IIA embolization [12, 13]. 

In the setting of EVAR, coils are the embolic 
agents of choice. Particle or liquid agents may flow 
into the distal branches of IIA and cause serious 
complications such as perineal necrosis or isch- 
emic radiculopathy. It has been suggested that com- 
plete cessation of antegrade flow in the target IIA 
during embolization is not necessary to prevent 
late endoleaks [12, 14]. Heye et al. embolized 53 
IIAs in 45 patients prior to EVAR [14]. In 30 of these 
patients, antegrade flow was still present at the end 
of the embolization procedure. No significant dif- 
ference was observed in the rate of type-II endoleaks 
among those patients who had complete versus par- 
tial embolization of the IIA. Similarly, Cynamon et 
al. observed only one retrograde leak among the 13 
patients with incomplete embolization ol IIAs [II]. 
While complete stasis of flow in the IIA may not be 
necessary, coil embolization should slow the flow 
sufficiently to cause thrombosis of the vessel after 
the deployment of the stent-graft. Obtaining access 
into the IIA after covering its origin may prove dif- 
ficult if a type-II leak develops. 

To achieve safe embolization, it is important to 
use accurately sized coils. Selection of a coil too 
small for the intended artery leads to its distal 
migration and occlusion of the non-target distal 
branches. Conversely, proximal dislodgement can 
occur in a short target area during the delivery 



and/or too long, 
inpatients with 



patent proxirr. 
or lateral sacr 
extended pro? 
risk of proxir. 



1 that is either too large 
maybe encounterec 

IIA branches such as iliolumbai 
arteries in which coils need to be 
nal to their origin. To reduce the 
coildislodgment, a coaxial system 
can be employed for better control over the deliv- 
ery. Use of detachable coils can also reduce the risk 
of coil misplacement when accurate deposition is 

Occasionally, communications between various 
branches of the IIA and the lumbar arteries may 
cause retrograde flow into the sac of an aortic aneu- 
rysm creating a type-II encloleak. Microcatheter tra- 
versal of the entire length of these communications 
may not always be possible. Under such circum- 
stances, liquid embolic agents have been employed 
to occlude the feeder arteries. As mentioned above, 
this practice may cause ischemic radiculopathy if the 
targeted vessels are either lateral sacral or iliolum- 
bar arteries. It may be more prudent to coil embo- 
lize these arteries and use alternative approaches to 
deal with the possible residual type-II endoleak (see 
Chap. 14). 

Manipulation of bulky devices in tortuous iliac 
the presence of atherosclerotic plaques or 
: of mural thrombus increases the risk of 
atherothrombotic embolization into the IIA or lower 
extremity circulations. Atherothrombotic macro or 
micro-embolization into the IIA may cause serious 
complications such as bladder, buttock, or colon 
infarction (see Sect. 15.2.2). Care must be taken to 
manipulation during EVAR or 
embolization of the IIAs. 



n the 5te;:t-Gr.il"[ Tre.itjn 




Fig. l.".'a-c. I- ";?.:■. iz;i:io:i of '.'.A berore .1 ■.:■ r I l o ?;ent 
graft impliintiition (courtesy of Dr Luc Stockx). a 

iliac angiogram Jemoiisir.iiing the internal 
and external iliac arteries. b.c Coil embolization of the 
proximal 1 1 A. Note the extension of the ai 
level of ili.'.c L"' i j'li i l." n i i i. ■ :"■. 



15.2.1.1 
Sequential \ 



■ Simultaneous Embolization of MAs 



Loss of flow in bilateral IIAs has been correlated 
with higher incidence of ischemic complications 
after EVAR [2, 15]. It has been suggested that a 
staged approach to IIA embolization may reduce 
the risks of developing symptoms [16]. This prac- 
tice would presumably allow for the development 
of collateral circulation prior to the interruption of 
flow in the contralateral IIA. Although this logic 
appears to make intuitive sense, Engelke and 
colleagues have made the opposite observation 
[17]. Among 16 patients who underwent bilateral 
IIA embolization, eight had simultaneous occlu- 



sion of IIAs and eight had sequential emboliza- 
tion. Patients with simultaneous embolization had 
a lower complication rate than those with staged 
embolization (12.5% vs 50%, respectively). Based 
on the available data, however, it is unclear if there 
are any advantages to staged versus simultaneous 
IIA embolization. 



15.2.2 

Complications 

The need to prevent endoleaks must be balanced 
against the necessity to preserve the blood supply 
to the pelvic structures. Although the majority of 



patients will remain asymptomatic after the loss of 
II A, maintenance of adequate pelvic blood flow has 
been a management problem in the open surgical 
treatment ot pal tents with AAA or aortoiliac disease. 
Occlusion of IIAs during or after such operations 
has been associated with rare but serious and often 
life-threatening complications such as spinal cord 
or lumbosacral plexus ischemia, buttock necrosis, 
or colorectal infarction [8-11]. Such complications 
have also been observed in the setting of EVAR and 
II A embolization (Table 15.1). These complications 
are discussed in more detail below. 



15.2.2.1 

Buttock Claudication 



This is the most common sequela of the reduction 
or loss of flow in the IIAs. The incidence varies 
from 10%-50% depending on the quality of col- 
lateral circulation, location of coil deposition and 
whether communications between anterior and 
posterior divisions of IIA have been interrupted. 
Review of the available literature on this issue sug- 
gests that those with embolization of bilateral IIAs 
have a higher chance of becoming symptomatic as 
compared with those who had unilateral emboliza- 
tion [2]. Despite this finding, status of the contra- 
lateral IIA at the time of unilateral embolization 
does not appear to affect the outcome [1], This con- 
clusion is consistent with the results of Iliopoulus 
et al. concluding that the branches of the ipsilateral 
external iliac and femoral arterial system provide 
a more significant collateral pathway than the con- 
tralateral IIA [18]. 

Cbudkationisa transient condition in the major- 
ity of these patients and tends to improve or resolve 
over time. Thigh and buttock claudication can last 
anywhere from a few weeks to few years. Resolu- 
tion occurs in 41%-77% of patients depending on 
the patients' level of activity and status of collateral 
circulation [1, 13, 19,20]. 



15.2.2.2 

Sexual Dysfunction 

Another common complication of the emboliza- 
tion of IIA is sexual dysfunction. In the surgical 
literature, interruption of flow in the IIAs bilater- 
ally has been shown to be associated with a higher 
rate of impotence as compared to the unilateral 
IIA [21-23]. This observation has also been made 



in patients undergoing endovascular treatment of 
AAA. Lin et al. in a prospective evaluation of penile 
brachial index (PBI) in 12 patients undergoing either 
unilateral (h=8) or bilateral (h=4) IIA embolization 
reported a significantly higher drop in PEI in those 
who had bilateral IIA occlusion [15]. Patients with 
unilateral IIA embolization experienced 13%±14% 
reduction in PBI (NS). Conversely, those with bilat- 
eral IIA occlusion had 39%±14% drop in their PBI 
(f<0.05). 

The reported incidence of sexual dysfunction 
varies between 2.5% to 36% after IIA flow interrup- 
tion (Table 15.1). The true risk of sexual dysfunc- 
tion may be higher than reported. The high rate of 
pre-existing sexual dysfunction among this patient 
population may mask the true incidence of this 
complication. Furthermore, the inherent inaccuracy 
of personal interviews and questionnaires in estab- 
lishing the diagnosis and causes of sexual dysfunc- 
tion introduces an unknown risk of error in results 
obtained in this fashion [24, 25]. 



15.2.2.3 
Colon Ischemia 

Ischemic colitis is a rare but serious complication 
after loss of flow in IIAs. Acute mesenteric ischemia 
develops in l%-3% of the patients undergoing sur- 
gery for AAA repair [7, 26]. The risk factors for the 
development of mesenteric ischemia in such patients 
include ruptured AAA and shock, prolonged operat- 
ing and cross-clamping times, and ligation of one or 
both IIAs [5, 7, 27]. It appears that the ligation or loss 
of the IMA does not significantly enhance the risk 
of colon ischemia in the presence of a normal SMA. 
This is due to the existence of collaterals between 
the two arteries. Prior bowel resection, however, 
may interrupt these collaterals and predispose the 
patient to the risk of complications. 

Colon ischemia has also been reported after IIA 
embolization [20, 28]. Karch et al. reported this 
complication in three of their 22 patients (14%) who 
had undergone IIA embolization [28]. All three 
patients had either accidental or intentional occlu- 
sion of bilateral IIAs during EVAR. The true risk of 
colon ischemia after IIA embolization, however, is 
difficult to quantify. This is due to the small number 
of reported cases and is likely to be substantially less 
than what was observed by Karch et al. and similar 
to that of the open surgical AAA repair. 

Although confounding risk factors for bowel 
ischemia such as significant blood loss, aortic 



Internal Iliac Artery Embokzi'.tion in I lie Steai-Gini'i Treatment of Aortoiliai 



Table 15.1. Summary of s" 
of .'.ortoiliac ;ine : .:rysa'.s 



idies reporting embolization of ir 



Au t ;'.!.'■■:' /yen 



Patients Un: Inter.;./ Percen:nge o: pnkems 
with IIA bilateral developing svmoioms 
emboliza- emboliza- „. .. , , : 



Razavi/2000 [I] 32 

Lee/2000 [19] 28 

Cynamo n/2000 [12] 32 

Chiado/2000 [3] 39 

Kakch/2000 [23] 22 

Yano/2001 [20] 103 

Wolpert/2001 [35] 18 

Mehta/2001 [36] 154 

Schoder/2001 [2] 55 

Lin/2002 [15] 12 



This refers : .c- the perceiiiage of p.Uienls vciUio-d prnor sex.;nl dysrti 
: Five of - 1 ' 1 mea .n tins smdv developed erectile dysfunction. 
AAA, Abdominal nor lie .inenrysas; IIA. inlemnl iliac aneurysm; NR, 



tuft 



o on- ien;s developed peri- 



1.5% Two pntie:v.s developed ischemic neuropathy 
etion who developed new symptoms. 
iot reported; S.v, symptoms. 



s-clamping, bowel retraction, and procedu 
jlatory instability are not typical features 



of 
endovascular approach, microembolization 
into the colonic vasculature can occur as a result 
of excessive endovascular manipulation causing 
bowel infarction. Dadian et al. [29] reported overt 
colon ischemia in eight (2.9%) of their patients after 
EVAR without IIA embolization. Pathologic exami- 
nation revealed evidence of atheroemboli in the 
colonic vasculature. Geraghty et al. made a simi- 
lar observation in four patients (1.7%) with bilat- 
erally patent IIAs [30]. These observations under- 
scores the importance of preservation of distal IIA 
flow when possible. 

We should emphasize, however, that the IMA 
exclusion or embolization in patients with SMA 
stenosis or prior partial colectomy where the collat- 
eral pathways between the IMA and SMA have been 
interrupted, is not advised [31]. 



15.2.2.4 

Perineal Ischemia/Nei 



Perineal skin necrosis is another rare complications 
olilA devascularizationand has been reported after 
IIA embolization [15]. This serious complication is 
associated more frequently with bilateral IIA occlu- 
sion. The major predisposing factor appears to be 
poor collateral circulation in chronically bed-ridden 
patients. 



15.2.2.5 

Lumbosacral Plexus Ischemia 

Embolization of the IIA or its branches (lumbosa- 
cral or lateral sacral arteries) may cause ischemia 
of the lumbosacral nerve roots. The pain associated 
with this condition resembles nerve root compres- 
sion and can be mistaken for buttock and thigh clau- 
dication. The pain and discomfort is usually more 
intense, lasts longer, and may be associated with 
ipsilateral weakness. This condition can be precipi- 
tated by unilateral IIA embolization and should be 
considered in patients with persistent symptoms. 



15.2.3 
Prevention 



Preventive measures such as surgical or endovas- 
cular revascularization of IIA may become neces- 
sary in patients who are at high risk of developing 
complications after IIA embolization (Table 15.2). 
Surgical bypass to IIA has been reported with good 
outcome in this setting [32]. Use of endografts with 
fenestrated iliac limbs is another alternative in such 
individuals. 

A patient's ability to tolerate IIA embolization 
maybe tested by temporary balloon occlusion of the 
target artery and measurement of the penile brachial 
index (PBI) pre and post IIA balloon occlusion. This 
can assess the risk of post procedure impotence. A 



V. K. Razav; 



1. Poor quantity or quality of collateral ciiviil.it ton 

a. > 70% Stenosis of the patent II A 

b. Diseased ips: lateral profunda or its superior bra 

c. Absent ipsilateral circumflex iliac 

d. Absence of a complete arc of Riolan 
J. Isolated iliac aneurysms 

3. Emnodzatioi; of bilateral I [As 

4. Embolization distal to the division of anterior and 
rior trunks of IIA 

5. Age > 75 years 

o. Atherothrontbotic enibolizjtLOii .1 n r j :~.g EVAK 



PBI of less than 0.7 may indicate vasculogenic impo- 
tence. Similarly, monitoring the superior rectal arte- 
rial signal using a transrectal Doppler probe during 
balloon occlusion of IIA will test the adequacy of 



of the signal 
may signal 
k of colonic 

rculation to 



mesenteric collaterals. Disappe; 
that does not reappear within 15 mil 
poor collateral circulation and a high r 
ischemia [33]. 

Another reliable measure of poor c 
colon is the direct quantification of r 
genation by a rectal probe [34]. A s 
rectal probe with an atraumatic tip i 
the rectum and oxygenation of the i 
sured. If the levels drop below a 
after balloon occlusion of the IIA, that patient is not 
a candidate for IIA embolization. 



15.2.4 
Conclusion 

Although the incidence of serious complications 
such as colonic, lumbosacral plexus, or buttock 
i low after IIA embolization, the inci- 
: of claudication and sexual dysfunction is 
enough to warrant preservation of the IIA cir- 
if possible. In final analysis, the decision 
whether to embolize an IIA or not should be weighed 
against the potential risks and benefits of the other 
therapeutic alternatives. The risk of development of 
such symptoms as claudication or sexual dysfunc- 
tion may outweigh the hazards of IIA r 
tion or aneurysm rupture and death if r. 






iiill disposable 7 ' 
s inserted into 

n critical level 8. 



: . Razavi M, DeGroot M.Olcott C, Sze l\ Kee 5. Semba C, Hake 
[vt irJOOOi Embolization ■.::' the internal iliac arterv in stent- 
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plications and outcome.] Vase Interv Radiol 11:561-566 

2.SchoderM, Zaunbauer L, Holzenbein T et al. (2001) Inter- 
na! iliac ai leiy emoojzotion before enci avascular repair of 
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cal results. Am J Roentgenol 177:599-605 

3.CriadoFJ, Wilson EP, Velazquez OC et al. (2000) Safety of 
■."■oil embolization of the interna! iliac artery in en.dovas- 
_" _r l.i i grafting of abdominal aortic aneurysms. I Vase Surg 
32:684-688 

4.Tefera G, turnipseed WD, Carr SC et al (2004) Is coil embo- 
lizaiion of hypogastric artery necessary during endovas- 
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18:143-146 

5-farvinen O, Laurikka J, Sisto T, Tarkka MR (1996) Intes- 
tinal ischemia following surgery for aorlo-iliac disrasr. 
A review of 502 consecutive aortic reconstructions. Vasa 
25:148-155 

6.PittalugaP, Batt M, Hassen-Khodja R, Declemy S, Le Bas P 
(ls!3Si !\evascular;zalion of internal iliac arteries cluiing 
aortoiliac surgery: a multicenter study. Ann Vase Surg 
12:537-543 

7.Bjorck M, Troeng T, Bergqvist D (1997) Risk factors for 
inlestiital isciraemia after aortoiliac surgery: a combined 
cohort and case-control study oi 2824 operations. Eur J 
Vase Endovasc Surg 13:531-539 

Iliopoulos JI, Howanitz PE, Pierce GE, Kueshkerian SM, 
Thomas JH, Hermreck AS (1987) The critical hypogastric 
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9. Gloviczki P, Cross SA, Stanson AW, Carmichael SW, Bower 
TC, Pairolero PC, Hallett )W, Jr, Toomey BJ, Cherry KJ Jr. 
(Is!9i) ischemic initiry to the spinal cord oi lumbosacral 
plrxtis a fir:' a or to- iliac reconstruction. Am J Surg 162:1 31 - 
136 

0. Hefty TR, Nelson KA, Hatch TR, Barry JM (1990) Acute 
lumbosacral olexopalhy in diabetic women after renal 
transplantation. J Urol 143:107-109 

l.Picone AL, Green RM, Ricotta JR, May AG, DeWeese ]A 
{i^Sm Spina! cord iscfiemia following operalions on the 
abdominal aorta. Vase Surg 3:94-103 

2.Cynamon J, Lerer D, Veith F et aL (2000) Hypogastric 
artery coil emrv.i/atioir prior to tiidoiuminal repaii ■ 
aneurysms and fistulas: buttock claudication, a ivcogmzed 
'."■ut possibly preventable complicatjon. I Vase Interv radio] 
11:543-545 

3. Kritpracha B, Pigott JP, Price CI et al. (2003) Distal internal 
iliac artery embolizalion: a procedure to avoid. I Vase Surg 
37:943-948 

4. Heye S, Nevelsteen A, Maleux G (2005) Internal iliac artery 
coil embolization in. lite prevention -oi potential type-2 
endoleak afl^r endovascuiar repair oi abdominal aortic 



Internal Iliac Artei'y imbolizal ion in I lie Siem-Grafi Treatment of Aortoiliac Aneurysm 



and iliac aneurysms: etfecl o: total occlusion versus resid- 
ual flow. I Vase Interv Radiol 16:235-239 

5. Lin PH, Bush RL, Chaikof EL et al. (2002) A prospective 
evaluation of hypogastric artery embolization in endovas- 
oular aortoiliac aneurysm repair. I Vase y.:rg 3i:i:s:j3-s.O:- 

6. Mehta M,Veith PJ, Darling RC et al. (2004) Effects of bilateral 
Irvpogaslrir erlerv inlerruplioii dur.ng entiovascular and 
open aortoiliac aneurysm repair, i Vase Surg 40:698-702 

7.Engelke C, Elford I.Morgan R A, Belli AM (2002) Internal 
iliac artery embolization w.i;-. bilateral occlusion before 
endervuscular aortoiliac aneurysm repair- clinical outcome 
of si m;: It;'. neons ;'.:id sequential intervention, j Vase Interv 
Radiol 13:667-676 

S.Iliopoulos JI, Herrareck AS, Thomas JH, Pierce GE (1989) 
Heniodvnamies ■.■]" the hypogastric arterial circulation. I 
Vase Surg 9:637-641; discussion 641 -642 

9. Lee CW, Kaufman JA, Fan CM et al. (2000) Clinical outcome 
of internal iliac artery occlusions during endovaseular 
treatment of aortoiliac aneurysmal diseases, i Vase Interv 
Radiol 11:543-545 

0. Yano OJ, Morrissey N, Eisen L et al. (2001 ) Intentional inter- 
na' iliac artery occlusion lo facilitate endovaseular repair 
□f aortoiliac aneurysms, j Vase Surg 34:204-211 

I.Burns JR, Houttuin E, Gregory JG, Hawatmeh IS, Sullivan 
TR (1979) Vascular-induced erectile impotence in renal 
transplant recipients. J Urol 121:721-723 

2.Gittes RE, Waters WB (1979) Sexual impotence: the over- 
looked complication of a second renal transplant. ) Urol 
121:719-720 

3. Billet A, Davis A.Linhardt GE Jr. Queral LA, Dagher FJ, Wil- 
liams GM (1984) The effects of bilateral renal transplanta- 
tion oil pelvic hemodynamics and sexual function.. Surgery. 
95:415-419 

4. Brannen GE, Peters TG, Hambidge KM, Kumpe DA, Kemp- 
czinski RF, Schroter GP, Weil R (1980) Impotence after 
kidney transplantation. Urology 15:138-146 

:■. Levy N"h ( ] '"<7.vi Sexua. adjustment io maintenance hemo- 
dialysis and renal Iransplantation: national survev by ques- 
tionnaire: oreli miliary rep 1 :-::. Trans Am Six Arrit intern 
Organs 19:138-143 



26. Brewster DC, Franklin DP, Cambria RP, Darling RC, Mon- 
cure AC, Lamuraglia GM, Stone WM, Abbott WM (1991) 
Intestinal ischemia complicating abdominal aortic surgery. 
Surgery 1 09:447-454 

27. Kim MW, Hundahl SA, Dang CR, McNamara I), Straehley 
CJ, Whelan TJ Jr. (1983) Ischemic colitis after aortic aneu- 
rysm ectomy. Ant I Surg 145:392-394 

28. Karen LA, Hodgson KJ, Mattos MA et al. (2000) Adverse 
consequences of internal iliac artery occlusion during 
end C'vu scalar repair of abdominal a or lie aneurysm, I Vase 
Surg 32:676-683 

29.Dadian N, Ohki T.Veith FJ et al. (2001] Overt colon, isch- 
emia after endovaseular repair: tfie importance of mic.ro- 
embolization as an etiology. 1 Vase Surg 34:9S6-99i! 

30. Geraghty Pi, Sanchez LA, Rubin BG et al. (2004) Overt isch- 
emic colitis after endovaseular repair of aortoiliac aneu- 
rysms. ] Vase Surg 40:413-418 

31. Crawford ES, Morris GC, Myhre HO, Roehm JO (1977) Celiac 
axis, superior mesenteric artery, and interior mesenteric 
artery occlusion: surgical cons id erai ions. Surgery >!J:S?o-8r.>!:- 

32. Faries PL, Morrissey N, Burks JA et al. (2001 ) Internal iliac 
artery revascularization as an adjunct to endovaseular 
repair of aortoiliac aneurysms. 1 Vase Surg 34:892-899 

33.IwaiT, Sakurazawa K, Sata S, Muraoka ¥, Inoue Y, Endo M 
i 1991 ) intra -opera tive monitoring of die pelvic circulation 
using a liansanal ["'oppler probe. Eur I Vase Surg 5:71 -74 

34.Benaron DA, Parachikov IH, Friedland S, Soetikno R, 
Brock-Utne J, van der Starre PJ, Nezhat C, Terris MK, 
Maxim PG, Carson JJ, Razavi MK, Gladstone HB, Fincher 
EF, Hsu CP, Clark FL, Cheong WF, Duckworth JL, Stevenson 
DK (2004) Continuous, noninvasive, and localized micro- 
vascular tissue oximetry using visib.e light spectroscopy. 
Anestiiesiology 100:1469-1475 

35. Wolpert LM, Dittrich KP, Hallisey MJ, et al. (2001 ) Hypog- 
asterie artery embolization in endovaseular AAA repait. j 
VascSurg33:1193-8 

36. Mehta M, Veith FJ, Ohki T, et al. (2001 ) Unilateral and bilat- 
eral hypogastric artery interruption during aortoiliac 
aneurysm repair in 154 patients; a relatively ii 
procedure. | Vase Surg .">."!( suppl'):S2 7-32 



Respiratory System 



16 Bronchial Artery Embolization 



6.1 Introduction 263 

6.2 Pathophysiology and Etiology 263 

6.3 Diagnostic Work-Up 264 
6.i.\ Conventional Radiography 264 

6.3.2 hULTopi:, :trochoscopy 264 

6.3.3 Cr." 26b 

6.4 Anatomy 265 

6.4.'. Bronchial A- :> ry Anatomy 265 

6.4.2 Non ■)r:ri. , :ii;'. Systemic Artery Anatomy 269 

6..- I(.'chnic|-i' . i bronchi ill Artery Embolization 269 

6.S.'. Krabolic Aji,tT.ls 273 



2/4 
mpli 

Conclusion 275 
kelerences 275 



275 



16.1 

Introduction 

Massive hemoptysis represents a major medical 
emergency that is associated with a high mortality. 

Rioir h ia I artery embolization was first described 
in the literature in the 1970s by Remy [1], and over 
time it has become a well established treatment for 
p.itients will] (massive) hemoptysis [2-5]. Techni- 
cal improvements in both catheters and embolizing 
agents have attributed to the increase of the safety of 
the procedure and it's applicability. 

In this chapter the pathophysiology and etiol- 
ogy of hemoptysis will be discussed, as well as the 
diagnostic work-up of patients suffering from severe 
bronchial bleeding. Anatomy of bronchial arterial 
supply will be described. The techniques, pitfalls, 
complications and results of bronchial artery embo- 
lization will be discussed. 



J. C. TAN DEN BEHG, MD, PllD 

Head or llie service of [meivtniiin.c AjJiobgy, ;.'speda,e 
!\rgicnii!e di Lugano, sede rjivico.Vu Te;serete 46, 
6900 Lugano, Switzerland 



16.2 

Pathophysiology and Etiology 

Expectoration of blood, or hemoptysis, is a poten- 
tially life threatening condition. Massive hemop- 
tysis in non-trauma patients is reported to carry 
35%-85% mortality. Death from hemoptysis is 
rarely caused by exsanguination, but rather by 
asphyxia that results from flooding of the airways 
and alveoli with blood [6]. Hemoptysis is consid- 
ered severe or massive when the total amount of 
blood expectorated exceeds 300-600 mL over a 24- 
h period [7-9]. Hemoptysis is defined to be trivial 
when only drops of blood or bloody sputum are 
present, and moderate with a blood loss of less then 
200mL/24h [7]. 

Hemoptysis has a propensity to recur if defini- 
tive therapy is not instituted. Patients presenting 
with massive hemoptysis who underwent medical 
therapy alone, had recurrence within 6 months after 
discharge, with a fatal outcome in about half of the 
patients [10]. 

In the vast majority (90%) of cases the source of 
the bleeding is the bronchial circulation. Bleeding 
from the pulmonary circulation (e.g. pulmonary 
arteriovenous ma ltorni.it ion, pnl monary endometri- 
osis, pulmonary aneurysm, injury from Swan-Ganz 
catheter [11, 12]) and hemorrhage directly from the 
aorta (e.g. aortobronchial fistula and ruptured tho- 
racic aneurysm) or non-bronchial systemic arterial 
supply to the lungs each account for 5% of the cases. 
Hemoptysis of pulmonary and direct aortic origin 
will not be discussed in this chapter. 

In most patients with hemoptysis the underlying 
cause is chronic or acute inflammatory lung disease, 
including pulmonary tuberculosis, bronchiectasis, 
cystic fibrosis and aspergilloma. All possible causes 
of hemoptysis are listed in Table 16.1. 

In patients with acute or chronic lung diseases 
(who constitute the majority of those presenting 
with hemoptysis) pulmonary circulation is reduced 
or completely blocked due to hypoxic vasoconstric- 
tion, thrombosis and vasculitis at the level of the 



i-iro rich ieota sis 
: NeiTOiiziisgj pneumoma 
Chronic bronchitis 
Lung abscess 

Aspeigi.losis/my.reiomj 
Tuberculosis 

Nontuberculous myoobacie: 
Cystic fibrosis 



Bronchial adenoma 
Bronchial carcinoid 
Metastatic disease 
Endometriosis 



bleeding [8, 14]. 



16.3 

Diagnostic Work-Up 

The most coiinisonlv i : s r- ■:! diagnostic modalities to 
find the cause of the hemoptysis and to identify the 
pulmonary lobes in which the bleeding is localized 
are conventional radiograph'.: fiberoptic bronchos- 
copy and CT. Knowledge of the localization of the 
bleeding is of importance for the interventionalist 
in order to facilitate the subsequent embolization 
procedure. 



CardicH-iJSitilar 

Severe left ventneubr :;eart faimre 

Mitral stenosis 

yiili]]c::;iiy embolis:Vj or infarction 

Aortic aneurysm 

Pulmonary aneurysm 

r-.- ... -...-. .. r fistula 

AV malformation 

lsir.ij!t':'iL .:■■■.. ns (e.g. Swaijn-'.r.anz; 



Wegener's jiranulor. 
Siys^i ii... lup. » erythema tos us 
■/..-'.::: • syndrome 

MliiilliDiiOltS 

Miojaihic pulmonary hemosiderosis 

Aspirated roieig: 1 . LVih" 

Pulmonary trauma or contusion 

Pos t-b i op sy ( tra ns thorac i c/ transbronch i a 1 ) 

"o"se of a:irii."oagu.ams,':^bri:;cly[;..-s 



pulmonary arterioles. This leads to proliferation 
and enlargement of the bronchial arteries in an 
attempt to compensate for the reduced pulmonary 
circulation. In patients with bronchiectasis blood 
circulation can increase and may represent as much 
as 30% of cardiac output [13]. In the inflamed sur- 
roundings the bronchial arteries are prone to rup- 
ture due to direct erosion by a bacterial agent in 
combination with the presence of a locally elevated 
blood pressure. The bronchial arteries being part of 
the systemic circulation implies that extravasation 
of blood into the bronchial tree occurs under sys- 



16.3.1 

Conventional Radiography 

Although frequently performed because of its avail- 
ability, the diagnostic yield of conventional radiog- 
raphy is low. In 17%-81% of patients with hemop- 
tysis radiographic findings are normal, or di 
help in localizing the bleeding source. Overall ches 
radiographs are diagnostic in about half of the 
[7, 8, 15]. 



16.3.2 

Fiberoptic Bronchoscopy 

Bronchoscopy is generally considered the modal- 
ity of choice in the diagnosis and management of 
patients with hemoptysis. It has (he advantage that it 
can identify central bronchial lesions, such as carci- 
noma, that generally are not considered candidates 
for bronchial artery embolization. Furthermore 
fiberoptic bronchoscopy can be used to administer 
vasoconstrictive drugs to control bleeding. Bron- 
choscopy can localize the bleeding site in up to 93% 
of cases, but the diagnostic accuracy of fiberoptic 
bronchoscopy drops considerably in patients who 
have a normal chest radiograph (range 0%-31%}. 
The overall diagnostic accuracy of bronchoscopy in 
all patients with hemoptysis (irrespective of find- 
ings at conventional radiography] is reported to be 
10%-43% [7, 16, 17]. Major source of difficulty is 
in patients with massive bleeding where blood may 
fill up all ipsilateral lobar bronchi and even the 
contralateral main stem bronchus. In patients with 
known causation of hemoptysis, in which the site 



Bronchial Artery Embolization 



of bleeding can be determined from conventio 

radiographs tiheroplie bronchoscopy has been dt 
onstrated to be of little added value [15]. 



CT offers the possibility to demonstrate both airway 
and vascular pathology (e.g. bronchiectasis, bron- 
chogenic carcinoma, aneurysmal disease of the tho- 
racic aorta}, and has been reported to be the modal- 
ity of first choice in patients with hemoptysis [18]. In 
patients who have a non-diagnostic fiberoptic bron- 
choscopy, CT can provide a diagnosis in half of the 
cases, while in patients with non- conclusive chest 
radiography this rate varies from 39% to 88% [16, 
17]. Localization of the bleeding site can be achieved 
in 63%-100% of all cases [7, 15]. Current multide- 
tector CT scanners also allow visualization of bron- 
chial and non-bronchial systemic artery anatomy, 
and may thus be of help for the 
plan the procedure [8, 13, 19, 20], 







CT of the thoracic aorta, 

clearly demonstrating the 
origin {arrowhead) and 

tal branches and bronchial 
artery (arrow) of right inter- 
cos tobronchial trunk 



16.4 
Anatomy 

16.4.1 

Bronchial Artery Anatomy 

Almost all bronchial arteries originate from the tho- 
racic aorta between the level of T4 and T7 [21, 22], 
with 90% originating between the upper border of T5 
and the lower border of T6 [23]. There are usually two 
bronchial arteries supplying the right. The first com- 
monly arises from the descending aorta as a common 
intercostobronchial trunk with the third right pos- 
terior intercostal artery, and has a poster olaterally 
lying orifice. This right intercostobronchial artery 
commonly has an initial vertical or oblique course 
upward. On CT it can be identified to the right of 
the retroesophageal space (Fig. 16.1] [13]. The second 
important artery is the common right and left bron- 
chial artery that arises from the anterior surface and 
supplies both lungs. On the left side a separate left 
bronchial artery is usually present, and arises from 
the anterolateral surface of the aorta. In a cadaveric 
study the right intercostobronchial trunk was pres- 
ent in 97.5% of cases, with an associated accessory 
right bronchial artery in 7.5% of cases. A common 
bronchial trunk was present in half of the cases, and 



the left bronchial arterial system was characterized 
by the presence of a direct left bronchial artery in 
76% of cases and a double left bronchial artery in 
20% (Fig. 16.2) [23]. It is extremely rare that a left 
bronchial artery arises from a common trunk of an 
intercostobronchial artery. 

At fluoroscopy in the AP-projection, the vast 
majority of the bronchial arteries have their origin 
at the level where the left main stem bronchus over- 
lies the aorta, slightly below the level of the tracheal 
carina (Fig. 16.3) [19,24]. 

Four classical bronchial artery patterns have been 
identified [8]: 

• Type Ir two bronchial arteries on the left, and one 
on the right (intercostobronchial trunk); present 
in 40% of cases. 

• Type II: one bronchial artery on the left and one 
interco.itobroiu dual artery on the right; present 
in 20% of cases. 

• Type III: two bronchial arteries on the left, and 
a bronchial artery and an intercostobronchial 
artery on the right; present in 20% of cases. 

• Type IV: one bronchial artery on the left, and 
a bronchial artery and an intercostobronchial 
artery on the right; present in 10% of cases. 

among the 
ight bronchial 



pulation that left and 




Fig. 16.2a-d. a Selective angiography of r'iel'.l i j ji c-i'irosi ob ro-nc K L;i 1 trr.nl-.: ca:he:cr tip at level of ostium i i r to iWjn ;.i\\ represen- 
tation of right Pro no hi.il artery din-iiii 1 ) and intercostal branch iciif.-al iin-pir!. b Selective angiographv of com iv.cn bronchial 
trunk; division into left and right bronchial a tie: v. c Selec:ive siigiography of right bronchia, aioery, ■: : i ti: n :. r i : it: directly from 
the aorta, d Selective angiograchv ^ let: bronchial artery, originating directly from the aorta 




Fig. 16.3. a Fluoroscopic image demolish Miing relatr mi snip of catheter tip with respect to left n 
l> Selective angicgi itpliy in same patient as ; a :: visualization of left bronchial artei y 



Bronchial Artery Embolizatioi 




Fig. 16.-1. a Ao: ::■: ,i: ■■;;. .1 ngi.-gi'jyjiv 1:'. patienl with ecaini on origin of : ight ano 1 el": 00 mm on earotio artery (iinrnri, and nghl 
stilvkivian artery (jmui /i L '<ii/) wit It origin ;st he lew! of die p 1' 0x1:1:.;! de^oenoi::g ihoracic joi 1,1 (arteria U:^oria). b ^eleodve 
angiography demons: rating ooivimo:i oicnchial t: -ink ivitli origin a: ".he lew! of die or i 10 a rob \ arrowhead) 



e from the aorta as a common trunk (up 
to 48%). 

The bronchial arteries supply the trachea, pul- 
monary airways (both intra- and extrapulmonary), 
regional lymph nodes, (visceral) pleura, esophagus, 
and vasa vasorum of aorta and pulmonary artery 

Many variations occur, and bronchial arteries may 
have their origins from the aortic arch (Fig. 16.4), 
internal thoracic or mammary artery (Fig. 16.5), 
thyrocervical and costocervical trunk, innominate 
artery, left subclavian artery and inferior thyroid 
artery, inferior phrenic artery or abdominal aorta 
[22]. A key finding in aberrant bronchial arteries, 
that distinguishes them anatomically and angio- 
graphically from non-bronchial systemic collateral 
vessels, is their course following the branching of 
the major bronchi [22]. Non-bronchial systemic col- 
lateral circulation (that can develop after successful 
embolization of bronchial arterial supply) usually 
enter the lung parenchyma through adjacent pleura 
or the pulmonary ligament, and have a typical course 
that does not parallel the bronchial tree. 

Communications between bronchial arteries and 
systemic vessels are ubiquitous, and can sometimes 
complicate an embolization procedure. The most 
commonly seen communication is that of a right 
intercostobronchial trunk with an anterior medul- 
lary artery that contributes to the vascular supply of 
the spinal cord through the anterior spinal artery. 
The anterior medullary arteries have a character- 
istic 'hairpin' configuration, and follow a course 



parallel to the spinal cord (Fig. 16.6) [25]. Other less 
commonly seen communications are with the left or 
right subclavian artery (Fig. 16.7} [26, 27], and right 
coronary artery (Fig. 16.8) [28]. 

Normal bronchial arteries have a diameter of 
less then 1.5 mm at their origin, and 0.5 mm at the 
level of the entrance into a bronchopulmonary seg- 
ment. Pathologic features of the bronchial artery are 




Fig. 16.5. i elective angiography of r j 1 e lefi internal n 

artery {arrowhead), giving off hcachial arterial branches 






Fig. 16.7. Selective angiography of right 
intercostobronchial trunk (arrow), demon- 
strating connection with the right subclavian 
artery [arrowhead) 



i"» <.*«■• 




* 



Fig. 16.ii. a i elective angiography of right inter - 
costooionchial trunk, early phase, b Selective 
angiography of ngfn ailercostobronchial trunk, 
late phase demonstrating thin arterial structure, 
with course par.tllel to vertebral column: .inte- 
rior spinal artery (arrowheads) 



Fig. 16.8. a Selective angiography of right bronchial artery 
(ai row ), early phase, cemonsl:a:ing connection with a vessel 
overlying the heart (iincnr/idti/i. b Selective angiography of 
right Lironciiia! .11 lerv. h.te phase: f'.c.c:.. l:.l:::g cai:e: n ■Ji-:a!.v 
of right coronary artery (arrowheads) 




Bronchial Artery Embolization 



hypertrophy (in a study comparing multi- detector 
row CT and selective angiography an average of one- 
third of the bronchial arteries showed dilatation 
over 1.5 mm [19]) and tortuosity (Fig. 16.9), neo- and 
hypervascularity, vascular blush, dense soft tissue 
staining (Fig. 16.10), shunting into the pulmonary 
vascular system (arterial or venous; Figs. 16.10 and 
16.11), extravasation of contrast medium into the 
alveoli or bronchial tree (Fig. 16.12) and formation 



of bronchis 
15,29-31]. 



artery aneurysm/pseudoaneurysm [9, 



16.4.2 

Non -bronchia I Systemic Artery Anatomy 

Several non-bronchial systemic arteries have been 
identified as possible sources of hemoptysis, espe- 
cially in patients afterrepe.it bronchial artery embo- 
lization, and inpatients who have concomitant pleu- 
ral involvement of disease. In one-third to 45% of 
patients a significant blood supply from n 
chial arteries contributes to the hemoptysis [32, 33]. 
Pathologic vessels may originate from intercostals 
arteries, branches of subclavian and axillary arteries 
(e.g. thyrocervical trunk; Fig. 16.13), internal n 
mary artery (Fig. 16.14), phrenic arteries (Fig. 16.15) 
and left gastric artery [34]. CT angiography can 
be useful in identifying pathologic vasculature in 
patients with pleural thickening and hemoptysis 
[8]. 




"e angiography of right intercostobronchial 
w), depicting pathologic blush [arrow- 
heads), and shunting ;o pu-monoi'y circulation [t 




Fig. 16.12. a S u pel s^c live rijig:- 'graphy of bronchia] 

of contrast into alveoli iiii ichWicii/) and bronchi (or 
medium in the bronchus (arrow) 



": 



Fig. 16.13. Selective cjiheleiization of thyrocervical trunk 
([ii run ), demoi]si:a:ing \-a;bol ogic mhancemem of left apical 
region and pulmonary shunting [arrowhead) 



osLC-nronchiiil artery, ,"!emoii^i:a:ing 
image. deciding to a J vantage pre?en 




Fig. 16.15. Selective angiography of right phrenii 

[tjrrowliend), connection wi:h pathologic intrapulmot 
se!s is clearly depicted (lirroic) 




Fig.16.14. Selective 
angiography of left 
internal mammary 
artery (a rrcwhead), 
with pleural con- 
nections supplying 

pathologic vascula- 



namic status, followed by the embolization proce- 
dure [6, 35]. 

After standard preparation the common femoral 
artery is punctured, an introduction sheath (4F or 
5 F), and a flush catheter is advanced into the upper 
part of the descending thoracic aorta. A diagnostic 
angiography is performed in an AP projection. The 
flush aortogram is used to identify any pathologic 
bronchial artery [36]. The injection rate is no less 
than 25 ml/s and lasts at least 2 s. The flush catheter 
is then exchanged for a selective diagnostic catheter 
that needs to have a minimum length of 100 cm, a 
lumen of 0.038" and should not have side holes. The 
latter is of utmost imiaorrance since in some cases 



t be adv; 



a the 



Bronchial Artery Embolization 



target vessel beyond a point at which the side holes 
are still at the level of the aorta (a position that would 
lead to inadvertent spill of embolic agents into the 
aorta). The most commonly used selective catheters 
are cobra-curved or Simmons-type catheters. The 
Simmons catheter can be used with the tip of the 
catheter pointing cranially in the descending tho- 
racic aorta (i.e. without reforming it's shape in the 
aortic arch; Fig. 16.16a), or in the classical way (after 
re-shaping in the arch). In the former configuration 
bronchial arteries that have an origin with an upward 
oriented, acute angle with respect to the aorta can 
be cannulated. Given the large variety in anatomy a 
range of diagnostic catheters should be at hand, and 
should include mammary catheters, multi-purpose 
and specific bronchial artery catheters. 

Selective angiography is then performed using 
hand-injection (frame rate 3/s). The selective angi- 
ography serves to establish the presence of patho- 
logic vasculature and to demonstrate any connec- 
tions to other vascular territories (e.g. anterior spinal 
artery). If any side branches of importance are pres- 
ent attempts should be made to advance the tip of 
the catheter beyond the point of the origin of these 
branches. This super-selective catheterization can 
be performed by advancing the 4-F catheter using a 
Glidewire where care should be taken not to create 
spasm or dissection. As an alternative amicrocathe- 
ter can be used, that is placed through the diagnostic 
catheter (co-axial system; Figs. 16. 16b, c, Fig. 16.17) 
and that is fixed to the diagnostic catheter with a 



Y-connector (Fig. 16.18). The latter also allows for 
continuous flushing of the guiding catheter. Alter- 
natively, a side hole can be created in a diagnostic 
catheter (at a distance from the tip as determined 
by the operator), which can serve as an exit for a 
microcatheter. This technique has been described to 
be helpful in the embolization of proximal subcla- 
vian arterial branches, when stable catheter position 
cannot be achieved in other ways [21]. In a similar 
fashion catheters with pre-fabricated side holes can 
be used in difficult anatomical situations [37]. 

Finally a microcatheter can be used as a "tapered" 
extension of a 4-F diagnostic catheter, in cases where 
the diameter of the ostium of the target vessel is 
smaller than the outer diameter of the diagnostic 
catheter (Fig. 16.19). 

Before proceeding to the embolization of the 
target vessel, stability ot the catheter tip and absence 
of backflow into the descending thoracic aorta 
should be confirmed by means of a test-injection 
using contrast medium. 

The embolic agents of choice are non- absorbable 
particles (see below). These particles are admin- 
istered through a three-way stopcock with small 
tubing that is connected to either the 4-F diagnostic 
catheter or microcatheter (Fig. 16.20). The embolic 
particles should be dispersed into contrast medium, 
in order to allow visualization of any backflow and 
to monitor for slowing of flow, which is indicative 
of progression of distal embolization. Preferably 
1-ml syringes are used. Advantages of the three- 




Fig. Hi. 1 6a --c. ii Seiecrive ca:he:. nation or ; igbi inlcico^coronchial i; Link with vruiv.ons type 1 rallied:; no: ice non-iefoirr.ed 
shape, with point ct ca:jieiei pointing upwards : : ri ron/icii:/;: rilling o: booh iniercostiil anc oronciiiiil hi miches. b Same poiir: 1 .: 
us in i a), after advancement ofi'.iiciocalheler ; : rr row) i:i:o;i£h 4-F diagnostic catheter iiii'oir/h'ii:/:. c Mipei selective angi' >gi .iphv 
through microcatheter; no flow into intercostal tranches is seen, with clear cepicrio:'. of oronchia! vasculature {arrow) 




Fig. 16.17. a Supersede live .ingiogript'.v 
of bronchial artery originating from left 
internal mammary artery (same patient 
as Fig. 1 6.5); diagnostic S-F mammary 
catheter (orron.'} and markers on micro- 
catheter (arrowheads) are clearly seen. 
b Control angiography after emboli- 
zation performed through diagnostic 
cathrter demonstrates aosen.ce o: f.ljisg 
of pathologic vasculature (arrowhead) 
and patency of distal internal mammary 
artery (arrow) 




Fig. 16.18. a Microcatheler i n> roiWjOiii/i introduced through ¥-c< 
U iir red a iio v.). l> Miciocilt.etei i ;inoii7jci (:/:!, with aco 'iiiL-anv.iig gi 
eter (nrroir!; this a. lows for rimer selective 



--!- diagnostic callietei 
i, protruding from diagnostic cath- 




Fig. 16.19. Micro catheter i.an;.nvh,.\id) protruding 
milli meters from the tip of diagnostic catheter (arrow.-); tt 
allows for ca [intuition c:' small diameter ostia of bionch: 



S.20. Three-way stopcock with tubing ianowhead), con- 
i (o two 1-ml syringes; one syringe is used for admin- 
on of the embolic agent mixed with contrast (arrow), 
the other syringe is used for lit. siting with saline 



Bronchial Artery Embolizi 



way stopcock are that frequent solution exchanges 
between two syringes can be performed to maintain 
the particles in a suspended condition, and that the 
catheter can be flushed easily with saline, without 
disconnecting the svrmge hi led with the mixture of 
contrast and microparticles. Care should be taken 
to keep only one syringe reserved for the embolic 
agent, in order to avoid inadvertent injection of 
embolic particles (e.g. during control angiography). 
Throughout the procedure regular angiographic 
controls should be performed, in order to detect 
appearance of previously not visible connections 
to other vascular territories such as the anterior 
spinal artery. After occlusion of peripheral bron- 
chial artery branches, which leads to an increase of 
resistance both distally and centrally, particles may 
reflux into side branches not detected initially [38, 
39]. After successful embolization of all pathologic 
bronchial arteries as visualized on the flush angiog- 
raphy in the above-described manner, it is recom- 
mended to perform another aortic angiography in 
order to scrutinize for any pathologic vessels previ- 
ously not visible. When present, these vessels should 
also be embolized. This approach helps in reducing 
the number of recurrences. 

In the future the need for flush aortography prior 
to and after embolization may be obviated, when 
the use of multi-detector row CT becomes more and 
more common. There are indications that the use of 
thin-section CT scanning reduces procedural time, 
as well as the potential iatrogenic risks of a selective 
search for ectopic bronchial or abnormal non-bron- 
chial systemic arteries [19]. 

Table 16.2 lists the materials most commonly 
used for bronchial artery embolization. 



16.5.1 

Embolk Agents 

Various embolic agents can be employed for bron- 
chial artery embolization, and include gelatin 
sponge, microspheres and coils. 

Absorbable gelatin sponge is readily available, 
inexpensive and easy to handle. Disadvantage is the 
fact that it is not radiopaque, and absorbable. The 
latter may lead to recanalization of the vessel treated, 
and thus to recurrences. Therefore gelatin sponge is 
not the embolic agent of first choice, although it can 
be used as an efficient temporary embolic agent. 

The most commonly used embolic agents are poly- 
vinyl alcohol particles. Polyvinyl alcohol particles 
are biocompatible and non-biodegradable and are 



Table 16.1. Cookbook: 



; : ugaos; Li catheters 
Hush : pigtail, universal flush) 
Selective: Cobra (C2 and C3) 

Simmons (type 1 and type 2) 
Mammary 
Multipurpose 
Bronchial 
Microcatheter (Progreai, Tracker. Transend, Prowler] 



Pressurized saline flush 

Three-way stopcock with tube 

1 ml Syringes 

Embolic agents 

Mi a a spheres isize range 100 um-'. SCO ..:;'.; Embosphere, 

!-iejd Block, [vo [on, Contour) 

Coils (oushable, fibred coils) 



considered to be a permanent embolic agent and the 
agent of first choice [38]. More recently tris-acryl gela- 
tin microspheres have become available. Use of these 
particles has been mainly in uterine fibroid emboli- 
zation, and experience in bronchial artery emboliza- 
tion is limited [40]. Tris-acryl gelatin particles can be 
administered more smoothly through micro-cath- 
eters, without the risk of plug-formation as can occur 
with the (older generation) polyvinyl alcohol parti- 
cles, and better penetration characteristics [41]. Both 
polyvinyl alcohol and tris-acryl gelatin particles are 
available in various diameters, ranging from 75 im to 
1000 im. Particles smaller than 350 im should be used 
with extreme caution, since particles smaller than 
this si/e mav pass broncliopulmoiiai y anastomoses, 
or may cause a very distal occlusion in normal periph- 
eral branches, that provide vascular supply to bronchi, 
esophagus etc. Occlusion of these branches may lead 
to bronchial or esophageal necrosis [25, 42]. 

Stainless steel or platinum coils and detachable bal- 
loonsarerarelyused as api unary ernholicagentinbron- 
chial artery embolization. Although these can be used 
to occlude a pathologic bronchial artery efficiently, use 
of coils precludes repeat embolization, which is often 
needed as patients are prone to distal collateralization 
(Fig. 16.21) [13, ■■!■■!]. The primary indication tor use of 
coils is in patients with a bronchial artery aneurysm. 
Secondly, in cases where a superselective position of a 
(micro) catheter cannot be reached, coils can be used 
to protect a normal distal vascular territory against 
inadvertent embolization [25]. 




Same patient as Fig. 16.13; 1 month after coil embolization of 

.cal trunk presenting with reciirrenl heT.op:ysis; notice presence 

■). b Late phase of selective angiography of the left subclavian 

of p.i ih::' logic enh.;:'ce:v.enr ( ■ r . " .■ : "■ i l i .in.- pulmonary shinning 

■/ji'ii;/!. c Selective rnigiography ^ I eh Mibc.ari.i:- unery showing filiiisg of 

ogic are; 1 , of apical vessels through vertebral itrrery (iinr.ir/icWi, C2-C3 

rals (uncjir) and Literal cervic.l branches irurivJ iinvirj; this situation 

.les repe.'.t err.r'ojzaiion 



Thrombin injection into the bronchial artery has 
been described, and has a theoretical advantage in 
patients where tortuosity of the target artery pre- 
cludes superselective catheterization [45]. However, 
given the rather unpred ictable behavior, and risk of 
peripheral embolization, this agent has not gained 
wide acceptance, the same as using absolute alcohol 
as an embolic agent. 



16.6 
Results 



Bronchial artery embolization is highly effective 
in the treatment of acute hemoptysis. Short-term 



no n- recurrence rates (with follow-up up to 1 month) 
range from 73% to 98% [1, 46, 47]. Technical suc- 
cess rates have increased by development of a more 
meticulous technique, using superselective emboli- 
zation, and performing control thoracic aortogra- 
phy as described above [14, 48]. Procedural failures 
are usually caused by inability to achieve a stable 
catheter position, or a position beyond the origin of 
spinal cord branches [38]. Recurrences at long-term 
follow-up can be as high as 52%, however, success 
rates of 100% can be achieved using repeat embo- 
lization and control of underlying disease either 
pharmacologically or surgically [25, 38, 47, 49-51]. 
Recurrence of hemoptysis may occur due to recana- 
lization of embolized vessels, incomplete emboli- 
ilarization by means of development 



Bronchial Artery Embolizatior 



of new collateral pathways, including development 
of contribution of non-bronchial systemic arterial 
supply [25]. The presence of anomalous bronchial 
arteries may also contribute to occurrence of recur- 
rences [52, 53]. 

The underlying disease is also of importance: 
patients with chronic tuberculosis more frequently 
suffer from recurrent hemoptysis, since the develop- 
ment of non-bronchial systemic collaterals is more 
extensive [33, 54]. However, repeat embolization in 
such patients, including treatment of non-bronchial 
collaterals often leads to satisfactory results [32, 
55-57]. 

Finally, operator experience in bronchial artery 
embolization is of crucial importance in achiev- 
ing high success and low complication rates. Given 
the low incidence of acute massive hemoptysis, the 
risk that each patient represents a new "learning" 
experience is not unimaginable [38], and therefore 
bronchial artery embolization should only be per- 
formed by skilled operators (at least five to ten cases 
a year). 



Rare complications as have been reported in 
literature are aortic and bronchial necrosis [58], 
bronchial stenosis [59], unilateral diaphragmatic 
paralysis [60], pulmonary infarction (especially 
in patients who have suffered pulmonary artery 
embolism), left main bronchial-esophageal fistula 
[61], and non-target embolization (colon, coronary 
and cerebral circulation) [62]. Especially the newer 
spherical embolic materials (tris-acryl gelatin) can 
traverse from the bronchial into the pulmonary cir- 
culation, and then through unoccluded pulmonary 
arteriovenous malformations into the systemic cir- 
culation [41]. 



16.8 
Conclusion 

Bronchial artery embolization is the treatment of 
choice in acute hemoptysis. 

Knowledge of bronchial and non-bronchial sys- 
temic circulation is mandatory to reduce complica- 
tions and to increase techni 



16.7 

Complications 



The most commonly occurring complication 
encountered after bronchial artery embolization is 
(transient) chest pain, being reported in 24% up to 
91% of cases. This is probably related to ischemia 
of embolized branches, and can be severe when 
intercostal branches are inadvertently embolized. 
Pleural pain can be avoided by using superselec- 
tive embolization techniques, with or without the 
use of large particles. The second most common 
lompluaison is dyspli;'i«i,i, .aused by emlx'l izi.it ion 
of esophageal branches, with a reported occurrence 
from 0.7% to 18.2% [30]. Spontaneous resolution of 
symptoms usually occurs. 

Incidentally subintimal dissection or perforation 
of the bronchial artery {caution with use of glide- 
wire-type guidewires) or dissection of the aorta may 
occur [29]. 

The most devastating complication is spinal 
cord ischemia, that has been reported to occur in 
1.4%-6.5% of patients treated with bronchial artery 
embolization [9, 30, 39]. The occurrence of this com- 
plication can be reduced by using a superselective 
embolization technique, performing regular con- 
trol angiograms before and after adm 
embolic agents as has been described abo^ 



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52. McPhersonS.Routh WD, Nath H, Keller FS ( 1990) Anoma- 
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53. Cohen AM, Antoun BW, Stern RC (1992) Left thyrocervi- 
cal trunk oionchia! jnerv supplying right In ng: scarce of 
recurrenl hemoptysis m cystic fiorosis. AIK Am | Roent- 
genol 158:1131-1 133 

54.Mossi F, Maroldi R, Battaglia G, Pinotti G.Tassi G (2003) 
Indicators predictive of success or" embolisation: analy- 
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105:48-55 



55.Antonelli M, Midulla F, Tancredi G, Salyatori FM, Bond 
E, Cimino G et al. (2002) Bronchial artery embolization 

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12:2056-2057 



17 Pulmonary Arteriovenous Malformations 

Jean-Pierre Pelage, Pascal Lacombe, Robert I. White Jr., and Jeffr, 



Introduction 279 
Epidemiology 280 
Clinical Manifestations of PAVMs 280 

Pulmonary Function Tests 281 

Imaging 281 

Contrast Material- Enhanced 

Echocardiography 2SI 

Chest Radiography 2S! 

Pulmonary Angiography 282 

Computed Tomography 282 

Mjg:~r".ii" Resonance Imaging j,v 

Which Diagnostic Approach to 

Suspected PAVMs? 283 

Classification of PAVMs 283 

Therapeutic Options and Rationale for 

Treatment 284 

Treatment Options 284 

Rationale for Treatment 284 

Procedure 285 

Preparation 285 

Techiucue or" Catheterization 1S5 

Embolization Materials 286 

Embolization Techniques 287 
. Anchor Technique 287 
! Scaffold Technique 287 
i Occlusion Balloon Assisted Technique 
I Vein of Galen Technique 289 
i Squirt Technique 290 
i Wire Push Technique 290 
7 Pulmonary Plow Redistribution 290 

Results 290 

Clinical Follow-up 290 

Imaging hollow-Up 292 

Complications: Descriptic 

Conclusion and Perspecd" 

References 294 



Prevention 292 



J.-P. Pelage, MD, PhD; P. Lacombe, MD 

Department of Radiology !-!6pilal Aiv.oioise Pare, 9, Avenue 

Charles De Gaulle, 92104 Boulogne Cedex, France 

R.I. White, Jr., MD 

Vale University School of Medicine, I 'ep.-itmen; of I ■■! agnostic 

Radiology, 333 Cedar Street, Room 5039 LMP, New Haven, CT 

06520, USA 

J. S. Pollak, MD 

Yale University School of Medicine, I jepaitmen; or" I >i agnostic 

Radiology, PO Box 20842, New Haven, CT 06504-8042, USA 



17.1 

Introduction 

Pulmonary arteriovenous malformations are caused 
by abnormal communications between pulmonary 
arteries and pulmonary veins, which are most com- 
monly congenital in nature [4, 20]. Although these 
lesions are uncommon, they are an important part 
of the differential diagnosis of common pulmonary 
problems such as hypoxemia and pulmonary nod- 
ules. These abnormal communications have been 
given various names including pulmonary arterio- 
venous fistulas, pulmonary telangiectases, and pul- 
monary arteriovenous malformations [20, 66]. 

Between 60% and 90% of patients with PAVM 
have hereditary hemorrhagic telangiectasia (HHT) 
but abnormal communications between blood ves- 
sels of the lung may also be found in a variety of 
acquired conditions [4, 20]. Right-to-left shunting 
as a result of communications between pulmonary 
arteries and pulmonary veins has been reported in 
hepatic cirrhosis, mitral stenosis, trauma and Fan- 
coni's syndrome [4, 35, 52, 70]. 

i'AVMs provide a direct capillary-tree communica- 
tion between the pulmonary and systemic circulations 
with three main clinical consequences: (1) pulmonary 
arterialblood passing through these right-to-left shunts 
cannot be oxygenated which may lead to hypoxemia, 
(2} the absence of normal filtering capillary tied allows 
particulate material (air bubbles or clots) to reach 
directly the systemic circulation (paradoxical embo- 
lism) with potential clinical sequelae in the cerebral 
circulation (transient ischemic attack, stroke, brain 
abscess), and (3) these abnormal vessels may rupture 
into the bronchus (hemoptysis) or the pleural cavity 
(hemothorax) particularly during pregnancy. 

Hereditary hemorrhagic telangiectasia (HHT i 
is a genetic disorder of blood vessels [21, 63]. Also 
known as Rendu- Osier- Weber syndrome, HHT is 
a condition which is transmitted in an autosomal 
dominant pattern, and characterized by arterio- 
venous malformations (AVM) in the skir 
membranes and visceral organs [4]. Thei 



types of HHT, type 1 and 2, caused by mutations in 
the endoglin and ALK-1 genes, respectively [20, 63, 
64].Theendoglinand ALK-1 genes code for proteins 
that are involved in proper blood vessel develop- 
ment. HHT has variable expression in each affected 
member of a family [21]. Mild to moderate epistaxis 
is the most common symptom of HHT [20, 21, 48]. 
To permit a high degree of clinical suspicion, recent 
international consensus diagnostic criteria have 
developed based on the four criteria of spontaneous 
recurrent epistaxis, mucocutaneous telangiectasia, 
visceral involvement (including PAVMs, hepatic, 
cerebral or spinal arteriovenous malformations} 
and an affected first degree relative [64]. The most 
common serious symptoms in adults are ischemic 
stroke, transient ischemic attack or brain abscess, 
due to PAVMs or hemorrhagic stroke or seizure 
due to cerebral arteriovenous malformation [20, 
21, 26, 41, 44]. Unfortunately, the underlying disor- 
der, HHT, is rarely identified by the family physi- 
cian, neurology specialist or diagnostic radiologist. 
The implications of the underlying disorder are 
not clearly presented to the family and as a result 
affected relatives may develop sudden catastrophic 
symptoms instead of receiving counseling, screen- 
ing, and treatment before complications occur. A 
crucial issue for families is that no child of a patient 
with HHT can be informed they do not have HHT 
unless they have had a molecular diagnosis. Pen- 
etrance is age-related and is nearly complete by 
the age of 40 [4, 49]. Other common symptoms in 
older adults include frequent nosebleeds and less 
commonly, gastrointestinal bleeding [20, 21, 48]. A 
smaller number of patients with HHT are affected 
by liver malformations, which can cause symptoms 
such as heart failure, abdominal pain, abnormal 
liver function tests or even cirrhosis [17, 20, 38]. 

The focus of this chapter will be mainly congeni- 
tal PAVM. We will discuss HHT predominantly as it 
relates to PAVMs. 



17.2 
Epidemiology 



PAVMs are not a common clinical problem. In an 
autopsy study, only three cases of PAVM were detected 
in 15,000 consecutive autopsies [20]. Around 10% of 
cases of PAVMs are identified in infancy or child- 
hood, followed by a gradual increase in the incidence 
through the fifth and sixth decades [20]. Approxi- 
mately 60%-90% of the cases of PAVM are associated 



with HHT [20, 29, 65, 77]. Conversely, approximately 
15%-35% of patients with HHT have PAVMs [22, 31, 
42,78].PAVMswerefound in only 4.6% of 324 patients 
with HHT from an endemic region in France but chest 
radiographs were not routinely performed [49]. 

With the onset of asymptomatic screening pro- 
grams in the United States and most European coun- 
tries, a much higher frequency of involvement is 
seen. It has been estimated that at least 30% of HHT 
patients have PAVMs, 30% have hepatic involvement 
and 10% cerebral involvement [14, 17, 22, 31]. 

About 10% of people with HHT die prematurely 
or are disabled due to complications of their vascular 
malformations. These "events" are preventable by early 
diagnosis, treatment, and tol low-up. Most patients are 
largely asymptomatic before their first serious com- 
plication. Approximately 50% of patients with HHT 
will have an arteriovenous malformation of the brain, 
lung, or liver, or a combination of two or three and will 
require therapy usually by a pluridisciplinary team 
consisting of internists and interventional radiologists 
with special expertise in this disorder. 

Because catastrophic cerebral events such as cere- 
bral abscess, transient ischemic attack or embolic 
stroke occur in patients with PAVMs regardless of 
the degree of respiratory symptoms, it is of para- 
mount importance to diagnose PAVMs to offer 
embolization as a means of pre 



17.3 

Clinical Manifestations of PAVMs 

Up to 55% of PAVMs are asymptomatic and those that 
are symptomatic can present in a remarkable vari- 
ety of ways [4]. Most of these clinical manifestations 
can be attributed to right-to-left shunting. Symptoms 
in early life may vary from being totally absent to 
severe [20]. In recent studies, about 70% of patients 
have symptoms referable to the PAVMs or underly- 
ing HHT [29, 65, 77]. Symptoms related to PAVM 
often develop between the fourth and sixth decades 
[20]. It is usually considered that the incidence of 
symptoms is higher in patients with multiple PAVMs 
rather than a single PAVM [20]. In the Mayo Clinic 
study, symptoms were seen in 37% of patients with 
a single PAVM and in 59% of patients with bilateral 
PAVM [67]. In addition, patients with diffuse PAVMs 
are almost always symptomatic [12, 20]. The most 
common complaint in symptomatic patients with 
PAVMs is epistaxis, caused by bleeding from mucosal 
telangiectases and reflects the high incidence of HHT 



Malformations 



in patients with PAVMs [20]. Dyspnea is the second 
most common complaint in patients with PAVMs 
particularly in those with large or diffuse PAVM. 
Dyspnea is seen in almost all patients who have asso- 
ciated cyanosis, clubbing, easy fatigability, or polycy- 
themia [3, 4, 20], Hemoptysis and hemothorax occur 
in roughly 10% of patients [1, 13, 77]. Less common 
complaints include chest pain, cough and migraine 
headaches [4, 20, 53]. Many of these symptoms are 
not specific and may be related to hypoxemia or cere- 
brovascular complications. Thus, the classic triad of 
dyspnea, cyanosis, and clubbing which is suggestive 
of PAVM was present in only 10% of patients with 
PAVM in one study [54]. It is estimated that 25% of 
patients with PAVMs experience transient ischemic 
attack or stroke and 10% experience cerebral abscess 
on presentation of PAVMs [64,77]. 

Since patients with clinically silent PAVMs are 
still at risk of hemorrhage and more commonly 
neurological sequelae due to paradoxical embolism, 
screening of asymptomatic patients should be per- 
formed. Neurologic complications in patients with 
untreated PAVMs are common and the incidence of 
stroke has been reported to be as high as 40% and 
brain abscess 20% with a mortality of up to 40% 
[8, 73]. These data illustrate the need for aggressive 
screening and treatment for PAVMS in patient with 
HHT. Complications associated with PAVMs can be 
limited if the condition is recognized and treated, 
with transcatheter embolization offering the safest 
method of treatment [20, 73]. 



17.4 

Pulmonary Function Tests 

Oxygenation is commonly affected in patients with 
PAVMs. In recent studies, 80%-100% of patients 
with PAVMs had either a Pao2 < 80 mm Hg or a Sa02 
< 97%-98% on room air [8, 20, 45]. Orthodeoxia 
which is the laboratory correlate of platypnea (rep- 
resents a decrease in Pa02 or Sa02 when going from 
the recumbent to the seated or upright position} is 
present in most patients with PAVMs [11, 20, 71]. 



planning particularly before embolization. Screen- 
ing methods vary between centers but are based 
on noninvasive methods to image the PAVMs or 
to detect the right-to-left shunt. Contrast-enhanced 
echocardiography is often used as the first line test 
in screening patients with HHT for intrapulmonary 
shunting because of its sensitivity greater than 95% 
[2, 43]. PAVMs may also be directly diagnosed using 
a variety of noninvasive imaging modalities includ- 
ing chest radiography, computed tomography (CT) 
and magnetic resonance imaging (MRI) [2, 4, 10, 30, 
43, 47, 56, 73]. Pulmonary angiography is still used 
for treatment planning in some centers [78], 



17.5.1 

Contrast Material-Enhanced Echocardiography 

Contrast echocardiography is an excellent tool for 
evaluation of cardiac and intrapulmonary shunts 
and is able to identify small right-to-left shunts [2, 
43, 61]. The technique (the so-called bubble study) 
consists in injecting 5-10 cc of agitated saline into 
a peripheral vein while simultaneously imaging the 
right and left atria [61]. In patients without right-to- 
left shunting, the contrast is visualized in the right 
atrium as a cloud of echoes and gradually dissipates 
as the bubbles become trapped in the pulmonary cir- 
culation [61]. Inpatients with intracardiac shunting, 
the contrast is visible in the left atrium within one 
cardiac cycle following its appearance in the right 
atrium. Conversely in patients with PAVMs, there is 
usually a delay of between three and eight cardiac 
cycles before contrast is visualized in the left atrium 
[2]. Diagnosis of PAVMs can be made with a high 
sensitivity probably close to 95%-100% for detect- 
ing clinically important (i.e., large) PAVMs [2, 46]. 
Contrast echocardiography detects the presence of 
PAVMs with a high sensitivity but is not correlated 
with the size, location, or number of PAVMs [2, 37, 
43]. Overdetection of clinically unimportant PAVM 
not requiring embolization may limit the use of con- 
trast echocardiography as the exclusive screening 
test for PAVM [2,20]. 



17.5 

Imaging 



Different in 
firm the dia 



iging techniques can be used to con- 
nosis of PAVMs but also for treatment 



17.5.2 

Chest Radiography 

Diagnosis of PAVMs may be suspected on chest radio- 
graphs because abnormal findings have been described 
in the majority of patients with PAVMs [56, 65]. The 
most common findings are peripheral circumscribed, 



noncalcified oval or round lesions connected by blood 
vessels to the hilum or the presence of nodules often 
described as coin lesions (Fig. 17.1). However, chest 
radiography can be normal in 20% of patients with 
smaUPAVMs[73].Inaddition,PAVMscanbe obscured 
by hemorrhage or atelectasis [20, 45]. 




Fig. 17.1. PAVM diagnosed on .; ci:esi radiograph. Plain chest 
radiograph showing ,i si:-g!e ! J AVM wiih smooth borders of 
the left lung (arrow) 



17.5.3 

Pulmonary Angiography 

In some centers, a complete diagnostic pulmonary 
angiography is performed prior to embolo therapy 
[78]. Selective injections in right and left pulmonary 
arteries in standard, oblique, and lateral projections 
are obtained. Outpatient pulmonary angiography 
in patients with diffuse 1'AVMs provides a basis for 
deciding which side to occlude first, to detail the 
anatomy, determine the best projection for occluding 
the PAVMs, and measure the feeding pedicles which 
helps to select the occlusion technique [76, 78]. 



17.5.4 

Computed Tomography 

When contrast echocardiography often used as a 
screening tool is positive, indicating a PAVM, thin 
section spiral chest CT should be performed to con- 
firm the diagnosis and evaluate if treatment is neces- 
sary [56]. The characteristic appearance of a PAVM 
on CT scans is the presence of a homogeneous, well- 
circumscribed, noncalcified nodule measuring up 
to several centimeters in diameter or the presence 
of a serpiginous mass connected with blood ves- 
sels (Fig. 17.2) [56]. The use of contrast- material is 
still a matter of debate because spiral CT and mul- 
tiplanar reconstructions allows easy identification 
of the feeding artery, aneurysm sac, and efferent 
veins without contrast injection [57]. Multiplanar 




Fig. 17.2a,b. PAVM diagnosed using CT with i 
intensity projection vieiv ib ) shows ; single PAVM of th- 
are easily identified 



Pulmonary 



Malrorinaiions 



and three-dimensional reconstructions, potentially 
useful to obtain precise angioarchitecture of PAVMs 
before embolization, may replace diagnostic pulmo- 
nary angiography (Fig. 17.2) [56, 57]. 



17.5.5 

Magnetic Resonance Imaging 

MRI of PAVMs has been evaluated less than CT. 
Conventional spin-echo MRI of pulmonary nod- 
ules or vascular lesions shows lesions with high 
signal intensity on T2-weighted images. Sev- 
eral techniques have been recently developed to 
improve sensitivity to flow [10, 30, 58]. The use 
of gradient-refocused echo MRI technique or MR 
angiography with venous or arterial signal elimi- 
nation or contrast injection has been reported with 
a high sensitivity [10, 30, 58]. The obvious advan- 
tage of MRI over CT is the absence of radiation 
exposure but its main limitations include expense 
and limited availability [20]. 



17.5.6 

Which Diagnostic Approach to Suspected 

PAVMs? 

Based on current scientific data, it seems that con- 
trast echocardiography is the best initial screening 
tool in patients with suspected PAVMs due to its 
excellent sensitivity and availability [19]. If the result 
is negative, the likelihood of significant PAVMs (i.e. 
requiring embolization) is low. The value of spiral 
CT in a screening algorithm is still considered low 
[53]. Conversely, all patients with positive echocar- 
diography should be evaluated using spiral CT in 
order to identify PAVMs amenable to embolization. 
In addition, initial CT will be used as a baseline 
study that can be compared with postembolization 
examinations [53, 56]. 

Treatment of PAVMs consists of transcatheter 
embolization performed by interventional radiolo- 
gists who are specially trained. Fibered platinum 
coils and in some instances balloons are placed in 
the feeding artery to thePAVM. 

Follow-up of patients with treated PAVM is criti- 
cal. By 3-6 months after treatment, the PAVM should 
be markedly reduced in size leaving a residual scar. 
Spiral chest CT should be repeated every 5 years in 
order to identify recanalization of embolized PAVMs 
and assess growth oiany small AVM, until the thresh- 
old size (3-mm diameter feeding artery) is reached. 



17.6 

Classification of PAVMs 

A classification of PAVMs based on segmental pul- 
monary artery anatomy was proposed by White et 
al. in 1983 [76]. PAVMs can be classified as either 
simple or complex [76]. In the initial classification, 
the simple type was defined as having a single seg- 
mental artery and draining vein [76]. The complex 
type of PAVM was defined as having two or more 
arieiies supplvntg (he PAVM and oiv or two drain- 
ing veins [76]. Based on CT findings, this classifica- 
tion has been modified subsequently [78]. A simple 
PAVM consists in single or multiple feeding arteries 
originating from a single segmental artery (Fig. 17.3) 
[78]. Conversely, in complex PAVMs, feeding arteries 
always originate from two or more segmental arter- 
ies (Fig. 17.4) [78]. Simple PAVMsusually account for 
80%-90% of PAVMs but simple and complexPAVMs 
are frequently seen in the same patient [76]. The 
majority of PAVMs are located in the lower lobes [20, 
77]. In some patients with simple and/or complex 
PAVMs, a diffuse pattern of PAVMs can be present. 
White et al. have described diffuse PAVMs when 
almost all segmental arteries have small PAVMs 
arising from subsegmental branches (Fig. 17.5) [76]. 
Patients with diffuse PAVMs usually have a more 
severe clinical presentation with exercise intoler- 
ance and profound cyanosis [12]. They are also at 
higher risk of neurologic complications [12], 



Simple PAVM 




Fig. 17.3a-c. Simple form of PAVM. The simple PAVM is sup- 
plied by one segmniial artery. The urtery lo the aneurysmal 
sac may consist of a single hrai'.ch iai, iniLiiple branches (b) or 
multiple orand'.es .■rising yioMnuliy from the same segmen- 
tal artery (c). (Reproduced from [76], w' " 




thoracic surgery [8, 65, 66]. Perioperative mortality 
varied from 0% to 9% [8, 54, 65, 66]. Postoperative 
follow-up is associated with 0%-10% recurrence rate 
in treated patients [8, 54, 65, 66]. Thus the disadvan- 
tages of surgery are the morbidity associated with a 
thoracotomy, the potential loss of normal pulmonary 
parenchyma surrounding the PAVM particularly in 
case of lobectomy or segmentectomy and the long 
hospital stay [54]. The first successful case of embo- 
lization of PAVMs was reported by Porstmann in 
1977. Since that time embolization has become the 
first line treatment and surgery is rarely indicated 
since embolization results in permanent occlusion 
of PAVMs in a vast majority of patients with minimal 



(Reproduced from complications i 






:ed hands [20]. 



17.7 

Therapeutic Options and Rationale for 

Treatment 

17.7.1 

Treatment Options 

The current preferred treatment for PAVMs consists 
of embolization using coils or other intravascular 
devices [28]. Surgical resection used to be the only 
method of treatment before 1977 [8,28,54,65,66]. 
Vascular ligations, local resection, segmentectomy, 
lobectomy, or pneumonectomy were performed [20]. 
Properly performed in well-selected patients, sur- 
gery is associated with minimal morbidity and mor- 
tality but carries at least the same risks as any other 



17.7.2 

Rationale for Treatment 

Indications for treatment of PAVMs include three 
broad categories: prevention of hemorrhage, 
improvement of hypoxemia in patients with exer- 
cise intolerance, and, most importantly, prevention 
of the complications associated with paradoxical 
embolism. Exercise intolerance consisting of dys- 
pnea and fatigue is difficult to quantify because 
most patients tolerate quite well significant hypox- 
emia. In most centers, the primary indication for 
embolization of PAVMs is prevention of neurologic 
complications. 

It is usually considered that PAVMs with feeding 
: (i.e. the artery leading to the malforma- 




„ 



Fig. I?.~a,h. L "■ iifu se PAVMs. a CT obtained Lit l lie level of both lower lobe? shows multiple PAVMs involving both '.vug*. 
b SeJei^ivs; !:'iei":io:' '.■:' pu.mon-.ii y lij icty to the middle lobe :on]iim^ :Jili: all segment,! I arteries supp-v <-:: : .d\ PAY' Kb. Nixe that 
multiple large PAVMs have already been embolization with coils 



Cion) that are 3 mm or greater in diameter, should 
be treated to prevent complications [20, 26, 77, 78]. 
The reason is that individuals with PAVM of this size 
or larger are at risk of stroke or transient ischemic 
attack due to passage of small clots through the mal- 
formation [73, 77]. The potential for brain abscess 
is reduced by treating all identified 3 mm diameter 
arteries leading to PAVMs, but not eliminated, hence 
the need for continued antibiotic prophylaxis before 
dental work [20]. Of interest, a recent case of neu- 
rological complication in a patient with two small 
PAVMs < 3 mm has been reported [72]. 

In patients with diffuse PAVMs, depending on the 
patient tolerance and the amount of iodinated con- 
trast used, multiple PAVMs canbeembolized during 
the same session. However, additional sessions are 
usually necessary to treat all the visible PAVMs. In 
these patients, embolotherapy may result in partial 
improvement of dyspnea, oxygenation, and shunt 
fraction. 

Finally, emergent embolization of PAVMs in 
patients with life-threatening complication such as 
pulmonary hemorrhage, hemothorax or hemoptysis 
can be discussed [1, 13, 18]. 

Women should be informed that PAVMs may 
enlarge during pregnancy and fatal hemorrhage 
from maternal PAVMs has been described [16, 20]. 
Altered hemodynamics and hormones found in 
pregnancy likely cause changes in PAVMs that pre- 
dispose them to deterioration [13, 18]. Most cases 
of PAVM deterioration seem to occur during the 
second or third trimester when blood volume and 
cardiac output are at their maximum [18]. The use of 
embolization in pregnant women has been reported 
in case of complications [18]. However, because of 
concerns about fetal radiation exposure; it is desir- 
able to screen women with HHT or previous PAVMs 
before pregnancy [13]. PAVMs should therefore be 
treated maximall;' before pregnancy [3, 20]. 



17.8 

Procedure 

17.8.1 
Preparation 

Unilateral femoral vein punctu re is performed under 
local anesthesia and a 7- or 8-F introducer sheath 
is placed. Mild sedation is usually used. Prophy- 
lactic antibiotics are given at the beginning of the 
procedure. Intravenous heparin (5000 IU) is given 



preprocedu rally supplemented with 1000-2500 IU 
hourly during catheterization. Continuous EKG, 
arterial pressure and Sa02 monitoring are obtained. 
Diagnostic angiography is still used by some inter- 
ventionalists to obtain precise segmental anatomy, 
to measure arterial diameter and to choose the pro- 
jection that best displays the PAVM [78]. A baseline 
pulmonary artery pressure is usually obtained at the 
beginning of the procedure. 



17.8.2 

Technique of Catheterization 

The method of catheterization has been extensively 
described by White et al. [77, 78]. The procedure 
first involves localization of the PAVM by angiogra- 
phy followed by catheterization of the feeding artery, 
advancement of the catheter tip to a point beyond any 
branches to normal lung and immediately proximal 
to the dilated venous portion and arterial occlusion 
using coils or balloons [77]. The development of 6- and 
7-F guide catheters (Gonadal, Cordis; Lumax, Cook) 
has greatly simplified access to PAVMs and stability 
of catheters when introducing balloons or standard 
pushable fibered coils (Fig. 17.6). Guide catheters sta- 
bilize one's position proximally in the feeding artery, 
in order to provide a controlled and precise delivery 
of coils through a coax ially placed 4- or 5-F catheters 
(Fig. 17.6). Multipurpose catheters (Cordis), Cobra 
catheters (Terumo) or Judkins right coronary cath- 
eters (Cook) are particularly suitable for catheterizing 
most PAVMs. For the right middle lobe or lingula, 
a Judkins Left coronary catheters may be useful to 
get access to the feeding artery (Fig. 17.6). Selective 
catheter positioning is achieved by advancing the 
catheter either directly or over a wire under fluoro- 
scopic guidance. Once a segmental artery has been 
selected, it is mandatory to aspirate blood through 
the catheter to prevent air or clot injections that may 
pass through the PAVM or enter the coronary circu- 
lation causing angina, bradycardia or electrocardio- 
graphic ST segment wave changes, if blood return 
is not obtained during aspiration, the catheter must 
be gently removed. The catheter must be carefully 
flushed using a heparinized solution before injection 
of iodinated contrast material. An underwater tech- 
nique must also be used for exchanges of wires to 
prevent air from going through the PAVM [40, 78]. 

The use of a coaxial microcatheter for cath- 
eterization and embolization may be needed to 
increase stability or to embolize the venous sac [9, 
79]. In addition, the use of a 




i-'ig. ! 7. ('■:!, b. !-riihol.z M.-in of a dng'. !ji' r'AV'.M. a 7 lie feeding ;ii leiv to a lingual r'AVM i ,!•■'.:: ^k i is sde.: lively ■.-.:L:etenzed using 
a left I u oliuis ?-r catheter iiin,:^ ) \vhic:'. js stabilized using .: 7-!-' guiding :a:iieiet i.iJC). bA?-: [liL^iOiJllielcj :s then :,uefullv 
advanced in the feeding aiteiy close to :hr aneurysmal sue {asterisk) 



the risk that the catheter may be dislocated during 
the advancement of macrocoils or balloons and the 
subsequent problem of coil deployment in inappro- 
priate vascular territory [9]. The risk of perforating 
the aneurysmal sac when superselective periph- 
eral catheterization is performed is reduced when 
microcatheters are used. Finally, a microcatheter 
is extremely helpful when a Judkins left coronary 
catheter is required to get access to the right middle 
lobe or lingula (Fig. 17.6}. 



17.8.3 

Embolization Materials 

Embolization needs to be carried out with devices 
large enough to occlude the feeding artery securely. 
In the first case reported by Porstmann in 1977 
[51], thePAVMwasembolized using hand-made steel 
coil. White et al. performed most of the early cases 
using different types of detachable balloon systems 
[75]. These devices initially developed for neuro- 
vascular and cardiovascular large-vessel occlusion 
are no longer available in most countries [27, 50, 
75]. Balloons had the advantage of providing total 
cross-sectional artery occlusion and recanalization 
due to early deflation was a rare event [50]. In the 
long-term, most of these balloons deflated but occlu- 
sion time was sufficient to obtain thrombosis of the 
PAVM. Experience with detachable balloons as well 
as newer occlusion devices, like the "Amplatzer", 



vascular plugs and the "Gianturco-Grifka vascu- 
lar occlusion device" suggested that cross sectional 
occlusion should be the goal for embolotherapy of 
PAVMs [15]. 

Nowadays, most groups favor the use of coils as 
the primary embolization agent. Initially only stain- 
less steel coils such as the Gi a nturco -Anderson- Wal- 
lace were available [11, 23, 55, 78]. More recently 
platinum coils available in fibered and nonfibered 
variants have become available (Fig. 17.7) [40]. The 
choice of a coil of a correct size is critical: too small, 
the coil may pass through the venous portion of the 
PAVM into the systemic circulation with potential 
disastrous consequences [78]. Too large, the coil 
may cause occlusion of proximal normal pulmo- 
nary arterial branches or may elongate leading to 
recanalization [33, 78]. After placement of the first 
coil, additional coils must be positioned until blood 
flow to the PAVM has ceased [78]. Packing of smaller 
coils in the center of the first placed coil is manda- 
tory to obtain complete cross-sectional occlusion 
and prevent recanalization (Fig. 17.8). If the number 
of coils is not sufficient recanalization may also 
occurbecause of insufficient thrombosis formation 
[33, 78]. 

The role of venous sac embolization remains 
unclear [79]. Venous sac closure is usually neces- 
sary in less than 1% of PAVMs when the artery to 
the PAVM is short (2 cm or less) and has high flow 
or uneven diameter and there is a risk of paradoxical 
embolization [6, 9, 78]. 



Mil] form at ions 




Fig. 17.8. Packing technique, in:;;: equate u.-cking of coils may 
be associated with central recanalization of the erabolized 
-AVM. Adequate racking consists of complete cross-sectional 



I VtncbaWe coils such as the Guglielmi coils (GDCs) 
have been occasionally used to perform embolization 
of the venous sac [9, 32]. A less expensive alternative 
to GDCs when repositioning or controlled placement 
is required is interlocking detachable coils [68]. The 
specific advantages of detachable coils is that they 
can be retracted if placed inundesired position. They 
can also be helpful to treat large high-flow fistulas 
that lack venous component [9]. The disadvantage 
of occluding the venous sac is the increased number 
of coils needed to pack the sac compared with the 



number of coils used in the occlusion of the feeding 
artery alone [9, 68]. Another approach to the embo- 
lization of the venous sac is the use of a temporary 
occlusion balloon catheter with a microcatheter 
placed into the aneurysm, the so-called vein of Galen 
technique (Fig. 17.9) [69]. Microcoils equivalent to the 
■ of the aneurysmal sac and exceeding the 
■of the draining vein are placed. 



17.8.4 

Embolization Techniques 

Different techniques for using pushable fibered 
coils have been developed. In general, these tech- 
niques for closing vessels 3-15 mm in diameter 
are equally applicable for all arterial occlusions in 
the systemic circulation as well. It is of paramount 
importance to achieve cross sectional occlusion at 
the time of initial therapy in order to reduce the 
risk of recanalization. The majority of arterial and 
venous occlusions can be performed using "cur- 
rent generation" 0.035 or 0.038-in. pushable fibered 
coils which produce reliable cross sectional occlu- 
sion, providing they are placed coaxially through 
a guide catheter and deployed into a dense mass of 
fibered coils. Rarely microcoils or detachable coils 
are required [79]. 



17.8.4.1 

Anchor Technique 

Thi.^ technique is used lor clem:; hi;ili-[lo'.v feed- 
ing arteries. It is also useful for routine occlusion if 
there is any concern about movement of the coil after 
deployment. The first centimeters of a long coil are 
anchored in a side branch immediately proximal to 
the site to be occluded (Fig. 17.10). The remaining 
coil is tightly packed into a "nest" and additional 
coils are added and packed until cross sectional 
occlusion of the artery is achieved (Fig. 17.11). 



17.8.4.2 

Scaffold Techniqui 



Using stainless steel or inconnel (European equiv- 
alent of stainless steel} high radial force coils, an 
"endoskeleton" is constructed within the artery to 
be occluded (Fig. 17.12). Usually the first high radial 
force coil should have a diameter 2 mm larger than 
the artery to be occluded. The occlusion is finished 




{. 17.9a-d. Vein or" Galen technique, a Right pulmoitarv artery liii^iogram: a large _ejilj.il PAVM udii) with a short and 
high -rlo.v feeding .1: ".ery is identified, b a temporary occlusion oalloon catheter i Hi is inflated occluding I he teed mg ai l^iy. A 
jl-F microca:he:er is placed in the aiieui ysnval sac (<utp n-'i). t a total of 12 vein of Galen and complex helical coils have teen 
deployed into the aneurysmal sac i ,in c ■■. j. d additional coils with a maximem diameter of 12 nun have been placed to obtain 
complete occlusion of [he sue (iiiti'ir! ; keprociuced from [<:■'■)]. with permission) 

by "packing" long fibered coils to achieve cross sec- 
tional occlusion (Fig. 17.12). 




17.8.4.3 
Occlusion Balloi 



t Assisted Technique 



This technique is often utilized in a high-flow 

PAVM or if the feeding artery is large (>12 mm). 

A temporary occlusion balloon catheter is placed 

to occlude the PAVM. The initial coils are placed 

centimeters of a long th h the balloon occlusion catheter are high 

immediately prtuomal ,. , ,- . , , ., , . 

be occluded. This technique prevents coil migra- radml force skinless or mconnel coils and they 



Fig. 17.10. Anchor technique. The 

coii are caref.illv pb.ced in a side br 



alsobi 



) the s 



red" in a side branch p 
to be occluded. After placing betweei 



Pulmonary Arteriovenous Mill format ions 




Fie. ! '.] 1 a,b. A . i .; 1 1 ■ .| -. _i :_i ] jrr. a A - : 1 1 : ."■ I . side ."'i:, :":.:.". d;.' '■:■!'. : ii:ii:ir.:...ilr.v proximal !.:■ Jir sile io be ::■ ."clnoeJ :. f" .: .■; idnyified. 
b The first centi meters of :. long coil are anchored in the side branch (arrow) 




Fig. 17.12a-c. Scaffold technique, a A large PAVM of the left 
lower lobe is identified i^iii'iri. b Willi dir use of a 7-F guid- 
ing catheter (GC) and a 5-F catheter, an "endo skeleton" .s 
constructed within the artery io be occluded using a high 
: a dial force coil uinvi; i.The first coil should have a di 
1 mm larger than ihe artery to be occluded, c 'he occlusion 
is finished by "flicking" long fiber ed coils to achi 
sectional occlusion (i 



two and three high radial force coils, the bal- 17.8.4.4 

loon occlusion catheter is deflated and a standard Vein of Galen Techniq 

coaxial guide catheter substituted. Embolization 

is then finished by "packing" long fibered coils 

to achieve cross sectional occlusion as previously 

described. 



hnique is used for occluding the aneurys- 
of short and/or high-flow PAVMs. Over- 
re injected through microcath- 



eters directly in the aneurysm of the PAVM [69]. 
The interventional radiologist should be aware of 
this technique even if it is not commonly used. In a 
recent study, the vein of Galen technique was used 
in six out of 650 consecutive patients only [69]. How- 
ever, it is particularly recommended in case of a 
short artery, usually less than 1-2 cm in length or 
when it is difficult to place safely snmdard fibered 
coils, because of high flow to the PAVM (Fig. 17.9). 



17.8.4.5 

Squirt Technique 

This technique is suitable for all fibered pushable 
s (0.018-in.) through microcatheters. The 
is loaded into the microcatheter and a 1-ml 
luer lock syringe with saline flush is attached to the 
hub of the microcatheter. Under fluoroscopic guid- 
ance the microcoil is delivered with small boluses of 
flush. Final adjustment of the microcoil can be done 
by moving the microcatheter before final delivery 
of the complete coil, if the initial deployment of the 
coil is distal to the site tor deployment. 



17.8.4.6 

Wire Push Technique 

For large lumen microcatheters, it is necessary to 
use a 0.021 or 0.025-in. pusher wire to avoid catheter 
occlusion. In the newer microcatheters (Renegade Hi- 
Flo, Boston Scientific; Progeat 2.7, Terumo or Embo- 
cath, Biosphere Medical), the use of standard 0.016- 
in. pusher wires will cause trapping of microcoils 
between the inner diameter of the microcatheter and 
the microcoil. To avoid this the "squirt technique" is 
utilized or a larger pusher wire is required. 



17.8.4.7 

Pulmonary Flow Redistribution 



This tech: 

to improve hyp> 

pattt 



i of dis 



ieveloped as an approach 
l patients with a diffuse 
; [62]. A temporary occlusion of 
lobar arteries of the most affected lobes (usually 
both lower lobes) is performed to determine if there 
is any improvement in oxygenation. In the patients 
whose Pa02 increases by at least 10 mm Hg, a per- 
manent lobar artery embolization is performed in 
order to obtain flow redistribution in the remaining 
(less affected) lobes [12]. 



17.9 
Results 

Long-term follow-up is indicated in all patients with 
PAVMs even after a successful therapy because of 
the risks of serial growth of small lesions and reper- 
fusion of embolized PAVMs [20, 33]. Clinical and 
imaging follow-up of patients treated with emboli- 
zation has been published in several studies origi- 
nating from a limited number of centers [11, 25, 40, 
50, 55]. 



17.9.1 

Clinical Follow-up 

Long-term follow-up of patients treated with embo- 
lization has been reported in several studies [11, 40, 
55, 60, 71, 77]. In a recent study, the long-term out- 
comes of embolization (mean follow-up 62 months), 
were successful in 83% of 112 treated patients overall 
and in 96% of patients in whom all angiographi- 
cally visible PAVMs were embolized [40]. During 
the follow-up after embolization major neurologi- 
cal complications such as cerebral abscess, transient 
ischemic attack, or stroke related to reperfused 
treated or new PAVMs have been reported [11, 25,40, 
77]. The long-term morbidity of reperfused PAVMs 
is unknown but some patients have already suffered 
from stroke because of recanalized PAVMs [40]. 

Repeat treatment is therefore indicated during 
the follow-up because of recanalization of previ- 
ously embolized PAVMs or enlargement of untreated 
PAVMs maybe seen in up to 13% of treated patients 
(Fig. 17.13) [33, 40]. Simple PAVMs are usually easy 
to occlude without risk of recanalization (Fig. 17.14). 
Different mechanisms accounting for reperfusion of 
embolized PAVMs have been described with follow- 
up CT [33]. These include recanalization of emboli- 
zed PAVMs due to insufficient packing, recruitment 
of adjacent normal branches and rarely systemic 
supply to the embolized PAVM (Fig. 17.15) [33, 59]. 

In most patients with diffuse PAVMs, improve- 
ment of dyspnea, oxygenation, and shunt fraction is 
not complete [12]. The residual shunt is believed to 
represent the shunt through small PAVMs [12]. Even 
if clinical and radiological evaluation is necessary, 
oxygen saturation tests are equally important to 
predict recurrence. It is recommended that patients 
with diffuse or non treated PAVMs be given antibi- 
otic prophylaxis before dental and surgical proce- 
dures to avoid seeding of PAVMs and subsequent 
development of brain abscess. 



s Malformations 




tig. I ■ .! y.i..b. !-!i.. 1 1 it- i'ii — :". : ■■:' -:.i. .! -AY M ■■..;■ ".' .■-: lb: .: -: be:'. . - e: ::>.-. i;a:io:: a large !-AVM : itsh'fiik) o: lite fight lower lobe. 
A small PAVM of the ugh: mic.dle lobe is seen iiii ten), b At I year later, there is s:gnihca:'.: enlaigemcm of the PAVM : iinrni). 
".e treated PAVM is seen 



\ \ ^A s 


Bl"<*v, 


^M**l«*. 


V 



Fig. 17.14a-c. Embolization of a simple form of PAVM. 
a Selective injection shows a simple form of PAVM with the 
aneurysmal sac i\: supplied by ■. ■ n e segmental artery ((iftl'ii'I. 
7 lie draining vein is seen i I':, b After embolization with coils, 
complete occlusion is seen, c Chest radiograph obtained 
j months after embolization shows letiacdcn of :Jjc- PAVM 





Fig. 17.15. a CT performed {- months nfl^r embolization of a 
complex PAVM of dir right uppei lobe allows recanalization 
'.■:' li'.e feeding arlei y Mi toui due to insufficient packing. The 
draining vein is still opacified i I'i. h Selective injection of the 
feeding artery confirms rec idealization i<irrpirj. Additional 
embolization has rieen performed to obtain complete cross- 
sectional occlusion 



mean follow-up of over 4 years (Fig. 17.14) [36]. In one 
large study, follow-up with CT scan 1 or more years 
after embolization showed that %%ott rested PAVMs 
were either undetectable or reduced in size [56]. This 
phenomenon is believed to be the result of thrombo- 
sis and retraction of the aneurysmal sac following 
embolization (Figs. 17.13, 17.14) [56]. Reperfusion of 
accurately embolized PAVMs is considered as a rare 
event, predominantly alio u as large and/or complex 
PAVMs [36, 40]. As previously mentioned, reperfu- 
sion may be due to several mechanisms. Insufficient 
cross-sechoniial occlusion (coil packing) at the tune 
of embolization is an obvious cause of recanalization 
(Fig. 17.14) [7, ii, 59]. Small accessor;' branches to the 
PAVM may be missed during the initial embolization 
or recruitment of initially normal branches adjacent 
to the PAVM may occur [33]. Small branches supply- 
ing the embolized PAVM may also be missed during 
follow-up CT evaluation particularly in the absence 
of contrast enhancement or because of coil-related 
artifacts [33, 59, 74]. Bronchial artery hypertrophy 
has been identified as a cause of reperfusion of small 
residual aneurysm after embolization [34]. Bronchial- 
to-pulmonary artery anastomoses may enter the pul- 
monary circulation distally to the embolized artery 
supplying the scarred region of the obliterated PAVM 
and may lead to future recanalization [7]. It is not 
known if the formation of systemic collaterals may 
place patients at risk for future hemoptysis [33]. 

Contrast echocardiography and MR perfusion 
imaging are probably too sensitive and remain positive 
in the majority of patients even after successful occlu- 
sion of all angiographic! I Iv visible PAVMs [37,47]. 



Rare reports of pulmonary hypertension follow- 
ng embolization have been published [24]. 



17.9.2 

Imaging Follow-Up 

Imaging lollov.-up ol treated patients in conjunction 
with clinical and physiological evaluation should 
be performed in order to document involution or 
reperfusion of embolized PAVMs but also to detect 
growth or enlargement of small PAVMs [5, 33, 57]. 
Small PAVMs can over time reach the threshold size 
for complications (Fig. 17.13). In one study of patients 
who underwent embolization of large PAVMs, 91% of 
treated PAVMs disappeared on chest radiograph at a 



Complications: Description and Prevention 



Complications following embolization of PAVMs 
have in general been infrequent and self-limited, par- 
ticularly in experienced hands [20, 40]. Most of the 
reported complications are minor and self-limited, 
most of these only require symptomatic treatment 
[20]. Pleuritic chest pain occurring in the first 24 h 
after embolization is the most frequent complication 
encountered in up to 13% ol treated patients [11, 20, 
40, 55, 77]. The incidence seems higher in patients 
presenting with large PAVMs [20, 36]. Pleural effu- 
sion has been reported in up to 12% of patients [40]. 
Pulmonary infarction has been observed in 3% of 
patients and most likely was related to occlusion of 
normal pulmonary arterial branches [55, 71, 7c>]. The 



i'lilnion.ify 



catheter tip should therefore be advanced distal to 
any arterial branch supplying normal lung paren- 
chyma as close as possible to the neck of the PAVM. 
Air embolism during embolization has been reported 
inup to4% of patients who developed transient symp- 
toms such as angina, bradycardia or perioral pares- 
thesia [11, 50, 71, 77]. Careful flushing of the catheters 
and observation of back bleeding before injection 
make this complication completely avoidable. 

Majoro^iiplicationssuchasparadoxicalemlX'liza- 
tion of a device and stroke are extremely rare. Device 
migration has been reported in about 1% of cases 
mainly with coils [11, 23, 40, 50, 55, 71]. Rare reports 
of balloon migrations have been published [11, 23, 40, 
50, 54]. Coil migration is more likely to occur in case 
of large (> 8 mm) or high-flow PAVMs and during the 
learning curve of the interventional radiologist [40, 
77]. These migrations may require additional inter- 
vention using an intravascular retrieval device. The 
use of occlusion balloon-assisted or vein of Galen 
techniques for short, large, or high-flow PAVMs may 
reduce the risk ot coil migration [69]. In all cases the 
first coil should be oversized in order to form a nest 
and prevent further coil migration. 

One report of cerebral infarction occurring 
1 week after coil embolization of a single PAVM has 
been recently published [39]. Clot migration from 
the embolized PAVM partially reperfused via a pre- 
viously embolized feeding pulmonary artery and 
a bronchial artery was the supposed mechanism 
accounting for this stroke [39]. 



17.11 

Conclusion and Perspectives 

Although embolization is a safe and effective treat- 
ment in the management of PAVMs, long-term 
follow-up of patients is mandatory to document 
aneurysmal retraction or reperfusion of treated 
lesions and to detect growth of small PAVMs reach- 
ing the threshold size for neurologic emboli. From 
a technical point of view, it is important to per- 
form the embolization with coils placed as dis- 
tally as possible in the feeding vessel to a PAVM 
close to the venous sac. This technique avoids the 
occlusion of branches to normal lung and reduces 
the rate of reperfusion and the risk of pleurisy or 
pulmonary infarction. In patients with localized 
PAVMs, prevention of neurological complications 
can be achieved in almost all cases if all PAVMs 
are occluded. Conversely in patients with diffuse 
PAVMs, multiple procedures will be necessary to 
improve the profound hypoxia, decrease the risks 
of neurological events and obtain an acceptable 
quality-of-life. 

Embolization ot PAVMs requires a specific exper- 
tise and should be performed by specially- trained 
interventional radiologists only. Pluridisciplinary 
management of PAVMs in HHT is mandatory in 
order to apply the appropriate treatment and to 
fully educate the patients and their family about the 
diagnosis, its clinical implications, and its heredi- 



Cookbook: 


1. Technique of catheter izatio 


n of PAVMs 










Indication 




First choice 




Second choice 




Simple or complex PAVM 

PAVM of the right middle loir 
Embolization of the venous s 


..^d. 


5-F ludkins right calheie:' 

5-F Judkins left catheter 
3-F Micro catheter 


5-F Cobra-shaped catheter 
5-F Multipurpose catheter 
j-F Mi era catheter 




2. Technique of embolization 


of PAVMs 










Indication 




First choice 




Second choice 




PAVM with normal flow 
PAVM with high flow 

PAVM with large feeding arte 




Scaffold technique 
Anchor technique 

Anchor technique 




Anchor technique 
Vein of Galen technique 

Occlusion balloon-assisted t- 


— 



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Subject Index 



absolute alcohol 24 



bleeding 50 

chr;imc pancreatitis 91 



adenomynsis 129,184 
aetrwisderol 26 
alpha agonist 228 
amenorrhea 135, 143 



.'V-p!.'.V 
spider 27 

- li g 3 ? 
.inih'" technique 38 
angiodysplasia 75,77 
anterior division of the internal il 
aortic puncture 249 
aortobronchial fistula 263 
arcofRiolan 247 
arcuate artery 108 



- malformation of the brain 280 

- shunt 53 

aspergilloma 263 
azygos artery 143 



balloon-occluded retrograd' 

(B-ORTO) 99,102 
bead block 189 
beta -emitting microsphere 190 
B-ORTO, see balloon-occluded retrograde 

obliteration 
bronchial artery 265,266,265,269 

- aneurysm 273 

- embolization 7,263 
--chest pain 275 
--coils 273 
--communications 267 

- complications 275 

- - detachable balloons 273 

- embolic agents 27.1 

- - gelatin sponge 272 

- - polyvinyl alcohol panicles 273 
--recurrences 274 

- - spherical embolic materials 27? 

- - spinal cord ischemia 275 

- - technical success 274 

- technique of embolization 169 
-- tris-acryl gelatin 273,275 






100 



cavernosal artery 228 

- artery 76 
-trunk 51,52,63 

cervicovaginal 
-branch 143 
-laceration 113 
channel 236,246 

-pancreatitis 93 

- pelvic pain 201 

- vaginal discharge 1 35 
clinical recurrence 188 
closure device 152 
coagulopathy 110 
coehac 91 

coil 26,80,112,287 

- anchor 27 
-cage 27 

- migration 293 

- packing 292 
collateral 246 
colon iscliemi 



256 



- bronchial trunk 267 
-iliac artery 253 

- intercostobronchial trunk 265 
complication 45 
contourSE 133,189 

contrast extravasation 53 
contrast-enhanced MR 136 
costocervical trunk 267 
CT guidance 248 
cya no a cry late 24 
cystic fibrosis 263 



-balloon 28,286 
-coil 61 
deiergeiiL-ty.^e sclerosant 

- eti'.anolamine oleate 2d 

- polidocanol 26 



I'll], see disseminated inlravosciLOf coagulotion 
dimethyl sulfoxide (DMSO) 25 
disseminated ijit: ovus^li l^i r coagulation (DIG) lOf 
DMSO, see dimethyl sulfoxide 

- pancreatic artery 92 

- penile artery 228 
■-:-y, ol-'inji 



.-. 



. i?.i,is: 



191 



Lyipha);ia 275 
Lyipntj 2K 

E 

e>cl ive embolization 4 
EmboCath 145 
EmboGold 19 
enrbolic 

- agent 5S 

- materials 4 
embolotherapy 15 

- complications 5 

- embolic materials 4 
rnrbo-phere 20, 116, 14 
rnrergencv enibc-jzaiioi 
emoinc embolization 56 
endoleak 253 
-angiography 245 

- angioplasty 249 

- balloon angioplasty 246,247 

- bare stent 249 
-biphasicCT 237 

- channel 247 

- classification 236 

- coil embolization 246 

- color Doppler ultrasound 237 

- CT angiography 237 

- delayed acquisition 237 

- embolization 246 

- endotensin 237 
-inflow 246 

- .arge Polmoz stent 246 

- lumbar arteries 236 

- MR angiography J 4? 
-MRI 245 

- other agents 248 
-outflow 246 

- proximal cuff 246 
-pseudo-endoleak 237 



-sac 247 
-seroma 249 
-SMA 247 

-stent-graft 247 

- surgical ligation 24 
-treatment 245 

- triphasic CT 237 
-rypel-III 236 
-rypelV-V 237 



endometrial 
-bleeding 129 
129 



endometriosis 131 

endotensin 237 

endovoscular aor:ic aneurysm repair (EVAR] 235 

epigastric artery 109 

esophageal artery 51 

ethanol alcohol 24 

ethanolamine oleate 26, 100 

ethibloc 25,248 

ethiodol 24 

tV'AR, see en c ''vascular aortic aneurysm reaair 



failure 188 
fibroid 

- perfusion 136 

- shrinkage 159 
-volume 136 
fresh frozen plasm; 



ices 00,100 
oduodenal 

-r.ographic anatomy 5! 
■ry 51,53,54,59,61,92 
oepiploic artery 51 , 92 
■r-s. ph i;a;er.. varices 53 
ointestinal 



lalshur 



100 



147 



zelfoa 



i 21,61,111,116,147,153 
-torpedo 65,179 

Giamurco coil J 5 , 22! 
Gianturco-Anderson-Wallace coil 236 
: "I K, see ^a ,; iO'i:\:r: : t.:'a. hemorrhage 
Glubran2 25,66 



; 24,54 



i6, 67, 6i 



sluebron : 

gluteal artery 109 

GnRH 126 ' 

G-i-gliemi detachable coil 35 

H 

haematemese 88 

haemobiaa 

- angiography 88 

malformations i 



■- 87 



-ct as 

- embolization 91 

- hepatic artery %i 

- iatrogenic 87 

- management 90 

- papillary artery 87 
helicobacter pylor 
hematochezia 62 



50 



Subject Index 



hemoglobinuria 101 
hemoptysis 7, 263 

- bronchial artery anatomy 265 

- bronchoscopy 264 

- causes of hemoptysis 264 
-CT 265 

- non-bronchial 269 
/.emorrfiaeic shock 43 
hemorrhoidal branch 76 

teriogram 90 



hepat 
hepat 



tery 



] , t-4, &S, «2 



v hemofih.L'.g!.: ir.angie' 



-vein 143,200 
u : I c- j :'.a. 

- mammary artery 267,270,272 

- pudendal artery 229 

- thoracic artery 267 
intracavitary fibroid 1 68 
inlramural 

- fibroid 143 

- leiomyoma 12S 
iodized oil 24 

ischemic radiculopathy 254 



- gastrointestinal bleeding 280 
-type 1/2 280 

-seizure 280 

- stroke 280 
histoacryl 65 
hydrophilic wire 80 
hyperaemia 53 
hypervascular tumor 58 
hysterectomy 113 

- complications 125 

- morbidity 125 
-mortality 125 



iliolumbar 109 

■MA, see inferior mesenteric anerv 
infarction 67 
infection 165 

- anterior pancreaticoduodenal artery Si 

- gluteal artery 142 

- hemorrhoidal 108 

- mesenteric artery (IMA) 75, 110, 236, 2 

- pancreaticoduodenal artery 92 

- phrenic artery 267 

- rectal artery 229 

- thyroid artery 267 
-vena cava 100 
inflammatory 

- bowel disease 75 
-lung disease 263 
inflow vessel 247 
mtercostiu hand: 27? 
intercostobronchial 

- artery 270 

-trunk 266,268,269,271 
internal iliac 
-artery 76,108 

- buttock claudication 256 
--coils 253,254 

- colon ischemia !:<*< 

- complication 255 

- embolization 253 
--EVAR 253 

- - lumbosai :i. pines ischemia 257 

- perineal isc hernia 257 

- perineal nocrosii l.-l 

- - sequential vs iim_ilane»us 255 

- - sexual dysfunction 256 



- bronchial artery 2<o 

- gastric artery 51, 63, 92 

- hepatic artery 92 
-ovarian vein 204 
-renal vein 204 
leiomyomata 126 
leiomyosarcoma 129, 168, 184 
lipiodol 24,191 

liquid agenl 23 

- absolute alcohol 24 

- cya no aery late 24 

- detergent-type sclerosants 26 
-ethibloc 25 

liver transplant 64 

lower gastrointestinal (LGI) bleeding 7,73 

- angiodvsplasia 75 

- clinical success 82 
-coil 80 

- embolic agents 79 

- ischemic complications S3 
-PVA 79 

- recurrent hemorrhage S3 

- surgery 82 

- technical success 82 



- vasospasm 81 
lumbar artery 236,254 
lumbosacral plexus ische: 
Lupron 179 

M 

mammary artery 267 
marginal artery 77 
MassTransit catheter 41 . 
melena 53,54,62 
menorrhagia 128 
methylene blue 228 
microcatheter 28 
microsphere 153,190 



middle hemorrhoidal 77, 108 

MRI detectable microsphere 191 

MRI-guided focused u nrasouitd fibroid ablation 126 



NBCA 249 
neovascularisation 53 
Nester coil 36 

neuroendocrine tumour 90 

nidus 247 

nitroglycerin 152 

non-spherical polyvinyl alcohol 153, 181 

lion- steroidal ;ii"il;-inri. !;•.'.;•.:. it. my ( NSAH'M I 34 

non-target embolization 163 

NSAID, see non-steroidal a nti- inflammatory 

nutcracker phenomenon 199,200 



onyx 25,248 

Osler-Rendu syndron 
-genetics 279 

outflow "vessel 246 



-artery 112,133,144,154,162,178, 
-failure 165 
-iliac vein 200 

-plexus 204 
-varicosity 200 
-vein 40,199,204 
--varice 131 

oxycel 23 



pampiniform plexus 21 5 
pancreatic 

- branch 76 

pancreatic;! magna artery 92 
pancreaticoduodenal 

paiiMeatkis 
-angiography 91 

- CT g::iced percutaneous thrombi: 1 . 

- CT g::;ced thrombin injection 95 

- pseud oaneurysm 91,93, 95 

- true aneurysm 95 

- ultrasound 91 

- visceral aneurysm 87, 95 
papillary artery 87 
paradoxical embolization 293 
particulate embolic ngenl 15 
-agglomeration 18 
-avitene 23 

- catheter occlusion 1 7 



- oxycel 23 

- polyvinyl alcohol i i: 

- microspheres 20 

- tnsacryl gel.'.tm microspheres 18 
particulate embolization 58 
PAVM 37 

pedunculated submucosal fibroid 169 

- congestion syndrome 199 
--CT 202 

- embolization 204 
--MRI 202 

- surgical treatments 204 

- ultrasound 202 

- infection 131 
-pain 134,199 

- varicose vein 200 
penel lai.ng trauma 44 
penile brachial index 257 
perineal 

-ischemia 257 
-necrosis 257 
phrenic artery 52,270 
placenta 

- praevia 110 
placenial abruption 110 
platelet 43 
platinum 



pleuritic ches: pain 292 

polidocanol 26 

polyvinyl alcohol (PVA] 16,79,112,116,146,159 

- microsphere 20 
portal hypertension 99 
post-embolization syndrome 6, 134 
postpartum hemorrhage 107 

- balloon occlusion 116 

- blood Iransfusion 1 1 1 



-DIG 108 

- embolotherapy 1 1 1 
-fertility 114 

- hysterectomy 113 

- inferior mesenteric artery 1 1 

- internal iliac ligation 1 13 

- pregnancy 114 

- uterine artery 108 

- uterine atony 108 

pressuri7jtion 249 

-color :■ .-.■.!.■ . 10 
-diagnosis 22> 

- - an.; i ■ v i 29 
-Doppltr 228 

- embuhilhtrapy 229 

- erect i It function 231 
-painful erection 227 
-pen c c":ras:!urd 228 
-posttraumatic 230 

- surfi. i! ij'.i':. 228 






nurys 



lusive priapism 227 
icro catheter 29 
ic embolization 56 



. 263 



is malformation 263,279 

— - anchor technique 287, 288 

— classification 283 

— clinical manifestations 280 
--coil 286 

— complex form 284 

— complications 292 
--CT 282 

— - detachable balloon 286 

— - echocardiography 261 

— - embolization 284,287 
--imaging 281 

— - imaging follow-up 292 

— occlusion balloon assisted technique . 

— oxygen saturation 290 

— - packing technique 287 

— paradoxical embolization 293 

— - Scaffold technique 287 
--simple 283 

— squirt technique 290 



— vein of Galen technique 289 

— wire push technique 290 

- endometriosis 263 

- How redistribution 290 
-infarction 275 
ous-'.afle fibered coil 35 
PVA. see polyvinyl alcohol 



ijdial artery 108 

RBC, see 99m labeled red blood cell 

red hlnrid cell (RBC), Wm labeled 54 

renal vein 218 

Kenju ;:iler-Weber syndrome 279 

Renegade Hi-Mo 41,145 

res:dual fibroid perfusion 160 

rest: -hah t embolic 193 

retained phcenta 110 

rel-u'vahk toil anchor 27 

right 

gastric artery 51,67 

hepatic artery 92 
- intercostobronchial artery 265 
-ovarian vein 208 
-renal vein 204 
round ligament 1 10 
sac 246 

sandwich embolization 57, 63 
Scaffold technique 39 
sclerosant 23,205 
scrotalvein 215 



short gastric artery 
SMA, see sup eric 
spasm 179,209 



spheric.:! enihol.c .igenl 

- polyvinyl alcohol microspher 

- tr is aery] gelatin microsphere: 
spherical PVA 146,182 
spider Amplatz device 28 
spinal cord 256 

- ischemia 275 
spleen 41,100 
splenicartery 63,76,92 

- pseudo.'.neurysm t; 4 
Squirt technique 39 
stainless steel coil 60 
stentgraft 28,235,253 
submucosal 
-fibroid 127,143 

- leiomyoma 128 

:;ub serosa! fibroid 143 

- gluteal artery 142 

- hemorrhoidal artery 77 

- mesenteric artery (SMA) 

- vesical 108 

surgical AAA repair 256 
Swan-Ganz 263 



., 52, (.2, 75,91, 247,257,7 



Uoid : 



tantalum 24 

technetium (Tc-99n 

thrombin 95,96 

thyrocervical trunk 267,270,274 

TIPS 99 102 

tissue adhesive 24 

toradol 134 

Tornado coil 36 



l:\iiisli: :v._\ii 



: 79 
247, 248 

venography 201 
trauma, penetrating 44 
trisacryl 

- collagen-coated microsphere 

- gelatin microsphere 18,189 
-microsphere 159 
tuberculosis 263 
tubo-ovarian anastomoses 1 44 
tungsten 24 

type-II endoleak 254 

U 

UAE, see uterine artery embolizi 
UFE 115 

upper GIH 49 

- carbon dioxide 52 

-CTA 54 

- embolization 56 
-gelfoam 61 

- Gianturco coils 60 
-glue 65 

- mortality rate 68 

- N-butyl2-cyanoacrylate u5 

- nuclear medicate 54 

- platinum mierocoils 60 



upper G1H (continued] 

- polyvinyl alcohol particles 58 

- therapeutic vasopressin 56 
-vasospasm 56 

- arteriography 50 

- endoscopy 50 

- surgery 50 

-artery 103,141 

- - arcuate artery 108, 143 
-- azygos artery 143 

- - cervicovaginal branch 143 

- - kekcine artery 143 

- intramural artery 143 

- radial artery 108 

- tubal branch 143 

- vaginal artery 143 
--variant 109 

- artery embolization (UAE) 19, 

- - angiographic endpoint 153 

- closure devices 1 51 
--PCApump 148 

- post-procedure pain 147 
--radiation 153 
--spasm 152 

-atony 108,110 
-bleeding 110 

- complications 1 34 

- contrast-enhanced MR 136 
-fibroid 125 

- - MR angiography ] 3 I 
--MRJ 131 

- - ultrasound 131 

-fibroid embolization 119,187 



178 

— clinical recurrence 188 

— - clinical success 1 77 

— complications 163 

— cost analysis 163 
--deaths 169 
--dissection 180 

— - dysmenorrhea 1 5>i 

— embolization 
--failure 178,1 
--fertility 171 

— - fibroid location 160, 183 

— infection 166 



myomectomy 170 



-late 

- limited embolization 

- menorrhagia 158 
-MRI 178 

- pelvic pain 158 

- post -emboli nation p.-i 

- pregnancy 171 

- pikmonaiy embolus 
159,177 



58 



- - residual perfusion 161 

- -spasm 179,182 

- technical success 1 57 

- urinary frequency 158 

- uterine functionality 194 

- - versus hysterectomy 169 

- fibroid pel fusion 136 

- in utero growth retardation 1 
-infertility 132 

-MR 131, 136 

- MH angk-griipky I 31 
-necrosis 165 

- ovarian failure 133 

- post-embolization syndrome 

- post-procedure 134 

- rupture 110 

- thromboembolic complication 

- ultrasound 131 
-vein 143 
-volume 136 



-artery 108,143 
-discharge 167,168 
-plexus 143 
varicocele 

- coil embolization 221 

- cyanoacrylates 222 

- deiad 1 .;."'k b:J'.'IV ; 111 

- diagnosis 216 

- grading system 216 

- hot (boiling) contrast sclerotherapy 220 

- pi'.thopriysiologie 216 

- perc.i^a neons embolization 1] 7 

- pregnancy 223 

- recurrence rate 223 

- sodium tetradecyl sulfate 221 

- spermatic veins 218,219 

- s : .;i'gk"iil kg.'.tion 1 1 7 
vasopressin infusion 73 

- inferior phrenic 100 

- pericardiacophrenic 100 
-portal 100 

- posterior gastric I 00 



100 

- short gastric : 
-splenic 100 



Wa'irr.Lin loop 111, 152 



List of Contributors 
Volume 1 



Hicham T.Abada, MD 

Department ot Imagine and Inrer.'i-niional Radiology 

Centre Hospitalier Rene Dubos 

6, Avenue de L' lie -de-France 

95303 Cergy Pontoise Cedex 

Douglas M. Coldweu, MD 

Professor of Radiology 

University of Texas Southwestern Medical Center 

5323 Harry Hines Blvd. 

Dallas, TX 75390-8834 

USA 

Michael D. Darcy, MD 
Professor of Radiology and Surgery 
Mallinckrodt Institute of Radiology 
Washington University School of Medicine 
510 South Kingshighway Boulevard 
Saint Louis, MO 63110-1076 
USA 

Luc Defreyne, MD 
Department of Vascular and 
Interventional Radiology 
Ghent University Hospital 
De Pintelaan 185 
9000 Ghent 
Belgium 

Arnaud Fauconnier, MD, PhD 
Department of Obstetrics and Gynecology, 
Centre Hospitalier de Poissy, 
10, rue du Champ Gaillard, 
78300 Poissy Cedex, 

Jafar Golzarian, MD 

Professor of Radiology 

Director, Vascular and Interventional Radiology 

University of Iowa 

Department of Radiology 

200 Hawkins Drive, 3957 JPP 

Iowa City, IA 52242 

USA 



David W. Hunter, MD 

Department of Radiology 

J2-447 Fair view-University Medical Center 

University of Minnesota 

500 Harvard Street S.E. 

Minneapolis, MN 55455 

USA 

Pascal Lacombe, MD 

Department of Radiology Hopital Ambroise Pare 

9, Avenue Charles De Gaulle 

92104 Boulogne Cedex 

Alexandre Laurent, MD, PhD 

Assistant Professor 

Center for Research in 

Interventional Imaging (Cr2i APHP-INRA) 

Jouy en Josas, 78352 

Lindsay Machan, MD 

Department of Radiology 

University of British Columbia Hospital 

2211 Wesbrook Mall 

Vancouver, BC V6T 2B5 

Canada 



Professor of Radiology 

University of Iowa Hospitals and Clinics 

Department of Radiology 

200 Hawkins Dr, 3957 JPP 

Iowa City, IA 52242 

USA 

Tony A. Nicholson, BScM, Sc, MB, ChB, FRCR 

Consultant Vascular Radiologist & Senior Lecture 

Leeds Teaching Hospitals NHS Trust 

Great George Street 

Leeds, LSI 3EX 

UK 



it of Contributors 



Jean-Pierre Pelage, MD, PhD 
Department of Radiology 
Hopital Ambroise Pare 
9,Avenue Charles De Gaulle 
92104 Boulogne Cedex 

Jeffrey S. Pollak, MD 

Yale University School of Medicine 

Department Diagnostic Radiology 

PO Box 20842 

New Haven, CT 06504-8042 

USA 

Mahmood K. Razavi, MD 

Director 

Center for Research and Clinical Tunis 

St. Joseph Vascular Institute 

Orange, CA 92868 

USA 

Jim A. Reekers, MD, PhD 

Department of Radiology, Gl-207 

Academic Medical Center 

University of Amsterdam 

Meibergdreef 9 

AZ 1105 Amsterdam 

The Netherlands 

Anne C. Roberts, MD 

University of California, San Diego Medical Center 

Division of Vascular and 

Interventional Radiology 

200 West Arbor Drive 

San Diego, CA 92103-8756 

USA 

GaliaT. Rosen, MD 

Department of Radiology 

J2-447 Fa irview- University Medical Center 

University of Minnesota 

500 Harvard Street S.E. 

Minneapolis, MN 55455 

USA 

Melhem J. Sharafuddin, MD 
Departments ot Radiology and Surgery, 3JPP 
University of Iowa Hospitals and Clinics 
200 Hawkins Drive 
Iowa City.IA 52242-1077 
USA 



Gary P. Siskin, MD 

Associate Professor of Radiology and 

Obstetrics & Gynecology 

Albany Medical College 

47 New Scotland Avenue, MC-113 

Albany, NY 12208-3479 

USA 

ShiliangSun,MD 
Department of Radiology 

University ot Iowa Hospitals and Clinics 
200 Hawkins Dr, 3955 JPP 
Iowa City, LA 52242 
USA 

Koji Takahashi, MD 
Department of Radiology 
Asahikawa Medical College 
2-1-1-1 Mid on;:; i '-'Li 
Asahikawa, 078-8510 



Jos C. van den Berg, MD, PhD 
Head of Service of Interventional Radiology 
Ospedale Regionale di Lugano, sede Civico 
Via Tesserete 46 



6900 Lugano 
Switzerland 



David A. Valenti.MD 

Royal Victoria Hospital 

McGill University Health Centre 

McGill University 

687 Pine Avenue West, Suite A451 

Montreal, Quebec H3A 1A1 

Canada 

Robert I. White, Jr., MD 

Yale University School of Medicine 

Department of Diagnostic Radiology 

333 Cedar Street, Room 5039 LMP 

New Haven, CT 06520 

USA 

Jeffrey J. Wong, MB ChB, BMedSc 

Senior House Officer 

Royal National Orthopaedic Hospital 

London 

UK 



Contents - Volume 2 



Vascular Malformatio 



1 Percutaneous Management of Hemangiomas ami Vascular Malformations 
Francis Marshalleck and Matthew S. foi 

2 Predominantly Venous Malformation 



Trauma and Iatrogenic Lesions 33 

3 Recognition and Treatment of Medical Emergencies in the Trauma Patient 

Lucy Wibben meyer and Melhem J. Sharafuddin 35 

4 Visceral and Abdominal Solid Organ Trauma 

Gary Siskin and Jafar Golzarian 43 

5 Embolization and Pelvic Trauma 

Jeffrey I.Wong and Anne C.Roberts 59 

6 Postcatheterization Femoral Artery Injuries 

Geert Maleux, Sam Heye, and Maria Thijs 69 

7 Iatrogenic Lesions 

Michael Darcy 79 



Visceral Aneurysm 

8 Embolization of Visceral Arterial Aneurysms 

Craig B. Glaiberman and D.Michael D. Darcy . 



Venous Ablation 

9 Endovenous Thermal Ablation of Incompetent Truncal Veins in Patients with 
Superficial Venous InsuElicieriy 
Neil M. Khilnani and Robert J. Min 



Em bolo therapy Applications in Oncology 127 

10 Chemo-Embolization for Liver 

Christos Georgiades and Jean Francois Geschwind 129 

1 1 Radioactive Microspheres for the Treatment of HCC 

Christos Georgiades, Riad Salem, and Jean-Francois Geschwind 141 

12 Yttrium-90Radioembolizationfor the Treatment of Liver Metastases 

Riad Salem, Kenneth G. Thurston, and Jean-Francois Geschwind 149 



306 Contents - Volume 2 

13 Portal Vein Embolization 

Alain J. Roche and Dominique Elias 163 

14 Embolotherapy for Neuroendocrine Tumor Hepatic Metastases 

Kong Teng Tan and John R.Kachura 177 

1 5 Bone Metastases from Renal Cell Carcinoma: Preoperative Embolization 
Shlliang Sun 189 

16 Embolotherapy for Organ Ablation 

David C. Madoff, Rajiv Verm a, and Kamran Ahrar 201 

17 Research and Future Directions in Oncology Embolotherapy 

Eleni Liapi and Jean-Francois H. Geschwind 221 



External Carotid 233 

18 Technical and Anatomical Considerations of the External Carotid System 

Paula Klurfan and Seon Kyu Lee 235 

19 End ova scu iar Management for Head and Neck Tumors 

Paula Klurfan and Seon-Kyu Lee 247 

20 Embolization of Epiiaxis 

Georges Rodesch, Hortensi a Alvarez, and Pierre Lasjaunias 257 

21 Diagnosis and End ova sen la i 1 Surgical Management of Carotid 
Blowout Syndrome 

John C.Chaloupka, Walter S. Lesley, Minako Hayakawa, 

and Shih-Wei Hsu 271 



Gene Therapy and Pediatrics . 



22 Embolotlu-rapv Applications in Gene Therapy 
James R.Duncan 



23 Embolotherapy in Pediatrics 

Josee Dubois and Laurent Garel . 



Subject Index 321 

List of Contributors 331 

Contents and List of Contributors of Volume 1 335 



List of Contributors -Volume 2 



KamhanAhhar.MD 

Section of Interventional Rr.diology 

Division of Diagnostic imaging 

The University or' Tex a 5 

MD Anderson Cancer Center 

1515 Hokombe Boulevard, Unit 325 

Houston, TX 77030-4009 

USA 



a,MD 



HoRTENSIA Al\ 

Service de Neuroradiologie Diagnostique 

et Therapeutique 

Hopital Bicetre 

78 rue due General Leclerc 

94275 Le Kremlin Bicetre 

France 



John C. Chaloupka, MD, FAHA, FACA 
Director of Interventional Neuroradiology 
Professor of Radiology and Neurosurgery 
University of Iowa Hospitals and Clinics 
University of Iowa Carver College of Medicii 
200 Hawkins Dr, 3893 JPP 
Iowa City, IA 52242 
USA 



Michael D. Darcy.MD 

Professor of Radiakigv .-no Surgery 
Pivision or I'i.igno-iii" Radiology 
Chief, intervention;- 1 Radiology Section 
Washington University School of Medicin 
Mallinckrodt Institute of Radiologv 
510 South Kingshighway, 6th Floor 
St.Louis,MO 63110 
USA 



Josee Dubois, MD 

Professor of Rad: okgv 
Pediairic and Interventi 
Department of Medical Imagii 
Hopital Ste-Justine 
3175 C6te Ste-Catherine Road 
Montreal, Quebec H3T 1C5 



James R. Duncan, MD, PhD 

Assistant Professor oi Radioloy and Surgerv 
Mallinckrodt Inst;- Lite or' Radiology and 
VVjshingro!; Umversiry School of Medici: 1 . ce 
510 S. Kingshighway Blvd 
St.Louis,MO 63110 
USA 

Dominique Elias.MD 

Head of Digestive Surgery Section 
Institu; Custave Rousssv 
39, Rue Camille Desmoulins 
94800 VillejuifCedex 
France 

Laurent Garel M ! '■ 

Professor .:■:' Radiology 

Pediatric and Interventional Radiologist 

f'eor.rtiuen: ot Medical k'jasiiia 

Hopital Ste-Justine 

3175 Cflte Ste-Catherine Road 

Montreal, Quebec H3T 1C5 



CHRISTOS S. GhOPLtI AI'JEiS. M I ''. I' I'll ■ 

Assist.':iit Professor or' Radiology and Surge: 1 ;" 
Johns Hopkins Medical Institutions 
Blalock 545, 600 North Wolfe Street, 
Baltimore, MD 21287 
USA 

Jean-Francois H. Geschwind, MD 

Associate Professor of K;\d:ok:gv. Surgery and Oncol 

Division of Vase u la r and Interventional Radiology 

The Russell H. Morgan Peva.-imeiit or' Radiolgy 

and Radiological Sciences 

Johns Hopkins Medical Institutions 

Blalock 545, 600 North Wolfe Street 

Baltimore, MD 21287 

USA 

Craig B. Glaiberman, MD 

Instructor, Radiology 

Division of Interventional Radiology 

Washington University School of Medicine 

Mallinckrodt Institute a: Radiology 

510 South K:ngshighwav. :-th Floor 

St.Louis,MO 63110 

USA 



List of Contributors - Volum 



,n,MD 
Professor of Rnd,ck-gy 
Director, Vascular and I 
University of Iowa 
Department of Radiology 
200 Hawkins Drive, 3957 JPP 
Iowa City.IA 52242 
USA 

Minako Hayakawa, MD 

Visiting Assistant Professor of Radiology 
University of Iowa Hospitals and Clinics 
University of Iowa Carver College of Medicine 
200 Hawkins Dr, 3893 JPP 
Iowa City.IA 52242 
USA 

SamHeye.MD 

Department of Radiology 
University Hosoituls Gnsthuisberg 
Herestraat 49 
3000 Leuven 
Belgium 

Shih-WeiHsu, MD 

Vismiig icholar, Universiiv of Iowa Hospitals 

11 lid Clink"? 

University of Iowa Carver College of Medicine 

200 Hawkins Dr, 3893 JPP 

Iowa City, IA 52242 

USA 



Assistant Professor, i ! e 

Radiology 

Chang Go.ng Meinona 

Kiiolisiuiig 

Taiwan 



.n,MD 

Associate Professor .:■"' Radiology 

I 'iecior. Section of intervenl ion a I Radiology 

Indiana University Hospital, UH0279 

Department of Radiology 

550 University Boulevard 

Indianapolis, IN 46202-5253 

USA 



:a,MD,FRCPC 
Division of Vascular and Interventional Radiologi 
I 'en a rt in en; of Medical !:v. aging 
Toronto General Hospital 
200 Elizabeth Street, Eaton South l-454d 
Toronto, ON M5G 2C4 
Canada 



NeilM. Khilnani.MD 

Cornell Vascular 

Weill Medical College of Cot 

416 East 55th Street 

New York, NY 10022 

USA 



FAN.MD 

ilNeur 



"adiolv C nnical Fellow 



Department of Medical Tin 
University of Toronto 
Toronto Western Hospital 
399 Bat hurst Street 
Toronto, Ontario M5T 2S8 
Canada 

Pierre Lasjaunias.MD, PhD 

Service de Neuroradiology I'lagnos" 
Hopital Bicetre 
78 rue due General Leclero 
94275 Le Kremlin Bicetre 

France 

SeonKyu Lee, MD, PhD 

Assistanl Professor and Staff Netiro 
', vp.u'ir.eiii :■:' \'ec'ical I maging 
University of Toronto 
Toronto Western Hospital 
#399 Bathurst Street 
Toronto, Ontario M5T 2S8 



Walter S. Lesley, MD 

Chief, Section of Surgical Neuroradiol 

Assistanl Profess;:'!" :■: Radiology 
Thr Te\..;s AJvM Uii.versiTy Health S.:. 
USA 



que et Therapeutique 



partment of Radio 



EleniLjapi.MD 

The Russed H. Morgan 
and Radiological Scene 
Johns Hopkins Medical 
Baltimore, MD 
USA 



David C. Madoff, MD 

Section of Interventional Radiology 

Division of Diagnostic Imaging 

The University of Texas 

MD Anderson Cancer Center 

1515 Holcombe Boulevard, Unit 325 

Houston, TX 77030-4009 

USA 

Geert Maleux, MD 

Department o'i Radiology 
University Hospitals Gasthtusnerg 
Herestraat 49 
3000 Leuven 
Belgium 



List of Contributors - Volume 2 



Francis Marshalleck, MD 

Assistant r [■■: Iv:;--:- .:■: Kadic-jgv 

Indiana University School of Medicine 

Indiana University Hospital 

Room 0279, 550 North University Boulevard 

Indianapolis, IN 26202 

USA 

Robert J. Min.MD 

Cornell Vascular 

Weill Medical College of Cornell University 

416 East 55th Street 

New York, NY 10022 

USA 



Anne C. Roberts, MD 

University of California. 5; 
Division of Vascular and I 
200 West Arbor Drive 
San Diego, CA 92103-8756 
USA 



i ". ! iego Medkol Center 
1 Radiology 



Alain J. Roche, MD 

Head of Interventional Radiology Section 

Professor, Inslitut Gastave Rousssv 
39, Rue Camille Desmoulins 
94800 VillejuifCedex 

Georges Rodesch, MD 

Service de Neurorodioloie I 'lognostique ei Titerapeuiique 

Hopital Foch 

40 rue Worth 

B.P. 36 

92150 Suresnes 

France 

Riad Salem,MD,MBA 

Assistant Professor of Radiology and Oncology 

Northwestern Memorial Hospital 

Department of Radiology 

676 North St. Claire, Suite 800 

Chicago, IL 60611 

USA 



Melhem J. Sharafuddin, MD 

University of loiva Hospitals and 
Department of Radiology 
200 Hawkins Dr, 3957 JPP 
Iowa City, IA 52242 
USA 



gSun.MD 
Associate Professor of Radiology 
Department of Radiology 
University of Iowa, College of Medic 
200 Hawkins Dr., 3955 JPP 
Iowa City, IA 52242 
USA 



Kong Teng Tan, MB, BCh, FRCS, FRCR 
Division of Vascular and Interventional R 

department t-A Medical i staging 

Toronto General Hospital 

585 University Avenue, NCSB 1C-563 

Toronto, ON M5G 2N2 

Canada 



Maria Thijs, MD 
Department of Radiology 
Universitv Hospital: Gasthuisberg 
Herestraat 49 

3000 Leuven 



Kenneth G. Thurston, Ma 
17 Bramble Lane 
West Grove, PA 19390 

USA 



Rajiv Verma.MD 

Section of Interventional Radiology 

Division of Diagnostic Imaging 

The University of Texas 

MD Anderson Cancer Center 

15 15 Hokombe Boulevard, Unit 325 

Houston, TX 77030-4009 

USA 



Lucy A. Wibbenmeyer, MD 

University of Iowa Hospitals and Clinic 

Department of Radiology 

200 Hawkins Dr. 

Iowa City, IA 52242 

USA 



Gary Siskin, MD 

Alianv Medical College 
Vascular Radio iogv, Alia 
47 New Scotland Avenue 
Albany, NY 12208-3479 
USA 



Jeffrey J. Wong, MB ChB, BMedSc 

University of California, ion Hi ego Medical Center 

Division of Vo sen I or and Interventional Radiology 

200 West Arbor Drive 

San Diego, CA 92103-8756 

USA 



MEDICAL RADIOLOGY Diagnostic Imaging and Radiation Oncology 



Titles in the series ,i/rv<i,fi published 



Diagnostic Imaging 



Radiology of the Upper Urinary Tract 

Edited by E.K.Lang 

The Thymus- Diagnostic Imaging, 

Functions, and Pathologic Anatomy 

Edited by E. Walter, E. Willich, 

and W.R. Webb 

Interventional Neuroradiology 

Edited by A. Valavanis 

Radiology of the Pancreas 

EditedbyA.L.Baert, 

:o-edned by G. Delorme 

Radiology of the Lower Urinary Tract 

Edited by E.K.Lang 

Magnetic Resonance Angiography 

Edited by I. P. Arlart, G. M. Bongartz, 

andG.Marchal 

Contrast-Enhanced MR) of the Breast 

S. Heywang-KBbrunner and R. Beck 

SpiralCToftheCheit 

Edited by M. Remy-lardin and J. Remy 

Radiological Diagnosis of Breast Diseases 

Edited by M. Friedrich and E.A. Sickles 

Radiology of theTrauma 

Edited by M. Heller andA.Fink 

Biliary Tract Radiology 

Edited by P.Rossi, 

co-edited by M.Brezi 

Radiological Imaging of Sports Injuries 

Edited by C. Masciocchi 

Modern Imaging of the Alimentary Tube 

Edited by A.R.Margulis 

Diagnosis and Therapy of Spinal Tumors 

Edited by P.R.AigraJ.Valk, 

Interventional Magnetic 
Resonance Imaging 

Edited by J.F. Debatin and G.Adam 
Abdomlnaland Pelvic MRI 
Edited by A. Heuck and M. Reiser 
Orthopedic Imaging 

Techniques and Applications 
Edited by A.M. Davies 

and H. Pettersson 



Radiology of the Female Pelvic Organs 

Edited by E.K.Lang 
Magnetic Resonance of the Heart 
and Great Vessels 
Clinical Applications 

Edited by i.Bogaert.A.J.Duerinckx, 

andF.E.Rademakers 

Modern Head and Neck Imaging 

Edited by S.K.Mukherii 

andl.A.Castelijns 

Radiological Imaging 

of Endocrine Diseases 

Edited by J.N. Bruneton 

in i" d I a I' o ran o;i wi:li K. F.;dovaiii 

andM.-Y.Mourou 

Trends in Contrast Media 

Edited bv H. S. Thomsen, 

R. N. Muller, and R. F. Mattrey 

Functional MRI 

Edited by C. T. W. Moonen 

andP.A.Bandettini 

Radiology of the Pancreas 

2nd Revised Edition 

Edited by A. L. Baert. Co-edited by 

G.DelormeandL.VanHoe 

Emergency Pediatric Radiology 

Edited by H.Carty 

Spiral CT of the Abdomen 

Edited by F. Terrier, M. Grossholz, 

and C.D.Becker 

Liver Malignancies 
Diagnostic and 
Interventional Radiology 

Edited by C.Bartolozzi 
andR.Lencioni 

Medical Imaging of the Spleen 

Edited by A. M. De Schepper 
and F-.Vanhoenacker 

Radiology of Peripheral Vascular Diseases 

Edited by E.Zeitler 

Diagnostic Nuclear Medicine 

Edited bv C. Sdiiepers 

Radiology of Blunt Trauma of the Chest 

P. Schnyder and M. Wintermark 

Portal Hypertension 

Diagnostic Imaging- Guided Therapy 

Edited by P. Rossi 

Co-edited by P. Ricci and L. Broglia 



Recent Advances in 
Diagnostic Neuroradiology 

Edited by Ph. Demaerel 

Virtual Endoscopy 

and Related 3D Techniques 

id::eJ bv ~:\ Rog.iLa. I. Tei'wis^ha 
Van Scheltinga, and B.Hamm 

MultisliceCT 

Edited by M. F. Reiser, M. Takahashi, 
M. Modi.", and R. Bruening 



TransfontanellarDoppler Imaging 
In Neonates 

A. Couture and C.Veyrac 

Radiology of AIDS 

A Practical Approach 

Edited by ]. W.A.J. Reeders 

and P.C.Goodman 

CT of the Peritoneum 

Armando Rossi and Giorgio Rossi 

Magnetic Resonance Angiography 

2nd Revised Edition 

Editedbyl.P.Arlart, 

G.M. Bongratz, and G. Marchal 

Pediatric Chest Imaging 

Ldi;ed bv Javier Lucava 

and Janet L. Strife 

Applications of Sonography 
In Head and Neck Pathology 

Edited by J. N. Bruneton 

in collaboration with C. Raffaelli 

and O. DassonviUe 



3D Image Processing 

Techniques and Clinical Applications 

Edited by D.Caramella 

and C.Bartolozzi 

Imaging of Orbital and 

Visual Pathway Pathology 

Edited by W. S. Muller-Forell 

Pediatric ENT Radiology 

Edited by S.J.King 
and A. E. Boothroyd 

Radiological Imaging of the Small Intestine 

Edited by N. C. Gourtsoyiannis 



MEDICAL RADIOLOGY Diagnostic Imaging and Radiation Oncology 

Titles in the series already published 



Imaging of the Knee 
Techniques and Applications 

EditedbyA.M.Davies 

andVN.Cassar-Pullicino 

Perinatal Imaging 

From Ultrasound (a MR Imaging 

Edited by Fred E.Avni 

Radiological Imaging of the Neonatal Chest 

Edited by V.Donoghue 

Diagnosticand Interventional 

Radiology in Liver Transplantation 

Edited by E. Biicheler, V. Nicolas, 

C.E.Broelsch,X.Rogiers, 

and G. Krupski 

Radiology of Osteoporosis 

Edited by S. Grampp 

Imaging Pelvic Floor Disorders 

Edited by C.I. Bartram 

and J. 0. L.DeLancey 

Associate Editors: S. Halligan, 

F.M.Kelvin, and J. Stoker 

Imaging of thePancreas 
Cystic and Rare Tumors 

Edited by C.Procacci 

and A.J. Megibow 

High Resolution Sonography 
of the Peripheral Nervous System 

Edited by S. Peer and G. Bodner 

Imaging of the Foot and Ankle 
Techniques and Applications 

EditedbyA.M.Davies, 
R.W.Wh'itehoiise, 
and J. P. R. Jenkins 

Radiology Imaging of the Ureter 

Edited by F. Joffre, Ph. Otal, 
and M. Soulie 

Imaging of the Shoulder 
Techniques and Applications 

Edited by A. M. Davies and J. Hodler 

Radiology of the Petrous Bone 

Edited by M. Lemmerling 

andS.S.Kollias 

Interventional Radiology in Cancer 

Edited by A.Adam, R. F. Dondelinger, 

and, P. R. Mueller 

Duplex and Color Doppier Imaging 

ofthe Venous System 

Edited by G.H.Mostbeck 



Mu It i detector-Row CT of the Thorax 

EditedbyU.J.Schoepf 

Functional Imaging ofthe Chest 

Edited by H.-U.Kauczor 

Radiology of the Pharynx 

and the Esophagus 

Edited by O.Ekberg 

Radiological Imaging 

In Hematological Malignancies 

Edited by A.Guermazi 

Imaging and Intervention in 

AbdomlnalTrauma 

Edited by R. F. Dondelinger 

MultisliceCT 

2nd Revised Edition 

Edited by M. F. Reiser, M. Takahashi, 

M.Modic, and C.R.Becker 

Intracranial Vascular Malformations 

and Aneurysms 

From Diagnostic Work-Up 

to Endovascular Therapy 

Edited by M.Forsting 

Radiology and Imaging ofthe Colon 

Edited by A.H. Chapman 



Dynamic Contrast -Enhanced Magnetic 
Resonance Imaging in Oncology 

Edited by A. Jackson, D. L. Buckley, 
and G.J. M.Parker 
Imaging in Treatment Planning 
forSinonasalDiseases 

Edited by R. Maroldi and P. Nicolai 

ClinicalCardlacMRI 

With Interactive CD-ROM 

Edited by J.Bogaert, 

S. Pym;"! j' ho wjki, ;\!idA.M. Tnylor 

Focal Liver Lesions 

Detection, Characterization, 

Ablation 

Edited by R. Lencioni, D. Cioni, 

and C. Bartolozzi 

Multidetector-RowCT Angiography 

Edited by C.Catalano 

andR.Passariello 

Paediatric Musculoskeletal Diseases 

With an Emphasis on Ultrasound 

Edited by D.Wilson 



Contrast Media in Ultrasonography 
Basic Principles and Clinical Applications 

Edited by Emilio Quaia 

MR Imaging in White Matter Diseases of the 

Brain and Spinal Cord 

Edited by M. Filippi, N. De Stefano, 

V. Dousset, and J. C. McGowan 

Diagnostic Nuclear Medicine 

2nd Revised Edition 

Edited bv C. Schieper:; 

Imaging ofthe Kidney Cancer 

Edited by A.Guermazi 

Magnetic Resonance Imaging in 

Ischemic Stroke 

Edited by R. von Kummer and T. Back 

Imaging of the Hip S Bony Pelvis 

Techniques and Appl ic.it icuis 

Edited by A. M. Davies, K. J. Johnson, 

andR.W.Whitehouse 

Imaging of Occupational and 

Environmental Disorders of the Chest 

Edited by P. A.Gevenois and 

P.DeVuyst 

Contrast Media 

Safety Issues and ESUR Guidelines 

Edited by H. S. Thorn sen 

Virtual Colonoscopy 

A l'i .uTiiiil Guide 

Edited by P. Lefere and 5. Gryspeerdt 

Vascular Embolotherapy 

A Comprehensive Appruach 

Volume 1 

Edited bv i. Gulznr :.'.]!. 'do -edited bv 

S.SunandM.I.Sharafuddin 

Vascular Embolotherapy 

A Comprehensive Approach 

Volume 2 

Edited by i. Golznri.'.n. Go -edited by 

S. Sun and M. i. Sharafuddin 

Head and Neck Cancer Imaging 

Edited by R.Hermans 

Vascular Interventional Radiology 

Current Evidence in Endovascular 

Surgery 

Edited bv H. G. Cowling 



4Q Springer 



MEDICAL RADIOLOGY Diagnostic Imaging and Radiation Oncology 

Titles in the series ahead) published 



Radiation Oncology 



Lung Canter 

Edited by C.W.Sci 

Innovations in Radiation Oncology 
EditedbyH.R.Withers 
and L.J. Peters 

Radiation Therapy 

of HeadandNeck Cancer 

Edited by G.E.Laramore 

Gastrointestinal Cancer- 
Radiation Therapy 
Edited by R.R. Dobelbower.Jr. 

Radiation Exposure 
and Occupational Risks 

Edited by E. Scherer, C. Streffer, 
and K.-R. Trott 

Radiation Therapy of Benign Diseases 

A Clinical Guide 

S.E. Order and S.S.Donaldson 

Interventional Radiation 

Therapy Techniques- Bra chytherapy 

Edited by R.Sauer 

Radlopathology of Organs andTlssues 

Edited by E. Scherer, C. Streffer, 

and K.-R. Trott 

Concomitant Continuous Infusion 

Chemotherapy and Radiation 

Edited bvM.Rotman 

and C. I. Rosenthal 

Intraoperative Radiotherapy - 

Clinical Experiences and Results 

Edited by F. A. Calvo, M. Santos, 

and L.W.Brady 

Radiotherapy of Intraocular 

andOrbitalTumors 

Edited by W.E.Alberti and 

R.H.Sagerman 

Interstitial and Intracavitary 

Thermoradiotherapy 

Edited by M. H. Seegenschmiedt 

and R.Sauer 

Non-Disseminated Breast Cancer 

Controversial Issues in Management 

Edited by G.H.Fletcher and 

S.H. Levitt 



Current Topics in 

Clinical Radiobiology of Tumors 

Edited by H.-P.Beck-Bornholdt 

Practical Approaches to 
Cancer Invasion and Metastases 
A Compendium of Radiation 
Oncologists' Responses to 40 Histories 
Edited by A. R. Kagan with the 
Assistance of R. J. Steckel 

Radiation Therapy in Pediatric Oncology 

EditedbyJ.R.Cassady 



Late Sequelae in Oncology 
Edited by J.Dunst and R. Sauer 

Mediastinal Tiirnnri. Update 1995 
Edited by D.E.Wood 
and G.R. Thomas, Jr. 

Thermoradiotherapy 

andThermochemotherapy 

Volume 1: 

Biology, Physiology, and Physics 

Volume 2: 

Clinical Applications 

HJile." :'y M.H. ?e egensihi'.'.irJt. 



P.Fes 



mden, and C.C. Verm 



Carcinoma of the Prostate 
Innovations in Management 

Edited by Z. Petrovich, L. Bae 
and L.W.Brady 

Radiation Oncology 
of Gynecological Cancers 

Edited by H.W.Vahrson 

Carcinoma of the Bladder 
Innovations in Management 



Blood Perfusion and 
Microenvironment of Human Tumors 
Implications for 
Clinical Radiooncology 

Edited by M.Molls and P.Vaupel 

Radiation Therapy of Benign Diseases 
A Clinical Guide 

2nd Revised Edition 

S.E. Order and S. S. Donaldson 



Carcinoma of the Kidney andTestis, 
and Rare Urologic Malignancies 
Innovations in Management 
Edited by Z. Petrovich, L. Baert, 
and L.W.Brady 

Progress and Perspectives in the 
Treatment of Lung Cancer 
Edited by P. Van Houtte, 

1. Klascersky, and P. Rocmans 

Combined Modality Therapy of 
Central Nervous System Tumors 
Edited by Z. Petrovich, L. W. Brady, 
\!. L. Apuzzo, and M. Bamberg 

Age-Related Macular Degeneration 
Current Treatment Concepts 
Edited by W. A. Alberti, G. Richard, 
andR.H.Sagerman 

Radiotherapy of Intraocular 
andOrbitalTumors 
2nd Revised Edition 
Edited by R.H.Sagerman, 
andW.E.Alberti 

Modification of Radiation Response 
Cytokines, Growth Factors, 
and Other Biolgical Targets 
Edited by C.Nieder, L. Milas, 
andK.K.Ang 

Radiation Oncology for Cure and Palliation 

R. G.Parker, N. A. Janjan, 
andM.T.Selch 

Clinical Target Volumes In Conformal and 
Intensity Modulated Radiation Therapy 
A Clinical Guide to Cancer Treatment 
Edited by V. Gregoire, P. Scalliet, 
and K. K. Ang 

Advances in Radiation Oncology 
In Lung Cancer 

Edited by Branislav Jeremic 

New Technologies In Radiation Oncology 

Edited by W. Schlegel, T. Bortfeld, 
and A.-L.Grosu 



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